"Edema" is the medical word for swelling. Any part of the body can become swollen when fluid accumulates in cavities or tissues. Commonly, swelling is the result of an injury, allergy, or infection.
Cerebral edema is when fluid builds up around the brain. This swelling exerts pressure on the brain, restricting the flow of blood, and therefore oxygen. Brain cells die when they are deprived of oxygen for too long, resulting in brain damage.
Infants may experience cerebral edema in relation to hypoxic-ischemic encephalopathy ("HIE"), brain damage from lack of oxygen during pregnancy or birth. Babies are at risk for HIE during labor, and it is a significant cause of disability and death in newborns.Causes of Cerebral Edema
Cerebral edema is a secondary to hypoxic-ischemic encephalopathy (HIE), also known as perinatal asphyxia. HIE is brain damage caused by a reduced supply of oxygenated blood to the brain. Oxygen deprivation, even for a few minutes, causes cells in the brain to die.
The chain of events put into motion by oxygen deprivation can also lead to cerebral edema. The reason why has to do with a cellular mechanism called the sodium-potassium pump.
Found in all animal cell membranes, the purpose of a sodium-potassium pump is to pull potassium into cells and push sodium out of cells. In neurons, for example, this creates the charge necessary in order to send electrical signals to other neurons throughout the brain and nervous system.
When deprived of oxygen, cells no longer have the energy to run sodium-potassium pumps. Lack of oxygen to the brain therefore causes an accumulation of sodium inside brain cells. When sodium flows into brain cells, it brings water along with it, leading to a buildup of fluid and swelling in the brain.
There are many reasons why an infant might be cut of from their supply of oxygen in the womb or during birth. Oxygen is supplied to the baby from the mother via the umbilical cord and placenta, and there are many ways in which this system can be disrupted. Circulation can be cut off due to placenta previa, breech presentation, or shoulder dystocia, among other issues. Pregnancies involving such abnormalities are at a higher risk for HIE and cerebral edema.Consequence of Cerebral Edema
A buildup of fluid and swelling puts pressure on the brain. This pressure further reduces the flow of blood and oxygen to the brain and damages nerves. Extreme pressure inside the skull can cause herniation, when part of the brain is pushed through its protective surroundings.
Infants who have experienced or are experiencing a brain injury like cerebral edema may exhibit a set of concerning symptoms after they are born. They might have less motor function than a normal baby, abnormal coloring, a low heart rate, or seizures.
Cerebral edema can have various consequences for an infant depending on the severity of the injury. Oxygen deprivation to an infant is extremely dangerous, and in the worst-case scenario, cerebral edema is fatal.
Infants with minor injuries may recover and develop without further problems. Others suffer the effects of neurological damage, including cognitive, sensory, and motor disabilities. Seizures, deafness, and cerebral palsy are examples of possible neurological conditions resulting from cerebral edema.Diagnosis and Treatment of Cerebral Edema
An Apgar test is used to evaluate an infant's health immediately after birth. The test is scored based on five criteria: skin color, pulse rate, reflexes, muscle tone, and respiration. A baby who is pink and crying will have a higher score, for example, than a baby who is pale and gasping. A low score indicates that the baby needs medical attention.
The baby may need to be transferred to a pediatric intensive car unit directly after they are born. In some cases, doctors will need to immediately attempt resuscitation and stabilization of the baby.
Even in milder scenarios, if the baby experienced a situation during pregnancy or birth that could have led to oxygen deprivation and displays certain symptoms, doctors may suspect cerebral edema or a similar brain injury.
Medications, surgery, and reduction in body temperature may be employed to reduce the amount of fluid and swelling in the brain. The faster the edema is treated, the lesser the risk of worsening injury and death.
Doctors will diagnose the extent of the injury. They will monitor the function of vital organs like the heart, kidneys, and liver. They will also observe the infant's sensory and motor function. Do they respond to light? Do they have low muscle tone? Are they having seizures? Lack of sensory and motor function and seizure activity is indicative of a brain injury. Doctors can also see what is happening inside the brain using technologies like CT scans.
Further treatment of cerebral edema depends on the types of issues that the brain injury causes. The effects of a brain injury from cerebral edema is hard to assess at first. An infant may improve or deteriorate in the days following birth.Cerebral Edema and Medical Malpractice
A fetal heart rate monitor is routinely used to track the pulse of a fetus during labor. It helps doctors notice when a baby's pulse drops below normal, indicating that they are not receiving enough oxygen and need to be delivered as quickly as possible.
Cerebral edema may be the result of medical negligence when a healthcare professional fails to notice or act within medical guidelines to address signs of oxygen deprivation. Delaying a c-section when it is clear that the baby is in distress wastes valuable time that could save them from a fatal or disabling brain injury.
Medical malpractice lawsuits provide families with the compensation they need to pay for past medical bills and the future care of their child.Cerebral Edema Settlements and Verdicts
- Illinois, 2019, $14,000,000 Settlement An expectant mother goes to the emergency room after her water breaks. Her pregnancy is high risk for a number of reasons. She has a history of stillbirth due to placental abruption, a dangerous situation when the placenta separates from the uterus. She also smoked in the beginning of the pregnancy. To make things worse, on her arrival at the hospital, she has high blood pressure readings and is diagnosed with preeclampsia, a high blood pressure condition that can progress into seizures. However, the electronic fetal monitor shows that her baby is doing well. The doctor orders the administration of the drug Pitocin, which increases and strengthens contractions. When used in excess, Pitocin can make contractions too strong, suffocating the baby. Later, the baby shows signs of oxygen deprivation, which progressively get worse. The placenta, like in the mother's first pregnancy, detaches from the uterus, causing severe pain for the mother and heightened risk for the baby. Despite this, the doctors do not perform a c-section and instead opt to deliver the baby vaginally. Once born, the baby does not have a heart rate for 15 minutes and does not breathe for 20 minutes. She has severe, permanent brain damage from hypoxic-ischemic encephalopathy and cerebral edema, requiring special care for the foreseeable future. The plaintiff claims that the doctors should not have continued to use Pitocin and should have performed an emergency c-section.
- Pennsylvania, 2016, $19,300,000 Settlement A pregnant woman goes to the hospital 34 weeks into her pregnancy. She is in pain and knows something is wrong. She is diagnosed with a placental abruption. Without proper function of the placenta, her baby is not receiving oxygen and is delivered via c-section. After she is born, the baby does not have a heartbeat for twenty minutes. Later, the extent of her injuries is discovered. The baby suffered severe hypoxia, cerebral edema, low heart rate, and other serious issues from the placental abruption. As a result, she has permanent neurological problems that will prevent her from walking, talking or feeding herself for the rest of her life.
- California, 2013, $9,975,000 Settlement A 37-year-old woman develops gestational diabetes during her second pregnancy, as she had during her first. Her diabetes and her age mean that the pregnancy is high-risk. Ten days before her due date, she complains of cramping. An obstetrician performs an ultrasound which appears normal. Six days before her due date, at another checkup, she complains that the baby is moving less than before and had been since the previous night. Another obstetrician performs a nonstress test, which monitors heart rate and movement. This test does not come back normal-the baby is not breathing. The mother is ordered to go to the hospital. However, a c-section is not performed until 2 hours after she arrives at the hospital. The baby has no heartbeat when she is finally born, and ultrasounds later reveal signs of cerebral edema. As a result of brain injuries that occurred during labor, the child has permanent cognitive and motor impairment. She has cerebral palsy, cannot speak clearly, and has seizures every day. The plaintiff alleges that the brain damage occurred thirty minutes before the c-section, meaning that it could have been prevented if the obstetricians and nurses had begun the operation sooner. The defendants did not act with appropriate urgency.
If you or a family member have been injured by a cerebral edema due to negligent medical care, you may be entitled to financial compensation. Call our medical malpractice attorneys today at 800-553-5053 or contact us online.SourcesScientific Studies
"Pathophysiology and treatment of cerebral edema in traumatic brain injury" by Ruchira Jha et al., Neuropharmacology, 2019.
"Evaluation of neonates suffered from cerebral edema in birth asphyxia by using transcranial Doppler" by Anup Kumar et al., International Journal of Medical and Health Research, 2018.
"Neonatal Hypoxic-ischemic Encephalopathy: A Radiological Review" by Shahina Bano et al., Journal of Pediatric Neurosciences, 2017.
"Hypoxic Ischemic Encephalopathy: Pathophysiology and Experimental Treatments" by Kimberly Allen and Debra Brandon, Newborn and Infant Nursing Reviews, 2011.
"Cytotoxic edema: mechanisms of pathological cell swelling" by Danny Liang et al., Journal of Neurosurgery, 2007.