Perinatal Asphyxia

Philadelphia Perinatal Asphyxia Injury Attorneys | Cohen, Placitella & Roth, PC

Perinatal Asphyxia | Johns Hopkins Medicine

Perinatal asphyxia results from a lack of oxygen either before, during, or after birth. Unfortunately, it is a common type of birth injuries, with potential impacts that can be severe, disabling, and even life threatening.     

At Cohen, Placitella & Roth, P.C.

, our birth injury attorneys understand how devastating this condition can be for you and your family, and the enormous costs that are often involved in caring for your child.

We provide the professional legal representation you need at a time your family needs it most, and can advise you on the best course of action to get the compensation you need to recover.         

What Causes Perinatal Asphyxia?

Healthline advises that it is important for physicians to carefully monitor both the mother’s and the baby’s oxygen level before and throughout the birthing process, to ensure they are receiving the proper amount of oxygen.

The infant’s heart rate should also be carefully monitored, as this is another key indicator of oxygen deprivation. In addition to slow heart rate, symptoms of perinatal asphyxia include difficulty breathing, skin that appears pale or blue, and weak muscle tone.

Common causes of the condition include the following:   

  • Low oxygen or low or high blood pressure in the mother during labor;
  • Long, difficult deliveries;
  • Infections of the mother or baby;
  • The placenta separating from the uterus, restricting oxygen flow;
  • The umbilical wrapping around the baby’s neck.

Babies with perinatal asphyxia must be closely monitored, and in severe cases, may require a ventilator to support breathing.

How Our Birth Injury Attorney Can Help

In addition to breathing issues, doctors at Johns Hopkins Medicine advise that infants with perinatal asphyxia may experience neurological problems, including coma and seizures, as well as problems with organ system functions, particularly with the circulatory, digestive and respiratory systems.

Doctors who fail to detect symptoms of perinatal asphyxia or take the appropriate steps to either prevent or respond to those symptoms may be held liable for any damages you suffer through a medical malpractice lawsuit. Compensation you may be able to claim includes:

  • Current and ongoing medical expenses, including rehabilitative therapy;
  • Lost wages if you or your spouse need to quit your job to care for your child;
  • Future losses in earning resulting from your child’s disability;
  • Compensation for pain, suffering, and emotional anguish resulting from your child’s injuries.  

Has Your Child Suffered A Birth Injury?

If your child suffers from perinatal asphyxia and you suspect your doctor’s actions led to the condition, contact Cohen, Placitella & Roth, P.C. today. Our birth injury attorneys can advise you on how to get compensation for the injuries your child suffered, while offering the personalized, professional representation you need to ensure your family’s rights are protected.


Mary Ann Wilson, PhD

Perinatal Asphyxia | Johns Hopkins Medicine


Mary Ann Wilson is a research scientist at the Kennedy Krieger Institute and an associate professor in the Departments of Neurology and Neuroscience at the Johns Hopkins University School of Medicine.


Wilson received her bachelor of arts in both art and physiology from the University of California at Berkeley before coming to Johns Hopkins for a doctoral degree in biochemistry, cellular and molecular biology, which she received in 1990. She held post-doctoral fellowships at Hopkins’ Department of Neuroscience and Kennedy Krieger Institute's developmental neuroscience lab before joining the research faculty at Kennedy Krieger Institute in 1994.


Wilson was elected to Phi Beta Kappa at UC-Berkeley in 1982, and received her degree in physiology with honors. She was awarded a pre-doctoral fellowship in systems and integrative biology at UC-Berkely in 1982, and was awarded a pre-doctoral fellowship in biochemistry, cellular and molecular biology at Hopkins in 1983.


Neurodevelopmental disorders such as cerebral palsy and autism are common chronic childhood disorders with no effective cure. Half a million children under the age of 18 in the United States have cerebral palsy, and one in 6 children have some form of developmental disability.

In term infants that suffer asphyxia at birth, low oxygen levels and low blood flow can cause hypoxic-ischemic encephalopathy, which is a major cause of cerebral palsy and related disabilities. Dr. Wilson’s research is focused on reducing brain damage in infants exposed to perinatal hypoxia-ischemia.

Therapeutic hypothermia is the first intervention to reduce brain injury in term infants after perinatal asphyxia, but protection is typically incomplete and rates of mortality and severe disability remain high.

There remains a critical need for complementary therapies that improve neuroprotection and address the negative effects of hypothermia and rewarming.


Wilson investigates molecular mechanisms of hypoxic ischemic injury in the developing brain and neuroprotective effects of drugs, hypoxic preconditioning, and hypothermia. She has investigated how changes in gene expression after a brief period of hypoxia reduce the vulnerability of the brain to a later, more severe HI insult. She also studies sex differences in brain injury mechanisms that are triggered by hypoxic ischemic injury in neonatal mice and has shown that there are sex-specific differences in the neuroprotective effects of some therapeutic interventions. Dr.

Wilson’s current work investigates the neuroprotective mechanisms engaged by hypothermia in neonates, with the goal of developing complementary therapies that enhance hypothermic neuroprotection.


Wilson also collaborates with Dr. William Baumgartner and colleagues to study brain injury after hypothermic circulatory arrest (HCA). This research uses an animal model of this surgical intervention, which is used for complex repairs to the heart or major vessels in infants and adults.

These studies have revealed inflammatory as well as apoptotic mechanisms that are activated after hypothermic circulatory arrest and have also identified serum biomarkers that can be used to detect brain injury early in the postoperative period.

Studies in collaboration with Drs. Kannan Rangaramanujam and Sujatha Kannan recently showed that dendrimer nanoparticles can be used to deliver therapy to injured neurons and activated microglia after hypothermic circulatory arrest.

This therapeutic approach holds great promise for prevention of brain injury after hypothermic circulatory arrest; Dr.

Wilson and her colleagues are also investigating dendrimer nanotherapy for treatment of neonatal hypoxic-ischemic brain injury.

Elsevier Fingerprint Engine Profile for Mary Ann Wilson

Research Publications

Zhang F, Trent Magruder J, Lin YA, Crawford TC, Grimm JC, Sciortino CM, Wilson MA, Blue ME, Kannan S, Johnston MV, Baumgartner WA, Kannan RM (2017). Generation-6 hydroxyl PAMAM dendrimers improve CNS penetration from intravenous administration in a large animal brain injury model. J Control Release. 249, 173-182.

Grimm JC, Magruder JT, Wilson MA, Blue ME, Crawford TC, Troncoso JC, Zhang F, Kannan S, Sciortino CM, Johnston MV, Kannan RM, Baumgartner WA (2016). Nanotechnology Approaches to Targeting Inflammation and Excitotoxicity in a Canine Model of Hypothermic Circulatory Arrest-Induced Brain Injury. Ann Thorac Surg. 102(3), 743-50.

Sweda R, Phillips AW, Marx J, Johnston MV, Wilson MA, Fatemi A (2016). Glial-Restricted Precursors Protect Neonatal Brain Slices from Hypoxic-Ischemic Cell Death Without Direct Tissue Contact. Stem Cells Dev. 25(13), 975-85.

Porambo M, Phillips AW, Marx J, Ternes K, Arauz E, Pletnikov M, Wilson MA, Rothstein JD, Johnston MV, Fatemi A (2015). Transplanted glial restricted precursor cells improve neurobehavioral and neuropathological outcomes in a mouse model of neonatal white matter injury despite limited cell survival. Glia. 63(3), 452-65.

Blue ME, Wilson MA, Beaty CA, George TJ, Arnaoutakis GJ, Haggerty KA, Jones M, Brawn J, Manmohan S, Lange MS, Johnston MV, Baumgartner WA, Troncoso JC (2014). Brain injury in canine models of cardiac surgery. J Neuropathol Exp Neurol. 73(12), 1134-43.

Mishra MK, Beaty CA, Lesniak WG, Kambhampati SP, Zhang F, Wilson MA, Blue ME, Troncoso JC, Kannan S, Johnston MV, Baumgartner WA, Kannan RM (2014). Dendrimer brain uptake and targeted therapy for brain injury in a large animal model of hypothermic circulatory arrest. ACS Nano. 8(3), 2134-47.

Falahati S, Breu M, Waickman AT, Phillips AW, Arauz EJ, Snyder S, Porambo M, Goeral K, Comi AM, Wilson MA, Johnston MV, Fatemi A (2013). Ischemia-induced neuroinflammation is associated with disrupted development of oligodendrocyte progenitors in a model of periventricular leukomalacia. Dev Neurosci. 35(2-3), 182-96.

Fatemi A, Wilson MA, Phillips AW, McMahon MT, Zhang J, Smith SA, Arauz EJ, Falahati S, Gummadavelli A, Bodagala H, Mori S, Johnston MV (2011). In vivo magnetization transfer MRI shows dysmyelination in an ischemic mouse model of periventricular leukomalacia.J Cereb Blood Flow Metab. 31(10), 2009-18. 

Arnaoutakis GJ, George TJ, Wang KK, Wilson MA, Allen JG, Robinson CW, Haggerty KA, Weiss ES, Blue ME, Talbot CC Jr, Troncoso JC, Johnston MV, Baumgartner WA (2011). Serum levels of neuron-specific ubiquitin carboxyl-terminal esterase-L1 predict brain injury in a canine model of hypothermic circulatory arrest. J Thorac Cardiovasc Surg. 142(4), 902-910.e1.

Johnston MV, Fatemi A, Wilson MA, Northington F (2011). Treatment advances in neonatal neuroprotection and neurointensive care. Lancet Neurol. 10(4), 372-82. 

Sharma J, Nelluru G, Wilson MA, Johnston MV, Hossain MA (2011). Sex-specific activation of cell death signalling pathways in cerebellar granule neurons exposed to oxygen glucose deprivation followed by reoxygenation. ASN Neuro. 3(2), .

Allen JG, Weiss ES, Wilson MA, Arnaoutakis GJ, Blue ME, Talbot CC Jr, Jie C, Lange MS, Troncoso JC, Johnston MV, Baumgartner WA (2010). Hawley H. Seiler Resident Award. Transcriptional profile of brain injury in hypothermic circulatory arrest and cardiopulmonary bypass. Ann Thorac Surg. 89(6), 1965-71.

Fatemi A, Wilson MA, Johnston MV (2009). Hypoxic-ischemic encephalopathy in the term infant. Clin Perinatol. 36(4), 835-58, vii. 

Weiss ES, Wang KK, Allen JG, Blue ME, Nwakanma LU, Liu MC, Lange MS, Berrong J, Wilson MA, Gott VL, Troncoso JC, Hayes RL, Johnston MV, Baumgartner WA (2009). Alpha II-spectrin breakdown products serve as novel markers of brain injury severity in a canine model of hypothermic circulatory arrest. Ann Thorac Surg. 88(2), 543-50.

Comi AM, Trescher WH, Abi-Raad R, Johnston MV, Wilson MA (2009). Impact of age and strain on ischemic brain injury and seizures after carotid ligation in immature mice. Int J Dev Neurosci. 27(3), 271-7. 

Gustavsson M, Mallard C, Vannucci SJ, Wilson MA, Johnston MV, Hagberg H (2007). Vascular response to hypoxic preconditioning in the immature brain. J Cereb Blood Flow Metab. 27(5), 928-38. 

Gustavsson M, Wilson MA, Mallard C, Rousset C, Johnston MV, Hagberg H (2007). Global gene expression in the developing rat brain after hypoxic preconditioning: involvement of apoptotic mechanisms? Pediatr Res. 61(4), 444-50. 

Comi AM, Highet BH, Mehta P, Hana Chong T, Johnston MV, Wilson MA (2006). Dextromethorphan protects male but not female mice with brain ischemia. Neuroreport. 17(12), 1319-22.

Comi AM, Johnston MV, Wilson MA (2005). Strain variability, injury distribution, and seizure onset in a mouse model of stroke in the immature brain. Dev Neurosci. 27(2-4), 127-33. 

Patra RC, Blue ME, Johnston MV, Bressler J, Wilson MA (2004). Activity-dependent expression of Egr1 mRNA in somatosensory cortex of developing rats. J Neurosci Res. 78(2), 235-44.

Comi AM, Weisz CJ, Highet BH, Johnston MV, Wilson MA (2004). A new model of stroke and ischemic seizures in the immature mouse. Pediatr Neurol. 31(4), 254-7.

Hagberg H, Wilson MA, Matsushita H, Zhu C, Lange M, Gustavsson M, Poitras MF, Dawson TM, Dawson VL, Northington F, Johnston MV (2004). PARP-1 gene disruption in mice preferentially protects males from perinatal brain injury. J Neurochem. 90(5), 1068-75.

Tsuji M, Wilson MA, Lange MS, Johnston MV (2004). Minocycline worsens hypoxic-ischemic brain injury in a neonatal mouse model. Exp Neurol. 189(1), 58-65.

Matsushita H, Johnston MV, Lange MS, Wilson MA (2003). Protective effect of erythropoietin in neonatal hypoxic ischemia in mice. Neuroreport. 14(13), 1757-61.

Nakajima W, Ishida A, Lange MS, Gabrielson KL, Wilson MA, Martin LJ, Blue ME, Johnston MV (2000). Apoptosis has a prolonged role in the neurodegeneration after hypoxic ischemia in the newborn rat. J Neurosci. 20(21), 7994-8004.

Wilson MA, Johnston MV, Goldstein GW, Blue ME (2000). Neonatal lead exposure impairs development of rodent barrel field cortex. Proc Natl Acad Sci U S A. 97(10), 5540-5.

Wilson MA, Kinsman SL, Johnston MV (1998). Expression of NMDA receptor subunit mRNA after MK-801 treatment in neonatal rats. Brain Res Dev Brain Res. 109(2), 211-20. 

Wilson MA, Molliver ME (1994). Microglial response to degeneration of serotonergic axon terminals. Glia. 11(1), 18-34.