eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Neonatology

Hypoxic-Ischemic Encephalopathy: Multimedia

Author: Santina A Zanelli, MD, Assistant Professor, Department of Pediatrics, Division of Neonatology, University of Virginia Health System
Coauthor(s): Dirk P Stanley, MD, Resident Physician, Department of Pathology, University of Virginia Health System; David Kaufman, MD, ECMO Director, Associate Professor of Pediatrics, Department of Pediatrics, Division of Neonatology, University of Virginia Health System
Contributor Information and Disclosures

Updated: Dec 15, 2008

Multimedia

Fetal response to asphyxia illustrating the initi...Media file 1: Fetal response to asphyxia illustrating the initial redistribution of blood flow to vital organs. With prolonged asphyxial insult and failure of compensatory mechanisms, cerebral blood flow falls, leading to ischemic brain injury.
Fetal response to asphyxia illustrating the initi...

Fetal response to asphyxia illustrating the initial redistribution of blood flow to vital organs. With prolonged asphyxial insult and failure of compensatory mechanisms, cerebral blood flow falls, leading to ischemic brain injury.

Pathophysiology of hypoxic-ischemic brain injury ...Media file 2: Pathophysiology of hypoxic-ischemic brain injury in the developing brain. During the initial phase of energy failure, glutamate mediated excitotoxicity and Na+/K+ ATPase failure lead to necrotic cell death. After transient recovery of cerebral energy metabolism, a secondary phase of apoptotic neuronal death occurs. ROS = reactive oxygen species.

Pathophysiology of hypoxic-ischemic brain injury ...

Pathophysiology of hypoxic-ischemic brain injury in the developing brain. During the initial phase of energy failure, glutamate mediated excitotoxicity and Na+/K+ ATPase failure lead to necrotic cell death. After transient recovery of cerebral energy metabolism, a secondary phase of apoptotic neuronal death occurs. ROS = reactive oxygen species.

Risk factors for neonatal encephalopathy.Media file 3: Risk factors for neonatal encephalopathy.
Risk factors for neonatal encephalopathy.

Risk factors for neonatal encephalopathy.

Severe acute hypoxic-ischemic neuronal change in ...Media file 4: Severe acute hypoxic-ischemic neuronal change in the basal ganglia is noted. Histologic examination reveals severe hypoxic-ischemic neuronal change, characterized by the presence of pyknotic and hyperchromatic nuclei, the loss of cytoplasmic Nissl substance, and neuronal shrinkage and angulation (arrow). These alterations begin to appear approximately 6 hours following hypoxic-ischemic insult. Reactive astrocytosis is evident approximately 24-48 hours after the primary hypoxic-ischemic event.
Severe acute hypoxic-ischemic neuronal change in ...

Severe acute hypoxic-ischemic neuronal change in the basal ganglia is noted. Histologic examination reveals severe hypoxic-ischemic neuronal change, characterized by the presence of pyknotic and hyperchromatic nuclei, the loss of cytoplasmic Nissl substance, and neuronal shrinkage and angulation (arrow). These alterations begin to appear approximately 6 hours following hypoxic-ischemic insult. Reactive astrocytosis is evident approximately 24-48 hours after the primary hypoxic-ischemic event.

Significant astrocytosis in the basal ganglia fol...Media file 5: Significant astrocytosis in the basal ganglia following hypoxic-ischemic insult is observed. An immunohistochemical stain for glial fibrillary acidic protein (GFAP) was performed on the same tissue shown in Media file 4 to demonstrate the prominent gliosis secondary to the hypoxic-ischemic event. GFAP is a useful marker to study astrocytic response to injury. This gliosis of the basal ganglia, along with subsequent hypermyelination, is responsible for the evolution of status marmoratus over months to years.
Significant astrocytosis in the basal ganglia fol...

Significant astrocytosis in the basal ganglia following hypoxic-ischemic insult is observed. An immunohistochemical stain for glial fibrillary acidic protein (GFAP) was performed on the same tissue shown in Media file 4 to demonstrate the prominent gliosis secondary to the hypoxic-ischemic event. GFAP is a useful marker to study astrocytic response to injury. This gliosis of the basal ganglia, along with subsequent hypermyelination, is responsible for the evolution of status marmoratus over months to years.

Bilateral acute infarctions of the frontal lobe a...Media file 6: Bilateral acute infarctions of the frontal lobe are shown. The infarctions depicted in the figure (arrows) are consistent with watershed infarctions secondary to global hypoperfusion. The lesions depicted in the image are consistent with an acute ischemic event, occurring within 24 hours of death. The regions most susceptible to hypoperfusion include the end-artery zones between the anterior, middle, and posterior cerebral arteries.
Bilateral acute infarctions of the frontal lobe a...

Bilateral acute infarctions of the frontal lobe are shown. The infarctions depicted in the figure (arrows) are consistent with watershed infarctions secondary to global hypoperfusion. The lesions depicted in the image are consistent with an acute ischemic event, occurring within 24 hours of death. The regions most susceptible to hypoperfusion include the end-artery zones between the anterior, middle, and posterior cerebral arteries.

A prior hypoxic-ischemic event involving the occi...Media file 7: A prior hypoxic-ischemic event involving the occipital lobe has resulted in a chronic lesion marked by dyslamination, neuronal loss, and disorganized arrangements of myelinated white matter fibers. Grossly, the lesion was marked by preserved gyral crests and involved sulci, resulting in prominent, mushroom-shaped gyri.
A prior hypoxic-ischemic event involving the occi...

A prior hypoxic-ischemic event involving the occipital lobe has resulted in a chronic lesion marked by dyslamination, neuronal loss, and disorganized arrangements of myelinated white matter fibers. Grossly, the lesion was marked by preserved gyral crests and involved sulci, resulting in prominent, mushroom-shaped gyri.

A Luxol-Fast Blue stain was performed on the same...Media file 8: A Luxol-Fast Blue stain was performed on the same tissue shown in Media file 7 to demonstrate the haphazard arrangement of myelinated white matter fibers projecting into the gray matter of the occipital cortex.
A Luxol-Fast Blue stain was performed on the same...

A Luxol-Fast Blue stain was performed on the same tissue shown in Media file 7 to demonstrate the haphazard arrangement of myelinated white matter fibers projecting into the gray matter of the occipital cortex.

Randomized controlled trials of therapeutic hypot...Media file 9: Randomized controlled trials of therapeutic hypothermia for moderate-to-severe hypoxic-ischemic enephalopathy (HIE).
Randomized controlled trials of therapeutic hypot...

Randomized controlled trials of therapeutic hypothermia for moderate-to-severe hypoxic-ischemic enephalopathy (HIE).

Periventricular leukomalacia is depicted. This cy...Media file 10: Periventricular leukomalacia is depicted. This cystic lesion, present in the cingulate cortex, is consistent with periventricular leukomalacia. Note the extensive hemorrhage within the cystic space as well as the hemosiderin-laden macrophages around the lesional rim.
Periventricular leukomalacia is depicted. This cy...

Periventricular leukomalacia is depicted. This cystic lesion, present in the cingulate cortex, is consistent with periventricular leukomalacia. Note the extensive hemorrhage within the cystic space as well as the hemosiderin-laden macrophages around the lesional rim.

Periventricular leukomalacia is depicted. This fi...Media file 11: Periventricular leukomalacia is depicted. This figure depicts the lesion seen in Media file 10 at higher magnification. Extensive hemosiderin and reactive astrocytosis is present surrounding the lesion (center of field). Note the proximity of the lesion to the ependymal lining of the lateral ventricle (far right).
Periventricular leukomalacia is depicted. This fi...

Periventricular leukomalacia is depicted. This figure depicts the lesion seen in Media file 10 at higher magnification. Extensive hemosiderin and reactive astrocytosis is present surrounding the lesion (center of field). Note the proximity of the lesion to the ependymal lining of the lateral ventricle (far right).

Summary of potential neuroprotective strategies.Media file 12: Summary of potential neuroprotective strategies.
Summary of potential neuroprotective strategies.

Summary of potential neuroprotective strategies.

More on Hypoxic-Ischemic Encephalopathy

Overview: Hypoxic-Ischemic Encephalopathy
Differential Diagnoses & Workup: Hypoxic-Ischemic Encephalopathy
Treatment & Medication: Hypoxic-Ischemic Encephalopathy
Follow-up: Hypoxic-Ischemic Encephalopathy
Multimedia: Hypoxic-Ischemic Encephalopathy
References

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Further Reading

Keywords

hypoxic-ischemic encephalopathy, neonatal Encephalopathy, hypothermia, HIE, perinatal asphyxia, birth asphyxia, neonatal asphyxia, hypoxia, acidosis, ischemia, cerebral blood flow, CBF, multiple organ failure, aspiration pneumonia, mental retardation, epilepsy, cerebral palsy, hemiplegia, paraplegia, quadriplegia, stupor coma, poor sucking, seizures, reperfusion injury, tricuspid regurgitation, pulmonary hypertension, renal failure, oliguria, tubular failure, electrolyte imbalances, necrotizing enterocolitis, delayed gastric emptying, thrombocytopenia, coagulopathy

Contributor Information and Disclosures

Author

Santina A Zanelli, MD, Assistant Professor, Department of Pediatrics, Division of Neonatology, University of Virginia Health System
Santina A Zanelli, MD is a member of the following medical societies: American Academy of Pediatrics, Society for Neuroscience, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Coauthor(s)

Dirk P Stanley, MD, Resident Physician, Department of Pathology, University of Virginia Health System
Disclosure: Nothing to disclose.

David Kaufman, MD, ECMO Director, Associate Professor of Pediatrics, Department of Pediatrics, Division of Neonatology, University of Virginia Health System
David Kaufman, MD is a member of the following medical societies: American Academy of Pediatrics, European Society for Paediatric Infectious Diseases, Medical Society of Virginia, Pediatric Infectious Diseases Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Ted Rosenkrantz, MD, Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine
Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Pediatric Society, Connecticut State Medical Society, Eastern Society for Pediatric Research, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Brian S Carter, MD, FAAP, Professor of Pediatrics (Neonatology), Vanderbilt University School of Medicine; Co-director, Pediatric Advance Comfort Team, Monroe Carell Jr Children's Hospital at Vanderbilt
Brian S Carter, MD, FAAP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, National Hospice and Palliative Care Organization, and National Perinatal Association
Disclosure: Nothing to disclose.

CME Editor

Carol L Wagner, MD, Professor of Pediatrics, Medical University of South Carolina
Carol L Wagner, MD is a member of the following medical societies: American Academy of Pediatrics, American Chemical Society, American Medical Women's Association, American Public Health Association, American Society for Bone and Mineral Research, American Society for Clinical Nutrition, Massachusetts Medical Society, National Perinatal Association, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Chief Editor

Ted Rosenkrantz, MD, Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine
Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Pediatric Society, Connecticut State Medical Society, Eastern Society for Pediatric Research, and Society for Pediatric Research
Disclosure: Nothing to disclose.

 
 
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