This document discusses shaken baby syndrome (SBS), examining the evidence for its diagnostic triad of encephalopathy, retinal hemorrhaging, and subdural hemorrhaging. Recent studies question the validity of SBS as a diagnosis and raise doubts about the mechanisms previously thought to cause each element of the triad. In particular, studies have found high rates of retinal bleeding and subdural hemorrhaging from other causes like birth trauma and accidental falls, challenging the idea that these signs are definitive evidence of abuse.
This document outlines a presentation on head injury/trauma given by students at the University of Gondar College of Medicine and Health Sciences. The presentation covers the definition, epidemiology, types, risk factors, causes, pathophysiology, clinical manifestations, diagnosis, differential diagnosis, management, and complications of head injury. It provides detailed descriptions and classifications of different types of head injuries including scalp lacerations, skull fractures, traumatic brain injury, focal injuries like epidural hematomas, and diffuse injuries such as concussions.
This document discusses the management of pediatric head injuries. Key points include:
- Pediatric head trauma can have lifelong implications and risks are higher for boys starting at age 5. Moderate to severe injuries increase risks of behavioral/cognitive issues.
- Differences from adults include epidemiology, types of injuries like birth injuries or abuse, and responses like malignant cerebral edema more common in young children.
- Management involves stabilizing the patient, assessing GCS and pupils, controlling ICP/CPP, monitoring for herniation, providing nutrition/seizure prophylaxis, and considering decompressive craniectomy for refractory elevated ICP.
Shaken baby syndrome typically involves head injuries in infants under 1 year old caused by violent shaking. This shaking causes shearing injuries in the brain due to rapid acceleration and deceleration forces. Characteristic findings include subdural and retinal hemorrhages seen in over 70% of cases. The immature anatomy of an infant's brain and skull makes it more susceptible to shearing injuries from shaking compared to older children.
Head injury refers to any damage to the structures of the head due to trauma. Common causes include falls, road accidents, assaults, and sports injuries. The severity can range from mild to severe based on the Glasgow Coma Scale. Treatment involves stabilizing the patient, monitoring for complications, and facilitating recovery through physiotherapy. Physiotherapy focuses on maintaining posture, range of motion, respiratory function, and encouraging remaining abilities through tailored exercises and activities. Outcomes depend on factors like duration of coma, age, and location of injuries in the brain.
The most common cause of death in young is non other than Head injury. The modern advances not only gave human mankind a luxury but with high velocity injury there is high burden of head injury too. This slide is updated with BTF 2016 guideline
The document discusses the history, pathophysiology, diagnosis, and treatment of traumatic axonal injury (TAI). TAI was first described in the mid-20th century and involves microscopic lesions in brain tissue resulting from mechanical impact. It involves both primary damage from the initial impact as well as secondary damage from chemical and metabolic changes. Diagnosis involves imaging like CT, MRI, and DTI to identify lesions in white matter tracts. Currently there is no specific treatment for TAI, but care focuses on stabilizing the patient and preventing increases in intracranial pressure to limit secondary damage.
This document outlines a presentation on head injury/trauma given by students at the University of Gondar College of Medicine and Health Sciences. The presentation covers the definition, epidemiology, types, risk factors, causes, pathophysiology, clinical manifestations, diagnosis, differential diagnosis, management, and complications of head injury. It provides detailed descriptions and classifications of different types of head injuries including scalp lacerations, skull fractures, traumatic brain injury, focal injuries like epidural hematomas, and diffuse injuries such as concussions.
This document discusses the management of pediatric head injuries. Key points include:
- Pediatric head trauma can have lifelong implications and risks are higher for boys starting at age 5. Moderate to severe injuries increase risks of behavioral/cognitive issues.
- Differences from adults include epidemiology, types of injuries like birth injuries or abuse, and responses like malignant cerebral edema more common in young children.
- Management involves stabilizing the patient, assessing GCS and pupils, controlling ICP/CPP, monitoring for herniation, providing nutrition/seizure prophylaxis, and considering decompressive craniectomy for refractory elevated ICP.
Shaken baby syndrome typically involves head injuries in infants under 1 year old caused by violent shaking. This shaking causes shearing injuries in the brain due to rapid acceleration and deceleration forces. Characteristic findings include subdural and retinal hemorrhages seen in over 70% of cases. The immature anatomy of an infant's brain and skull makes it more susceptible to shearing injuries from shaking compared to older children.
Head injury refers to any damage to the structures of the head due to trauma. Common causes include falls, road accidents, assaults, and sports injuries. The severity can range from mild to severe based on the Glasgow Coma Scale. Treatment involves stabilizing the patient, monitoring for complications, and facilitating recovery through physiotherapy. Physiotherapy focuses on maintaining posture, range of motion, respiratory function, and encouraging remaining abilities through tailored exercises and activities. Outcomes depend on factors like duration of coma, age, and location of injuries in the brain.
The most common cause of death in young is non other than Head injury. The modern advances not only gave human mankind a luxury but with high velocity injury there is high burden of head injury too. This slide is updated with BTF 2016 guideline
The document discusses the history, pathophysiology, diagnosis, and treatment of traumatic axonal injury (TAI). TAI was first described in the mid-20th century and involves microscopic lesions in brain tissue resulting from mechanical impact. It involves both primary damage from the initial impact as well as secondary damage from chemical and metabolic changes. Diagnosis involves imaging like CT, MRI, and DTI to identify lesions in white matter tracts. Currently there is no specific treatment for TAI, but care focuses on stabilizing the patient and preventing increases in intracranial pressure to limit secondary damage.
- The document provides guidance on assessing and managing facial nerve palsy, which can be caused by various upper or lower motor neuron lesions.
- In patients presenting with facial weakness, the first priority is to determine if it is caused by an upper motor neuron lesion by checking for signs such as limb weakness or ataxia.
- For lower motor neuron lesions, the causes include Bell's palsy (idiopathic), infections like Ramsay Hunt syndrome, and tumors. Bell's palsy is diagnosed after ruling out other causes.
- Treatment depends on the cause but may include corticosteroids for Bell's palsy within 72 hours, antivirals for Ramsay Hunt syndrome
This document discusses the radiological pathology of seizure disorders. It describes various developmental anomalies, neoplasms, infections, immune-mediated disorders, cerebrovascular diseases, and trauma that can cause seizures. Specific conditions mentioned include cortical dysplasia, tuberous sclerosis, Sturge-Weber syndrome, neuronal migration disorders, vascular malformations, infections, and immune-mediated Rasmussen's encephalitis. The document provides detailed descriptions of the histopathological findings and MRI/CT appearances of different lesions that can underlie seizure disorders.
This document discusses multiple topics related to traumatic brain injury (TBI) and neurocritical care, including:
1. It defines TBI and provides classifications based on severity, location, mechanism of injury, and clinical presentation. Mild TBI is associated with a GCS of 13-15 while severe TBI is GCS <9.
2. It discusses specific injuries like subarachnoid hemorrhage, subdural hematomas, and diffuse axonal injury that commonly result from TBI.
3. Neurocritical care involves intensive care management of life-threatening neurological illnesses and injuries in a specialized unit to address the unique needs of critically ill neurological patients.
This document provides an overview of pediatric neuro-ophthalmology and various conditions that can cause visual impairment or loss in children. It discusses cortical visual impairment, congenital optic nerve anomalies, swollen optic discs, brain tumour related visual loss, optic atrophy, pupil abnormalities, and ocular motor nerve palsies. Evaluation and management are outlined for many of the conditions. The seminar aims to review specific topics like optic nerve hypoplasia, morning glory disc anomaly, optic disc coloboma, intracranial hypertension, optic neuritis, and brainstem gliomas among others.
Head injury or traumatic brain injury- Dr Dhaval Gohil- nimhansdhavalgohil11
This document provides an overview of traumatic brain injury (TBI), including epidemiology, pathophysiology, classification, imaging, and management. It discusses the primary and secondary injuries that occur with TBI, common findings on CT such as epidural, subdural, and intracerebral hemorrhages, and complications like increased intracranial pressure. Initial management focuses on the ABCDE approach and preventing secondary insults like hypoxia and hypotension.
This document discusses classifications of traumatic brain injury (TBI). It describes several classification systems including:
- Glasgow Coma Scale (GCS) which grades severity as mild, moderate or severe.
- Mayo classification which defines moderate-severe TBI based on features like loss of consciousness over 30 minutes.
- Outcome-based classifications like Glasgow Outcome Scale which grades outcome on a scale from death to good recovery.
Pathophysiology of primary injury from mechanical forces and secondary injury from physiological changes are outlined. Initial stabilization priorities and neurological assessment techniques are also reviewed.
This document discusses diffuse axonal injury (DAI), a type of traumatic brain injury seen in fatal TBI cases. It provides a historical perspective on DAI and reviews the pathology, including microscopic findings. DAI involves damage to axons throughout the brain and is graded based on its severity and location. While commonly seen in fatal TBI, the pathology of mild DAI requires further study. The document also describes a unique brain tissue archive containing over 2,000 traumatic brain injury cases accrued over decades that has been used in over 150 publications to better understand DAI and its association with neurodegenerative conditions.
1) Head trauma can cause permanent injury, with motor vehicle crashes and falls being common causes. Approximately 30% of those with moderate head trauma have at least one other significant concurrent injury.
2) Primary brain injury results directly from trauma and causes bleeding, tearing and shearing of brain tissue. Secondary brain injury can occur later and includes hypoxia, swelling and increased pressure inside the skull.
3) Various types of head injuries are discussed, including scalp lacerations, skull fractures, concussions, contusions and bleeding within or around the brain. The Glasgow Coma Scale is used to assess level of consciousness.
Craniocerebral trauma is a leading cause of death and disability in children, most commonly resulting from road traffic accidents, falls, or assaults. Head injuries can cause skull fractures, hemorrhages such as epidural or subdural hematomas, and diffuse axonal injuries that may require neurosurgical intervention. Secondary injuries like increased intracranial pressure, edema, or hypotension can further damage the brain if not properly managed.
Presentation by Dept of Surgery Eko Hospitals, Ikeja, Lagos Nigeria on the 1st of July 2015. Prepared by Dr. Ajayi Babajide (Junior Resident Family Medicine.)
This document provides an outline and introduction for a presentation on imaging head trauma. It discusses the significance of craniocerebral injuries and concepts related to brain volume and pressure. It also distinguishes between primary and secondary brain injuries. The document outlines recommendations for when to perform imaging for minor, moderate and severe head injuries, as well as indications for different imaging modalities like CT and MRI. It concludes by noting that information is intended for education and further discussion of traumatic brain pathology will continue in Part 2.
Seminar presentation on HEAD INJURY its introduction definition causes risk factors pathophysiology symptoms classification complications diagnostic evaluation treatment and management topic of subject medical surgical nursing
Post traumatic headache can occur after mild, moderate, or severe traumatic brain injury (TBI). The most common symptom is headache, which usually resolves within 3 months but can become chronic. Headaches occurring after TBI are often indistinguishable from primary headache disorders like tension-type headache or migraine. Post traumatic headache accounts for about 4% of all secondary headaches. Treatment involves both pharmacological and non-pharmacological approaches based on the type of headache, and may include abortive medications, prophylactic medications, nerve blocks, trigger point injections, and behavioral therapies. Managing any comorbid conditions is also important for optimal treatment of post traumatic headache.
This document provides an overview of head injuries, including:
1) Trauma is a common cause of death, with head injuries contributing to over half of trauma fatalities and being the leading cause of death among young adults. Road traffic accidents, falls, and assaults are common causes.
2) Pathologies include contusions, hemorrhages, shearing of brain tissue, and edema. The Glasgow Coma Scale is used to classify head injury severity. Injuries can be open or closed.
3) Complications involve skull fractures, cerebral injuries, and damage to cranial nerves. Specific hemorrhages like epidural, subdural, and subarachnoid hematomas can cause mass
This document provides information on nursing management of patients with head injuries. It begins with objectives of teaching nurses to provide care for head injury patients. It then covers anatomy and physiology of the brain, definitions and classifications of head injuries, causes and risk factors, mechanisms of injury, clinical manifestations, diagnostic assessments, potential complications, medical and surgical management including surgery, and nursing management with a focus on patient assessment and monitoring.
This document provides information on head injuries. It begins by defining different types of head injuries from minor scalp lacerations to major trauma involving brain contusions and lacerations. It then discusses causes, presentations, investigations, management strategies and complications for various head injury types including skull fractures, epidural and subdural hematomas, subarachnoid hemorrhage, and intracerebral hemorrhage. Nursing management focuses on airway protection, maintaining cerebral perfusion, preventing secondary injuries, and supporting recovery.
Abusive head trauma: SBU report and beyond Felice D'Arco
A short presentation summarising the main findings of the consensus paper on abusive head trauma, the controversies raised by the SBU report about triad and "shaken baby syndrome" and main criticisms moved against SBU report. A useful summary for radiologists and clinicians involved in child abuse.
Presented at the Pediatric Neuroradiology PanLondon Sunset Meeting July 2019
Head injuries can range from minor lacerations to life-threatening conditions like skull fractures and cerebral compression. The document outlines the different types of head injuries including concussions, contusions, compressions, skull fractures, subdural hematomas, and epidural hematomas. It describes the symptoms of each type of injury and emphasizes that even seemingly minor head trauma requires medical monitoring since complications can arise. Immediate first aid involves stabilizing the victim's head and neck and controlling any bleeding while seeking emergency help.
Traumatic brain injury and shaken baby syndromeAlison Stevens
Shaken baby syndrome is a serious form of physical child abuse seen most commonly in children under 2 years old, especially under 6 months. It is defined as vigorous shaking of an infant leading to whiplash-induced intracranial and intraocular bleeding with no external signs of trauma. Children may present with irritability, inappetence, sleepiness, seizures or being unresponsive. Diagnosis can be made when asymptomatic subarachnoid hemorrhage is found on CT scan. Retinal hemorrhages are also frequent. Management requires a thorough history and neurological examination for signs of abuse while considering the child's welfare.
Barnes Pd, Krasnokutsky M. Cns Imaging In Suspected Abuse. Top Magn Reson Ima...alisonegypt
This document summarizes an article on imaging of the central nervous system in cases of suspected nonaccidental injury in children. It discusses how radiologists must consider both accidental and nonaccidental causes when evaluating imaging findings. While some findings like subdural hemorrhages are commonly seen in nonaccidental injury cases, they can also occur in accidental injuries or medical conditions. The diagnosis of nonaccidental injury relies on correlation of clinical history, imaging, and other evidence, as imaging alone cannot determine intent. The topic remains controversial as evidence questioning the shaking mechanism and criteria used to diagnose abuse has grown.
- The document provides guidance on assessing and managing facial nerve palsy, which can be caused by various upper or lower motor neuron lesions.
- In patients presenting with facial weakness, the first priority is to determine if it is caused by an upper motor neuron lesion by checking for signs such as limb weakness or ataxia.
- For lower motor neuron lesions, the causes include Bell's palsy (idiopathic), infections like Ramsay Hunt syndrome, and tumors. Bell's palsy is diagnosed after ruling out other causes.
- Treatment depends on the cause but may include corticosteroids for Bell's palsy within 72 hours, antivirals for Ramsay Hunt syndrome
This document discusses the radiological pathology of seizure disorders. It describes various developmental anomalies, neoplasms, infections, immune-mediated disorders, cerebrovascular diseases, and trauma that can cause seizures. Specific conditions mentioned include cortical dysplasia, tuberous sclerosis, Sturge-Weber syndrome, neuronal migration disorders, vascular malformations, infections, and immune-mediated Rasmussen's encephalitis. The document provides detailed descriptions of the histopathological findings and MRI/CT appearances of different lesions that can underlie seizure disorders.
This document discusses multiple topics related to traumatic brain injury (TBI) and neurocritical care, including:
1. It defines TBI and provides classifications based on severity, location, mechanism of injury, and clinical presentation. Mild TBI is associated with a GCS of 13-15 while severe TBI is GCS <9.
2. It discusses specific injuries like subarachnoid hemorrhage, subdural hematomas, and diffuse axonal injury that commonly result from TBI.
3. Neurocritical care involves intensive care management of life-threatening neurological illnesses and injuries in a specialized unit to address the unique needs of critically ill neurological patients.
This document provides an overview of pediatric neuro-ophthalmology and various conditions that can cause visual impairment or loss in children. It discusses cortical visual impairment, congenital optic nerve anomalies, swollen optic discs, brain tumour related visual loss, optic atrophy, pupil abnormalities, and ocular motor nerve palsies. Evaluation and management are outlined for many of the conditions. The seminar aims to review specific topics like optic nerve hypoplasia, morning glory disc anomaly, optic disc coloboma, intracranial hypertension, optic neuritis, and brainstem gliomas among others.
Head injury or traumatic brain injury- Dr Dhaval Gohil- nimhansdhavalgohil11
This document provides an overview of traumatic brain injury (TBI), including epidemiology, pathophysiology, classification, imaging, and management. It discusses the primary and secondary injuries that occur with TBI, common findings on CT such as epidural, subdural, and intracerebral hemorrhages, and complications like increased intracranial pressure. Initial management focuses on the ABCDE approach and preventing secondary insults like hypoxia and hypotension.
This document discusses classifications of traumatic brain injury (TBI). It describes several classification systems including:
- Glasgow Coma Scale (GCS) which grades severity as mild, moderate or severe.
- Mayo classification which defines moderate-severe TBI based on features like loss of consciousness over 30 minutes.
- Outcome-based classifications like Glasgow Outcome Scale which grades outcome on a scale from death to good recovery.
Pathophysiology of primary injury from mechanical forces and secondary injury from physiological changes are outlined. Initial stabilization priorities and neurological assessment techniques are also reviewed.
This document discusses diffuse axonal injury (DAI), a type of traumatic brain injury seen in fatal TBI cases. It provides a historical perspective on DAI and reviews the pathology, including microscopic findings. DAI involves damage to axons throughout the brain and is graded based on its severity and location. While commonly seen in fatal TBI, the pathology of mild DAI requires further study. The document also describes a unique brain tissue archive containing over 2,000 traumatic brain injury cases accrued over decades that has been used in over 150 publications to better understand DAI and its association with neurodegenerative conditions.
1) Head trauma can cause permanent injury, with motor vehicle crashes and falls being common causes. Approximately 30% of those with moderate head trauma have at least one other significant concurrent injury.
2) Primary brain injury results directly from trauma and causes bleeding, tearing and shearing of brain tissue. Secondary brain injury can occur later and includes hypoxia, swelling and increased pressure inside the skull.
3) Various types of head injuries are discussed, including scalp lacerations, skull fractures, concussions, contusions and bleeding within or around the brain. The Glasgow Coma Scale is used to assess level of consciousness.
Craniocerebral trauma is a leading cause of death and disability in children, most commonly resulting from road traffic accidents, falls, or assaults. Head injuries can cause skull fractures, hemorrhages such as epidural or subdural hematomas, and diffuse axonal injuries that may require neurosurgical intervention. Secondary injuries like increased intracranial pressure, edema, or hypotension can further damage the brain if not properly managed.
Presentation by Dept of Surgery Eko Hospitals, Ikeja, Lagos Nigeria on the 1st of July 2015. Prepared by Dr. Ajayi Babajide (Junior Resident Family Medicine.)
This document provides an outline and introduction for a presentation on imaging head trauma. It discusses the significance of craniocerebral injuries and concepts related to brain volume and pressure. It also distinguishes between primary and secondary brain injuries. The document outlines recommendations for when to perform imaging for minor, moderate and severe head injuries, as well as indications for different imaging modalities like CT and MRI. It concludes by noting that information is intended for education and further discussion of traumatic brain pathology will continue in Part 2.
Seminar presentation on HEAD INJURY its introduction definition causes risk factors pathophysiology symptoms classification complications diagnostic evaluation treatment and management topic of subject medical surgical nursing
Post traumatic headache can occur after mild, moderate, or severe traumatic brain injury (TBI). The most common symptom is headache, which usually resolves within 3 months but can become chronic. Headaches occurring after TBI are often indistinguishable from primary headache disorders like tension-type headache or migraine. Post traumatic headache accounts for about 4% of all secondary headaches. Treatment involves both pharmacological and non-pharmacological approaches based on the type of headache, and may include abortive medications, prophylactic medications, nerve blocks, trigger point injections, and behavioral therapies. Managing any comorbid conditions is also important for optimal treatment of post traumatic headache.
This document provides an overview of head injuries, including:
1) Trauma is a common cause of death, with head injuries contributing to over half of trauma fatalities and being the leading cause of death among young adults. Road traffic accidents, falls, and assaults are common causes.
2) Pathologies include contusions, hemorrhages, shearing of brain tissue, and edema. The Glasgow Coma Scale is used to classify head injury severity. Injuries can be open or closed.
3) Complications involve skull fractures, cerebral injuries, and damage to cranial nerves. Specific hemorrhages like epidural, subdural, and subarachnoid hematomas can cause mass
This document provides information on nursing management of patients with head injuries. It begins with objectives of teaching nurses to provide care for head injury patients. It then covers anatomy and physiology of the brain, definitions and classifications of head injuries, causes and risk factors, mechanisms of injury, clinical manifestations, diagnostic assessments, potential complications, medical and surgical management including surgery, and nursing management with a focus on patient assessment and monitoring.
This document provides information on head injuries. It begins by defining different types of head injuries from minor scalp lacerations to major trauma involving brain contusions and lacerations. It then discusses causes, presentations, investigations, management strategies and complications for various head injury types including skull fractures, epidural and subdural hematomas, subarachnoid hemorrhage, and intracerebral hemorrhage. Nursing management focuses on airway protection, maintaining cerebral perfusion, preventing secondary injuries, and supporting recovery.
Abusive head trauma: SBU report and beyond Felice D'Arco
A short presentation summarising the main findings of the consensus paper on abusive head trauma, the controversies raised by the SBU report about triad and "shaken baby syndrome" and main criticisms moved against SBU report. A useful summary for radiologists and clinicians involved in child abuse.
Presented at the Pediatric Neuroradiology PanLondon Sunset Meeting July 2019
Head injuries can range from minor lacerations to life-threatening conditions like skull fractures and cerebral compression. The document outlines the different types of head injuries including concussions, contusions, compressions, skull fractures, subdural hematomas, and epidural hematomas. It describes the symptoms of each type of injury and emphasizes that even seemingly minor head trauma requires medical monitoring since complications can arise. Immediate first aid involves stabilizing the victim's head and neck and controlling any bleeding while seeking emergency help.
Traumatic brain injury and shaken baby syndromeAlison Stevens
Shaken baby syndrome is a serious form of physical child abuse seen most commonly in children under 2 years old, especially under 6 months. It is defined as vigorous shaking of an infant leading to whiplash-induced intracranial and intraocular bleeding with no external signs of trauma. Children may present with irritability, inappetence, sleepiness, seizures or being unresponsive. Diagnosis can be made when asymptomatic subarachnoid hemorrhage is found on CT scan. Retinal hemorrhages are also frequent. Management requires a thorough history and neurological examination for signs of abuse while considering the child's welfare.
Barnes Pd, Krasnokutsky M. Cns Imaging In Suspected Abuse. Top Magn Reson Ima...alisonegypt
This document summarizes an article on imaging of the central nervous system in cases of suspected nonaccidental injury in children. It discusses how radiologists must consider both accidental and nonaccidental causes when evaluating imaging findings. While some findings like subdural hemorrhages are commonly seen in nonaccidental injury cases, they can also occur in accidental injuries or medical conditions. The diagnosis of nonaccidental injury relies on correlation of clinical history, imaging, and other evidence, as imaging alone cannot determine intent. The topic remains controversial as evidence questioning the shaking mechanism and criteria used to diagnose abuse has grown.
Barnes pd, krasnokutsky m. cns imaging in suspected abuse. top magn reson ima...Alison Stevens
This document summarizes the challenges in diagnosing non-accidental injury (NAI) or child abuse based solely on central nervous system (CNS) imaging findings. It notes that the imaging findings in NAI often overlap with accidental injuries or other medical conditions. Additionally, the mechanisms and manifestations of traumatic CNS injury have both primary and secondary components, and can present as either focal or diffuse injuries across acute and chronic timeframes. Due to these complexities, medical imaging alone cannot reliably diagnose intentional injury, and requires correlation with clinical history and other investigative findings to determine if abuse occurred.
1) Shaken baby syndrome (SBS) is a common form of non-accidental head injury in infants caused by violently shaking the baby.
2) The characteristic findings of SBS are diffuse encephalopathy, subdural hemorrhage, and retinal hemorrhage in the absence of an adequate explanation.
3) SBS is estimated to occur 100-200 times annually in Germany and can result in death or long-term impairment in survivors. Proper diagnosis requires understanding of the underlying pathophysiology and a multidisciplinary approach.
Shaken baby syndrome a biomechanics analysis of injury mechanismsVera Moreira
This document presents a biomechanical analysis of injury mechanisms in shaken baby syndrome (SBS). The analysis finds that the rotational velocity and acceleration levels described in the SBS literature would subject an infant's head to forces exceeding the structural failure limits of the infant cervical spine. It also finds that shaking can cause cervical spine injury at much lower force levels than described in SBS literature. This is inconsistent with the reported rarity of cervical spine injuries in SBS cases. The findings suggest a re-evaluation of SBS diagnostic criteria is needed.
Pediatric head trauma is a major public health issue that can cause long-term physical, cognitive, and behavioral impairments. Boys are at higher risk than girls generally until age 10. Children with moderate to severe head injuries have high rates of behavioral and cognitive problems. Management of pediatric head injuries differs from adults due to differences in epidemiology, injury types, and responses to injury. Intensive care focuses on controlling intracranial pressure and maintaining adequate cerebral perfusion pressure to prevent secondary brain injury.
1) Neurogenic shock describes the sudden loss of autonomic tone due to spinal cord injury, which results in decreased systemic vascular resistance and vasodilation, causing hypotension.
2) It occurs most commonly with injuries above T6 due to loss of sympathetic tone. Aggressive management is needed to treat hypotension and avoid further spinal cord injury.
3) Treatment involves fluid resuscitation as well as vasoactive drugs like phenylephrine, norepinephrine, or vasopressin to increase blood pressure. Bradycardia may also occur and is treated with atropine, chronotropic drugs, or pacing in severe cases.
Aspectos neuroqx de infeccion del snc 2012Residentes1hun
This document discusses central nervous system (CNS) infections that neurosurgeons commonly encounter, including their pathogenesis, microbiology, surgical indications, and treatment. It summarizes several key CNS infections:
- Intracerebral abscesses can rapidly cause severe neurologic deficits or death and require prompt evaluation, imaging, and treatment.
- Subdural empyema is an uncommon but potentially life-threatening infection that typically requires prompt surgical decompression, culturing, and antibiotics.
- The organisms causing meningitis vary by the age of presentation and require prompt treatment with differing antibiotics.
- Herpes simplex encephalitis requires very rapid recognition, diagnosis, and antiviral treatment to prevent
Moyamoya disease (MMD) is a rare and unique cerebrovascular disease. The term “moyamoya” is Japanese and refers to a hazy puff of smoke or cloud. In people with moyamoya disease, this is how the blood vessels appear in the angiogram. MMD is characterized by the progressive stenosis of the distal internal carotid artery (ICA) resulting in a hazy network of basal collaterals called moyamoya vessels. This may be a consequence of Mutations in a few genes. In addition, MMD is also associated with many genetically transmitted disorders, including neurofibromatosis, Down syndrome, Sickle cell anemia, and Collagen vascular disease. It follows bimodal age distribution. Younger populations present with ischaemic symptoms, whereas adults show hemorrhagic symptoms The exact cause remains unknown. Immune, genetic and other factors contribute to this disease. It follows complex pathophysiology resulting in neovascularization as a compensatory mechanism. Diagnosis is based on cerebral angiography using the DSA scale. Treatment involves managing symptoms with medicine or surgery, improving blood flow to the brain, and controlling seizures. Revascularization helps to rebuild the blood supply to the underside of the brain.
Presentation1.pptx, radiological imaging of peri natal acute ischemia and hyp...Abdellah Nazeer
This document discusses radiological imaging of neonatal acute ischemia and hypoxic ischemic encephalopathy. It describes different types of imaging techniques including CT, MRI, DWI, and ASL and how they can be used to identify areas of injury over time in neonates who experience a stroke. Risk factors for neonatal stroke are also reviewed. Imaging findings include restricted diffusion, cortical laminar necrosis, and reversal of gray-white matter attenuation on CT. MRI is useful for assessing injury to deep gray matter structures and cortical border zones.
This document discusses acquired brain injury (ABI) in children, including causes, incidence, developmental factors, classification, management, and recovery stages. ABI can be traumatic (e.g. from motor vehicle accidents) or non-traumatic (e.g. from strokes or tumors). Incidence is higher in males and low socioeconomic groups. Children's brains are more susceptible to injury due to anatomical differences. Management focuses on preventing secondary brain damage by maintaining oxygen, blood pressure, intracranial pressure, and cerebral perfusion pressure. Recovery proceeds through initial unresponsive/coma, early response, agitated/confused, and higher-level response stages.
Shaken baby syndrome is a form of child abuse that occurs when an infant is violently shaken. It often results in retinal hemorrhages, subdural hematomas, and brain injuries. The shaking causes the infant's brain to impact the skull, damaging blood vessels and brain tissue. Retinal hemorrhages are a hallmark sign and can range from mild to completely filling the retina. Other eye findings include retinal folds, schisis cavities, and vitreous hemorrhage. While external injuries may be absent, the combination of eye and brain injuries strongly indicates shaken baby syndrome even without a reported history of trauma. Survivors often have permanent disabilities, and up to 29% of victims die from their injuries.
The document summarizes traumatic brain injury (TBI), including the primary mechanical injury and subsequent secondary injuries. It describes the pathophysiology of contusions, hematomas (epidural, subdural, intracerebral), diffuse axonal injury, and concussions. It discusses classification systems for TBI severity and outlines the mechanisms of injury, including contact forces, inertial loading, rotational acceleration, and angular acceleration. Factors affecting injury extent and outcomes are also summarized.
The document summarizes recent developments in understanding child abuse relevant to ophthalmologists. It discusses several issues:
1) Minor trauma like rough play cannot cause the clinical picture of shaken baby syndrome, as the forces required to cause retinal hemorrhage are considerable.
2) Acute hypoxia alone has not been shown to result in the shaken baby syndrome picture. Hypoxia coupled with circulatory collapse may produce fatal brain swelling.
3) Cervical injuries alone do not cause retinal bleeding. However, inflicted cervical spine injury coupled with circulatory collapse has the potential to induce hypoxic brain injury.
This review article summarizes the ophthalmic findings associated with inflicted childhood neurotrauma, also known as shaken baby syndrome. The most common ophthalmic finding is retinal hemorrhage, which is present in approximately 80% of cases and usually occurs at all levels of the retina. Other acute findings include vitreous hemorrhage, optic nerve sheath hemorrhages, and macular retinoschisis lesions. Late findings seen in survivors include optic atrophy, retinal pigmentary changes, macular holes, and high myopia. The extent and severity of ocular injuries correlates with neurologic outcome and prognosis. The differential diagnosis of retinal hemorrhages in infants is limited, as many medical conditions are readily
This case discusses a 22-month-old female patient diagnosed with asymmetric dyskinetic cerebral palsy. MRI images show bilateral cystic necrosis of the lateral putamen and globus pallidus, likely due to perinatal hypoxia/ischemia. This resulted in an extrapyramidal form of cerebral palsy. Cerebral palsy is caused by nonprogressive brain defects or lesions early in development. Perinatal factors cause 70-80% of cases. Basal ganglia injury can result in dyskinetic cerebral palsy phenotypes.
Minor and moderate head injuries in childrenNabil Khalil
This document provides an overview of current management strategies for mild head injuries in pediatric patients. It discusses the definition of mild head injury, epidemiology, mechanisms of injury, clinical evaluation, diagnostic evaluation including X-rays and CT scans, treatment including criteria for admission, and neurobehavioral outcomes. Key differences in traumatic brain injuries between children and adults are also reviewed.
This document discusses hydrocephalus, which is an excess of cerebrospinal fluid in the brain that increases pressure. It can be caused by various disorders and makes diagnosis complex. The document covers epidemiology, pathophysiology, causes, symptoms, investigations, treatment, and prognosis. Hydrocephalus can be treated with surgical placement of a ventriculoperitoneal shunt, though lifelong follow-up is often needed, especially in children. Outcomes depend on type of hydrocephalus, with seizures associated with poorer outcomes and lower IQ. About 60% of children can attend school, and 40% may lead normal lives with treatment.
This document discusses the concept of "inflicted brain injury", formerly known as "shaken baby syndrome". It argues that the diagnosis has been adopted through consensus rather than scientific evidence, and that key features used to identify abuse such as retinal hemorrhages can also be caused by medical conditions. The author asserts that differential diagnoses including nutritional deficiencies must be specifically excluded before concluding abuse. The document questions the evidence and assumptions underlying the diagnosis and stresses the importance of considering alternative explanations to avoid inappropriate accusations of child abuse.
Multiple sclerosis is a chronic disease of the central nervous system characterized by multiple areas of inflammation and demyelination in the brain, spinal cord, and optic nerves. It commonly begins in young adults and is the most common chronic neurological condition affecting young people. Lesions appear separated in space and time throughout the central nervous system. Common symptoms include visual disturbances, limb weakness, and sensory changes. The cause is thought to involve an environmental trigger in a genetically susceptible individual, leading to an immune-mediated process. While there is no cure, treatment focuses on managing relapses, modifying the disease course, and controlling symptoms.
Similar to Dr. waney squire shaken baby syndromee (20)
Sue Amphlett founded Parents Against Injustice in 1985 after her family was wrongly accused of child abuse. Her youngest daughter had fractures from minor falls but doctors initially suspected abuse. This led to an investigation where Sue and her family felt marginalized as strangers passed judgement on them. The process was long, traumatic and damaging as they tried to prove their innocence without support. Most people caught up in similar situations lose self-esteem and cannot cope as their life structure revolves around their children. Sue felt the process focused too much on child protection and not enough on properly investigating allegations and supporting families impacted.
court applications under the children's actAlison Stevens
This document provides information about mediation and the requirement to attend a Mediation Information and Assessment Meeting (MIAM) before applying to family court regarding disputes over children or finances.
It states that applicants are now legally required to consider mediation through attending a MIAM before submitting a court application, to explore if mediators can help resolve arrangements. Exceptions include cases involving domestic violence, where evidence must be provided.
It provides details on what mediators do, how mediation can help give more control and be less stressful than court. It provides information on finding mediators and mediation services online or by scanning a QR code, and that MIAM attendance is free if qualifying for legal aid.
Applicants
This document provides guidance on the rules for McKenzie Friends in family court proceedings. It summarizes that litigants in person have a right to reasonable assistance from a layperson known as a McKenzie Friend. The presumption is in favor of allowing a McKenzie Friend unless fairness or justice require otherwise. A McKenzie Friend may provide moral support, take notes, help with paperwork, and quietly advise on legal points, but cannot address the court or examine witnesses without permission. The court has discretion to grant rights of audience or litigation to McKenzie Friends in some cases.
The document provides an overview of child protection processes and offers tips for dealing with a child protection situation. It explains that child protection focuses on assessing adults for risk to children and that the local authority has a duty to investigate potential harm and intervene even without prosecution being likely. It describes the roles of various professionals involved like social workers, police, and solicitors. Key tips include remaining calm, keeping records, listening to professionals, and understanding what the social services consider in their assessments of the home and family environment.
The document discusses guidelines for McKenzie Friends (MKFs) assisting litigants in family court proceedings. It provides an overview of current legislation regarding MKFs, their role and responsibilities, and best practices. Key points include:
- MKFs can provide support to litigants but cannot act as their legal representative or address the court without special permission.
- Litigants have a strong presumption to receive assistance from an MKF unless fairness or justice say otherwise. Objections from other parties do not outweigh this presumption.
- It is best practice for potential MKFs to introduce themselves to the judge assigned to the case in advance whenever possible to avoid objections from other parties.
- Applications to
The document sets out the code of practice for social care workers in the UK. It outlines six key responsibilities for social care workers: 1) protect service users' rights and interests, 2) establish trust with service users, 3) promote independence while preventing harm, 4) respect service users' rights while preventing harm to others, 5) uphold public trust in social care services, and 6) be accountable for their work and improve their skills. It also provides guidance on how the public can complain about a social care worker's conduct.
1) The author and her partner had twins via IVF who both had medical issues from birth. Their daughter stopped breathing at 4 months old and was diagnosed with a seizure, but the author believed it was related to acid reflux.
2) A few days later, both twins were found to have subdural bleeding and fractures through medical imaging at the hospital. The parents were accused of non-accidental injury (NAI) by hospital staff.
3) Over many months, the parents fought accusations from social services and underwent supervised care of their children. Eventually, the author was diagnosed with Ehlers-Danlos syndrome (EDS), which she believed explained her children's health issues, but authorities remained skeptical
1) The document discusses several cases of infants who experienced fractures, retinal hemorrhages, and brain injuries. In each case, the injuries were attributed to Shaken Baby Syndrome but the author argues they were actually due to an autoimmune response triggered by vaccination or infection.
2) The author's hypothesis is that vaccination or infection damages the beta cells in the pancreas, causing hypoinsulinemia. This inhibits cellular uptake of vitamin C, leading to "tissue scurvy" and failure of proteins involved in coagulation. This results in the bruising, bleeding, and fractures seen in the "triad".
3) Blood tests in the cases showed markers of coagulation disorders, vitamin deficiencies, and
This document is a quotation from G.A. Pindar & Son (NZ) Ltd for printing a 300-page book titled "Shaken Baby Syndrome". The quotation includes specifications for the physical book, project scope, pricing assumptions, preliminary pricing broken down by quantity, project sequence, and notes on pricing, production process, and terms of trade. Key details are the 300 page extent, paperback binding, 4 color cover and 1 color internal print, and pricing of $17.28 per book for a 2,000 unit print run in New Zealand or $12.75 per book for a 3,000 unit print run in China.
This document summarizes 6 case studies of children who experienced fractures, retinal hemorrhages, and brain injuries. In each case, the injuries were initially attributed to non-accidental trauma (such as shaken baby syndrome), but laboratory tests revealed evidence of autoimmune reactions, vitamin deficiencies, and coagulation disorders following vaccination or childhood illness. The document argues that fractures, hemorrhages, and encephalopathy in these cases were actually caused by an autoimmune response to antigenic stimulation from vaccines or infections, rather than abuse.
This document establishes a pilot scheme for care and supervision proceedings and other proceedings under Part 4 of the Children Act 1989. The pilot scheme will assess new practices and procedures to support the 26 week time limit for these types of cases. It modifies various Family Procedure Rules and Practice Directions to implement the pilot scheme, including establishing case management hearings and timelines. Courts can choose to begin participating in the pilot scheme on one of four start dates between July 2013 and October 2013.
This document outlines the key stages and timelines of the court process for care, supervision, and other Part 4 proceedings based on the Public Law Outline. It includes:
1) The typical stages and timelines for proceedings, including case management hearings, issues resolution hearings, and final hearings, with the aim of resolving proceedings within 26 weeks.
2) Relevant rules, practice directions, and guidance that must be considered in applying the Public Law Outline.
3) Clarification that the court has flexible powers to direct the process, including holding hearings without notice or resolving stages at different times than outlined, based on each case's specific circumstances.
PAIN aims to ensure fair treatment of families and strict procedures by authorities. It accepts not all families are innocent but takes no sides except the child's best interest. However, it advocates for families' rights which can be overlooked.
The document discusses unexplained fractures in children that may indicate brittle bone disease rather than non-accidental injury. It summarizes 128 cases referred to the author related to unexplained fractures in children living in the UK. In many cases, the author determined the children had forms of brittle bone disease like osteogenesis imperfecta or temporary brittle bone disease. For those returned to parents, no subsequent evidence of non-accidental injury was found in long-term follow-ups of over 400 patient-years. The document concludes some rare cases of brittle bone disease can be difficult to diagnose but falsely accusing parents of abuse in such cases can cause significant harm to families.
This document presents two case reports of infants who were diagnosed with shaken baby syndrome but may have had alternate explanations. Both infants' mothers had nutritional deficiencies during pregnancy and smoked. The infants were formula fed without vitamin C supplements. Both experienced apparent life-threatening events after vaccines and developed bruising, fractures, and other findings commonly associated with shaken baby syndrome. However, the author proposes the infants may have had vitamin C deficiency, as their symptoms and laboratory results resembled Barlow's disease or scurvy. The author argues vitamin C deficiency should be considered before diagnosing shaken baby syndrome.
Three cases of infants and children presenting with concerning medical issues are described. All three cases had signs of metabolic dysfunction, including prolonged prothrombin time and liver abnormalities. One case also presented with the "triad" of subdural hemorrhage, retinal hemorrhage, and encephalopathy. The document concludes that these presentations may have been caused by deficiencies or abnormalities of vitamins C, D, and K resulting from malnutrition or liver dysfunction, rather than presumed abuse as initially diagnosed.
Bruising forensic study adc.2009.177469.fullAlison Stevens
This study examined autopsy reports of 135 infants between 7-364 days old to determine the significance of bruising. The researchers found that 21 infants (15.6%) had bruising, and of those, 17 (81%) also had other injuries. Only 9 of the 114 non-bruised infants (8%) had other injuries. Bruising was significantly associated with other injuries and homicide. Bruising had a sensitivity of 65% and specificity of 96% for detecting other injuries, increasing to 71% sensitivity at <6 months when independent mobility is limited. The presence of bruising in infants is a significant marker for other injuries including homicide.
1. Shaken Baby Syndrome adult head injury in road traffic accidents. Following
Guthkelch’s paper, the “shaken baby syndrome” has
become widely accepted as a form of child abuse [1].
Introduction
The diagnosis “shaken baby syndrome” (SBS) has
The Triad of Injuries
been widely accepted for over 30 years, but recent The three elements of the triad are encephalopathy,
evidence from biomechanical and clinical observa- RH, and SDH.
tional studies questions the validity of the syndrome.
Retinal Hemorrhages (RHs)
Definition RHs have been regarded as an important indicator
The diagnosis of SBS is based on the clinical triad of inflicted injury, but many other causes of reti-
of encephalopathy, retinal hemorrhage (RH), and nal bleeding are recognized in infants, for example
subdural hemorrhage (SDH) in infants, usually under after normal birth, raised intracranial pressure, blood
six months of age, who may die unexpectedly or dyscrasias, hemoglobinopathies, extracorporeal mem-
survive with greater or lesser degrees of neurolog- brane oxygenation, cataract surgery, and accidental
ical damage [1]. The term non-accidental head injury trauma [8]. Postmortem indirect ophthalmoscopy has
(NAHI) has been preferred as it has no implications shown RHs to be more common after natural dis-
for mechanism of injury. Other features often associ- ease and accidental injury than after inflicted injury
ated include a sole carer at the time of collapse and [9]. These authors also noted that infants suspected
a clinical history that is incompatible with the sever- to have been abused were more likely to have oph-
ity of the injuries. The diagnosis of inflicted injury thalmological examination in life than infants with
becomes less problematic if there is objective evi- accidental injuries or natural diseases. This bias read-
dence of violence, such as bruises, fractures, or burns, ily distorts the true incidence of RH in non-accidental
but objective evidence of trauma has not always been injury. Indeed Vinchon [10] noted in his study of
necessary in making the diagnosis. infant head injury that “In the construct of our study
Central to the assessment of these cases is whether we could not obviate the circularity bias, and the eval-
the triad of findings can be regarded as diagnostic uation of the incidence of RH in child abuse remains a
of abuse with any degree of certainty. This review self-fulfilling prophecy”. These authors did, however,
examines the evidence base for each element of suggest that the extent and nature of retinal bleeds
the triad and the current biomechanical evidence may be more important as indicators of inflicted head
regarding mechanisms of infant head injury and its injury than their existence per se [10].
pathological investigation. The main hypotheses for genesis of RH are that
it is the result of venous obstruction, which in turn
may result from compression of the optic nerve
History by raised intracranial or intravascular pressure, even
transiently, or that the tissues of the retina are torn
SDH has been associated with child abuse since the during the act of shaking. This latter hypothesis does
mid-19th century [2]. Kempe described SDH with not withstand biomechanical scrutiny [11].
multiple skeletal injuries and bruises as the bat-
tered child syndrome and Caffey described long bone Encephalopathy
fractures and SDH [3–5], but it is Guthkelch [6]
who developed the hypothesis that the whiplash–like This term may be widely interpreted to include a
movements during shaking cause the characteristic range of clinical manifestations from feeding dif-
bilateral thin film SDH of the syndrome. He based ficulties, vomiting, and sleepiness to seizures and
his hypothesis, that shaking causes tearing of the fulminating cerebral edema.
cerebral bridging veins leading to SDH, on the biome- The specific neuropathological features of trau-
chanical studies of Ommaya [7] who was researching matic brain injury are contusions and traumatic
2. 2 Shaken Baby Syndrome
(a) (b)
Figure 1 (a) Acute axonal injury. Bands of BAPP expression in an infarcted area of brain in acute hypoxic-ischemic
injury. (b) Axonal swellings expressing BAPP restricted to the pontine cortico-spinal tracts, considered to indicate traumatic
damage
axonal injury. Hypoxic-ischemic injury and brain injury due to the specific intracranial pathophysiology
swelling are frequently seen but are not specific for before the skull bones fuse [19].
trauma. Contusions are very uncommon in infant Damage to the cervical nerve roots has been
brain trauma in the absence of skull fractures. Identifi- documented as part of the pathology of shaking injury
cation of axonal injury now depends on the immuno- [14]. It has not been established that this is the result
cytochemical demonstration of beta amyloid precur- of shaking, as cervical cord displacement resulting
sor protein (BAPP). This is a very sensitive marker of from brain swelling may also cause traction on nerve
interruption of normal axonal flow but may be upreg- roots in the region. Autopsy studies in man and
ulated after hypoxic–ischemic injury and metabolic primates have shown that the spinal cord is displaced
disruption as well as trauma (Figure 1). Distinction during extension and flexion of the neck [20, 21]
of traumatic axonal expression of BAPP from other and it remains a possibility that hyperextension and
flexion could cause traction damage to nerve roots
causes is fraught with difficulty, and depends in part
throughout the length of the spinal cord, but this has
on its distribution [12], [13], [14]. Neuropathological
not been documented in living infants.
studies have shown that in babies who die following
NAHI, the underlying brain pathology is widespread
hypoxic-ischemic injury and not diffuse traumatic Subdural Hemorrhage (SDH)
axonal injury as previously believed [12, 13]. In this
SDH is perhaps the most important and consistent
series axonal injury was seen in a limited distribu- component of the triad. In the acutely sick infant, it
tion in the lower brainstem and in only a minority is frequently the first clinical sign, identified on brain
of cases. Radiological studies have confirmed these scan, to raise the question of abuse. There are no
pathological observations [15]. specific imaging patterns that can distinguish inflicted
This observation is important as traumatic axonal from accidental intracranial injury [22, 23].
injury will lead to immediate loss of function causing Autopsy and imaging studies show that infant
clinical symptoms from the time of trauma. In SDH is usually a thin bilateral film and not a thick,
contrast, hypoxic-ischemic injury and ensuing brain unilateral space occupying clot as seen in traumatic
swelling take variable periods of time to develop SDH in older children and adults [12, 13, 24]. This
and a baby so damaged may not show immediate raises the question of whether the two forms have the
symptoms. Even fatal brain trauma may present with same etiology and anatomical source.
a lucid interval between injury and clinical collapse
[16, 17]. Lucid intervals are more frequently seen Causes of Subdural Hemorrhage. The common-
in infants less than two years of age [18], reflecting est cause of SDH in infants is said to be trauma
the very different responses of the infant brain to [25] although a recent study has shown a significant
3. Shaken Baby Syndrome 3
incidence (26%) of birth-related SDH [26]. Other intracranial damage including retinal and intracranial
causes in infants include benign enlargement of hemorrhage after falls from levels as low as 3 ft [10,
the extracerebral spaces (BEECS), clotting disorders, 17, 30–33]. While most babies may suffer little from
hemorrhagic disease of the newborn, rare metabolic an apparently trivial fall, this is clearly not always
diseases, vascular malformations, and neurosurgical the case.
procedures [25, 27].
Birth-Related SDH
Traumatic SDH Three studies, using magnetic resonance imaging
Proposed traumatic causes of infant SDH are inflicted (MRI), have shown a surprisingly high incidence
injury such as shaking and/or impact and accidental of SDH after birth in asymptomatic infants. Whitby
injuries such as falls. Impact includes blunt impact of identified SDH in the first two days of life in 9%
an object on the head and that resulting from a fall [32], while SDH was seen in up to 46% of otherwise
or striking the moving head on a rigid surface. The normal neonates using higher resolution MRI scan-
biomechanical aspects of these injuries are discussed ning [26, 34]. With regard to method of delivery,
below. The vast majority of cases described as SBS ventouse or instrumental deliveries have been asso-
have evidence of impact [28]. While the pathologist ciated with a higher incidence of intracranial injury
may be able to determine features indicative of [35, 36]. Towner [37] found an increased incidence
impact, it is not, of course, possible to distinguish of intracranial hemorrhage after instrumental delivery
accidental from non-accidental injuries by pathology. with ventouse or forceps and emergency caesarean
section, but the incidence was lower after caesarean
Low-Level Falls section before labor had begun. However, it should
Low-level falls have the potential, albeit only rarely, be noted that all of Looney’s cases followed normal
to cause SDH in infants and young children. Absolute vaginal delivery [26].
height is not as important a criterion for injury as While neonates with SDH may be asymptomatic
the exact nature of the fall for a particular infant, [26, 35] they may also have signs in the neonatal
in a particular circumstance [29]. The effects of period including unexplained apnoea, dusky episodes,
twisting, rotation, or crushing of the structures of the hypotonia, seizures, and lethargy [38].
neck are crucial in terms of outcome. Biomechanical
studies show that falls even from low levels of Sources of SDH. Traditional belief is that in SBS
3–4 ft can generate far greater forces in the head the SDH results from tearing of the superficial bridg-
than shaking [11]. There are a number of case series ing veins as they cross from the brain to the dural
demonstrating that infants and children may suffer sinuses [6] (Figure 2). This has never been proved.
Figure 2 Infant bridging veins may be visualized by opening the skull very carefully, but they are readily torn in normal
autopsy procedures. (Picture courtesy of Dr P. Lantz)
4. 4 Shaken Baby Syndrome
Indeed it is very difficult to find documented evidence alternative sites of origin exist, the dura itself and
of torn bridging veins at surgery or at autopsy. Cush- the old subdural membranes (Figure 4).
ing, who operated on neonates with SDH and sub-
sequently performed the autopsies wrote “In two of Dural Hemorrhage
the cases I have examined I have satisfied myself that The dura is composed of two leaflets, the periosteal
such ruptures were present. A positive statement, how- and the meningeal dura, separated by a thin vascular
ever, cannot be given even for these cases, since the channel, which widens to form the large dural sinuses
dissection and exposure, difficult enough under any [44]. There are particularly extensive venous sinuses
circumstances, owing to the delicacy of the vessels is in the posterior falx, [45] a frequent site of high signal
the more so when they are obscured by extravasated on brain scans in asphyxiated infants. Bleeding into
blood” [39]. More recently Maxeiner [40] addressed the falx is well recognized in asphyxiated infants
the problem by injecting radio-opaque dye into the [46]. It has long been acknowledged that optic
veins at autopsy to assess their integrity after remov- nerve sheath hemorrhage arises from the dura [47]
ing the top of the head in one piece, hard-boiled egg and more recently the dura was proposed as the
source of intracranial SDH in infants [48] (Figure 5).
style. This approach is not widely used as it destroys
Careful microscopic examination of the dura confirms
much of the brain and injection pressures need to be
that intradural bleeding is common in asphyxiated
carefully monitored if the veins are not to be ruptured
infants, particularly in the dural folds of the falx and
artifactually.
tentorium close to the large venous sinuses [49]. In
Volpe [41] said that SDH was by no means some cases intradural bleeding leaks out on to the
always traumatic and suggested that in neonates subdural surface leading to macroscopically evident
without tentorial tears the bleeding may arise from subdural haematoma [50].
the tributary veins of the dural sinuses. Autopsy
studies from the older literature show bridging vein Healing Subdural Membranes
rupture is uncommon, Craig described 62 neonatal Healing of SDH is by formation of a thin, vascu-
SDH, of which only 3 had torn bridging veins, lar membrane consisting of fibroblasts, macrophages,
all of those with overriding sutures [42]. Larroche which often contain altered blood products, and wide
described 700 autopsies 18% with SDH. [43] She thin-walled capillaries with a potential to rebleed
noted an association with hypoxic-ischemic injury [51] (Figure 6). It is uncommon in infants to see a
(Figure 3). She did not identify torn veins. double layered membrane around a localized mass
If SDH does not arise from torn bridging veins, of resolving clot, as seen in the elderly, probably
what other sources may there be? Two obvious because the infant SDH usually forms as a thin film
Figure 3 Fresh subdural blood seen after birth asphyxia. (Picture courtesy of Dr I. Scheimberg)
5. Shaken Baby Syndrome 5
Arachnoid Superior sagittal sinus Intradural fluid channel
granulation
Lateral lacuna of
sagittal sinus
Dura
Inner dural plexus
Subarachnoid
space Cortical
draining vein
Arachnoid barrier
membrane Falx
Figure 4 Diagram representing a coronal slice through the brain and dura indicating the intradural sinuses and their
relationship to cortical surface veins, arachnoid granulations, and intradural fluid channels
(a) (b)
Figure 5 (a) The dura is thickened and congested and there is patchy subarachnoid and subdural blood. Autopsy 44 h
after collapse following choking episode. (Courtesy of Dr I. Sheimberg.) (b) H & E stained section of falx showing it to
be destroyed by massive acute bleeding
rather than as a mass lesion. Contrast injection is and be influenced by the method of treatment of
required to identify the membranes radiologically the acute hematoma. Surgical evacuation or tap-
[52]. In some cases, acute SDH leads to accumu- ping may prevent later reaccumulation of fluid [53,
lation of fluid in the subdural space. The reasons 54]. The period of time for redevelopment of sub-
for this are unknown. Fluid collections may result dural fluid collections may be long, between 15
from immaturity of the arachnoid granulations and and 111 days [55]. It is likely that an important
impaired cerebrospinal fluid (CSF) absorption [22], contribution to chronic subdural fluid accumulation is
6. 6 Shaken Baby Syndrome
(a) (b)
(c)
Figure 6 (a) Dural surface showing a very thin yellow-brown membrane, which has partly lifted during removal of the
brain. Head injury four weeks prior to death. (b) H & E stained section of acute bleed overlying a chronic membrane, which
consists of some six layers of fibroblasts between which are macrophages and new capillaries (three days after collapse
with acute SDH) (c) Same section stained with CD34 to show endothelial cells. Note capillaries growing into the fresh clot
repeated rebleeding and oozing from a chronic sub- Distribution. In the first few days after bleeding,
dural membrane [56, 57]. subdural blood sediments under the influence of
There is little information regarding the potential gravity and undergoes secondary redistribution to the
for birth-related SDH to evolve into chronic fluid most dependent part, the posterior falx and tentorium
collections. Whitby followed nine cases with a repeat [59]. Radiological studies show that subdural blood
scan at one month; none had developed a chronic tracks down around the spinal cord [60] and, if the
collection [35]. Rooks followed 18 cases for up to 3 spine of babies with intracranial SDH is examined at
months, one developed a further subdural bleed [34]. autopsy, blood is regularly seen in the subdural space
However these studies could not identify membranes and around sacral nerve roots in the most dependent
as contrast was not used. Chronic membranes have parts of the dural sac (Figure 7).
been seen at autopsy in up to 31% of infants dying
unexpectedly without previous clinical evidence of
chronic SDH [58]. In view of the potential for acute Differential Diagnosis of SBS
accidental SDH to evolve into a chronic collection
several months later [55], it would appear likely that The most common causes of the triad are impact,
the same pattern would follow birth-related SDH. At birth-related SDH, BEECS, coagulopathies, apnoea,
this time, we simply have insufficient information. asphyxia and choking, acute life-threatening events
7. Shaken Baby Syndrome 7
(a) (b)
Figure 7 (a) A collection of fresh subdural blood at the dorsal aspect of the sacral spinal cord. Baby died within hours
of inflicted abdominal injury with acute and chronic subdural hemorrhage. (b) Microscope section showing an elliptical
collection of fresh blood dorsal to the spinal cord. The blood is within a chronic subdural membrane indicated by the iron
pigment, stained here by Perl’s stain. Baby died three weeks after traumatic subdural hemorrhage
(ALTEs), osteogenesis imperfecta, osteopenia of Biomechanics
prematurity, and metabolic diseases [14, 28, 61,
62, 63]. Biomechanics is the application of principles of
physics to biological systems and has been the main-
stay of research into motor vehicle safety for six
Choking/Asphyxia decades. It was just such research into noncontact
head injury from rear-end shunts that stimulated
In a considerable number of cases, vomiting and/or Guthkelch to formulate his hypothesis for SBS in
reflux are described at the time of collapse, and 1971 [6]. Ommaya [7] had caused concussion, SDH,
in some there is a history of feeding difficulties, and white matter shearing injury (diffuse axonal
gastroesophageal reflux, and choking or apnoeic injury) in primates by whiplash. Guthkelch suggested
episodes [14, 62]. SBS is commonly diagnosed in the that the rotational forces of shaking would cause
first three months of life, the age of peak incidence of tearing of bridging veins and bilateral subdural bleed-
sudden infant death syndrome. Inhalation of feed or ing, although Ommaya himself warned that “It is
vomit may play a part in sudden infant death [64] and improbable that the high speed and severity of the
awake apnoea is associated with gastroesophageal single whiplash produced in our animal model could
reflux [65]. The physiological response to aspiration be achieved by a single manual shake or even a short
may be dramatic; foreign material on the larynx series of manual shaking of an infant in one episode”.
causes laryngospasm, which is associated with startle, More recent studies using “crash test dummies”
cessation of respiration, hypoxaemia, bradycardia, indicate that impact generates far more force than
and a doubling of blood flow to the brain [66]. shaking (Figure 9) and that impact is required to
These circumstances, with or even without vigorous produce SDH [68]. Cory and Jones [69] generated
resuscitation, may cause reperfusion injury and a pre- forces that exceeded the injury threshold for concus-
existing healing subdural membrane may bleed. The sion, but not for SDH or axonal injury. Their adult
dura itself may become hemorrhagic and ooze blood shaker volunteers fatigued after 10 seconds. While
into the subdural space (Figure 8). As long ago as they concluded that “It cannot be categorically stated,
1905, Cushing suggested that coughing, choking, and from a biomechanical perspective, that pure shak-
venous congestion may explain some forms of infant ing cannot cause fatal head injuries in an infant”,
SDH [39], a hypothesis recently revived by Geddes, they noted that in their experiments there were chin
[48, 67]. and occipital contacts at the extremes of the shaking
8. 8 Shaken Baby Syndrome
(a) (b)
Figure 8 (a) Cortical vein thrombosis. Infant died 10 days after collapse following two choking episodes. Several surface
veins are thrombosed (arrows). (b) Section of thrombosed vein shows a network of new capillaries growing into the
periphery of the thrombus (CD31)
Peak head acceleration (g)
125
100 From adult male’s arms
76.2 cm
Inflicted slamming
style impacts onto
75 surfaces noted
50.8 cm
Bed – mattress
Leather sofa
50
25.4 cm
25
Free fall impacts onto
carpeted stairs
(fall heights noted)
0
Figure 9 Comparative forces generated by dropping or shaking and slamming a dummy representing a six-month-old
infant (C Van Ee, personal communication 2007)
motion that could have caused impact. These authors It is likely that the forces required to cause intracra-
expressed their concerns regarding the difficulties in nial injury will also damage the weak infant neck
extrapolating to human infants the findings in both [71]. In road traffic accidents, infants who suffer sin-
dummy and animal models. Biomechanical studies gle severe hyperextension forces have cervical frac-
have shown that falls and impact to the head pro- tures, dislocations, spinal cord injury, and torn nerve
duce significant rotational forces when the impacting roots, not SDH [72–74].
forces are not aligned through the center of gravity
of the head, due to hinging of the head on the Investigation of Shaken Baby Syndrome
neck. Shaking is not necessary to cause rotational
acceleration. SBS or NAHI is most likely to occur in an infant
Neck injuries may be underreported in babies dying suddenly under the age of six months. Autopsy
dying after severe abuse [70]. In Ommaya’s study, should be performed with careful consideration of
11 of 19 primates had neck injuries; these were adult this diagnosis and appropriate steps taken to support
animals with mature neck structure and musculature. or exclude it. The records of pregnancy and delivery
9. Shaken Baby Syndrome 9
must be carefully studied to look for any evidence of evidence of intradural bleeding and rupture onto
complications that could mimic NAHI. These include the subdural surface. This may be the source of
pregnancy disorders such as oligohydramnios, fetal significant subdural blood.
hypokinesia, and prematurity, which lead to osteope- The brain must be fixed for detailed histological
nia and predispose to fractures. The birth history and examination.
method of delivery are important as SDH may arise In all of these cases, the time between collapse
at this time while being entirely asymptomatic in and death may play a significant part in the final
the neonatal period. Head circumference charts are pathology. A baby who has collapsed and becomes
important; head circumference measurements taken at apnoeic with subsequent cardiopulmonary rescusci-
birth and in the subsequent weeks may reflect abnor- tation (CPR) and ventilation will be shocked and
mal head growth, which can indicate an accumulating suffer multiorgan failure with altered clotting, loss
subdural fluid collection and a propensity to rebleed. of integrity of vessels and membranes, oozing of
The clinical history may give clues to other prob- blood into intracranial compartments, including the
lems in the early weeks of life. Vomiting, feeding subarachnoid and subdural spaces, and development
problems, and apnoeic episodes and ALTEs may of the “respirator brain”.
indicate difficulties with coordination of breathing, Review of the brain imaging in life is essential
sucking and swallowing, and vulnerability to chok- in assessing, as far as possible, just how much
ing. Any event that threatens life may also potentially hemorrhage occurred at the time of collapse and how
end it. much may be the result of subsequent secondary
The history of the baby’s terminal collapse must changes. It is recognized that SDH may continue to
also be carefully examined. Parents may describe bleed after initial onset [75] especially if a baby is
events that reveal a cause for collapse. In any other very sick. Finding a large clot at autopsy may suggest
field of medicine, the clinical history is regarded as traumatic rupture of a large vessel, but comparison
the cornerstone of diagnosis and it should not be with early brain scans may indicate that the bleed was
disregarded without serious critical evaluation. only minor at the outset, indicating a slower oozing
The autopsy can reveal evidence of trauma such process with different implications for causation. It
as deep bruises and fractures not seen in clinical is becoming increasingly obvious that not all SDH
examination. The examination of the intracranial arises from traumatic rupture of blood vessels.
contents is paramount. The scalp and skull require
careful examination for evidence of bruising and Acknowledgment
fractures. Suture separation due to raised intracranial
pressure and wormian bones can be mistaken for I would like to thank Dr Irene Scheimberg and Dr Pat Lantz
fractures. When the cranium is opened, the presence for providing pictures and Dr Chris Van Ee for valuable
of any intracranial bleeding must be noted. Unclotted discussion and for preparing Figure 8.
blood may escape from the subdural space as the
skull is opened and be mistaken for bleeding from the References
dural sinuses. It is important to note the volume and
nature of blood and the presence of xanthochromia, [1] American Academy of Pediatrics Committee on child
indicating older bleeding. As the cranium is opened, abuse and neglect: shaken baby syndrome: inflicted
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