Head Injuries Past Paper 2024 PDF

Thursday, 21st November 2024 Head Injuries Dr Heidi Okkers Year 2 21st November 2024 Pathology HEAD INJURIES LEARNING OUTCOMES Describe the various types of scalp injuries. Describe the types and complications of skull fractures. Describe the types and pathology of brain haemorrhage. Des...

Thursday, 21st November 2024 Head Injuries Dr Heidi Okkers Year 2 21st November 2024 Pathology HEAD INJURIES LEARNING OUTCOMES Describe the various types of scalp injuries. Describe the types and complications of skull fractures. Describe the types and pathology of brain haemorrhage. Describe the features and types of cerebral contusion. Describe the causes and pathology of diffuse axonal injury. Describe the pathophysiology of raised intracranial pressure. Describe the types and effects of brain swelling. Describe the pathology of alcohol related head injury. THE SIGNIFICANCE OF HEAD INJURIES? Clinical Pathological Legal  CLINICAL SIGNIFICANCE  HEAD INJURIES (H.I.) Head injury is the most common cause of attendance to A&E in Ireland 90% of al HI attendees minor 40 – 50% are children Minor head injury – rarely associate with long term complications 0.2% of HI will die – usually severe HI http://www.hse.ie/eng/health/az/H/Head-injury,-minor/  HEAD INJURY IN IRELAND 19,000 new brain injuries annually 10,000 people are hospitalised with traumatic brain injuries annually 8000-8,500 new strokes happen every year 300 new brain tumours per annum 120,000 people living with disabilities after brain injury https://www.abiireland.ie/wp-content/uploads/delightful-downloads/2019/11/ABII-Report- 2018.pdf PATHOLOGICAL SIGNIFICANCE  HEAD INJURIES (H.I.) Commonest cause of death in young adults in developed countries 50% of deaths in 15-19 year olds Accident, Suicide, Homicide THE CENTRAL NERVOUS SYSTEM Dampens impact/shock waves - protects Protective but rigid – no expansion and if broken, potentially dangerous. Sub - arachnoid space contains CSF - cushion, leeway for expansion http://my-ms.org/anatomy_brain_part4.htm  SPECTRUM OF INJURIES  Surface  Scalp/Face  Skull  Meninges  Dura mater  Arachnoid  Brain SCALP AND FACIAL INJURIES  INJURY TO FACE OR SCALP Blunt Force Trauma Bruise External or subcutaneous punch, kick, fall Abrasion Imprints e.g. Stamping Lacerations Linear or specific e.g. hammer. Sharp Force Trauma Incised wounds – Surface injury. Stab wounds – Potential brain injury.  COMPLICATIONS FOR SCALP INJURIES Haemorrhage The scalp is highly vascular and death can be due to acute blood loss. Due to blood obstructing the airways. Fractured skull Bleeding around brain Extradural, subdural, subarachnoid ANY SURFACE INJURY MAY CAUSE... Injury to brain Diffuse itself damage Hypoxia, Contusions axonal injury, oedema Lacerations Haemorrhage SKULL FRACTURES  SKULL  Fractures  Simple  Compound  Indicate amount of force used  Not necessarily life-threatening  SKULL FRACTURES  Types  Linear - simple fall  Comminuted - more force, scalp damage  Depressed - usually direct blow, focused  Basilar – fall from height, RTA  Ping-pong – neonates  Diastatic – along skull sutures  May indicate size and shape of weapon  Severity α Force  Line of least resistance  SKULL FRACTURES HIGH VELOCITY IMPACT Produces Penetrating or Depressed Fractures FLAT IMPACTS Produce Linear, Non-Displaced Fractures RISK OF SKULL # WITH BFT DEPENDS ON Severity of Blow Speed of impact Object involved in impact Weight, shape, consistency Thickness of Hair, scalp, skull! Age of Victim Elasticity, brittleness of bone  COMPLICATIONS OF A #  CSF leakage Basal fractures  Infections  Extradural haemorrhage “Black Eyes”/Panda Eyes Frontal fracture **Children’s skull may deform and not break, but can cause massive internal damage** THE MENINGES  MENINGEAL INJURY Tears Associated with fractured skull Haemorrhage With or without fracture  EXTRADURAL HAEMORRHAGE Blood between skull & dura 90% # petrous temporal bone Above or behind ear May occur with no # (children)  MENINGEAL INJURY - EDH Source of bleeding Arterial Middle meningeal artery is the commonest. Venous Diploic channels of skull Small veins  MENINGEAL INJURY - EDH High mortality  50% associated with intracerebral bleeding Treatable  But intellectual / emotional disability if treatment delayed Problems Fall v accelerated fall e.g. assault associated with alcohol in young males  EDH – LUCID INTERVAL Affected individual has “conscious” period after the HI. Then collapses and dies usually within a few hours. Usually EDH. Sometimes in acute subdural haemorrhage.  SUBDURAL HAEMORRHAGE Blood between dura and arachnoid Classification Acute Subacute 3 - 14 days Chronic > 14 days Source of Bleeding Bridging vein Occasionally venous sinus May not be obvious at PM or surgery  SUBDURAL HAEMORRHAGE Elderly, alcoholics Children ‘Shaken baby’ May be a birth-related injury Whiplash injury  SDH - PROBLEMS Less clearly associated with impact injury Not necessarily associated with fracture Due to shearing forces Can take several hours for symptoms Slow evolution – venous bleed  SUBARACHNOID HAEMORRHAGE Blood over surface of brain, beneath arachnoid Cause Tearing of pial vessels between brain and arachnoid Shearing or rotational injury  SUBARACHNOID HAEMORRHAGE Minor SAH Indication of HI May have been concussed or ‘knocked out’ Significant SAH Severe trauma Damage to neck – vertebral arteries Rupture of aneurysm inside skull Extension of intracranial bleed  TSAH – VERTEBRAL ARTERIES Basal SAH Transmural tear of vertebral artery at the relevant site, usually without preexisting pathology Biomechanically and temporally consistent evidence of blunt impact Hyperextension and/or rotation of the head and neck DD: Non-traumatic rupture from intracranial vertebral artery dissection, abnormal vessel THE BRAIN  BRAIN INJURY Localised Generalised or diffuse Depends on type of H.I. Direct force Rotational forces Acceleration/deceleration  BRAIN DAMAGE Primary Sustained at time of impact Cortical contusions and lacerations. Diffuse axonal/vascular injury. Secondary Early – Hypoxia, Ischaemia, Brain swelling, formation of intracranial haematoma Late – Epilepsy, Infection  LOCALISED BRAIN INJURY Surface Lacerations - Contusions Direct injury frontal and (bruises) temporal CONTUSIONS Bruising on the surface of the brain. Fractures. Involve the crests of gyri and may be superficial. May extend into underlying white matter and form a haematoma. Coup and contrecoup contusions  BRAIN – SURFACE INJURIES Fracture contusion Directly under a # Coup contusion No #, but contusion at site of impact Contre-coup contusion Bruising opposite site of impact Usually frontal/temporal following occipital trauma  BRAIN – SURFACE INJURIES Impact front of head Few injuries Impact top of head Injury of base of brain Impact of side of head injury sides of brain, worse opposite Impact back of head injury at back, severe injury front of brain  BRAIN – SECONDARY INJURY INTRACEREBRAL HAEMORRHAGE Usually surface injuries overlying small bleed Burst lobe – usually fatal Differential diagnosis: Spontaneous intracerebral haemorrhage Associated with hypertension, specific sites  BRAIN – INTERNAL INJURY Deep intracerebral heamorrhage Indirect injury Associated with motion of head, eg.RTA. Due to tearing of vessels In young persons may not be associated with severe external damage BRAIN – INTERNAL INJURY Diffuse/generalised damage Primary Damage Diffuse axonal injury (DAI) + Diffuse vascular injury (DVI)  DAI/DVI Acceleration/deceleration. Shearing/rotational forces. RTA Falls from height Simple falls/assaults Range of outcomes from concussion ➔ persistent vegetative state  DAI-BRAIN Gliding contusions When brain rubs against projecting/hard surfaces Haemorrhage corpus callosum + brain stem (dorsolateral quadrants) The forces generated by violent shaking or rotational injury (as in a passenger ejected from a moving vehicle) can produce stretching of axons in cerebral white matter. The force may be strong enough to shear off axons, the ends of which retract into globoid shapes that appear with this silver stain of white matter as "retraction balls". SECONDARY DAMAGE FROM GENERALISED/DIFFUSE CEREBRAL INJURY  CEREBRAL OEDEMA A clinico-pathological state that is characterised by an increase in brain water content (above the normal brain water content of approximately 80%). Occurs in response to brain insult. Increases brain volume → raised intracranial pressure (ICP). Raised ICP decreases cerebral perfusion pressure leading to cerebral ischemia. Cerebral oedema may result in brain herniation due to the associated mass effect.  PATHOPHYSIOLOGY OF CEREBRAL OEDEMA Cerebral injury →cascade of events initiated at molecular level→ accumulation of fluid in the brain’s intracellular and extracellular spaces. Fluid compartments of the brain: Cerebral vessels (blood brain barrier). Cerebrospinal fluid (in the ventricular system) Interstitial fluid (brain parenchyma) Intracellular fluid (neurons and glial cells).  CEREBRAL OEDEMA Vasogenic oedema. Due to breakdown of the BBB secondary to mechanical disruption. Cytotoxic/ionic/cellular oedema. Due to cellular energy failure with anaerobic metabolism. Intact BBB. Usually due to hypoxia or ischaemia.  CEREBRAL OEDEMA Interstitial/hydrocephalic oedema. Due to increased intraventricular pressure and transependymal migration of CSF into extracellular space. Seen in meningitis, SAH, normal pressure hydrocephalus and obstructing mass in relation to ventricular outflow. Osmotic/hypostatic oedema. Due to imbalance of osmolality between serum plasma and brain parenchyma, eg SIADH. Hydrostatic oedema. BRAIN SWELLING  BRAIN SWELLING A separate entity from cerebral oedema, but often occurring simultaneously following cerebral insult. Due to engorgement of the cerebral vessels: Increased intravascular blood volume. Can lead to cerebral oedema. May be Delayed (esp. in children) RAISED INTRACRANIAL PRESSURE  RAISED INTRACRANIAL PRESSURE Caused by: Localised mass lesions: Extradural, subdural, intracerebral haemorrhage. Obstruction to major venous sinuses: depressed fractures, venous thrombosis. Focal oedema secondary to trauma, infection, tumour. Diffuse brain oedema: diffuse head injury, SAH, meningitis, near drowning. Neoplasms. Abscess. Disturbance of CSF circulation: obstructive hydrocephalus, communicating hydrocephalus. Idiopathic intracranial hypertension. CLINICAL FEATURES OF RAISED ICP Headache Alteration in mental state; lethargy, irritability, abnormal social behaviour. Vomiting. Pupillary changes. Unilateral ptosis or third and sixth nerve palsies. Fundoscopy: Pappiloedema flame-shaped haemorrhages. Retinal haemorrhages may be seen. ** BEWARE WITH LUMBAR PUNCTURE**  RAISED INTRACRANIAL PRESSURE Compensatory Mechanisms: Displacement of blood Displacement of CSF Loss of Brain Tissue  RAISED INTRACRANIAL PRESSURE Increase Cerebral Pushes fluid oedema and pressure inside out displacement skull Pressure on brainstem - Herniate haemorrhage  Head Injury Raised Brain Swelling Cerebral intracranial Oedema Pressure Herniation Brain stem haemorrhage and death OTHER SECONDARY DAMAGES  Hypoxic damage Facial injuries - inhaling blood. Blood loss from injuries. Cardiac arrest. Seizures. In severe head injury: Pulmonary oedema. Gastric erosions. Acute pancreatitis.  CAUSE OF DEATH Brain Damage Raised Intra Cranial Pressure Others Associated injuries Haemorrhage Inhalation Bronchopneumonia I.H.D etc. ALCOHOL & HEAD INJURIES  ALCOHOL AND HEAD INJURIES Many accidents and assaults occur in the setting of excessive alcohol intake. 35-81% of individuals with TBI were alcohol intoxicated and 42% of the TBI were heavy drinkers before injury Intoxication Worse outcome, even with relatively minor head trauma Muscle Laxity “Unprotected” when fall  Concussion Period of post-injury apnoea lengthened by alcohol intoxication. Recurrent falls – Chronic subdural haemorrhages. End stage liver disease – coagulation disorders. BRAINSTEM AND SPINAL CORD INJURIES  BRAINSTEM INJURIES Function Midbrain: regulates eye movements. Pons: co-ordinates facial movements, hearing and balance. Medulla oblongata: regulates your breathing, heart rhythm, blood pressure and swallowing. CAUSES OF INJURY Inflammation: encephalitis Vascular: thrombo-emboli, occlusions, trauma, hypertension Traumatic brain injury – herniation Falls Sudden cardiac death Tumours CLINICAL FEATURES Loss of reflexes, balance and gait issues. Impaired vision, dizziness and loss of sense of smell. Altered heart rate and irregular breathing. Paralysis and coma. EFFECTS Coma – BS has a network of neurons (RAS) Locked-In syndrome – severely damaged brainstem Swallowing problems Respiratory issues Sensory problems SPINAL CORD INJURIES Causes Compression damage - falls Hyperflexion and hyperextension Road traffic collisions Assaults Diving accidents Sport related injuries (incl. horse riding) Categorized Complete Incomplete  Cervical cord and cervicomedullary injuries are features of non- accidental whiplash injuries that can result from the shaking of infants Age at the time of injury, neurological status at the time of injury and extent of injury were identified as predictors of survival Closed SCIs are the most common traumatic cord lesions in clinical practice, and are associated with fracture or dislocation of the spine due to: consequence of hyperflexion/hyperextension movements, compressive forces, such as a fall from height landing on the top of the skull rotational movements, causing fracture dislocations, typically associated with thoracolumbar lesions  Fracture of the spinal column Cross-section of cervical spinal resulting in direct compression cord, showing central of haemorrhagic infarction after a the spinal cord contusional spinal cord injury QUESTIONS?