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Head injuries
- 1. Head Injury- Clinical Manifestations, Diagnosis and Management AHMED JEMAL CLINICAL-1(HO) JAN 5,2015
- 2. Head Injury • Any degree of traumatic brain injury ranging from scalp laceration to LOC to focal neurological deficits
- 3. Head Injury • Causes – Motor vehicle accidents – Falls – Assaults – Sports-related injuries – Firearm-related injuries
- 4. Head Injury • High potential for poor outcome • Deaths occur at three points in time after injury: – Immediately after the injury – Within 2 hours after injury – 3 weeks after injury
- 5. Head Injury TYPES: • Scalp laceration • Skull Fractures • Minor Head Trauma Concussion and post-concussion syndrome • Major Head Trauma: Cerebral contusion Laceration
- 6. Head Injury • Scalp lacerations – The most minor type of head trauma – Scalp is highly vascular → profuse bleeding – Major complication is infection
- 7. Head Injury • Skull fractures – Linear Skull Fracture – Depressed Skull Fracture – Diastatic Skull Fracture – Basal Skull Fracture – Compound Skull Fracture – Compound elevated Skull Fracture – Growing Skull Fracture
- 8. Head Injury • Skull fractures – Location of fracture alters the presentation of the manifestations – Facial paralysis – Conjugate deviation of gaze – Battle’s sign, Raccoon eyes
- 9. Battle’s SignBattle’s Sign Fig. 55-13
- 10. Head Injury • Basal Skull fractures – CSF leak (extravasation) into ear (Otorrhea) or nose (Rhinorrhea) – High risk infection or meningitis – “HALO Sign ” on clothes of linen – Possible injury to Internal carotid artery – Permanent CSF leaks possible
- 11. Investigations X-ray CT scan: standard modality MRI Bleeding from the ear or nose in cases of suspected CSF leak -"halo" or "ring" sign , when dabbed on a tissue paper CSF leak - analyzing the glucose level and by measuring tau-transferrin.
- 12. Management Pre-hospital care: • Patients with severe head injuries should be assumed to have a cervical spine (C-spine) injury and immobilized with until clinical and radiographic studies can prove otherwise • Minimize CSF leak – Bed flat – Never suction orally; never insert NG tube; never use Q-Tips in nose/ears; caution patient not to blow nose • Place sterile gauze/cotton ball around area Definitive Rx: • Measures to reduce ICP • Supportive management • Surgery
- 13. Head Injury • Minor head trauma – Concussion : head injury with a temporary loss of brain function concussion can cause a variety of physical, cognitive , and emotional symptoms. Cause: Sudden acceleration and deceleration injury eg: Car accident, sports injury, bicycle accident etc
- 14. Head Injury Types of Head Injuries Concussion Presentation: Physical-headache, LOC, Amnesia, s/s of ↑ ICP(Cushing’s triad) , convulsions Cognitive : confusion, irritability, behavioral changes
- 15. Head Injury • Minor head trauma – Postconcussion syndrome • 2 weeks to 2 months • Persistent headache • Lethargy • Personality and behavior changes
- 16. Head Injury • Major head trauma – Includes cerebral contusions and lacerations – Both injuries represent severe trauma to the brain
- 17. Head Injury • Major head trauma – Contusion • The bruising of brain tissue within a focal area that maintains the integrity of the pia mater and arachnoid layers associated with multiple micro-hemorrhages, small vessel bleed into brain tissue – Lacerations • Involve actual tearing of the brain tissue • Intracerebral hemorrhage is generally associated with cerebral laceration
- 18. Head Injury Cerebral Contusion Cerebral Laceration
- 19. Head Injury Pathophysiology • Diffuse axonal injury (DAI) – Widespread axonal damage occurring after a mild, moderate, or severe TBI – Seen in half the cases of head injury – Process takes approximately 12-24 hours
- 20. Head Injury Pathophysiology • Diffuse axonal injury (DAI) – Clinical signs: ∀↓ Level of Consciousness ∀↑ ICP • Decerebration or decortication • Global cerebral edema • 90% regain consciousness from severe DAI
- 21. Intracranial Hemorrhage Extra- axial hemorrhage • Epidural hematoma • Subdural hematoma- Acute Chronic • Subarachnoid hemorrhage Intra-axial hemorrhage • Intra-parenchymal hemorrhage • Intra-ventricular hemorrhage
- 22. Epidural hematoma – Results from bleeding between the dura and the inner surface of the skull – MC type of traumatic Intracranial bleed, rarely occurs spontaneously – A neurologic emergency – Bleed is Venous or arterial origin
- 23. Epidural hematoma Source of Bleed : Temperoparietal locus (most likely) - Middle meningeal artery Frontal locus - anterior ethmoidal artery Occipital locus - transverse or sigmoid sinuses Vertex locus - superior sagittal sinus Clinical Features: • LOC>>> Lucid Interval >> unconsciousness • s/s of raised ICP • Focal neurological deficit • s/s of cerebral herniation
- 24. Subdural hematoma – Occurs from bleeding between the dura mater and arachnoid layer of the meningeal covering of the brain – Source of bleed: Bridging veins; May be caused by an arterial hemorrhage – Much slower to develop into a mass large enough to produce symptoms. Cause: Acceleration-deceleration injury, direct trauma, Risk factors: Elderly, dementia, alcoholics, shaken baby syndrome, pts on anticoagulants
- 25. Subdural hematoma – Acute subdural hematoma(<72hrs) • High mortality • Associated with major direct trauma (Shearing Forces) Clinical Features: Headache, fluctuating LOC, confusion, dilated fixed pupil, deviated gaze CT scan: hyperdense
- 26. Subdural hematoma – Subacute subdural hematoma • Occurs within 4-21 days of the injury • Failure to regain consciousness may be an indicator CT scan: Isodense or hypodense – Chronic subdural hematoma(>3wks) • Develops over weeks or months after a seemingly minor head injury, probably from repeat minor bleeds CT scan : hypodense
- 27. Epidural and Subdural HematomasEpidural and Subdural Hematomas Fig. 55-15 Epidural Hematoma Subdural Hematoma
- 28. Epidural and Subdural HematomasEpidural and Subdural Hematomas Hematoma type Epidural Subdural Location Between the skull and the dura Between the dura and the arachnoid Involved vessel Temperoparietal (most likely) - Middle meningeal artery Frontal - anterior ethmoidal artery Occipital - transverse or sigmoid sinuses Vertex - superior sagittal sinus Bridging veins Symptoms Lucid interval followed by unconsciousness Gradually increasing headache and co nfusion CT appearance Biconvex lens- limited by suture lines Crescent shaped- crosses suture lines Fig. 55-15
- 29. Subarachnoid Hemorrhage Causes: • Rupture of Berry aneurism(MCC) • Trauma (fracture at the base of the skull leading to internal carotid aneurysm) • Amyloid angiopathy • Blood dyscrasias • Vasculitis Clinical Features: • Explosive or thunderclap headache, “worst headache of my life”, • nausea and vomiting, decreased LOC or coma. • Signs of meningeal irritation
- 30. Intracerebral Hemorrhage (ICH) Intracranial hemorrhage is hemorrhage that occurs within the brain tissue itself; an intra-axial hemorrhage. Two main types: 1)Intraparencymal hemorrahge- ICH extending into brain parenchyma; MCC- HTNsive vasculopathy 2)Intra-ventricular hemorrhage- ICH extending into ventricles; MCC –trauma Causes: Hypertensive vasculopathy(70-80%) Ruptured AVM Trauma Blood dyscracias
- 31. Intracerebral Hemorrhage (ICH) Clinical presentation: Rapidly progressive severe headache, building over several minutes, often accompanied by focal neurological deficits, nausea and vomiting, decreased level of consciousness. S/S depend site of hemorrhage: Basal ganglia/internal capsule - hemiparesis, dysphasia Cerebellum - ataxia, vertigo Pons - cranial nerve deficits, coma Cerebral cortex - hemiparesis, hemisensory loss, hemianopsia, dysphasia
- 32. Complications • Neurological deficits or death • Seizures • Obstructive Hydrocephalus • Spasticity • Urinary complications • Aspiration pneumonia • Cushing’s ulcer • Neuropathic pain • Deep venous thrombosis • Pulmonary emboli • Cerebral herniation
- 33. Cerbral Herniation Brain herniation is a deadly side effect of very high intracranial pressure that occurs when a part of the brain is squeezed across structures within the skull. “Brain herniation represents mechanical displacement of normal brain relative to another anatomic region secondary to mass effect from traumatic, neoplastic, ischemic, or infectious etiologies. “
- 34. Cerbral Herniation Supratentorial herniation 1. Uncal 2. Central (transtentorial) 3. Cingulate (subfalcine) 4. Transcalvarial Infratentorial herniation 5. Upward (upward cerebellar or upward transtentorial) 6. Tonsillar (downward cerebellar)
- 35. Cingulate Herniation The most common type, the innermost part of the frontal lobe is scraped under part of the falx cerebri, the dura mater at the top of the head between the two hemispheres of the brain. Cingulate herniation can be caused when one hemisphere swells and pushes the cingulate gyrus by the falx cerebri. Cingulate herniation is frequently believed to be a precursor to other types of herniation
- 36. Uncal Herniation common subtype of cerebral herniation following raised ICP Innermost part of the temporal lobe, the uncus, can be squeezed so much that it moves towards the tentorium and puts pressure on the brainstem, most notably the midbrain Clinical feature: • Compression of I/L CN III- I/L fixed dilted pupil • Compression of I/L PCA- C/L homonymous hemianopsia • Compression of C/L crus cerebri- I/L hemiparesis • Duret hemorrhage
- 37. Diagnostic Studies CT scan – • A GCS score less than 15 after blunt head trauma warrants a patient with no intoxicating consideration of an urgent CT scan.
- 38. CT findingsCT findings Fig. 55-15 Epidural Hematoma Subdural Hematoma
- 39. CT findingsCT findings Fig. 55-15 Subarachnoid hemorrhage Intracerebral hematoma
- 40. Diagnostic Studies • MRI – superior for demonstrating the size of an acute subdural hematoma. • Cerebral angiogram if hemorrhage is confirmed (not necessary in case of classic hypertensive hemorrhage • Cervical spine X-ray • EEG • Lumbar Pucture
- 41. Management 1) Supportive Measures: • Endotracheal intubation for patients with decreased level of consciousness and poor airway protection. • Cautiously lower blood pressure to a MAP less than 130 mm Hg, but avoid excessive hypotension.[10] • Rapidly stabilize vital signs, and simultaneously acquire emergent CT scan. • Maintain euvolemia, using normotonic rather than hypotonic fluids, to maintain brain perfusion without exacerbating brain edema • Avoid hyperthermia. • Facilitate transfer to the operating room or ICU.
- 42. Management 2) Decrease cerebral edema: • Modest passive hyperventilation to reduce PaCO2 • Mannitol, 0.5-1.0 gm/kg slow iv push • Furosemide 5-20 mg iv • Elevate head 20-30 degrees, avoid any neck vein compression • Sedate and paralyze if necessary with morphine and vecuronium (struggling, coughing etc will elevate intracranial pressure)
- 43. Management 3) Surgical Evacuation of hematoma: • No surgical intervention if collection <10ml Indication of surgical decompression: • The GCS score decreases by 2 or more points between the time of injury and hospital evaluation • The patient presents with fixed and dilated pupils • The intracranial pressure (ICP) exceeds 20 mm Hg Exception : In Subdural hematoma with GCS=15- hematoma >10mm ,or >5mm midline shift ---- requires Surgical decompression SAH: whn a cerebral aneurysm is identified on angiography, clipping and coiling is done to prevent re-bleed
- 44. Management Sugical Decompression contd.. Types: • Burr-hole • Craniotomy- bone flap is temporarily removed from the skull to access the brain • Craniectomy – in which the skull flap is not immediately replaced, allowing the brain to swell, thus reducing intracranial pressure • Cranioplasty - surgical repair of a defect or deformity of a skull.
- 45. Management 4) Medical therapy: • Antihypertensives - reduce blood pressure to prevent exacerbation of intracerebral hemorrhage in hypertensive encephalopathy. Eg Nicardipine, labetolol; CCB help relieve vasospasm in SAH and decrease further damage • Diuretics - Mannitol, CAI • Anticonvulsants – reduce frequency of seizures and prophylaxis of seizures eg: Fosphenytoin • Antipyretics- to Rx fever and pain relief eg: Acetaminophene • Antidote- VitK/FFP for warfarin overdose; protamine for heparin overdose • Antacids- prophylaxis for Cushing’s gastric ulcer eg: Famotidin • Glucorticoids may help reduce the head and neck ache caused by the irritative effect of the subarachnoid blood.
- 46. Preventive Measures Health Promotion • Prevent car and motorcycle accidents • To Wear safety helmets
- 47. Rehabilitation Ambulatory and Home Care • Nutrition • Bowel and bladder management • Spasticity • Dysphagia • Seizure disorders • Family participation and education
- 48. References: • Harrison's Principles of Internal Medicine • Medscape Reference http://emedicine.medscape.com • US National Library of Medicine National Institutes of Health http://www.ncbi.nlm.nih.gov
Notas del editor
- A skull fracture is a break in one or more of the eight bones that form the cranial portion of the skull, usually occurring as a result of blunt force trauma. Linear skull fractures are breaks in the bone that transverse the full thickness of the skull from the outer to inner table, are usually fairly straight and involve no displacement of the bone A depressed skull fracture is a type of fracture usually resulting from blunt force trauma, such as getting struck with a hammer, rock or getting kicked in the head. These types of fractures, which occur in 11% of severe head injuries, are comminuted fractures in which broken bones are displaced inward. Diastatic fractures occur when the fracture line transverses one or more sutures of the skull causing a widening of the suture Basilar skull fractures, are basically linear fractures that occur in the floor of the cranial vault (skull base), which require more force to cause than other areas of the neurocranium. Thus they are rare, occurring as the only fracture in only 4% of severe head injury patients. A fracture which occurs in conjunction with an overlying laceration which tears the epidermis and the meninges or runs through the paranasal sinusesand the middle ear structures, resulting in the outside environment being in contact with the cranial cavity is termed a compound fracture. A compound elevated skull fracture is a rare type of skull fracture where the fractured bone is elevated above the intact outer table of the skull A growing skull fracture (GSF) also known as a craniocerebral erosion or leptomeningeal cyst[14] due to the usual development of a cystic mass filled with cerebrospinal fluid is a rare complication of head injury usually associated with linear skull fractures of the parietal bone in children under 3.
- other than a fracture at the vertex that might be missed by CT scan and picked up by a plain film, skull x-ray is of no benefit when a CT scan is obtained. CT scan is the criterion standard modality for aiding in the diagnosis of skull fractures : MRI or magnetic resonance angiography is of ancillary value for suspected ligamentous and vascular injuries.
- Role of surgery is limited in the management of skull fractures. Infants and children with open depressed fractures require surgical intervention. At times, craniectomy is performed if the underlying brain is damaged and swollen.
- is the most common type of traumatic brain injury.
- is the most common type of traumatic brain injury.
- the pia-arachnoid membranes are torn over the site of injury in laceration and are not torn in contusion. Cerebral lacerations usually accompany other brain injuries and are often found with skull fractures on both sides of the head common in penetrating and perforating head trauma
- the pia-arachnoid membranes are torn over the site of injury in laceration and are not torn in contusion. Cerebral lacerations usually accompany other brain injuries and are often found with skull fractures on both sides of the head common in penetrating and perforating head trauma
- Diffuse axonal injury (DAI) is one of the most common and devastating types of traumatic brain injury,[1] meaning that damage occurs over a more widespread area than in focal brain injury. DAI, which refers to extensive lesions in white matter tracts, is one of the major causes of unconsciousness and persistent vegetative state after head trauma.[2] It occurs in about half of all cases of severe head trauma and also occurs in moderate and mildbrain injury.[3] the major cause of damage in DAI is the disruption of axons, the neural processes that allow one neuron to communicate with another.
- Often due to trauma, the condition is potentially deadly because the buildup of blood may increase pressure in the intracranial space, compress delicate brain tissue, and cause brain shift. The condition is present in one to three percent of head injuries.[1] Between 15 and 20% of epidural hematomas are fatal .Epidural hematoma is usually found on the same side of the brain that was impacted by the blow, but on very rare occasions it can be due to a contrecoup injury.[1]
- After the epidural hematoma begins collecting, it starts to compress intracranial structures which may impinge on the CN III.[3] This can be seen in the physical exam as a fixed and dilated pupil on the side of the injury.[3] The eye will be positioned down and out, due to unopposed CN IV and CN VI innervation. a lucid interval is a temporary improvement in a patient&apos;s condition after a traumatic brain injury, after which the condition deteriorates. A lucid interval is especially indicative of an epidural hematoma. An estimated 20 to 50% of patients with epidural hematoma experience such a lucid interval
- As the brain shrinks with age, the subdural space enlarges and the veins that traverse the space must travel over a wider distance, making them more vulnerable to tears.
- Acute subdural hematomas are less than 72 hours old and are hyperdense compared with the brain on computed tomography scans. The subacute phase begins 3-7 days after acute injury; the surgical literature favors 3 days, whereas the radiological literature favors 7. Subacute subdural hematomas are isodense or hypodense compared with the brain. Chronic subdural hematomas are 21 days (3 wk) or older and are hypodense compared with the brain. However, subdural hematomas may be mixed in nature, such as when acute bleeding has occurred into a chronic subdural hematoma.
- kinds
- kinds
- Central herniation In central herniation, the diencephalon and parts of the temporal lobes of both of the cerebral hemispheres are squeezed through a notch in the tentorium cerebelli.[5][7] . [edit]Cingulate herniation Subfalcine herniation on CT In cingulate or subfalcine herniation, the most common type, the innermost part of the frontal lobe is scraped under part of the falx cerebri, the dura mater at the top of the head between the two hemispheres of the brain.[5][8] Cingulate herniation can be caused when one hemisphere swells and pushes the cingulate gyrus by the falx cerebri.[4] This does not put as much pressure on the brainstem as the other types of herniation, but it may interfere with blood vessels in the frontal lobes that are close to the site of injury (anterior cerebral artery), or it may progress to central herniation.[5]Interference with the blood supply can cause dangerous increases in ICP that can lead to more dangerous forms of herniation.[9] Symptoms for cingulate herniation are not well defined.[9] Usually occurring in addition to uncal herniation, cingulate herniation may present with abnormal posturingand coma.[4] Cingulate herniation is frequently believed to be a precursor to other types of herniation.[9] [edit]Transcalvarial herniation In transcalvarial herniation, the brain squeezes through a fracture or a surgical site in the skull.[4] Also called &quot;external herniation&quot;, this type of herniation may occur during craniectomy, surgery in which a flap of skull is removed, preventing the piece of skull from being replaced.[1] [edit]Upward herniation Increased pressure in the posterior fossa can cause the cerebellum to move up through the tentorial opening in upward, or cerebellar herniation.[5] Themidbrain is pushed through the tentorial notch. This also pushes the midbrain down. [edit]Tonsillar herniation In tonsillar herniation, also called downward cerebellar herniation,[4] or &quot;coning&quot;, the cerebellar tonsils move downward through the foramen magnum possibly causing compression of the lower brainstem and upper cervical spinal cord as they pass through the foramen magnum.[5] Increased pressure on the brainstem can result in dysfunction of the centers in the brain responsible for controlling respiratory and cardiac function.
- Subfalcine herniation on CT In cingulate or subfalcine herniation, the most common type, the innermost part of the frontal lobe is scraped under part of the falx cerebri, the dura mater at the top of the head between the two hemispheres of the brain.[5][8] Cingulate herniation can be caused when one hemisphere swells and pushes the cingulate gyrus by the falx cerebri.[4] This does not put as much pressure on the brainstem as the other types of herniation, but it may interfere with blood vessels in the frontal lobes that are close to the site of injury (anterior cerebral artery), or it may progress to central herniation.[5]Interference with the blood supply can cause dangerous increases in ICP that can lead to more dangerous forms of herniation.[9] Symptoms for cingulate herniation are not well defined.[9] Usually occurring in addition to uncal herniation, cingulate herniation may present with abnormal posturingand coma.[4] .[9] [edit]Transcalvarial herniation In transcalvarial herniation, the brain squeezes through a fracture or a surgical site in the skull.[4] Also called &quot;external herniation&quot;, this type of herniation may occur during craniectomy, surgery in which a flap of skull is removed, preventing the piece of skull from being replaced.[1] [edit]Upward herniation Increased pressure in the posterior fossa can cause the cerebellum to move up through the tentorial opening in upward, or cerebellar herniation.[5] Themidbrain is pushed through the tentorial notch. This also pushes the midbrain down. [edit]Tonsillar herniation In tonsillar herniation, also called downward cerebellar herniation,[4] or &quot;coning&quot;, the cerebellar tonsils move downward through the foramen magnum possibly causing compression of the lower brainstem and upper cervical spinal cord as they pass through the foramen magnum.[5] Increased pressure on the brainstem can result in dysfunction of the centers in the brain responsible for controlling respiratory and cardiac function.
- Central herniation In central herniation, the diencephalon and parts of the temporal lobes of both of the cerebral hemispheres are squeezed through a notch in the tentorium cerebelli.[5][7] Transtentorial herniation can occur when the brain moves either up or down across the tentorium, called ascending and descending transtentorial herniation respectively; however descending herniation is much more common.[1] Downward herniation can stretch branches of the basilar artery (pontine arteries), causing them to tear and bleed, known as a Duret hemorrhage. The result is usually fatal.[7]Radiographically, downward herniation is characterized by obliteration of the suprasellar cistern from temporal lobe herniation into the tentorial hiatus with associated compression on the cerebral peduncles. Upwards herniation, on the other hand, can be radiographically characterized by obliteration of the quadrigeminal cistern. Intracranial hypotension syndrome has been known to mimic downwards [edit]Transcalvarial herniation In transcalvarial herniation, the brain squeezes through a fracture or a surgical site in the skull.[4] Also called &quot;external herniation&quot;, this type of herniation may occur during craniectomy, surgery in which a flap of skull is removed, preventing the piece of skull from being replaced.[1] [edit]Upward herniation Increased pressure in the posterior fossa can cause the cerebellum to move up through the tentorial opening in upward, or cerebellar herniation.[5] Themidbrain is pushed through the tentorial notch. This also pushes the midbrain down. [edit]Tonsillar herniation In tonsillar herniation, also called downward cerebellar herniation,[4] or &quot;coning&quot;, the cerebellar tonsils move downward through the foramen magnum possibly causing compression of the lower brainstem and upper cervical spinal cord as they pass through the foramen magnum.[5] Increased pressure on the brainstem can result in dysfunction of the centers in the brain responsible for controlling respiratory and cardiac function.
- Patients with possible subdural hematoma should be examined for related injuries (using guidelines established by the American College of Surgeons Committee on Trauma), such as cervical spine fracture, spinal cord injury, or long-bone fractures. Although magnetic resonance imaging (MRI) is superior for demonstrating the size of an acute subdural hematoma and its effect on the brain, noncontrast head CT is the primary means of making a diagnosis and suffices for immediate management purposes.
- Early treatment in patients presenting with spontaneous intracerebral hemorrhage is important as it may decrease hematoma enlargement and lead to better neurologic outcome
- Stupor is a state of partial or near complete unconsciousness in which the patient is lethargic, immobile, and has a reduced response to stimuli.[3] Coma is a state in which the patient is totally unconscious and cannot be aroused even with strong stimuli.[4] Persistent vegetative state is a condition in which awake patients are unconscious and unaware of their surroundings and the cerebral cortex is not functioning.[5] A vegetative state can result from diffuse injury to the cerebral hemispheres of the brain without damage to the lower brain and brainstem. The vegetative state is considered permanent if it persists for 12 months after TBI or 3 months after causes other than trauma.[6] A minimally conscious state is a condition in which patients have a reduced level of arousal and may appear, on the surface, to be in a persistent vegetative state but are capable of demonstrating the ability to actively process information. Locked-in syndrome is a condition in which a patient is aware and awake, but cannot move or communicate due to complete paralysis of the body.[7] Voluntary control of eye movements or blinking may be spared, permitting the detection of conscious awareness and enabling the establishment of functional communication.[7] Brain death is the irreversible loss of measurable brain function, with loss of any integrated activity among distinct areas of the brain.[8] Breathing and heart function must be maintained with assistive devices.[8] Disorders of consciousness affect a significant number of people who suffer severe TBI; of those with severe TBI discharged from a hospital, 10-15 are in a vegetative state, and of this number only half regain consciousness within one to three years.[6]