Head Injury (Traumatic Brain Injury) - types, complications and management

this presentation provides in-depth knowledge regarding head injuries, types of head injuries their complications, and management. management is discussed from medical, surgical, and nursing points of view.

1. Head injury (traumatic brain injury) Medical-Surgical Nursing Viresh Sunil Mahajani M. Sc Medical Surgical Nursing (Cardiovascular and Thoracic Nursing) Institute of Nursing Education, Mumbai

2. Anatomical review Neurons Primary functional unit of nervous system. Three main characteristics Excitability Conductivity Influence Three main parts- Cell body Multiple dendrites An axon

3. Cell body contains nucleus and cytoplasm. It is the metabolic centre of neuron. Dendrites are the short processes that extends from cell body. They receive impulses or signals from other neurons. Axons are the long projections that extends from cell body. They carry impulses away from the cell body towards other neurons or end organs like smooth muscles, striated muscles and glands. These axons may be mylinated or unmylinated . Myline sheet is a white lipoprotein substance that acts as an insulator For conduction of impulses.

4. Glial cells/ Neuroglial cells Supporting cells of the Nervous system. Provide support, protection and nourishment to the neurons of the nervous system. Constitutes almost half of the mass of brain and spinal cord. Two types – Microglial cells and Macroglial cells.

5. Microglial cells – Microphage of nervous system. Capable of phygocytosis Mobile with in brain. Capable of multiplication when brain injury occurs. Macroglial cells – Three types- Astrocytes, oligodendrocytes, ependymal cells. Astrocytes – Found in gray matter Provide structural support to neurons Forms blood brain barrier along with endothelium of blood vessels Plays important role in synaptic transmissions.

6. Oligodendrocytes – Found in white matter Specialized cell that helps to produce myline sheet of nerve fibers in CNS. Schwann cells produce same action in peripheral nervous system.

7. Ependymal cells – Present along the lines of brain ventricles
Aids in secretion of cerebrospinal fluid.

8. Most of the primary CNS tumors are of glial cells. Primary malignancy of neurons are reare .

9. Brain

10. Brain has three major intracranial components – Cerebrum Cerebellum Brain stem

11. Cerebrum Cerebrum is divided into left and right hemisphere. Each hemisphere is divided into four lobes – frontal, parietal, temporal and occipital lobe. Frontal lobe controls higher cognitive function, memory, concentration, voluntary movement and motor functions. Frontal lobe contains broca’s area that controls speech production. Parietal lobe contains sensory cortex that interprets Spatial information Occipital lobe processes information related to sight Temporal lobe processes somatic, visual and auditory data.

12. Mid brain Med brain is located in the inner side of the cerebrum. It consists of basal ganglia, thalamus, hypothalamus and limbic system.

13. Basal ganglia Located centrally to cerebrum and mid brain. Responsible for initiation, execution and completion of voluntary movement, learning, emotional response and autonomic movements like salivation, blinking and swinging hands while walking. Thalamus Placed just above the brain stem. Major relay centre for sensory input from the body, face, Retina, cochlear and taste receptors. Motor relay centre that connects cerebellum and basal ganglia to frontal cortex. Hypothalamus Located inferior to thalamus, in front of midbrain. Exert direct influence on release of pituitary hormones.

14. Hypothalamus It also contains center for regulation of appetite, body temperature, water regulation, circadian rhythm and expression of emotions. Limbic system Located neart the inner surface of cerebral hemisphere Responsible for emotional responses, feeding behaviour, and sexual behaviour.

15. Brain stem

16. Brain stem It consists of midbrain, pons and medulla oblongata. It is the nuclei of cranial nerve III to nerve XII. Vital centre for respiratory, vasomotor and cardiac functions. Contains reticular system that facilitates communication among brain stem, reticular formation and cerebral cortex. Functions of reticular system is to relay sensory information, influence the excitatory and inhibitory control of spinal motor neurons amd controlling vasomotor and respiratory activity. Brain stem also contains center for regulating arousal and sleep wake transition. It also contains center for sneezing, coughing, hiccups, vomiting, sucking and swallowing.

17. It is located in posterior cranial fossa. It co-ordinates voluntary movements and maintaine trunk stability and equilibrium. It receives information from cerebral cortex, muscles, joints, and inner ear. It influences motor activity through axonal connection to thalamus, motor cortex and brain stem and descending pathways. Cerebellum

18. Ventricles and cerebrospinal fluid

19. Brain contains four interconnected fluid filled cavities called ventricles. This cavity extends centrally through the full length of the spinal cord. This cavity is filled with the fluid called as cerebrospinal fluid. Avarage volume of CSF is 150 ml. CSF is produced by chlorid plexuses located within fourth ventricle of the brain. Avarage rate of CSF production is 500 ml/day Absorption of CSF occurs through arachinoid villiv that are located within subarachnoid space.

20. Cerebral circulation

21. Blood supply to the brain is supplied by Internal carotid arteries Vertebral arteries Internal carotid artery on entering into cranial cavity splits into two branches –anterior cerebral artery and medial cerebral artery. Anterior cerebral artery supplies blood to the medial and frontal portion of frontal lobe. Mid cerebral artery supplies blood to the outer portion of frontal lobe, parietal lobe and superior temporal lobe. Two vertibral arteries join to form basilar artery. Basilar arteries are joined to left and right internal carotid arteries by posterior communicating arteries.

22. Both left and right internal carotid arteries are joined anteriorly by anterior communicating artery. From the posterior communicating arteries arises posterior cerebral arteries. Posterior cerebral arteries supplies blood to the medial portion of occipital lobe and inferior temporal lobe. The structure formed by internal carotid arteries, anterior and posterior communicating arteries and basilar artery resembles the circular structure. This structure is called as circle of Willis. This structure is considered as a safety valve for blood flow.

23. Meninges Meninges are the protective membranes that surrounds brain and spinal cord. There are three layers of meninges – Dura matter, Arachinoid matter and pia matter.

24. Dura matter is the thick outermost layer of meninges. The space between dura matter and arachinoid matter is called subdural space. Arachinoid layer is the fragile web like membrane that lies between dura matter and pia matter. It is vascular inner most layer of meninges. The space between arachinoid matter and pia matter is called as subarachnoid space. This space is filled with CSF. Pia matter is the innermost layer of the meninges.

25. Skull Skull is the protective compartment in which brain lies . Skull is made up of 8 cranial bones and 14 facial bones 8 cranial bones are- Frontal bones- 1 Parietal bones -2 Temporal bones-2 Occipital bone-1 Ethmoid bone-1 Sphenoid bone-1 Cranium is the safety Vault of the brain that protects brain from external injury.

26. Head injury

27. Head injury Any injury or trauma to the scalp skull or the brain tissue is referred as head injury. It is broader term used to describe any damage to the head region as a result of trauma. Head injury can be classified as – Scalp laceration Skull fracture Traumatic brain injury.

28. Scalp laceration Scalp is a soft tissue that covers to the cranial vault. Scalp is made up of 5 layers S- Skin C- Connective tissue A- Aponeurosis and muscle L- Losse Areolar tissue P- Periosteum Laceration is a type of injury caused due to blunt trauma causing tear of skin and underlying tissue. Scalp laceration refers to the injury to the scalp due to the trauma.

29. As scalp contains many blood vessels with poor constrictive abilities most scalp laceration are associated with profused bleeding. Thus a large size scalp laceration can be life threatening and should be treated as emergency. Such scalp wounds can be potential portals of entery for organisms that can lead to intracranial infection. Therefore is such patient arrived in emergency department, wounds should be irrigated properly before suturing to remove foreign bodies and to reduce the risk of infection.

30. Skull fracture Fracture of the bones of the skull bones is called as skull fracture. Skull fracture can be described as – Linear or depressed fracture Simple, comminuted or compound fracture Closed fracture or open fracture Type of fracture depends on velocity, momentum, direction and shape of injury causing agent and site of impact.

31. Head injury (traumatic brain injury) Injury to the brain tissue is referred as tarumatic brain injury. Brain injuries are mainly of two types depending on gross involvement of brain tissue in the injury. Diffuse injury (Generalized brain injury) Focal injury (Localised brain injury) Brain injury is also classified as minor, moderate and sever injury.

32. Diffuse injury When damage to the brain tissue cannot be localized to any one particular area then such a injury is referred as diffuse brain injury. There are two main types of diffused brain tissue injury – Concussion Diffuse axonal injury.

33. Concussion A sudden transient mechanical head injury with disruption of neural activity and a change in level of consciousness is called concussion. Concussion is a minor head injury. Typical signs of concussion are- Brief disturbance of level of consciousness Amnesia regarding the event Headache All these symptoms last for very short duration of time. One the symptoms are resolved,the patient is discharged from the medial facility with an instruction to notify the health care provider if any symptoms persist or any behavioural changes occur.

34. Post concussion syndrome – In some patients with history of concussion, symptoms such as headache, lethargy, personality and behavioural changes, shortening of attention span, decreased short term memory and changes in intellectual abilities may persist for the period from 2 weeks to 2 months . Appearance of such symptoms is referred as post concussion syndrome. This syndrome can affect the patient’s ability to perform activities of daily living.

35. Diffuse axonal injury Widespread axonal damage occuring after mild, moderate or sever head injury is referred as diffuse axonal injury. Such a damage is mostly found around the axons of the subcortical white matter of cerebral hemisphere, basal ganglia, thalamus and brain stem region. During DAI, trauma changes the functioning of the axons, resulting in to axona swelling and disconnection of the axons. All this phenomenon occurs approximately 12-24 hours after the trauma and may persist longer.

36. Clinical manifestations of DIA Decreased level of consciousness Global cerebral edema Increased intracranial pressure Decortication and decerebration Aproximately 90% of patients with DAI remains in persistent vegitative state.

37. Focal injury Injury to the any one perticular part of the brain can be termed as focal injury. Focal injury can be in form of laceration of brain tissue, contusion, hematomas, and cranial nerve injury. Laceration – Actual tearing of the brain tissue is called as laceration of brain tissue. Contusion – bruising of the brain tissue within focal area is called as contusion. Hematomas – Collection of blood and formation of blood clots within or outside the brain tissue, or meninges is called hematomas.

38. Laceration of brain tissue Actual tearing of the brain tissue is called as laceration of brain tissue. It is usually associated with the depressed and open fracture and the penetrating injuries. In such conditions, tissue damage is sever and surgical repair is impossible, because of non regenerative nature of brain tissue. Cerebral laceration may result into intracerebral hemorrhage , followed by hematoma formation and cerebral edema and seizure. Such an hematoma is manifested as space occupying lesion, accompanied by unconscious, hemiplaai on contralateral side and dilated pupils on ipsilateral sides. As hematoma expands signs of increased ICP becomes more severe.

39. Laceration brain injury Tissue damage Haemorrhage from laceration Cerebral oedema Formation of Hematoma Compression of blood vessels Increased intracranial pressure Decreased blood flow to brain. Compression of blood vessels Decrease blood and oxygen supply to brain. Death of brain cells Edema around necrotic cells Further Increase In ICP

40. Compression of brain stem and respiratory centre Accumulation of CO2 Vasodilation Increased blood flow to brain Further increase in ICP DEATH

41. Contusion Bruising of the brain tissue with in the focal area is called as Contusion. It is usually associated with the closed head injury . Contusion is usually contain areas of hemorrhage , infraction, necrosis and edema . It frequently occurs alon the site of fracture. In contusion often the phenomenon of coup and countrecoup injury occurs.

42. Coup and countercoup injury The high energy or high impact injury that occurs due to Brain moving inside the skull can be called as Coup and countercoup injury. In such injury, damage (contusion or laceration) is found in two or more areas. Primarily in the area of direct impact of brain on skull (Coup) and secondary on the opposite side of the primary injury due to bounce back action of the brain within cranial cavity (countercoup). Such a patient show’s multiple contusion sites during radiological studies. Such injuries are often severe and overall prognosis of such patient’s is always poor.

43. Contusions may bleed, rebleed leading to the formation of hematoma, increase in ICP, increased cerebral edema and finally leading to death of brain tissue if not managed properly within short period of time. Patients may also exhibit symptoms of convulsions.

44. Complications of Head injury Epidural hematoma Subdural hematoma Intracerebral hematoma

45. Epidural hematoma

46. Epidural hematoma Hematomas formed due to bleeding between dura matter and the skull’s inner surface is referred to as Epidural Hematoma. Approximately about 2 % to 4% of traumatic brain injuries are Epidural Hematomas. It us usually associated with the linear fracture crossing major arteries in dural space. It can be arterial or venous in origin. If of venous origin hematoma develops slowly when compared to the arterial one. Initial clinical presentation of a patient with Epidural Hematoma is with the following complaint s- Initial loss of consciousness f/b decreased level of consciousness Headache Nausea and vomiting

47. Management of patients with Epidural Hematoma Conservative approach Sometimes the epidural hematoma may be small enough not to generate or increase any kind of Intracranial pressure. It is recommended that patients who exhibit an EDH that measures less than 30 mL, is less than 15 mm thick, and has less than 5-mm midline shift, with no focal neurologic deficit and with GCS greater than 8, can be treated nonoperatively with medication. Such hematoma can be managed conservatively by allowing the body to respond and absorb the hematoma. Such patients are needed to be monitored closely for any emergency new symptoms related to increased ICP. Repeated CTs are advised to observe the growth or reduction in the size of the hematoma and decisions are taken as per.

48. Medical management Osmatic diuretic (mannitol) to reduce increasing Intracranial pressure. Monitoring and Maintaining fluid and electrolyte levels within normal limits. Antiepileptic drugs to prevent incidents of convulsions. Corticosteroid to prevent inflammation due to injury Surgical management Surgical management includes rapid intervention to evacuate the hematoma and prevent cerebral herniation. Craniotomy and hematoma evacuation are done for Surgical removal of hematoma and reducing ICP

49. Subdural hematoma on CT

50. Subdural hematoma Hematoma formed between dura mater and arachnoid matter i.e. within the subdural space is referred to as a subdural hematoma It usually results due to injury to the brain tissue and its blood vessels. Approximately 50% of brain injuries and 60% of deaths are due to SDH. Most of the Subdural hematomas are formed due to injury to the veins that drain blood from the surface of the brain to the sagittal sinuses. As being venous in origin, subdural hematomas are mostly slow growing. Size of the hematoma mostly determines the clinical presentation and prognosis of the patient. It is often observed that the injury causing subdural hematoma may also cause Brain injury and may lead to cerebral edema. Resulting in increased ICP and increased risk of morbidity and mortality.

51. Subdural hematomas are classified as – Acute subdural hematoma –It develops within 24-48 hours after injury. Subacute Subdural hematoma –It develops 2 to 14 days after the injury. Chronic subdural hematoma –It develops over weeks or months after a seemingly minor head injury.

52. Intracranial hematoma

53. Intravertebral hematoma Bleeding and formation of hematoma with the brain tissue is called as intracerebral injury. Approximately 16% of traumatic brain injuries are intracerebral injuries. ICH mostly occurs in the frontal and temporal lobes of the brain.

54. Diagnostic studies CT scan MRI XRAY

55. Nursing Management

56. Nursing assessment Glasgow coma scale Vital signs Neurological examination Systemic examination Determining CSF leaking

57. Possible nursing diagnosis Ineffective airway clearance Impaired gas exchange Risk of ineffective tissue perfusion Deficit fluid volume Imbalance nutrition Risk of injury Risk of impaired skin integrity Disturbed sleep patterns Ineffective coping Knowledge deficient.

58. Recent research in traumatic brain injury management Prehospital Tranexamic Acid Use for Traumatic Brain Injury Primary aim: To determine the efficacy of two dosing regimens of TXA initiated in the prehospital setting in patients with moderate to severe TBI (GCS score ≤12). Primary hypothesis: The null hypothesis is that prehospital administration of either of two dosing regimens of TXA in patients with moderate to severe TBI will not increase the proportion of patients with a favorable long-term neurologic outcome compared to placebo, based on the GOS-E at 6 months. Secondary aims: To determine differences between TXA and placebo in the following outcomes for patients with moderate to severe TBI treated in the prehospital setting with 2 dosing regimens of TXA:

59. Clinical outcomes: ICH progression, DRS at discharge and 6 months, GOS-E at discharge, 28-day survival, frequency of neurosurgical interventions, and ventilator-free, ICU-free, and hospital-free days. Safety outcomes: Development of seizures, cerebral ischemic events, myocardial infarction, deep venous thrombosis, and pulmonary thromboembolism. Mechanistic outcomes: Alterations in fibrinolysis based on fibrinolytic pathway mediators and degree of clot lysis based on TEG. A multi-center double-blind randomized controlled trial with 3 treatment arms: Bolus/maintenance: 1 gram IV TXA bolus in the prehospital setting followed by a 1 gram IV maintenance infusion initiated on hospital arrival and infused over 8 hours. Bolus only: 2 grams IV TXA bolus in the prehospital setting followed by a placebo maintenance infusion initiated on hospital arrival and infused over 8 hours. Placebo: Placebo IV bolus in the prehospital setting followed by a placebo maintenance infusion initiated on hospital arrival and infused over 8 hours.

60. bibliography Lewis’s Medical-Surgical Nursing, Assessment, and Management of Clinical Problems, Volume -2, Fourth Edition, ELSEVIER Publication, Harding, Kwong , Robert, Hagler, Reinisch , Chintamani, Page No –1348-1355. Brunner and Suddharths , Textbook of Medical-Surgical Nursing, Volume -2, Edition –Second, Wolters Kluwer Publication, Suresh K. Sharma, S. Madhavi, Page No –1630-1644. Lippincott Manual of Nursing Practice, South Asian Edition, Sandra M. Nettinaand Suresh K Sharma, Wolters Kluwer Publication, page no-973-975. https://emedicine.medscape.com/article/248840-treatment#d9 https://my.clevelandclinic.org/health/diseases/21183-subdural-hematoma https://www.mayo.edu/research/clinical-trials/cls-20192462