Download as PDF, PPTX
![References
•
•
•
•
•
•
•
•
•
Principles and Practice of Surgery
Nelson Essentials of Pediatrics
Bailey and Love’s Short Practice of Surgery
MedlinePlus Medical Encyclopedia
Medscape
Lye CL, Shores EA. Traumatic brain injury as a risk factor for Alzheimer's
Disease: a review. Neuropsychology Rev. 2000;10:115–29. [PubMed] [Google
Scholar] [Ref list]
BMJ JOURNALS
Traumatic Brain Injury in the Accident and Emergency Department of a
Tertiary Hospital in Nigeria - J.K.C. Emejulu, C.M. Isiguzo, C.E. Agbasoga, C.N.
Ogbuagu. Department of Surgery, Nnamdi Azikiwe University Teaching Hospital,
Nnewi, Anambra State, South East NIGERIA.
Dhandapani S, Manju D, Sharma B, Mahapatra A. Prognostic significance of
age in traumatic brain injury. J Neurosci Rural Pract. 2012 May;3(2):131-5.
doi: 10.4103/0976-3147.98208. PMID: 22865961; PMCID: PMC3409980.](https://image.slidesharecdn.com/traumaticbraininjuryicupdf-220904144033-fbcaa852/75/TRAUMATIC-BRAIN-INJURY-ICUpdf-pdf-49-2048.jpg)
![General intensive care activities
•
•
•
Similar to other patients in the intensive care, TBI
victims should receive the usual daily care as
follows:
- Raising head of bed to 30° - 45°: that would
reduce ICP and improves CPP [125]; and lower the
risk of ventilator-associated pneumonia (VAP).
- Keeping the head and neck of the patient in a
neutral position: this would improve cerebral
venous drainage and reduce ICP.](https://image.slidesharecdn.com/traumaticbraininjuryicupdf-220904144033-fbcaa852/75/TRAUMATIC-BRAIN-INJURY-ICUpdf-pdf-96-2048.jpg)
![REFERENCES
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1. Brunner, L. S., Suddarth, D. S., Smeltzer, S. C. O., & Bare, B. G. (2004). Brunner &
Suddarth's textbook of medical-surgical nursing (10th ed.). Philadelphia: Lippincott
Williams & Wilkins.
2. Understanding Increased Intracranial Pressure Medically reviewed by Susan W. Lee,
DO
— Written by Elea Carey and Rachael Zimlich, RN, BSN on February 28, 2022,
available
on https://www.healthline.com/health/increased-intracranial-pressure
2. Shaikh F, Waseem M, Boling AM. Head Trauma (Nursing) [Updated 2022 May 15]. In:
StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-.
Available
on https://www.ncbi.nlm.nih.gov/books/NBK568699/](https://image.slidesharecdn.com/traumaticbraininjuryicupdf-220904144033-fbcaa852/75/TRAUMATIC-BRAIN-INJURY-ICUpdf-pdf-119-2048.jpg)
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- 1. TRAUMATIC BRAIN INJURY SURG SLTET DANS MEDICAL OFFICER ICU NNRH OJO
- 2. Outline • • • • • • • • Introduction/Definition Epidemiology Relevant anatomy andphysiology Aetiology Classification Pathophysiology Prognosis References
- 3. Introduction • • • • • Head injury isdefined as damage to the brain, skull, scalp or any other structure of the head as a result of a traumatic insult. While the term ‘head injury’ is most often associated with traumatic brain injury (TBI), head injuries also involves injury to the bones, muscles, blood vessels, skin, and other structures of the head. Head injury is one of the major reasons for emergency treatment and is associated with high mortality and disability. It is commonly caused by road traffic accidents (RTAs) Detection and classification of severity is difficult, making prognosis poor
- 4. Epidemiology • • • • • • – – – – – – – – Traumatic brain injury(TBI) is a leading cause of disability in all regions of the globe. 4 million people experience head trauma annually. The global incidence rate of TBI is estimated at 200 per 100 000 people per year; however, this rate is uncertain and a likely underestimate. Severe head injury is the most frequent cause of trauma death (75-80% mortality) In one study, Accident and Emergency Department (A&E) incidence rate was put at 2710 per 100,000 per year in our environment, far higher than the A&E figures of 453 and 394 per 100,000 per year for UK and US, respectively. Incidence in Lagos state is about 450/100000 per year. At Risk population: Males 15-24 Infants Young Children Elderly Low income individuals Unmarried individuals Individuals with a history of substance abuse Individuals who have suffered a previous TBI
- 5. Anatomy and physiology • • • • • • • • • • SCALP Highlyvascularised Protected by hair Made up of 5 layers: Skin Connective tissue (dense) Aponeurotic layer Loose connective tissue Periosteum of the skull Blood vessels are found in the dense connective tissue layer. Accounts for inability of the vessels to constrict when lacerated and thus makes the scalp prone to profuse bleeding
- 6. Anatomy and physiology • • • SKULL Bonystructure that covers and protects the brain Composed of eight bones separated by sutures: - Frontal - Parietal (2) - Occipital - Temporal (2) - Sphenoid - Ethmoid Temporal bone has three processes - Mastoid - Styloid - Zygomatic
- 8. Anatomy and physiology • • • • Brain Weighsabout 1.5 kg (apprx. 2 % of the total body mass) Composed of neurons, glial cells and blood vessels It is supplied by a network of vessels called the ‘circle of Willis’ It takes about 20-22% of the cardiac output and uses 20 % of total blood glucose supply.
- 9. Anatomy and physiology • • • • Thebrain has 4 lobes: frontal, parietal, temporal, occipital Has 4 ventricles: lateral (right and left), third and fourth ventricle Between the skull and the brain are the meninges (dura mater, arachnoid membrane, pia mater) Divided into 4 parts: cerebrum, diencephalon (thalamus, hypothalamus), brainstem (midbrain, pons, medulla oblongata), and cerebellum
- 10. Anatomy and physiology • • • • – – – Cranialvolume fixed Brain (80%) Blood vessels & blood (12%) CSF (8%) Increase in volume of one component compensates by decrease of another Inability to compensate = increased ICP Compensating for intracranial pressure Compress venous blood vessels Reduction in free CSF Brain herniation
- 11. Anatomy and physiology • • • – – • • • • • • Factorsaffecting ICP Intracranial vasculature Cerebral Edema Systemic Blood Pressure Low BP = Poor Cerebral Perfusion High BP = Increased ICP Reduced respiratory efficiency (hypoventilation) Carbon Dioxide Fever Pain Head posture Agitation
- 12. Anatomy and physiology • – • – – – – – • – Roleof Carbon Dioxide Increase of CO2 in CSF Cerebral Vasodilation Encourage blood flow Reduce hypercarbia Reduce hypoxia Contributes to ICP Reduced levels of CO2 in CSF Cerebral vasoconstriction Results in cerebral anoxia
- 13. Aetiology of headinjuries • • • • • • • • Mostly caused by RTAs Domestic falls Assault Sports-related injuries Recreational accidents Firearm- related injury Gunshot to the head Stab injuries
- 14. Classification of headinjury • Based on brain communication with external environment Closed - Skull not compromised and brain not exposed (dura mater intact) Open - Skull compromised and brain exposed (dura mater breeched)
- 15. Classification of headinjury • 1. 2. 3. 4. Based on mechanism: - Blunt Injury Baseball injury Motor vehicle collisions Assaults Falls - Crush injury - Penetrating Bullet or missile (gunshots, explosions) Sharp non-missile (stabbing)
- 16. Classification of headinjury • • • Classification based on anatomy Scalp Injuries Cranial Injuries Brain Injuries
- 17.
- 18. Scalp injuries • • Bleeds brisklydue to high vascularity Shock: children and adult with underlying pathology
- 19. Cranial Injury • Traumamust be extreme to fracture
- 20. Cranial Injury • – – – • Basal Skull Unprotected Spacesweaken structure Relatively easier to fracture Basal Skull Fracture Signs • • • • Battle’s sign Racoon eyes Bleeding from external orifices (eyes, ears, nose) CSF leakage (dura tear leading to CSF drainage through an external passageway) - CSF otorrhea (ear) - CSF rhinorrhea (nose) - CSF orbitorrhea (eye)
- 21. Cranial Injury • • • • • • Battle’s sign RetroauricularEcchymosis Associated with fracture of auditory canal and lower areas of skull Racoon eyes Bilateral Periorbital Ecchymosis Associated with orbital fractures
- 22. Basilar Skull Fracture Battle’ssign Raccoon eyes 22 Head Trauma -
- 23. Cranial Injury • – • – – Basilar Skull Fracture Maytear dura Permit CSF to drain through an external passageway May mediate rise of ICP Evaluate for “Target” or “Halo” sign
- 24. Crainial Injuries Penetrating trauma 24 HeadTrauma - Bullet fragments
- 25. Brain injury • • • • • • • The NationalHead Injury Foundation defines brain injuries as “a traumatic insult to the brain capable of producing physical, intellectual, emotional, social and vocational changes.” Classification: Direct Primary injury caused by forces of trauma Most primary injuries are from blunt trauma or from movement of brain inside skull Indirect Secondary injury caused by factors resulting from the primary injury
- 26. Brain injury • • • – • – Direct braininjury Immediate damage due to force Fixed at time of injury Coup force Injury at site of impact Contrecoup force Injury on opposite side from impact
- 27. Brain injury • – • • i. ii. • – • • • Direct BrainInjury Categories: Focal Occur at a specific location in brain Cerebral Contusion Intracranial Hemorrhage Epidural hematoma Subdural hematoma Intracerebral Hemorrhage Diffuse Pathology distributed throughout brain Concussion Moderate Diffuse Axonal Injury Severe Diffuse Axonal Injury
- 28. Focal Brain Injury • – – – – – – CerebralContusion Blunt trauma to local brain tissue Capillary bleeding into brain tissue Common with blunt head trauma Results from Coup-countercoup injury There is bruising of brain tissue leading to rapid and severe swelling. There is prolonged unconsciousness and confusion and amnesia is profound.
- 29. Brain Injuries • • • • • • • Cerebral contusion Bruisingof brain tissue Swelling may be rapid and severe Level of consciousness Prolonged unconsciousness, profound confusion or amnesia Associated symptoms Focal neurological signs May have personality changes 29 Head Trauma -
- 30. Focal Brain Injury • i. – – • – – IntracranialHemorrhage Epidural Hematoma Bleeding between dura mater and skull Involves arteries Middle meningeal artery most common Rapid bleeding & reduction of oxygen to tissues Herniates brain toward foramen magnum
- 31. Focal Brain Injury • • • • Acuteepidural hematoma Bleeding is arterial in origin and temporal fracture is common. Onset is minutes to hours. There is initial loss of consciousness followed by “lucid interval”. There is associated ipsilateral dilated fixed pupil, signs of increasing ICP, contralateral paralysis, and death.
- 32. Focal Brain Injury • – • • – • – SubduralHematoma Bleeding within meninges Beneath dura mater & within subarachnoid space Above pia mater Slow bleeding Superior saggital sinus Signs progress over several days with slow deterioration in mentation.
- 33. Focal Brain Injury • • • • Acutesubdural hematoma Bleeding is venous in origin. Onset of bleeding is hours to days. There is fluctuations in consciousness with associated headaches and focal neurologic signs. Common among alcoholics, elderly and those taking anticoagulants.
- 34. Focal Brain Injury • • • • • Intracerebralhemorrhage Bleeding could be arterial or venous and surgery is not often helpful There is rupture within the brain Alterations in level of consciousness is common. Associated symptoms vary with region and degree of hemorrhage, and is similar to that of stroke (headache and vomiting). The signs and symptoms worsen over time.
- 35. • – – – Types Concussion Moderate Diffuse AxonalInjury Severe Diffuse Axonal Injury
- 36. Diffuse Brain Injury • – • • • • – • • • • Concussion Mildform of Diffuse Axonal Injury (DAI) Nerve dysfunction without visible structural anatomic injury to the brain Level of consciousness Variable period of unconsciousness or confusion Followed by return to normal consciousness Transient episode of Confusion, Disorientation, Event amnesia Momentary loss of consciousness manifesting as Retrograde short-term amnesia May repeat questions over and over Associated symptoms Dizziness, headache, ringing in ears, and/or nausea
- 37. Diffuse Brain Injury • • • • • • • Diffuseaxonal injury Usually as a result of severe blunt trauma - Most common injury from severe blunt head trauma Diffuse injury Generalized edema No structural lesion Associated symptoms Unconscious No focal deficits
- 38. Diffuse Brain Injury • – • • • – – – – – ModerateDiffuse Axonal Injury Same mechanism as concussion Additional: Minute bruising of brain tissue Unconsciousness May exist with a basilar skull fracture Signs & Symptoms Unconsciousness or Persistent confusion Loss of concentration, disorientation Retrograde & Antegrade amnesia Visual and sensory disturbances Mood or Personality changes
- 39. Diffuse Brain Injury • • – • • – – – SevereDiffuse Axonal Injury Brainstem Injury Significant mechanical disruption of nerve cells Cerebral hemispheres and brainstem High mortality rate Signs & Symptoms Prolonged unconsciousness Cushing’s reflex Decorticate or Decerebrate posturing
- 40. Extremity Posturing • • Decorticate Arms flexed andlegs extended Decerebrate Arms extended and legs extended 40 Head Trauma -
- 41. Indirect Brain Injury • • • • Dueto response to primary injury Results from hypoxia or decreased perfusion Develops over hours Can be prevented by proper management of primary injuries
- 42. Indirect Brain Injury • • • • Indirectbrain injury Results from hypoxia or decreased perfusion Response to primary injury Develops over hours Management Good prehospital care can help prevent 42 Head Trauma -
- 43. Pathophysiology of headinjury
- 44. Pathophysiology of headinjury • – – – • – » » » – » » » Increased intracranial pressure Compresses brain tissue Compromises blood supply Herniates brainstem Signs & Symptoms Upper Brainstem Vomiting Altered mental status Pupillary dilation Medulla Oblongata Respiratory Cardiovascular Blood Pressure disturbances
- 45. Effect of TraumaticBrain Injury on Age • (1) (2) • • • • • TBI may interact negatively with aging in at least 2 ways: Recovery after TBI is more limited for older than younger survivors; Older individuals who have suffered a TBI are at higher risk for progressive cognitive decline. First, advanced age at the time of injury may result in less complete recovery compared to younger persons with comparable injuries. While the mechanisms of this phenomenon are not known, it may be due simply to less capacity for compensation or reduced cognitive reserves, with increasing age. Prospective, longitudinal outcome studies are required to determine whether functional outcomes of TBI improve more slowly, or even decline, among older individuals over time. ‘In patients with TBI, an increasing age is significantly associated with unfavorable outcome at 6 months, in stepwise manner centered on a threshold of 40 years, independent of other prognostic factors.” – Dhandapani et al. “The study reaffirms that outcome of head injury worsens with advancing age and indicates that severity of head injury and higher frequency of multi-system trauma may contribute to worse outcome in older patients.” – Odebode et al. MORTALITY IN TBI – The highest mortality rate (32.8 cases per 100,000) is found in persons aged 15 – 24 years. The mortality rate in patients who are elderly (65 years or older) is about 31.4 individuals per 100,000 people.
- 46. Prognosis • • Prognosis depends onthe severity of the injury This can be assessed using the Glasgow coma outcome scale
- 47. Prognosis • Glasgow comaoutcome scale Score Description 1 Death 2 Persistent vegetative state: patient exhibits no obvious cortical function 3 Severe disability(conscious but disabled): patient depend upon others for daily support due to mental or physical disability or both 4 Moderate disability(disabled but independent): Patient is independent as far as daily life is concerned. The disabilities found include varying degrees of dysphagia, hemiparesis, or ataxia, as well as intellectual and memory deficits and personality changes 5 Good recovery: resumption of normal activity even though there may be minor neurological or psychological deficits
- 48. THANK YOU FORLISTENING
- 49. References • • • • • • • • • Principles and Practiceof Surgery Nelson Essentials of Pediatrics Bailey and Love’s Short Practice of Surgery MedlinePlus Medical Encyclopedia Medscape Lye CL, Shores EA. Traumatic brain injury as a risk factor for Alzheimer's Disease: a review. Neuropsychology Rev. 2000;10:115–29. [PubMed] [Google Scholar] [Ref list] BMJ JOURNALS Traumatic Brain Injury in the Accident and Emergency Department of a Tertiary Hospital in Nigeria - J.K.C. Emejulu, C.M. Isiguzo, C.E. Agbasoga, C.N. Ogbuagu. Department of Surgery, Nnamdi Azikiwe University Teaching Hospital, Nnewi, Anambra State, South East NIGERIA. Dhandapani S, Manju D, Sharma B, Mahapatra A. Prognostic significance of age in traumatic brain injury. J Neurosci Rural Pract. 2012 May;3(2):131-5. doi: 10.4103/0976-3147.98208. PMID: 22865961; PMCID: PMC3409980.
- 51. MANAGEMENT OF TBI SURGSLT LO MAJOLAGBE
- 52.
- 53. INTRODUCTION • TBI isdefined as a non degenerative, non congenital insult to the brain from an external mechanical force, possibly leading to a permanent or temporary impairment of cognition, physical and psychosocial functions with an associated diminished or altered state of consciousness.
- 54. INTRODUCTION • • – It is oftenused synonymously with head injury which may not be associated with neurological deficits. National Head Injury Foundation “A traumatic insult to the brain capable of producing physical, intellectual, emotional, social and vocational changes.”
- 55.
- 56. 5 6 Head Trauma - CLINICALFEATURES / PRESENTATIONS
- 57. HEAD TRAUMA – – Open Skull compromised andbrain exposed Closed Skull not compromised and brain not exposed 5 7 Head Trauma -
- 58.
- 59. ECCHYMOSIS • – • • – • • Basal Skull FractureSigns Battle’s Signs Retroauricular Ecchymosis Associated with fracture of auditory canal and lower areas of skull Raccoon Eyes Bilateral Periorbital Ecchymosis Associated with orbital fractures
- 60. BASILAR SKULL FRACTURE Battle’ssign Raccoon eyes 6 0 Head Trauma -
- 61. BASILAR SKULL FRACTURE • – • BasilarSkull Fracture May tear dura Permit CSF to drain through an external passageway
- 62. SIGNS & SYMPTOMSOF BRAIN INJURY • – – – • • • – – – Altered Mental Status Altered orientation Alteration in personality Amnesia Retrograde Antegrade Cushing’s Reflex Increased BP Bradycardia Erratic respirations Vomiting Without nausea Projectile Body temperature changes Changes in pupil reactivity Decorticate posturing
- 63. SIGNS & SYMPTOMSOF BRAIN INJURY – • – • – • – » – » » – • Frontal Lobe Injury Alterations in personality Occipital Lobe Injury Visual disturbances Cortical Disruption Reduce mental status or Amnesia Retrograde Unable to recall events before injury Antegrade Unable to recall events after trauma “Repetitive Questioning” Focal Deficits Hemiplegia, Weakness or Seizures
- 64. SIGNS & SYMPTOMSOF BRAIN INJURY • – – • – – – • Upper Brainstem Compression Increasing blood pressure Reflex bradycardia Vagus nerve stimulation Cheyne-Stokes respirations Pupils become small and reactive Decorticate posturing Neural pathway disruption
- 65. SIGNS & SYMPTOMSOF BRAIN INJURY • – – – • – – Middle Brainstem Compression Widening pulse pressure Increasing bradycardia CNS Hyperventilation Deep and Rapid Bilateral pupil sluggishness or inactivity Decerebrate posturing
- 66. SIGNS & SYMPTOMSOF BRAIN INJURY • – – • – – – Lower Brainstem Injury Pupils dilated and unreactive Ataxic respirations Erratic with no pattern Irregular and erratic pulse rate Hypotension Loss of response to painful stimuli
- 67. INVESTIGATIONS • • • • • • • Plain films (X-ray) of the skull Computer tomography (CT) scan (non-contrast) Magnetic Resonance Imaging (MRI) Carotid angiography Electroencephalography Echoencephalography Exploratory burr hole craniotomy
- 68. INVESTIGATIONS - Lateral CervicalSpine X- ray
- 69.
- 70. INVESTIGATIONS – CRANIALCTS SCANS
- 71. MANAGEMENT PROTOCOL • • • • • • Primary surveyand Resuscitation Airway Maintenance and C-spine protection Breathing Circulation and control of Hemorrhage Rapid Neurologic Survey Exposure-Remove all clothes
- 72. MANAGEMENT PROTOCOL • • • • • • • Secondary Survey DetailedSystemic Examination Xrays: Chest, spine CT Scan Other Xrays Laboratory Tests Tetanus Immunization
- 73. MANAGEMENT PROTOCOL • • • • • • Definitive Care Immediate,early initial intervention which focus on detection of primary injury and prevention and treatment of secondary injury. Focus of management: Prevent elevated ICP Avoid hypotension (show to increase morbidity and mortality) Minimize cerebral metabolic rate of O2 consumption
- 74. Factors that decreasecerebral oxygen supply • • • • • Anemia Hypoxemia Systemic hypotension Low cardiac output Elevated intracranial pressure
- 75. Factors that increasecerebral oxygen demand • • • • • Seizure Fever Agitation Pain Excitatory neurotransmitters
- 76. MANAGEMENT PROTOCOL INICU • • It can be classified on the basis of neurological assessment using Glasgow Coma Score into, mild (13/15), moderate (9-12/15) and severe (3-8/15). Moderate to severe TBI often require admission to the Intensive care unit (ICU).
- 77. MANAGEMENT PROTOCOL INICU • • Severe traumatic brain injury (TBI) is currently managed in the intensive care unit with a combined medical-surgical approach. Treatment aims to prevent additional brain damage and to optimize conditions for brain recovery. The goal of ICU management of TBI is the prevention of secondary brain injuries such as hypotension, hypercapnia, hypertension, hypo/hyperglycemia and hyperthermia
- 78.
- 79. MANAGEMENT • – – • • • TIME IS CRITICAL IntracranialHemorrhage Progressing Edema Increased ICP (5 to 15mmhg – 7.5 to 20cmH2O) CPP = MAP – ICP (60 to 80mmhg) Cerebral Hypoxia Permanent Damage
- 80. MANAGEMENT • • • • • • • • • For unconscious patients:Airway maintenance with endotracheal intubation in cases of respiratory distress Tracheostomy in anticipated long periods of unconsciousness Assist ventilation High-flow oxygen One breath every 6–8 seconds SpO2 >95% Maintain EtCO2 at 35 mmHg Fluid administration for traumatic brain injury, GCS <9 Titrate to 110–120 mmHg systolic with or without penetrating hemorrhage to maintain Cerebral perfusion pressure (60 to 80mmhg).
- 81. MANAGEMENT • • • • Hyperventila tion : Indications forhyperventilation TBI GCS <9 with decerebrate posturing TBI GCS <9 with dilated or nonreactive pupils TBI initial GCS <9, then drops >2 points Age group Physiologic respiratory rate Hyperventilation respiratory rate Adult 8–10 per minute 20 per minute Children 15 per minute 25 per minute Infants 20 per minute 30 per minute If signs resolve, stop hyperventilation. Capnography Maintain EtCO <30 mmHg, but >25 mmHg
- 82. MEDICAL THERAPY • • • • • Anticonvulsants(5-15% post-traumatic Seizures) Immediate,Early(first wk), Late Seizures Prophylaxis beneficial in first week Risk factors for late seizures: early seizures, depressed skull fractures and intracranial haematoma Mannitol Lasix Barbiturates Steroids
- 83. SURGICAL THERAPY • • • • • Wound debridement Surgicalevacuation of Intracranial haematoma and contusions Elevation of compound depressed fracture Repair of Venous sinus injuries Decompressive craniectomy for patients with raised intracranial pressure
- 84. MONITORING • Monitoring ofpatients with severe TBI is essential for the guidance and optimization of therapy. The rationale of monitoring is early detection and diagnosis of secondary brain insults, both systemic and intracranial. Therefore, monitoring of patients with severe TBI must comprise both general and specific neurologic monitoring.
- 85. MONITORING • • • • • • • • • • • • Mental State examination– COMJS GCS Pupillary reflex ICP monitoring (Intraventricular – EVD) Brain tissue oxygen tension monitor (PbtO2) – delivery and consumption Vital signs ABG O2 saturation Capnography Temperature Blood sugar FOUR SCORE
- 86. • • Reactive: ICP increasing Nonreactive(altered LOC): increased ICP PUPILLARY REFLEX Both dilated • • Nonreactive: brainstem Reactive Unilaterally dilated 8 6 Head Trauma - Eyelid closure • Slow: cranial nerve III
- 87.
- 88.
- 89. GLASGOW COMA SCALE Suspectsevere brain injury GCS <9 8 9 Head Trauma - *Decorticate posturing to pain **Decerebrate posturing to pain
- 90. EXTREMITY POSTURING – – Decorticate Arms flexed andlegs extended Decerebrate Arms extended and legs extended 9 0 Head Trauma -
- 91. GLASGOW COMA SCALE • • • • • Sumof the Scores in the 3 categories Best Score 15 Worst Score 3 Score is related to severity Score is related to outcome
- 92. INCREASING ICP 9 2 Head Trauma- Vital Sign with Increasing ICP 1. Respiration Increase, decrease, irregular 2. Pulse Decrease 3. BP Increase, widening pulse pressure • CUSHING’S TRIAD
- 93.
- 94.
- 95. General intensive careactivities • Prior to suctioning the patient through the endotracheal tube (ETT), preoxygenation with a fraction of inspired oxygen (FiO2) = 1.0, and administration of additional sedation are recommended to avoid desaturation and sudden increase in the ICP. Suctioning ETT must be brief and atraumatic.
- 96. General intensive careactivities • • • Similar to other patients in the intensive care, TBI victims should receive the usual daily care as follows: - Raising head of bed to 30° - 45°: that would reduce ICP and improves CPP [125]; and lower the risk of ventilator-associated pneumonia (VAP). - Keeping the head and neck of the patient in a neutral position: this would improve cerebral venous drainage and reduce ICP.
- 97. General intensive careactivities • • • - Avoiding compression of internal or external jugular veins with tight cervical collar or tight tape fixation of the endotracheal tube that would impede cerebral venous drainage and result in an increase in the ICP. - Turning the patient regularly and frequently with careful observation of the ICP - Providing eye care, mouth and skin hygiene
- 98. General intensive careactivities • • • - Implementing all evidence-based bundles for prevention of infection including VAP and central line bundle . - Administrating a bowel regimen to avoid constipation and increase of intra-abdominal pressure and ICP. - Performing physiotherapy
- 99. DIAGNOSIS • • • • • • • • History taking Mechanism ofinjury Loss of consciousness or amnesia Level of consciousness at scene and on transfer Evidence of seizures Probable hypoxia or hypotension Pre-existing medical conditions Medications (especially anticoagulants) Illicit drugs and alcohol
- 100. DIAGNOSIS • • • • • • • Examination General Close examination ofthe skull for external evidence of injury Check for pallor-suggestion for bleeding Check mouth odour for alcohol, acetone(suggestive of uncontrolled DM), mousy(hepatic failure), urea( uraemia). Level of consciousness using the GCS Ears and nose- bleeding or CSF leakage (suggestive basal skull fracture)
- 101. COMPLICATIONS • • • – – • Personality changes -Frontal lobe injury Visual disturbances - Occipital lobe injury Altered mental status Retrograde amnesia Antegrade amnesia Focal deficit- hemiplegia, weakness or seizures
- 102. COMPLICATIONS • Cerebral herniation syndrome Brainforced downward CSF flow obstructed, pressure on brainstem Level of consciousness Decreasing, rapid progression to coma Associated symptoms Ipsilateral pupil dilatation, out-downward deviation Contralateral paralysis or decerebrate posturing Respiratory arrest, death
- 103. COMPLICATIONS • • • • • • Cranial nerve injuries Cerebraloedema Cerebral abscess Post traumatic epilepsy Post traumatic headaches Infection - Meningitis
- 104. GLASGOW COMA SCALE • • • • • • • • • GoodRecovery: 5 Return to pre-injury level of function Moderate Disability : 4 Diminished level of function but Cares for self Severe Disability : 3 Unable to care for self Vegetative State : 2 No awareness of self or environment Death : 1
- 105. FOLLOW UP • In-patientrehabilitation follow up is important especially for moderate - severe head injury.
- 106. CONCLUSION • • • • Head injury isone of the major reasons for emergency treatment and is associated with high mortality and disability It is commonly caused by road traffic accidents(RTAs) Time is critical in the management of head injuries. Requires continuous monitoring & evaluation and follow up.
- 108. NURSING MANAGEMENT OFA PATIENT WITH TRAUMATIC BRAIN INJURY SMSN TIMOTHY RM INTENSIVE CARE UNIT (ICU), NIGERIAN NAVY REFERENCE HOSPITAL, OJO, LAGOS.
- 109. Introduction • It isestimated that between 750 000 and one million individuals with head injuries attend accident and emergency (A&E) departments in the UK every year. Approximately 150 000 to 200 000 are admitted to hospital and, of these, 5% require admission to a neurosurgical unit (Flint, 1997).
- 110. Nursing Management inCritical Care • The critical-care nurse needs to be alert to the potential problems that may be encountered by the brain- injured patient, who may be at risk of sudden deterioration at any time. This involves taking an holistic view of the patient.
- 111. 1. Respiratory care: • • Hypoxiaafter head injury is common for a number of reasons: inadequate airway clearance leading to poor tidal volumes, associated chest trauma and aspiration and hypermetabolic state post-injury, which will increase tissue oxygen.
- 112. Haemodynamic/fluid management: • Theminimum monitoring required for a critically head-injured patient should include continuous arterial blood pressure monitoring (rather than non-invasive methods in order to enable measurement of CPP), core body temperature, respiration rate and pattern and continuous ECG.
- 113. Temperature control: • • In head-injuredpatients with hypoxia and ensuing ischaemia, the oxygen demand of brain tissue escalates (Chambers, 1999). The brain’s metabolic rate increases by approximately 7% for each degree centigrade increase in temperature(Johnson, 1999). This elevated metabolism increases cerebral blood volume, thereby increasing ICP (Hickey, 1997). There may also be damage to the temperatureregulating centre in the hypothalamus, which may cause body temperature to fluctuate (Wong, 2000).
- 114. Positioning: • • Positions that restrictvenous drainage from the brain through the internal jugular vein may cause a significant rise in ICP (Johnson, 1999). In a comprehensive review of the literature, Beitel (1998) found that elevation of the head from 15 to 30 degrees was associated with a mean decrease in ICP in all patients.
- 115. Nutritional support: • • Severe headinjury is associated with a hypermetabolic state with, in some cases, the metabolic rate increasing by as much as 40 to 100% (Hinds and Watson, 1996). It is therefore important to begin feeding as early as possible, preferably enterally. The feeding tube should always be passed via the orogastric route in head-injured patients, unless a basal skull fracture has been definitively ruled out (Withington, 1997).
- 116. Other Nursing Interventionsinclude; • • • • • • • • • • a. Maintaining the airway b. Protecting the patient. c. Providing mouth care. d. Maintaining skin and joint integrity. e. Preserving corneal integrity f. Preventing urinary retention g. Promoting bowel function h. Providing sensory stimulation i. Check Nose and Ear for CSF leak. j. Administrator medications as prescribed.
- 117. SIGNS OF RAISEDINTRACRANIAL PRESSURE (ICP) • • • • • • • • • • • • * Headache * Nausea * vomiting * Increased blood pressure * Decreased mental abilities * Confusion * Double vision * Pupils that don’t respond to changes in light * Shallow breathing * Seizures * Loss of consciousness * Coma
- 118. Conclusion • • Nursing care ofthe head-injured patient can present many challenges for the critical care nurse and, as a consequence, a thorough knowledge of the dynamics of ICP and the factors associated with its increase is required (Johnson, 1999). Thank you for listening.
- 119. REFERENCES • • • • • • • • • 1. Brunner, L.S., Suddarth, D. S., Smeltzer, S. C. O., & Bare, B. G. (2004). Brunner & Suddarth's textbook of medical-surgical nursing (10th ed.). Philadelphia: Lippincott Williams & Wilkins. 2. Understanding Increased Intracranial Pressure Medically reviewed by Susan W. Lee, DO — Written by Elea Carey and Rachael Zimlich, RN, BSN on February 28, 2022, available on https://www.healthline.com/health/increased-intracranial-pressure 2. Shaikh F, Waseem M, Boling AM. Head Trauma (Nursing) [Updated 2022 May 15]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available on https://www.ncbi.nlm.nih.gov/books/NBK568699/