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Head trauma

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Presented at AWS General Hospital, supervised by dr. Arie Ibrahim SpBS

Presented at AWS General Hospital, supervised by dr. Arie Ibrahim SpBS

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  • 1. HEAD TRAUMA Dr. Isa Basuki Department of Surgery, AWS General Hospital Faculty of Medicine, MulawarmanUniversity
  • 2. INTRODUCTION  Head trauma orTraumatic brain injury (TBI) is a disruption or alteration of brain function due to external forces  The external forces creating the injury may be the result of:  acceleration or deceleration,  direct compression,  penetrating objects,  combined effects,  complex mechanisms
  • 3. INTRODUCTION  It may produce:  fractures,  contusion,  subarachnoid hemorrhage (SAH),  subdural hemorrhage (SDH),  epidural hemorrhage (EDH),  Intraparenchymal hemorrhage (IPH),  diffuse axonal injury (DAI).  All injuries and symptoms should be taken seriously
  • 4. EPIDEMIOLOGY  Approximately 1.4 million people per year sufferTBI  1.1 million are treated and released, 240,000 are hospitalized, and 50,000 die  Common causes:  Falls (28%),  Motor vehicle accidents (20%),  Pedestrian impact (19%),  Assault (11%)  Age distribution with the greatest risk in 0–4 and 15- to 19-year-olds.  Males have 1.5 times the risk of females
  • 5. PATHOPHYSIOLOGY  Primary injuries  disruption of scalp (lacerations),  bone (cranial vault, skull base, facial bones),  vasculature (SDH/EDH/IPH/intraventricular hemorrhage [IVH], traumatic aneurysm),  brain parenchyma (contusion, DAI)  Secondary injuries  hypoxemia,  ischemia,  initial hyperemia,  cerebral edema,  expansion of hemorrhages  increased intracranial pressure (ICP),  seizures,  metabolic abnormalities  systemic insults
  • 6. GENERAL PRINCIPLES
  • 7. SYSTEMIC EVALUATION AND RESUSCITATION  Assessment and treatment often begins in the prehospital setting  The basic principles of trauma resuscitation  rapid assessment and maintenance of an airway, breathing, and circulation  medical and surgical history should be obtained including:  the events preceding a trauma,  a description of the accident scene,  accurate description of the patient’s neurological baseline,  any subsequent changes to the neurological status
  • 8. SYSTEMIC EVALUATION AND RESUSCITATION  In the newborn or premature infant  cephalohematoma may allow enough displacement of blood to produce hemodynamic instability  Raccoon’s eyes (periorbital ecchymosis),  Battle’s sign (postauricular ecchymosis), suggest a basilar skull fracture  otorrhea/rhinorrhea  Puncture wounds  penetrating injury to the brain, spinal cord, sympathetic plexus, or vasculature  Bruits of the carotid artery  carotid dissection or carotidcavernous fistula
  • 9. NEUROLOGICAL EXAMINATION  Accurate neurological examination is essential  The exam may be limited due to:  patient’s age  level of education  native language  presence of sedative or paralytic medication • Illicit drugs • hypotension • hypoxia • hypothermia • hypoglycemia
  • 10. PUPILLARY RESPONSE  parasympathetic, pupilloconstrictor, and light reflex (pupillary reflex) can be easily and rapidly assessed in the unconscious patient  Damage to the Edinger–Westphal nucleus or uncal compression of CN III at the tentorial notch  pupillary dilatation (≥4 mm)  Direct orbital trauma can also result in pupillary dilation/fixation in the absence of temporal lobe herniation or intracranial hypertension (ICHTN).
  • 11. GLASGOW COMA SCALE  standard for objective measurement ofTBI severity  three parameters:  best eye opening [E]  best verbalization [V],  best motor function [M]  GCS = 13 – 15  mildTBI  GCS = 9 – 12  moderateTBI  GCS = 3 – 8  severeTBI  If the patient is intubated  1 for the verbal component and the overall scored is annotated with a “T.”  Examples: M4/VT/E2 = 4 + 1 + 2 = 7T
  • 12. GLASGOW COMA SCALE (RECOMMENDED FOR AGE ≥4)
  • 13. GLASGOW COMA SCALE FOR CHILDREN (RECOMMENDED FOR AGE <4)
  • 14. RADIOGRAPHIC EVALUATION
  • 15. PLAIN X-RAYS  For evaluating and clearing the cervical spine.  The spine is imaged from the occiput toT1 and a C-collar  AP, lateral and odontoid views are the most useful  T- and L-spine films are obtained based on:  mechanism of injury,  degree of neurological deficits,  pain
  • 16. CT SCAN  CT scan findings after trauma:  SDH, EDH, SAH, IPH, IVH  contusions  hydrocephalus  cerebral edema or anoxia  skull fractures  ischemic infarction (if >12 hours old)  mass effect  midline shift  Indications for an initial post- traumatic CT scan:  GCS ≤ 14  unresponsiveness,  focal deficit,  amnesia for the injury,  altered mental status,  signs of basilar skull fracture
  • 17. MRI  better parenchymal resolution  can evaluate infarction, ischemia, edema, and DAI  helpful to determine ligamentous injury of the spine or traumatic cord injury  generally performed after the initial trauma evaluation and resuscitation have been completed  Disadvantages:  limited availability  slower image acquisition time  increased cost
  • 18. CLASSIFICATION AND SURGICAL MANAGEMENT OF SPECIFIC INJURIES
  • 19. SKULL FRACTURES  can be described by:  The state of the overlying scalp (closed or open),  The number of bone fragments (simple or compound),  The relationship of bone fragments to each other (depressed or nondepressed),  Whethert the fracture enters or widens an existing cranial suture (diastatic, more common in children), and whether it involves the cranial vault or skull base  lower force impacts (falls from standing)  more linear, closed, and without dural laceration  Higher force impacts (MVA, falls from heights, penetrating trauma)  compound, open fractures with underlying dural or cerebral injury  “Ping-pong” fractures are greenstick-type fractures usually seen in newborns
  • 20. CT bone windows showing ping-pong skull fracture. The multiple nondisplaced linear lucencies are normal sutures.
  • 21. SKULL FRACTURES  Associated clinical signs of:  calvarial skull fractures  gross deformity and palpable skull fracture in patients with open scalp lacerations  Basilar skull fractures  postauricular or periorbital ecchymosis, hemotympanum or laceration of the external auditory canal, and CSF rhinorrhea or otorrhea  Cranial nerve injuries:  fractures of the cribriform plate (CN I, anosmia)  optic canal (CN II, visual deficit)  temporal bone (CNVII, facial weakness; or CNVIII, hearing loss)  Severe basilar skull fractures  pituitary gland injury  endocrinopathies
  • 22. SKULL FRACTURES  Direct injury to vasculature that penetrates the skull base   Arterial dissection,  Traumatic aneurysm formation,  Traumatic carotid-cavernous sinus fistula with symptoms:  cranial neuropathies  chemosis  bruits  Strokes
  • 23. SKULL FRACTURES RADIOGRAPHIC DIAGNOSIS  Differential Diagnosis of Fractures on Skull X-Rays
  • 24. SKULL FRACTURES RADIOGRAPHIC DIAGNOSIS  Most skull fractures are discovered by CT scan  Plain films may be superior to CT scan in discovering linear calvarial fractures parallel to the skull base  CT angiograms/venograms to assess   fractures involving skull base foramen containing vasculature (e.g., carotid canal, foramen magnum)  fractures that cross major venous sinuses (superior sagittal or transverse sinuses, jugular foramen).  Closed, nondisplaced fractures do not require immediate intervention  Open skull fractures should be debrided and carefully inspected and all should receive antibiotics
  • 25. SKULL FRACTURES  Relative indications for surgical elevation of a depressed skull fracture:  depression of more than 8–10 mm or more than the thickness of the skull  Focal neurological deficit clearly attributable to compressed underlying brain,  Significant intraparenchymal bone fragments (implying dural laceration),  Persistent deformity after all swelling has subsided  Current recommendations:  surgical repair  open fractures depressed greater than the thickness of the cranium  nonoperative management  open depressed cranial fractures if there is no evidence of dural penetration
  • 26. CT bone windows showing a depressed skull fracture that required surgical elevation and dural repair. The patient also had an underlying brain contusion and presented with a receptive aphasia
  • 27. SKULL FRACTURES  Indications for surgery:  significant intracranial hematoma,  depression >1 cm,  frontal sinus involvement,  Gross cosmetic deformity,  wound infection,  pneumocephalus,  gross wound contamination
  • 28. FOCAL CEREBRAL INJURIES CEREBRAL CONTUSION  Injuries to the superficial gray matter of the brain  External forces   acceleration of the intact skull or fractured skull fragments toward the brain surface or  the brain continues to move toward the rapidly decelerating skull and dural folds of the falx or tentorium  “Coup” lesions  ipsilateral to the impact site  adjacent calvarial fractures  “Contrecoup” lesions  opposite the coup lesion  rebounding brain striking the inner table of the skull  CT scans  patchy, hyperdense lesions with a hypodense background
  • 29. FOCAL CEREBRAL INJURIES INTRAPARENCHYMAL HEMORRHAGE  8.2% of allTBI and up to 35% of severeTBI cases  Delayed traumatic intracerebral hemorrhage (DTICH)  approximately 20% of cases and most occur within 72 hours of the initial trauma  Indications for surgical decompression:  neurological decline referable to theTICH lesion  TICH > 50 cm3  GCS = 6 – 8 with frontal or temporal contusions >20 cm3 with midline shift ≥5 mm and/or cisternal compression on CT scan  Surgical procedures range  Localized frontal or temporal craniotomy with resection of underlying focal clot  Extensive craniectomies with duraplasty, evacuation of severely contused brain, or temporal lobectomy
  • 30. FOCAL CEREBRAL INJURIES EPIDURAL HEMORRHAGE  blood collects in the potential space between the dura and inner table of the skull  1% of all head trauma admissions and in 5–15% of patients with fatal head injuries  more common in males (M:F = 4:1)  usually occurs in young adults  90% of EDHs are due to arterial bleeding  fracture at the middle meningeal artery groove  10% are due to venous bleeding  violation of a venous sinus by an occipital, parietal, or sphenoid wing fracture
  • 31. FOCAL CEREBRAL INJURIES EPIDURAL HEMORRHAGE  Location of EDH:  lateral convexity of a cerebral hemisphere (70%),  frontal (5–10%),  parieto-occipital (5–10%),  posterior fossa locations (5–10%)  CT scan   hyperdense, biconvex (lenticular) mass adjacent to the inner table of the skull (84%)  medial edge being straight (11%)  crescentic  resembling an SDH (5%)  Additional associated findings  SDHs and cerebral contusion
  • 32. CT showing epidural hemorrhage. Note the biconvex- or lenticular-shaped hemorrhage. On the bone windows this was adjacent to a diastatic left lambdoid suture.
  • 33. FOCAL CEREBRAL INJURIES EPIDURAL HEMORRHAGE  Clinical presentation:  Brief post-traumatic loss of consciousness (LOC)  40%  Lucid interval (80%)  Obtundation  Contralateral hemiparesis,  Ipsilateral (85%) pupillary dilatation (60%)  Kernohan’s phenomenon (a false localizing sign)   local hemispheric mass effect  compression of the contralateral brainstem against the tentorial notch  ipsilateral hemiparesis  Mortality   unilateral EDH (5–12%)  Bilateral EDH (15–20%)  no lucid interval (20%)  posterior fossa location (25%)  concurrent acute SDH (25–90%)
  • 34. FOCAL CEREBRAL INJURIES EPIDURAL HEMORRHAGE  Rapid diagnosis and intervention when indicated  optimize the outcome  Guidelines:  Surgical  EDH of >30 cm3 should be evacuated regardless of GCS score  Conservative EDH of <30 cm3 and <15 mm of thickness and >5 mm midline shift (frequent neurological examinations and serial CT scan)  Relative indications  EDHs that are neurologically symptomatic or have a maximal thickness >1 cm.  Absolute indication  acute EDH in coma (GCS ≤ 8) and anisocoria  Craniotomy  complete clot evacuation with meticulous hemostasis and use of tackup sutures to decrease the potential epidural space
  • 35. FOCAL CEREBRAL INJURIES SUBDURAL HEMORRHAGE  blood collects between the arachnoid and inner dural layer  Type/variants:  hyperacute (<6 hours),  acute (6 hours to 3 days),  subacute (3 days to 3 weeks),  chronic (3 weeks to 3 months)  Etiologies:  traumatic stretching and tearing of cortical bridging veins  coagulopathy,  subdural dissection of ICH,  rupture of a vascular anomaly (AVM, aneurysm, cavernoma, dural AV fistula) into the subdural space
  • 36. CT showing an acute subdural hemorrhage. Note that crescentic hemorrhage crosses under the right coronal suture.
  • 37. APPEARANCE OF SDH ON CT AND MRI
  • 38. FOCAL CEREBRAL INJURIES SUBDURAL HEMORRHAGE  Guidelines suggestion for SDH evacuation:  acute SDH with thickness >1 cm or a midline shift >5 mm regardless GCS score  acute SDH <1 cm thick and midline shift <5 mm and in coma (GCS ≤8) if:  GCS decreases by 2 points.  pupils that are asymmetric or fixed/dilated.  the ICP ≥20 mm Hg.  Craniotomy  ASAP, may require craniectomy and duraplasty for ICP control  Mortality  50% to 90% (related more to the underlying injury, increased in the elderly and in patients on anticoagulants)  Outcome  mortality improvements from 66–90% down to 30–59% if the patient was operated on in less 4 hours
  • 39. FOCAL CEREBRAL INJURIES SUBARACHNOID HEMORRHAGE  blood located between the pial and arachnoid membranes  results from venous tears in the subarachnoid space  33% of patients with moderate head injury and is found in nearly 100% of trauma patients at autopsy.  CT scan  sulcal hyperdensity  MRI  FLAIR hyperintensity  Clinical presentation  headache, emesis, and lethargy  Treatment  supportive using IV fluids, anticonvulsants, and nimodipine (to prevent vasospasm)
  • 40. CT with arrow pointing to a small traumatic subarachnoid hemorrhage in left central sulcus
  • 41. CT AND ANGIOGRAM OF ICH
  • 42. DIFFUSE CEREBRAL INJURIES CONCUSSION  an alteration of consciousness resulting from nonpenetrating injury to the brain  Classic symptoms:  headache  confusion  amnesia  LOC  Additional symptoms:  Deficits of motor function (incoordination, stumbling),  Speech (slowed, slurred, incoherent),  Memory or processing (amnesia, short-term memory loss, difficulty concentrating or focusing, inattention, perseveration, easy distractibility),  Orientation (vacant stare, “glassy eyed,” unable to orient to time/date),  Irritability
  • 43. CONCUSSION GRADING
  • 44. DIFFUSE CEREBRAL INJURIES CONCUSSION  Physiological responses  transient increase in cerebral blood volume due to loss of vascular autoregulation  mild cases  mild cerebral swelling, or hyperemia  more severe cases  malignant cerebral edema  elevated ICPs refractory to nearly all measures and 50–100% mortality  “second impact syndrome”  CT scan  subtle or nonexistent and include mild diffuse swelling secondary to hyperemia  Treatment  recognition of injury
  • 45. DIFFUSE CEREBRAL INJURIES DIFFUSE AXONAL INJURY  traumatic axonal stretch injury caused by overlying cerebral cortex and underlying deep brain structures moving at different relative speeds  Mild  axonal stretching + transient neuronal dysfunction  Severe  axonal shearing + permanent neuronal damage  80%  microscopic and nonhemorrhagic with impaired axonal transport and delayed axonal swelling  CT scans  normal (50–80%) or hyperdense petechial hemorrhage (20–50%)  MRI  multifocal hyperintense T2 at frontal lobes (67%), corpus callosum (20%), and brainstem (10%)  Prognosis generally related to the patient’s age, presenting neurological status, and trajectory of neurological improvement.
  • 46. MANAGEMENT OF TRAUMATIC BRAIN INJURY
  • 47. MEDICAL MANAGEMENT  Basic measures:  ICU setting with frequent monitoring of:  vital signs,  fluid intake and output  neurological examinations (as permitted)  Multiple invasive lines for:  blood pressure (arterial line),  volume assessment (Swan–Ganz),  administration of fluids, medication, or nutrition (central venous catheter),  urine output or temperature (Foley catheter),  ICP,  cerebral tissue oxygenation, or cerebral blood flow (CBF)
  • 48. MEDICAL MANAGEMENT  kept normothermic and euvolemic with isotonic fluids  GI prophylaxis against Cushing’s (stress) ulcer  head of bed should be elevated to 30–45°  neck should be kept midline  cervical collar and endotracheal tube stabilizer   prevent compression of the jugular veins  promote venous outflow from the head
  • 49. BLOOD PRESSURE AND OXYGENATION  single episode of hypoxemia (apnea, cyanosis or O2 saturation <90% in the field, or PaO2 < 60 mmHg) or hypotension (SBP < 90 mmHg)  predictor of worse outcome  Oxygen saturation and blood pressure monitoring  started in the field and continued at hospital setting  Goal  identifying, avoiding, and rapidly correcting hypoxemia or hypotension  Oxygen administration  start as early as possible (may require endotracheal intubation)  isotonic or hypotonic saline, plasma, colloid, blood, or intravenous pressors  to avoid hypotension
  • 50. INTRACRANIAL PRESSURE ASSESSMENT  modified Monro–Kellie hypothesis   Assuming that the skull is completely inelastic, the ventricular space is confluent  pressures are equally and readily transmitted throughout the intracranial space  balance between the brain, blood volume, and CSF in the intracranial space  Increases in the volume or addition of new components  compensatory decreases in other constituents to maintain the same ICP  Mildly increased, localized pressure in the brain  neurological dysfunction of the immediate area  severe pressure increases  local tissue compression, shift of intracranial structures, subfalcine and transtentorial herniation  most severe  compression at the level of the brainstem, occlusion of brainstem vasculature, infarction, and death.
  • 51. ICP MONITORING  Normal ICPs:  <10–15 mm Hg in adults  3–7 mm Hg in children  1.5–6 mm Hg in infants  ICP monitoring is recommended for:  patients with severeTBI (GCS= 3 – 8)  abnormalCT scan or with severeTBI  considered in patients without an accurate neurological examination due to sedatives, paralytics, or general anesthesia required  Higher mortality  ICP persistently above 20 mm Hg.
  • 52. ANALGESICS AND SEDATIVES  Pain and agitation can cause increased sympathetic tone, increased temperature, and hypertension   increased venous and ICP,  increased metabolic demand,  resistance to controlled ventilation  may require sedatives or psychotropic medication to prevent self-injurious behavior and dislodgement of airway, vascular lines, or monitoring equipment  If on ventilators, may require sedatives or paralytics to allow appropriate lung excursion or timing of breath patterns.  side effects  hypotension, alteration or obliteration of the neurological examination, and rebound ICP elevation
  • 53. ANALGESICS AND SEDATIVES AGENTS ADVANTAGES Haloperidol relatively nonsedating quality  useful for agitation fentanyl and its related derivatives (remifentanil, sufentanil) short acting, reversible, and conducive to administration by continuous infusion  for acute and longer-term analgesia Midazolam short-acting benzodiazepine  effective for sedation of the ventilatedTBI patient. Propofol hypnotic anesthetic with rapid onset and a very short half- life  facilitates rapid neurological assessment, reduces cerebral metabolism and oxygen consumption and exerts a neuroprotective effect
  • 54. HYPEROSMOLARTHERAPY  Mechanism of Mannitol:  first few minutes  produces immediate plasma expansion with reduced hematocrit and blood viscosity  improved rheology, and increased CBF and O2 delivery  reduces ICP  Over the next 15–30 minutes  produces an osmotic effect with increased serum tonicity and withdrawal of edema fluid from the cerebral parenchyma.  Bolus  ICP reduction is evident at 1–5 minutes and peaks at 20–60 minutes  Initial bolus of mannitol  1 g/kg  Subsequent administration at smaller doses and longer intervals (i.e., 0.25–0.5 g/kg Q 6 hours)  Furosemide may also be used synergistically with mannitol
  • 55. HYPEROSMOLARTHERAPY  Serum osmolality should be monitored (>320 mOsm/L  use of mannitol should be restricted)  Larger dose (1,4 g/kg) improved outcome of the comatose patients with:  operative subdural hematomas  operative intraparenchymal temporal lobe hemorrhages  abnormal pupillary dilatation
  • 56. HYPERTONIC SALINE  lower ICP through two mechanisms: 1. oncotic pressure gradient, across the BBB, results in mobilization of water from brain tissue and hypernatremia 2. rapid plasma dilution and volume expansion, endothelial cell and erythrocyte dehydration, and increased erythrocyte deformability  improvements in rheology, CBF, and oxygen delivery  Administration:  continuous infusion of 25–50 mL/h of 3% saline  bolus infusions of 10–30 mL of 7.2%, 10%, or 23.4% saline solution  Onset  minutes and may last for hours  Serum sodium and osmolality levels should be aggressively followed  central pontine myelinolysis (most often in patients with preexisting, chronic hyponatremia)  may also induce or exacerbate pulmonary edema in patients with underlying cardiac or pulmonary deficits
  • 57. HYPERVENTILATION  lowers PCO2 with subsequent vasoconstriction, reduction of cerebral volume, and reduction in ICP  Time of onset  30 seconds to 1 hour,  Peak effect  8 minutes and may last up to 15–20 minutes  should be avoided during the first 24 hours postinjury  CBF is most reduced  after the first 24 hours  short-term, mild HPV (PCO2 = 30 – 35)  ICP control  moderate HPV should be avoided  Prophylactic HPV (PCO2 ≤ 25) is contraindicated  increased ischemia and worse outcomes
  • 58. DECOMPRESSIVE CRANIECTOMY  The bone is removed, the lesion is resected, and the dura and bone are replaced  Severe cases  diffuse cerebral edema, contusions of large size in eloquent areas, or multiple, coalesced contusions  leave the bone flap off.  Most common  unilateral hemispheric  Bifrontal and bilateral hemispheric craniectomies  based on the location and severity of the underlying lesion(s)  The dura is opened widely and areas of noneloquent contused and devitalized brain can be removed if required  hemispheric technique  at least 12-cm cranial flap is removed
  • 59. CT of a bilateral hemispheric decompressive craniectomy performed in a patient with severe edema from a likely second impact syndrome.
  • 60. BARBITURATES  Benefit:  decreasing metabolic demand for oxygen (CMRO2)  decreasing free radicals and intracellular calcium  lowering ICPs  Side effects:  immunosuppression  hypotension (reduced sympathetic tone and mild cardiodepression)  Patients exclusion:  hemodynamic instability,  sepsis,  respiratory infection,  cardiac risk factors
  • 61. BARBITURATES  loading dose   10 mg/kg over 30 minutes  followed by a 5 mg/(kg h) infusion for 3 hours  maintenance dose  1 mg/(kg h)  Serum barbiturate levels  3–4 mg%
  • 62. HYPOTHERMIA  Improve outcome in patients with severeTBI through reduction of:  cerebral metabolism,  ICP,  inflammation,  lipid peroxidation,  excitotoxicity,  cell death,  Seizures  Side effects:  Decreased cardiac function  thrombocytopenia  elevated creatinine clearance  pancreatitis  shivering
  • 63. HYPOTHERMIA  patients who were hypothermic on admission had improved outcomes when hypothermia was maintained  target temperature  32–33°C (maintained for greater than 48 hours)  patients should be closely monitored for electrolyte abnormalities, hypocoagulability, and cardiac rhythm alterations  Rewarming  very slow (not exceeding more than 1° per 24 hours)
  • 64. STEROIDS  Glucocorticoids are not recommended  Side effects of steroid:  coagulopathies,  hyperglycemia,  increased infection
  • 65. SPECIFIC SYSTEM CONSIDERATIONS
  • 66. NUTRITION  All injured patients show an increase in basal energy expenditure (BEE)  Patients who are sedated and paralyzed  120–130% of baseline  Comatose patients (GCS ≤8) with isolated head injury  140% (range 120–250%)  at least 15% of calories should be supplied as protein  nutritional replacement should start by 72 hours postinjury  Enteral feeding is preferred over parenteral nutrition  enhanced immunocompetence and a reduced risk profile  Total parenteral nutrition   if enteral feeding is not possible  if higher nitrogen intake is required
  • 67. INFECTION  Source of infection:  gross wound contamination  immunosuppression,  iatrogenically from open surgical procedures,  intubation for mechanical ventilation,  invasive monitoring equipment  Antibiotic coverage should be targeted toward specific organisms  Perioperative antibiotics  only recommended for the first 24 hours
  • 68. COAGULOPATHY PROPHYLAXIS  Coagulopathies should be rapidly and aggressively treated  normal coagulation profile.  Effects of warfarin anticoagulation may be reversed by:  vitamin K,  fresh frozen plasma (FFP),  prothrombin complex concentrate  Effects of heparin may be reversed with protamine sulfate  Thrombocytopenia or platelet deactivation may be treated with donor platelet transfusion
  • 69. DVT PROPHYLAXIS  Neurological risk factors for DVT and PE:  stroke  spinal cord injury,  prolonged surgery  prolonged bed rest  incidence of DVTs in neurosurgical patients  19% to 50%.  Prophylactic measures   passive range of motion,  early ambulation,  rotating beds,  electrical stimulation of calf muscles  Pharmacologic anticoagulation  increase the effectiveness of DVT prophylaxis  Low-molecular-weight heparins can be added to pneumatic compression boots (PCBs) without significantly increased risk of hemorrhage
  • 70. ALGORITHM FOR MANAGEMENT OF MINOR BRAIN INJURY
  • 71. ALGORITHM FOR MANAGEMENT OF MODERATE BRAIN INJURY
  • 72. ALGORITHM FOR INITIAL MANAGEMENT OF SEVERE BRAIN INJURY
  • 73. OUTCOME GLASGOW OUTCOME SCORE
  • 74. PROGNOSIS  Worse prognosis when:  bilaterally dilated (> 4 mm)  absent pupillary light reflexes,  absent oculocephalic or oculovestibular reflexes,  increased injury severity scale (> 40),  extreme age (> 60 and possibly < 2),  hypotension (SBP < 90 mmHg , worse with concomitant hypoxemia),  abnormalCT scan (extensive tSAH, compression or obliteration of basal cisterns),  persistent ICP > 20 mm Hg,  elevated ICP during the first 24 hours  lower GCS subscores (motor ≤3, eye opening ≤2, verbal response ≤2)
  • 75. BRAIN DEATH DETERMINATION AND ORGAN DONATION  Brain death  the absence of any observable neurological activity in the brain and the irreversibility of cessation of the cardiopulmonary system or the entire brain.  Requirements  No complicating conditions:  Hypothermia <32.2°C,  Hypotension [SBP<90]  Exogenous sedatives,  Paralytics  drug/alcohol  Hepatic encephalopathy,  Hyperosmolar coma,  Atropine  Recent CPR/shock/anoxia
  • 76. BRAIN DEATH DETERMINATION AND ORGAN DONATION  Patient’s condition:  fixed, dilated pupils  no observable corneal, oculocephalic, oculovestibular, gag, or cough reflexes  no movement to deep central or peripheral pain  no spontaneous breathing is seen on disconnection from the ventilator with PaCO2 >60 mm Hg (i.e., apnea test).  Head-injured patients who progress to brain death may be candidates for organ donation  Organ donation can provide family members with a slightly more positive conclusion to a series of unfortunate events.
  • 77. REFERENCES 1. Mattox K, Moore E, Feliciano D.Trauma, Seventh Edition. McGraw Hill Professional; 2012. 2. Jr HRJ Jr, Srinivasan J, Allam GJ, Baker RA. Netter’s Neurology. Elsevier Health Sciences; 2011. 3. American College of Surgeons, Committee onTrauma. ATLS, advanced trauma life support for doctors: student course manual. 8th ed. Chicago, IL: American College of Surgeons; 2008. 
  • 78. THANKYOU

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