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

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

8. GENERAL PRINCIPLES

9. 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

10. 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

12. 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

14. 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).

15. 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

17. GLASGOW COMA SCALE (RECOMMENDED
FOR AGE ≥4)

18. GLASGOW COMA SCALE FOR CHILDREN
(RECOMMENDED FOR AGE <4)

19. RADIOGRAPHIC EVALUATION

20. 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

21. 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

22. 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

23. CLASSIFICATION AND SURGICAL
MANAGEMENT OF SPECIFIC
INJURIES

24. 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

25. CT bone windows showing ping-pong skull
fracture.
The multiple nondisplaced linear lucencies are
normal sutures.

26. 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

27. 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

28. SKULL FRACTURES
RADIOGRAPHIC DIAGNOSIS
 Differential Diagnosis of Fractures on Skull X-Rays

29. 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

30. 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

31. 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

32. SKULL FRACTURES
 Indications for surgery:
 significant intracranial hematoma,
 depression >1 cm,
 frontal sinus involvement,
 Gross cosmetic deformity,
 wound infection,
 pneumocephalus,
 gross wound contamination

33. 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

34. 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

35. 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

36. 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

37. CT showing epidural hemorrhage. Note the biconvex- or lenticular-shaped hemorrhage.
On the bone windows this was adjacent to a diastatic left lambdoid suture.

38. 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%)

40. 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

41. 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

44. CT showing an acute subdural hemorrhage. Note that crescentic hemorrhage
crosses under the right coronal suture.

45. APPEARANCE OF SDH ON CT AND MRI

46. 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

48. 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)

49. CT with arrow pointing to a small traumatic subarachnoid
hemorrhage in left central sulcus

50. CT AND ANGIOGRAM OF ICH

51. 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

52. CONCUSSION GRADING

53. 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

54. 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.

56. MANAGEMENT OF
TRAUMATIC BRAIN INJURY

57. 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)

58. 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

59. 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

60. 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.

62. 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.

64. 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

65. 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

66. 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

67. 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

68. 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

69. 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

70. 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

71. CT of a bilateral hemispheric decompressive craniectomy
performed in a patient with severe edema from a likely
second impact syndrome.

72. 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

73. 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%

74. 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

75. 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)

76. STEROIDS
 Glucocorticoids are not recommended
 Side effects of steroid:
 coagulopathies,
 hyperglycemia,
 increased infection

77. SPECIFIC SYSTEM
CONSIDERATIONS

78. 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

79. 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

80. 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

81. 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

82. ALGORITHM FOR MANAGEMENT OF
MINOR BRAIN INJURY

83. ALGORITHM FOR MANAGEMENT OF
MODERATE BRAIN INJURY

84. ALGORITHM FOR INITIAL MANAGEMENT
OF SEVERE BRAIN INJURY

85. OUTCOME
GLASGOW OUTCOME SCORE

86. 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)

87. 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

88. 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.

89. 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.


90. THANKYOU