Head Trauma. Minor head trauma (Glasgow Coma Scale [GCS] score of 14 to 15) or presence of any intracranial contusion, hematoma, or laceration

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1 Minor head trauma (Glasgow Coma Scale [GCS] score of 14 to 15) or presence of any intracranial contusion, hematoma, or laceration Moderate head injuries (GCS of 9 to 13) Severe head injuries (GCS of 8 or less)

2 External physical signs of head trauma not always present in the patient who has sustained serious underlying traumatic brain injury (TBI).

3 Cerebral Hemodynamics Blood-Brain Barrier. The normal pressure exerted by the CSF is 65 to 195 mm H2O or 5 to 15 mm Hg.

4 Cerebral Hemodynamics Blood-Brain Barrier. Head Trauma Hypertension, alkalosis, and hypocarbia promote cerebral vasoconstriction; hypotension, acidosis, and hypercarbia cause cerebral vasodilation.

5 Cerebral Hemodynamics Pco2 Over time, injured vessels lose their responsiveness to hypocarbia become vasodilated. increased brain swelling and mass effect.

6 Cerebral Hemodynamics Po2 Low Po cerebral vessels dilate vasogenic edema. So hypoxia should be treated

7 Cerebral Perfusion Pressure & BP Head Trauma CPP is estimated as MAP minus ICP. CBF remains constant when CPP is 50 to 160 mm Hg. If CPP falls below 40 mm Hg, the autoregulation of CBF is lost----ischemia So hypotension & increased ICP should controlled

8 Primary and Secondary Brain Injury Primary ---- damage that occurs at the time of head trauma. it causes permanent mechanical cellular disruption and microvascular injury. Secondary brain injury results from intracellular and extracellular derangements All currently used acute therapies for TBI are directed at reversing or preventing secondary injury.

9 Secondary Brain Injury Influence the outcome Common secondary systemic insults in trauma patients include Hypotension Hypoxia Anemia. hypercarbia, hyperthermia, coagulopathy, and seizures.

10 Secondary Brain Injury Head Trauma All Bad Hypotension doubles the mortality Hypoxia, defined as a Po2 less than 60 mm Hg Anemia When anemia (hematocrit less than 30%) occurs in patients with severe head injury, the mortality rate increases Brain Trauma Foundation, American Association of Neurological Surgeons, Joint Section on Neurotrauma and Critical Care : Guidelines for the management of severe traumatic brain injury. J Neurotrauma 2000; 17:471.

11 Contributing events in the pathophysiology of secondary brain injury.

12 Altered Levels of Consciousness hallmark of brain insult Causes hypoxic Hypotension intoxication consumed before the injury.

13 Cushing's Reflex Progressive hypertension associated with bradycardia and diminished respiratory effort D/T acute, potentially lethal rises in ICP. The full triad of hypertension, bradycardia, and respiratory irregularity is seen in only one third of cases of life-threatening increased ICP.

14 Cerebral Herniation When increasing ICP cannot be controlled, the intracranial contents shift and herniate through the cranial foramen. Herniation can occur within minutes to days mortality approaches 100% without rapid implementation of temporizing emergency measures and definitive neurosurgical therapy.

15 Uncal Cerebral Herniation The most common a form of transtentorial herniation. hematomas in the lateral middle fossa or the temporal lobe. the third cranial nerve is compressed; ipsilateral anisocoria, ptosis, impaired extraocular movements, and a sluggish pupillary light reflex As the herniation progresses, compression of the ipsilateral oculomotor nerve eventually causes ipsilateral pupillary dilation and nonreactivity.

16 Uncal Cerebral Herniation contralateral Babinski's Contralateral hemiparesis decerebrate posturing eventually occurs; LOS & change in respiratory pattern, and cv system. Herniation that is uncontrolled progresses rapidly to brainstem failure, cardiovascular collapse, and death. Kernohan's notch syndrome When hemiparesis is detected ipsilateral to the dilated pupil and the mass lesion, it causes false-localizing motor findings

17 CLINICAL FEATURES, History mechanism comorbid factors. Past medical history, Medications level of consciousness, course Witnessed posttraumatic seizures apnea

18 Acute Neurologic General Examination Identification of life-threatening injuries and of neurologic changes in the immediate posttrauma period. mental status GCS pupillary size Responsiveness motor strength and symmetry. neurologic assessment in the immediate posttrauma period serves as a baseline

19 Glasgow Coma Scale The GCS assesses a patient's best eye, verbal, and motor responsiveness. limitations. Hypoxia, hypotension, and intoxication can falsely lower the initial GCS. Intubation Periorbital edema Extremity fractures Decisions on continued resuscitation should not be based on the initial GCS

20 Pupillary Examination must be done early A large fixed pupil suggests herniation syndrome Limitations: Traumatic mydriasis, resulting from direct injury to the eye and periorbital structures, may confuse the assessment of the pupillary responsiveness.

21 Motor Examination: Posturing Head Trauma A false-localizing motor examination can be caused by contralateral cerebral parenchymal injury occurring simultaneously with the expanding mass lesion or by Kernohan's notch syndrome occult extremity trauma spinal cord injury nerve root injury motor movement should be elicited by application of noxious stimuli.

22 Motor Examination: Posturing Decorticate posturing implies injury above the midbrain. Decerebrate posturing is the result of a more caudal injury and therefore is associated with a worse prognosis.

23 Brainstem Function respiratory pattern pupillary size eye movements The oculocephalic response The oculovestibular response (cold water calorics) (CN) examination is often limited to the pupillary responses (CN III), gag reflex (CNs IX and X) corneal reflex (CNs V and VII). Facial symmetry (CN VII) with noxious stimuli.

24 Clinical Characteristics of Basilar Skull Fractures Blood in ear canal Hemotympanum Rhinorrhea Otorrhea Battle's sign (retroauricular hematoma) Raccoon sign (periorbital ecchymosis) Facial paralysis Decreased auditory acuity Dizziness Tinnitus Nystagmus Cranial nerve deficits

25 Clinical prognostic indicators initial motor activity pupillary responsiveness Age premorbid condition secondary systemic insult The prognosis cannot be reliably predicted by the initial GCS or initial CT scan.

26 MANAGEMENT, Laboratory Tests complete blood count Electrolytes Glucose coagulation studies. ECG

27 MANAGEMENT, Neuroimaging Head Trauma non contrast-enhanced head CT scan. Emergency management decisions are strongly influenced by these acute CT scan findings. MRI is better than CT in detecting posttraumatic ischemic infarctions subacute nonhemorrhagic lesions contusions axonal shear injury lesions in the brainstem or posterior fossa

28 MANAGEMENT Out-of-Hospital Care The goals of the out-of-hospital management are necessary airway interventions to prevent hypoxia establishing intravenous (IV) access to treat trauma-related hypotension. GCS pupillary responsiveness and size level of consciousness motor strength and symmetry.

29 MANAGEMENT All head-injured patients should have a cardiac monitor as they are transported from the accident scene.

30 MANAGEMENT, Airway Rapid sequence intubation (RSI) If possible, a brief neurologic examination Lidocaine (1.5 to 2 mg/kg IV push) may help Thiopental may also be effective but should not be used in hypotensive patients. Etomidate (0.3 mg/kg IV) a short-acting sedative-hypnotic agent has beneficial effects on ICP by reducing CBF and metabolism. minimal adverse effects on blood pressure

31 MANAGEMENT, Hypotension rarely caused by head injury in adult spinal cord injury, neurogenic hypotension may occur. fluids do not produce clinically significant increases in ICP; SO should never be withheld in the head trauma patient with hypovolemic hypotension for fear of increasing cerebral edema and ICP normal saline or lactated Ringer's solution or hypertonic saline

32 MANAGEMENT, Hyperventilation Head Trauma only in patients demonstrating neurologic deterioration. onset of action is within 30 seconds peaks within 8 minutes after the Pco2 drops to the desired range. Pco2 should not fall below 25 mm Hg

33 MANAGEMENT, Mannitol Head Trauma for increased ICP Mannitol (0.25 to 1 g/kg) occur within minutes peak about 60 minutes after bolus administration. The ICP-lowering effects of a single bolus may last for 6 to 8 hours.

34 MANAGEMENT, Mannitol It is an effective volume expander It also promotes CBF by reducing blood viscosity and microcirculatory resistance. It is an effective free radical scavenger, Limitation renal failure or hypotension if given in large doses. paradoxical effect of increased bleeding into a traumatic lesion by decompressing the tamponade effect of a hematoma.

35 MANAGEMENT, Hypertonic Saline Head Trauma also improves hemodynamics by plasma volume expansion, reduction of vasospasm by increasing vessel diameter, and reduction of the posttraumatic inflammatory response. Concerns osmotic demyelinization syndrome acute renal failure Coagulopathies Hypernatremia red blood cell lysis.

36 MANAGEMENT, Barbiturates Head Trauma If other methods unsuccessful, it may be added in the hemodynamically stable patient. Pentobarbital is the barbiturate most often used

37 MANAGEMENT, Steroids Head Trauma No evidence indicates that steroids are of benefit in head injury.

38 MANAGEMENT, Seizure Prophylaxis immediate posttrauma seizures ---no predictive value for future epilepsy early seizures can cause Hypoxia Hypercarbia release of excitatory neurotransmitters increased ICP

39 MANAGEMENT, Seizure Prophylaxis Lorazepam (0.05 to 0.15 mg/kg IV, over 2 to 5 minutes up to a total of 4 mg) has been found to be most effective at aborting status epilepticus Diazepam (0.1 mg/kg, up to 5 mg IV, every 10 minutes up to a total of 20 mg) is an alternative. For long-term anticonvulsant activity, phenytoin (13 to 18 mg/kg IV) or fosphenytoin (13 to 18 phenytoin equivalents/kg) can be given.

40 MANAGEMENT, Seizure Prophylaxis In a review published in the Cochrane database, the use of antiepileptic drugs reduced the risk of early seizures by 66%. all paralyzed head-injured patients should have prophylactic anticonvulsant & Continuous electroencephalographic monitoring

41 Indications for Acute Seizure Prophylaxis in Severe Head Trauma Depressed skull fracture Paralyzed and intubated patient Seizure at the time of injury Seizure at emergency department presentation Penetrating brain injury Severe head injury (Glasgow Coma Scale score 8) Acute subdural hematoma Acute epidural hematoma Acute intracranial hemorrhage Prior history of seizures

42 MANAGEMENT, Antibiotic Prophylaxis Infection may occur as a complication of penetrating head injury open skull fractures complicated scalp lacerations. Not indicated in BSF

43 MANAGEMENT, Disposition Consultation Neurosurgical consultation should be obtained as soon as possible to help direct the patient's subsequent management.

44 MANAGEMENT, Transfer Head Trauma Severely head-injured patients require admission to an institution capable of intensive neurosurgical care and acute neurosurgical intervention.

45 COMPLICATIONS AFTER HEAD INJURY Neurologic Complications Seizures common in the acute or subacute period. Acute posttraumatic seizures are usually brief After the acute seizure, the patient often has no additional seizure activity. In the subacute period, 24 to 48 hours after trauma, seizures are caused by worsening cerebral edema, small hemorrhages, or penetrating injuries.

46 COMPLICATIONS AFTER HEAD INJURY Meningitis after Basilar Fractures In patients with a CSF leak after basilar fracture, early meningitis,within 3 days of injury) Pneumococci Ceftriaxone or cefotaxime Vancomycin if a high regional pneumococcal resistance exists. Gram-negative------more than 3 days after trauma A third-generation cephalosporin, with nafcillin or vancomycin added to ensure coverage of Staphylococcus aureus. Prophylactic antibiotics are not currently recommended Lapointe M, et al: Basic principles of antimicrobial therapy of CNS infections. In: Cooper PR, Golfinos JG, ed. Head Injury, 4th ed.. New York: McGraw- Hill; 2000:483.

47 COMPLICATIONS AFTER HEAD INJURY Brain Abscess CT. A ring pattern The treatment is usually operative drainage. The patient with cerebritis may respond to IV antibiotics. Common organisms are S. aureus and gramnegative aerobes Cranial Osteomyelitis wuth penetrating injury to the skull.

48 COMPLICATIONS AFTER HEAD INJURY Medical Complications DIC The injured brain is a source of tissue thromboplastin that activates the extrinsic clotting system. Neurogenic Pulmonary Edema

49 Medical Complications Cardiac Dysfunction Head Trauma COMPLICATIONS AFTER HEAD INJURY can be life threatening and require aggressive therapy. cardiac dysrhythmia after head injury is supraventricular tachycardia, diffuse large upright or inverted T waves, prolonged QT intervals, ST segment depression or elevation, and U waves. Dysrhythmias in head-injured patients often resolve as ICP is reduced. Standard ACLS

50 Contusions: Are bruises on the surface of the brain, usually caused by impact injury. Epidural Hematoma (EDHs): Are blood clots that form between the inner table of the skull and the dura. Subdural Hematoma (SDHs): are blood clots that form between the dura and the brain.

51 Traumatic Subarachnoid Hemorrhage (TSAH): is defined as blood within the CSF and meningeal intima. Intracerebral Hematoma (ICHs): are formed deep within the brain tissue All types of head injuries with cranial hematoma should be admitted initially to critical care area with neurosurgical consultation.

52 Initial resuscitation of patient with severe head injury: treatment options

53 Severe and Moderate Head Injuries All patients with severe or moderate head injury require serial neurologic examinations Acute herniation syndrome manifested by neurologic deterioration should initially be managed with short-term hyperventilation, to a Pco2 of 30 to 35 mm Hg, with monitoring and then surgical intervention as soon as possible. Long-term hyperventilation is not indicated. Mannitol should be used only in patients with increasing ICPs or acute neurologic deterioration. Secondary systemic insults such as hypoxia and hypotension worsen neurologic outcome after severe and moderate head trauma and should be corrected as soon as detected

54 Severe and Moderate Head Injuries For adult patients, hypotension in the presence of isolated severe head injury is a preterminal event. Hypotension usually results from comorbidity, and its cause should be sought and treated. The Glasgow Coma Scale is a useful clinical tool for following headinjured patients' neurologic status, but because of its limitations, the initial GCS in the emergency department cannot reliably predict prognosis after acute head injury. Head-injured patients who have been chemically paralyzed do not have clinical manifestations of seizures; anticonvulsants should be given prophylactically. Most talk and deteriorate patients who present with moderate head injury have subdural or epidural hematomas. Early detection, CT scan, and expedient surgical intervention are the keys to a good outcome.

55 Minor Head Trauma The decision to perform CT scans on patients with minor head trauma should be individualized but based on consideration of high- and moderate-risk criteria.

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