Head Trauma PDF

| 14.02.23 - 13:46 1000 Head Trauma 60 Head Trauma – General Information, Grading, Initial Management 60.1 Head trauma – general information 60.1.1 Introduction 56–60% of patients with GCS score ≤ 8 have 1 or more other organ system injured.1 25% have “surgi- cal” lesions. There is a 4–5% incidence of associated spine fractures with significant head injury (mostly C1 to C3). When a detailed history is unavailable, remember: the loss of consciousness may have preceded (and possibly have caused) the trauma. Therefore, maintain an index of suspicion for e.g., aneurysmal SAH, hypoglycemia, etc. in the diﬀerential diagnosis of the causes of trauma and associated coma. Brain injury from trauma results from two distinct processes: 1. primary brain injury: occurs at time of trauma (cortical contusions, lacerations, bone fragmenta- tion, diﬀuse axonal injury, and brainstem contusion) 2. secondary injury: develops subsequent to the initial injury. Includes injuries from intracranial hematomas, edema, hypoxemia, ischemia (primarily due to elevated intracranial pressure (ICP) and/or shock), vasospasm Since impact damage cannot be influenced by the treating neurosurgeon, intense interest has focused on reducing secondary injuries, which requires good general medical care and an under- standing of intracranial pressure (p. 1036). 60.1.2 Delayed deterioration ≈ 15% of patients who do not initially exhibit signs of significant brain injury may deteriorate in a delayed fashion, sometimes referred to as patients who “talk and deteriorate,” or when more lethal, patient who “talk and die.”2 Etiologies: 1. ≈ 75% will exhibit an intracranial hematoma a) may be present on initial evaluation and can then worsen b) may develop in a delayed fashion delayed epidural hematoma (EDH) (p. 1075) delayed subdural hematoma (SDH) (p. 1081) delayed traumatic contusions (p. 1072) 2. posttraumatic diﬀuse cerebral edema (p. 1026) 3. hydrocephalus 4. tension pneumocephalus 5. seizures 6. metabolic abnormalities, includes: a) hyponatremia b) hypoxia: etiologies include pneumothorax, MI, CHF… c) hepatic encephalopathy d) hypoglycemia: including insulin reaction e) adrenal insuﬃciency f) drug or alcohol withdrawal 7. vascular events a) dural sinus thrombosis (p. 1594) b) carotid (or rarely, vertebral) artery dissection (p. 1578) c) SAH: due to rupture of aneurysm (spontaneous or posttraumatic) or carotid-cavernous fistula (CCF) (p. 1519) d) cerebral embolism: including fat embolism syndrome (p. 1013) 60 8. meningitis 9. hypotension (shock) 60.2 Grading Despite many (valid) criticisms, the initial post-resuscitation Glasgow Coma Scale (GCS) score (▶ Table 18.1) remains the most widely used and perhaps best replicated scale employed for the | 14.02.23 - 13:46 Head Trauma – General Information, Grading, Initial Management 1001 assessment of head trauma. Problems with this type of scale include that it is an ordinal scale that is non parametric (i.e., does not represent precise measurements of discrete quantities), it is non-linear, and it is not an interval scale, so that for example, a decrease of 2 points in one parameter is not neces- sarily equal to a decrease in 2 points of another.3 Thus, performing mathematical manipulations (e.g., adding components, or calculating mean values), while often done, is not statistically sound.4 ▶ Stratification. There are a number of schemes to stratify the severity of head injury. Any such cat- egorization is arbitrary and will be imperfect. A simple system based only on GCS score is as follows: GCS 14–15 = mild GCS 9–13 = moderate GCS ≤ 8 = severe More elaborate systems (e.g., ▶ Fig. 60.1 3) may incorporate factors in addition to the GCS. Minimal Mild Moderate Severe GCS = 15 GCS = 14 4 13 GCS = 9–1 GCS = 3–8 No loss of conscious- OR OR ness (LOC) GCS = 15 5 plus EITHER EITHE Critical† No amnesia LOC ≥ 5mins Brief LOC (< 5 mins) GCS = 3–4 OR Impaired OR alertness or memory al neurologi Focal neurologic deficit Concussion * Abbreviations: LOC = loss of consciousness, GCS = Glasgow Coma Scale score. † “Critical” designation is used by some to indicate the most severe injuries (GCS=3-4). Fig. 60.1 Sample stratification scheme for head injury severity.3 60.3 Transfer of trauma patients It is sometimes necessary for a neurosurgeon to accept a trauma patient in transfer from another institution that is not equipped to handle major neurologic injuries, or to transfer patients to other facilities for a variety of reasons. ▶ Table 60.1 lists factors that should be assessed and stabilized (if Table 60.1 Factors to assess in head injured patients Clinical concern Items to check Steps to remedy hypoxia or hypoventilation ABG, respiratory rate intubate any patient who has hypercarbia, hypoxemia, or is not localizing hypotension or hypertension BP, Hgb/Hct transfuse patients with significant loss of blood volume anemia Hgb/Hct transfuse patients with significant anemia seizures electrolytes, ASM correct hyponatremia or hypoglycemia; administer levels ASMs when appropriatea 60 infection or hyperthermia WBC, temperature LP if meningitis is possible and no contraindications (p. 1811) spinal stability spine X-rays spine immobilization (spine board, cervical collar & sandbags…); patients with locked facets should be reduced if possible before transfer asee Seizures (p. 480), as well as Posttraumatic seizures (p. 504) | 14.02.23 - 13:46 1002 Head Trauma possible) prior to transfer. These items should also be evaluated in trauma patients about whom a neurosurgeon is consulted in his or her own E/R, as well as in patients with other CNS abnormalities besides trauma (e.g., SAH). 60.4 Management in E/R 60.4.1 General measures Blood pressure and oxygenation Practice guideline: BP and oxygenation Level II5: monitor BP and avoid hypotension (SBP < 90 mm Hg) Level III5: monitor oxygenation and avoid hypoxia (PaO2 < 60 mm Hg or O2 saturation < 90%) Hypotension Hypotension (shock) is rarely attributable to head injury except: in terminal stages (i.e., with dysfunction of medulla and cardiovascular collapse) where enough blood has been lost from scalp wounds to cause hypovolemia (exsanguination) in infancy, where enough blood can be lost intracranially or into the subgaleal space to cause shock Hypotension (defined as a single SBP < 90 mm Hg) doubles mortality, hypoxia (apnea or cyanosis in the field, or PaO2 < 60 mm Hg on ABG) also increases mortality,6 and the combination of both triples mortality and increases the risk of bad outcome. SBP < 90 mm Hg may impair CBF and exacerbate brain injury and should be avoided (p. 1050). Early use of paralytics and sedation (prior to ICP monitoring) Practice guideline: Early sedation and paralysis Level III7: sedation and neuromuscular blockade (NMB) can be helpful for transporting the head- injured patient, but they interfere with the neuro exam Level III7: NMB should be used when sedation alone is inadequate The routine use of sedatives and paralytics in neurotrauma patients may lead to a higher incidence of pneumonia, longer ICU stays, and possibly sepsis.8 These agents also impair neurologic assess- ment.7,9 Use should therefore be reserved for cases with clinical evidence of intracranial hyperten- sion (see ▶ Table 60.2), for intubation, or where use is necessary for transport or to permit evaluation of the patient (e.g., to get a combative patient to hold still for a CT scan).10 Table 60.2 Clinical signs of IC-HTNa 1. pupillary dilatation (unilateral or bilateral) 2. asymmetric pupillary reaction to light 3. decerebrate or decorticate posturing (usually contralateral to blownb pupil) 4. progressive deterioration of the neurologic exam not attributable to extracranial factors 60 aItems 1–3 represent clinical signs of herniation. The most convincing clinical evidence of IC-HTN is the witnessed evolution of 1 or more of these signs. IC-HTN may produce a bulging fontanelle in an infant. b“blown pupil”: fixed & dilated pupil | 14.02.23 - 13:46 Head Trauma – General Information, Grading, Initial Management 1003 Intubation and hyperventilation Indications for intubation in trauma; also see Practice guideline: Intubation – indications (p. 1003): 1. depressed level of consciousness (patient cannot protect airway): usually GCS ≤ 7 2. need for hyperventilation (HPV): see below 3. severe maxillofacial trauma: patency of airway tenuous or concern for inability to maintain patency with further tissue swelling and/or bleeding 4. need for pharmacologic paralysis for evaluation or management Practice guideline: Intubation—indications Level III11: secure the airway (usually by endotracheal intubation) in patients with GCS ≤ 8 who are unable to maintain their airway or who remain hypoxic despite supplemental O2 Cautions regarding intubation: 1. if basal skull fracture through cribriform plate is possible, avoid nasotracheal intubation (to avoid intracranial entry of tube). Use orotracheal intubation 2. prevents assessment of patient’s ability to verbalize9 e.g., for determining Glasgow Coma Scale score. This ability should be noted (none, unintelligible, inappropriate, confused, or oriented) prior to intubation 3. risk of pneumonia: see Practice guideline: Antibiotics for intubation (p. 1003) regarding antibiotics Practice guideline: Antibiotics for intubation Level II12: periprocedural antibiotics for endotracheal intubation reduce the risk of pneumonia, but do not alter length of stay or mortality Hyperventilation (HPV) Practice guideline: Early/prophylactic hyperventilation Level II13: prophylactic hyperventilation (PaCO2 ≤ 25 mm Hg) is not recommended Level III hyperventilation (HPV) before ICP monitoring is established should be reserved as a temporizing measure13 for patients with signs of transtentorial herniation (see ▶ Table 60.2) or progressive neurologic deterioration not attributable to extracranial causes7 HPV should be avoided during the first 24 hrs after TBI (when CBF is often dangerously decreased)13 1. since HPV may exacerbate cerebral ischemia, HPV should not be used prophylactically (p. 1052) 2. prior to ICP monitoring, HPV should only be used briefly when CT or clinical signs of IC-HTN are present10 (see ▶ Table 60.2 for clinical signs) a) when appropriate indications are met: HPV to PaCO2 = 30–35 mm Hg b) HPV should not be used to the point that PaCO2 < 30 mm Hg (this further reduces CBF but does not necessarily reduce ICP) 3. acute alkalosis increases protein binding of calcium (decreases ionized Ca + + ). Patients being 60 hyperventilated may develop ionized hypocalcemia with tetany (despite normal total [Ca]) | 14.02.23 - 13:46 1004 Head Trauma Mannitol in E/R Practice guideline: Early use of mannitol Level III7,14: the use of mannitol before ICP monitoring is established should be reserved for patients who are adequately volume-resuscitated with signs of transtentorial herniation (see ▶ Table 60.2) or progressive neurologic deterioration not attributable to extracranial causes Indications in E/R, see also more details (p. 1053): 1. evidence of intracranial hypertension (see ▶ Table 60.2) 2. evidence of mass eﬀect (focal deficit, e.g., hemiparesis) 3. sudden deterioration prior to CT (including pupillary dilatation) 4. after CT, if a lesion that is associated with increased ICP is identified 5. after CT, if going to O.R. 6. to assess “salvageability”: in patient with no evidence of brainstem function, look for return of brainstem reflexes Contraindications: 1. prophylactic administration is not recommended due to its volume-depleting eﬀect. Use only for appropriate indications (see above) 2. hypotension or hypovolemia: hypotension can negatively influence outcome.10 Therefore, when intracranial hypertension (IC-HTN) is present, first utilize sedation and/or paralysis, and CSF drainage. If further measures are needed, fluid resuscitate the patient before administering man- nitol. Use hyperventilation in hypovolemic patients until mannitol can be given 3. relative contraindication: mannitol may slightly impede normal coagulation 4. CHF: before causing diuresis, mannitol transiently increases intravascular volume. Use with cau- tion in CHF, may need to pre-treat with furosemide (Lasix®) ℞: bolus with 0.25–1 gm/kg over < 20 min (for average adult: ≈ 350 ml of 20% solution). Peak eﬀect occurs in ≈ 20 minutes (p. 1053) (for follow-up dosing). Prophylactic antiseizure medications (ASMs) Practice guideline: Prophylactic antiseizure medications after TBI Level II15,16,17: prophylactic phenytoin, carbamazepine, phenobarbital, or valproate18 do not prevent late PTS Level II: ASMs17 (e.g., phenytoin, valproate, or carbamazepine15,16,18) may be used to decrease the incidence of early PTS (within 7 days of TBI) in patients at high risk of seizures after TBI (see ▶ Table 60.3); however, this does not improve outcome Routine use of prophylactic antiseizure medications (ASMs) in traumatic brain injury (TBI) is ineﬀec- tive in preventing the late development of posttraumatic seizures (PTS) i.e., epilepsy, and has been shown to not be useful except in certain circumstances.15,16 Table 60.3 Conditions with increased risk of posttraumatic seizures 1. acute subdural, epidural, or intracerebral hematoma (SDH, EDH or ICH) 60 2. open-depressed skull fracture with parenchymal injury 3. seizure within the first 24 hrs after injury 4. Glasgow Coma Scale score < 10 5. penetrating brain injury 6. history of significant alcohol abuse 7. ± cortical (hemorrhagic) contusion on CT | 14.02.23 - 13:46 Head Trauma – General Information, Grading, Initial Management 1005 See details on using (p. 506) and discontinuing (p. 506) prophylactic ASMs following TBI. ▶ Table 60.3 reiterates the markers for patients at increased risk of early PTSs. 60.4.2 Neurosurgical exam in trauma General information It is not possible to outline a physical exam that is universally applicable. Major trauma must be assessed rapidly, often under chaotic circumstances, and must be individualized based on patient’s medical stability, type of injury, degree of combativeness, use of pharmacologic paralytics (p. 1002), the needs of other caregivers attending to other organ injuries, the need to triage in the event of multiple patients requiring simultaneous attention… The following describes some features that should be assessed under certain circumstances with the understanding that this must be individualized. This addresses only craniospinal injuries, and assumes that general systemic injuries (internal bleeding, myocardial and/or pulmonary contu- sion…) as well as orthopedic injuries (long bone and pelvic fractures…) will be treated by other members of a “trauma team.” Although organized here in outline form, the most eﬃcient order of examination is usually dictated by circumstances unique to each situation. General physical condition (oriented towards neuro assessment) 1. visual inspection of cranium: a) evidence of basal skull fracture (p. 1064): raccoon’s eyes (AKA Panda bear sign): periorbital ecchymoses Battle’s sign: postauricular ecchymoses (around mastoid air sinuses) CSF rhinorrhea/otorrhea (p. 418) hemotympanum or laceration of external auditory canal b) check for facial fractures Le Fort fractures (p. 1067): palpate for instability of facial bones, including zygomatic arch orbital rim fracture: palpable step-oﬀ c) periorbital edema, proptosis 2. cranio-cervical auscultation a) auscultate over carotid arteries: bruit may indicate carotid dissection b) auscultate over globe of eye: bruit may indicate traumatic carotid-cavernous fistula CCF; see Carotid-cavernous fistula (p. 1519) 3. physical signs of trauma to spine: bruising, deformity 4. evidence of seizure: single, multiple, or continuing (status epilepticus) Neurologic exam 1. cranial nerve exam a) optic nerve function (p. 1014) if conscious: serial quantitation of vision in each eye is important.19 A Rosenbaum near vision card is ideal (see inside back cover), otherwise use any printed material. If patient cannot see this, check if they can count fingers. Failing this, check for hand motion vision and lastly light perception. Children may develop transient cortical blindness lasting 1–2 days, usually after a blow to the back of the head if unconscious: check for aﬀerent pupillary defect (p. 592), best demonstrated with swing- ing flashlight test (p. 591). Indicates possible optic nerve injury funduscopic exam: check for papilledema, pre-retinal hemorrhages, retinal detachment, or retinal abnormalities suggestive of anterior optic nerve injury. If a detailed exam is required, pharmacologic dilatation with mydriatics (p. 593) may be employed; however, this precludes pupillary exam for a variable period of time, and should be undertaken advisedly b) pupil: size in ambient light; reaction to light (direct & consensual) c) VII: check for peripheral VII palsy (p. 1064) (facial asymmetry of unilateral upper and lower facial muscles) 60 d) VI: abducens palsy (p. 598) following trauma may occur as a result of ↑ ICP or with clival frac- tures (p. 1065) | 14.02.23 - 13:46 1006 Head Trauma 2. level of consciousness/mental status a) Glasgow coma scale for quantitating level of consciousness in poorly responsive patient (see ▶ Table 18.1) b) check orientation in patient able to communicate 3. motor exam (assesses motor tracts from motor cortex through spinal cord) a) if patient is cooperative: check motor strength in all 4 extremities b) if uncooperative: check for appropriate movement of all 4 extremities to noxious stimulus (diﬀerentiate voluntary movement from posturing or stereotypical spinal cord reflex). This also assesses sensation in an unresponsive patient c) if any doubt about integrity of spinal cord: also check “resting” tone of anal sphincter on rectal exam, evaluate voluntary sphincter contraction if patient can cooperate, check anal wink with pinprick, and assess bulbocavernosus reflex (p. 1130) (see Neurological assessment, for details) 4. sensory exam a) cooperative patient: check pinprick on trunk and in all 4 extremities, touch on major dermatomes (C4, C6, C7, C8, T4, T6, T10, L2, L4, L5, S1, sacrococcygeal) check posterior column function: joint position sense of LEs b) uncooperative patient: check for central response to noxious stimulus (e.g., grimace, vocaliza- tion…, as opposed to flexion-withdrawal, which could be a spinal cord mediated reflex) 5. reflexes a) muscle stretch (“deep tendon”) reflexes if patient is not thrashing: e.g., preserved reflex indi- cates that a flaccid limb is due to CNS injury and not nerve root injury (and vice versa) b) check plantar reflex for upgoing toes (Babinski sign) c) in suspected spinal cord injury: the anal wink and bulbocavernosus reflex are checked on the rectal exam (see above) 60.5 Radiographic evaluation of TBI in the E/R 60.5.1 General information An unenhanced (i.e., non-contrast) CT scan of the head usually suﬃces for patients seen in the emer- gency department presenting after TBI or with a new neurologic deficit. Enhanced CT or MRI may be appropriate after the unenhanced CT in some circumstances, but are not usually required emer- gently (exceptions include: suspected ischemic stroke, significant brain edema on non-contrast CT suggesting a neoplasm that cannot be demonstrated without contrast). Other tests: angiography may be needed acutely in certain circumstances, primarily in penetrat- ing head trauma. Skull X-rays are usually inadequate for primary evaluation, but may be helpful in certain situations, for example with some retained foreign bodies. Spine imaging: victims of TBI are often at risk for concomitant spine injuries. Spine imaging is covered in brief below and in detail under Spine Trauma. See also special considerations in concussion (p. 1023). 60.5.2 Indications for initial brain CT ▶ Initial imaging inconcussion (p. 1019) or mild TBI. There is not uniform agreement about when to obtain an admitting imaging study (usually a noncontrast head CT scan) with mild TBI and con- cussion. Some recommendations for adults are provided below. For patients ≤ 16 years see Pediatric head injuries (p. 1099). Also see Initial imaging for moderate to severe TBI (p. 1008) for indications for CT in severe TBI and for specific conditions excluded from the mTBI guidelines (e.g., penetrating skull trauma). The American College of Emergency Physicians (ACEP) guidelines (p. 1007) 20 for initial imaging for mTBI in patients ≥ 16 years age is based on previously published rules (including the Canadian CT Head Rule (p. 1007) for GCS = 13-15, and the New Orleans Criteria (▶ Table 60.5) for GCS = 15, which are included below for completeness since they are validated and in common use). The ACEP guide- 60 lines have not been validated. | 14.02.23 - 13:46 Head Trauma – General Information, Grading, Initial Management 1007 Practice guideline: initial head CT with mTBI (ACEP policy) Noncontrast head CT for patients ≥ 16 years age with GCS = 14-15 following non-penetrating TBI are indicated only if one or more of the following is present Level I20: For patients with LOC or posttraumatic amnesia headache vomiting age > 60 years intoxication (alcohol or drugs) short-term memory deficits physical signs of trauma above the clavicle posttraumatic seizure GCS < 15 focal neurologic deficit coagulopathy (including anticoagulants/antiplatelet drugs)* Level II20: For patients without LOC or posttraumatic amnesia focal neurologic deficit vomiting severe headache age ≥ 65 years signs of basal skull fracture (includes hemotympanum, “raccoon’s eyes” (p. 1065), CSF rhinor- rhea or otorrhea, Battle’s sign (p. 1065)) GCS < 15 coagulopathy (including anticoagulants/antiplatelet drugs)* dangerous mechanism of injury: pedestrian hit by motor vehicle, ejection from automobile, fall from height > 3 feet or > 5 stairs *data regarding the risk of adverse outcome in anticoagulated patients after mTBI is limited and of low quality21 Canadian CT Head Rule (CCTHR) for mild TBI (GCS = 13-15) (▶ Table 60.4)22 is a validated23 decision rule that may be used to determine if an initial head CT is indicated for mild TBI (Glasgow Coma Scale score (GCS) = 13-15) in patients ≥ 16 years age who have a witnessed loss of consciousness, amnesia or confusion after a TBI who do not have exclusionary criteria listed in the table footnote. ★ The CCTHR is 100% sensitive for injuries requiring neurosurgical intervention.23 Table 60.4 Canadian CT Head Rule (CCTHR)22 Head CT is indicated for patients ≥ 16 years age with GCS = 13-15 from witnessed TBI, only if one or more of any of the following are present*: High-risk criteria (“CT is mandatory”22)(presence of any 1 often requires neurosurgical intervention) GCS < 15 at 2 hours post injury suspected open or depressed skull fracture signs of basal skull fracture (includes hemotympanum, “raccoon’s eyes” (p. 1065), CSF rhinorrhea or otorrhea, Battle’s sign (p. 1065)) 2 or more episodes of vomiting age ≥ 65 years Medium risk criteria (presence of any 2 often have clinically important findings on CT) amnesia before injury > 30 minutes dangerous mechanism of injury: pedestrian hit by motor vehicle, ejection from automobile, fall from height > 3 feet or > 5 stairs 60 * exclusionary criteria for the CCTHR (i.e., these patients were not studied): age < 16, coagulopathy including anticoagulants/antiplatelet drugs, seizure, penetrating skull trauma, focal neurologic deficit, unstable vital signs, return for reassessment of the same injury, pregnancy. NB: intoxication (drugs or alcohol) reduces the sensitivity of the CCTHR to 70%24 | 14.02.23 - 13:46 1008 Head Trauma New Orleans Criteria (NOC) for head CT(▶ Table 60.5)25 may be used for GCS = 15. It may be more sensitive than the CCTHR for showing clinically significant CT findings (99% vs. 87.3%), but it is less specific (5.6% vs. 39.7%). Table 60.5 New Orleans Criteria25 for head CT scan Head CT scan is indicated for patients with TBI and GCS = 15 only if one or more of the following are present: 1. headache 2. vomiting 3. age ≥ 60 years 4. drug or alcohol intoxication 5. persistent anterograde amnesia (short-term memory deficits) 6. visible trauma above the clavicle 7. seizure ▶ Indications for imaging in pediatrics with mTBI26 : See Pediatric head injuries (p. 1099). ▶ Initial imaging for moderate to severe TBI 1. brain CT is indicated in TBI with any of the following risk factors: a) GCS ≤ 14 b) unresponsiveness c) depressed level of consciousness not clearly due to EtOH, drugs, metabolic abnormalities, pos- tictal state, etc. d) coagulopathy including anticoagulants/antiplatelet drugs e) seizure f) penetrating skull trauma g) focal neurologic deficit h) unstable vital signs i) polytrauma j) suspected nonaccidental trauma (i.e., child abuse) k) patients intoxicated with alcohol or other drugs (due to unrealiability of clinical assessment) l) deteriorating neurologic status 2. assessment prior to general anesthesia for other procedures (during which neurologic exam can- not be followed in order to detect delayed deterioration) 60.5.3 CT findings in trauma The main emergent conditions to rule out (and brief descriptions): 1. blood (hemorrhages or hematomas): a) extra-axial blood: surgical lesions are usually ≥ 1 cm maximal thickness epidural hematoma (EDH) (p. 1072): usually biconvex and often due to arterial bleeding. Unlike SDH, EDH may cross dural barriers such as the the falx or tentorium (▶ Fig. 64.2) subdural hematoma (SDH) (p. 1000): usually crescentic, usually due to venous bleeding. May cover larger surface area than EDH (dural adherence to inner table limits extension of EDH). Chronology of SDH: acute = high density, subacute ≈ isodense, chronic ≈ low density b) subarachnoid blood: trauma is the most common cause of subarachnoid hemorrhage (SAH). Unlike aneurysmal SAH (aSAH) (p. 1453) where blood is typically thickest near the circle of Willis, traumatic SAH (tSAH) usually appears as high density spread thinly over the convexity, filling sulci (▶ Fig. 60.2) or basal cisterns. However, when the history of trauma is not clear, a CTA (or catheter arteriogram) may be indicated to R/O a ruptured aneurysm (that might have precipitated the trauma in some cases) c) intracerebral hemorrhage (ICH): increased density in brain parenchyma d) hemorrhagic contusion (p. 1071): often “fluﬀy” inhomogeneous high-density areas within brain parenchyma, usually adjacent to bony prominences (frontal and occipital poles, sphe- 60 noid wing). Typically less well-defined than primary ICH e) intraventricular hemorrhage (p. 1454): present in ≈ 10% of severe head injuries.27 Associated with poor outcome; may be a marker for severe injury rather than the cause of the poor out- come. Use of intraventricular rt-PA has been reported for treatment28 2. hydrocephalus: enlarged ventricles may sometimes develop following trauma https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:46 Head Trauma – General Information, Grading, Initial Management 1009 Fig. 60.2 Traumatic subarachnoid hemorrhage (tSAH) in a 22-year-old patient following an assault, demonstrating an example of tSAH (yellow arrow- heads) overlying the high left convexity. Image: noncontrast axial CT, brain windows. 3. cerebral swelling: obliteration of basal cisterns (p. 1109), compression of ventricles and sulci… 4. evidence of cerebral anoxia: loss of gray-white interface, signs of swelling 5. skull fractures (best appreciated using bone windows): a) basal skull fractures (including temporal bone fracture) b) orbital blow-out fracture c) calvarial fracture (CT may miss some linear nondisplaced skull fractures especially if the frac- ture is in the same plane as the CT slice) linear vs. stellate open vs. closed diastatic (separation of sutures) depressed vs. nondepressed: CT helps assess need for surgery 6. ischemic infarction (stroke): findings are usually minimal or subtle if < 24 hrs since stroke (DWI MRI is the test of choice for this) 7. pneumocephalus: may indicate skull fracture (basal or open convexity) 8. shift of midline structures (due to extra- or intra-axial hematomas or asymmetric cerebral edema): midline shift (p. 1110) can be associated with altered levels of consciousness ▶ Marshall CT classification of TBI. The Marshall CT classification (▶ Table 60.6 29 has 6 categories of TBI severity based on the presence or absence of the factors shown below on a non-contrast head CT. The Marshall score was devised for descriptive purposes, the “Rotterdam score” ▶ Table 60.7 30 is a stronger predictor of outcome. 1. intracranial abnormalities 2. CT evidence of increased ICP as demonstrated by a) midline shif (MLS) > 5 mm and/or b) compression of basal cisterns 3. presence or absence of mass lesions (contusions/hemorrhages) 4. planned evacuation of mass lesions ▶ Rotterdam score for TBI. The Marshall score was devised for descriptive purposes, and while it was subsequently shown to correlate with outcome parameters, including mortality, outcome pre- diction is stronger with the specific CT findings identified by recursive partitioning analysis in the “Rotterdam score” (▶ Table 60.7) which is calculated from a non-contrast head CT obtained within 4 hours of injury. There is evidence that the worst CT scan obtained during the admission has greater 60 predictive value.31 The points from ▶ Table 60.7 are summed, and the predicted 6-month mortality is shown in ▶ Table 60.8. https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:46 1010 Head Trauma Table 60.6 Marshall CT classification of TBI severity29 Category Description Mortality30 I - diffuse injury no visible pathology 6.4% II - diffuse injury MLSa = 0 to 5 mm 11% basal cisterns remain visible no high or mixed density lesions ≥ 25 cm3 esti- mated volumeb, may include bone fragments & foreign bodies III - diffuse injury (swelling) MLS = 0 to 5 mm 29% basal cisterns compressed or completely effacedc no high or mixed density lesions ≥ 25 cm3 IV - diffuse injury (shift) MLS > 5 mm 44% no high or mixed density lesions ≥ 25 cm3 V - evacuated mass lesion any lesion evacuated surgically 30% VI - non-evacuated mass lesion high or mixed density lesions ≥ 25 cm3 34% not surgically evacuated a“MLS” = midline shift (p. 1110) bto estimate volume of mass on CT (p. 1616) cto assess the basal cisterns (p. 1109) Table 60.7 “Rotterdam score” for CT findings in TBI Feature Points Score normal 0 basal cisterns (p. 1109) compressed 1 (0 - 2) absent 2 0–5 mm 0 midline shift (MLS) (p. 1110) (0 - 1) > 5 mm 1 absent 0 epidural mass lesion (0 - 1) present 1 absent 0 intraventricular blood or traumatic SAH (tSAH) (0 - 1) present 1 add 1 pointa +1 Rotterdam score → TOTAL (1 - 6) aone point is added to all scores to bring the range from 1 to 6 in a nod to the original Marshall score Table 60.8 Mortality associated with total “Rotterdam scores”a Score Mortality number & % 1 0/36 (0%) 2 41/600 (6.8%) 3 122/773 (16%) 4 121/465 (26%) 5 138/261 (53%) 6 69/114 (61%) a6-month mortality 60 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:46 Head Trauma – General Information, Grading, Initial Management 1011 60.5.4 Follow-up CT Routine follow-up CT (when there is no indication for urgent follow-up CT, see below): 1. it is our practice to perform a “stability scan” (a repeat head CT) with ≈ 24 hours (usually about 6-12 hours) for patients who are clinically stable but had findings on initial head CT of: traumatic SAH, small SDH or EDH, intraparenchymal contusions 2. for patients with severe head injuries: a) for stable patients, follow-up CTs are usually obtained between day 3 to 5 (some recommend at 24 hrs also) and again between day 10 to 14 b) some recommend routine follow-up CT several hours after the “time zero” CT (i.e., initial CT done within hours of the trauma) to rule out delayed EDH (p. 1075), SDH (p. 1081), or trau- matic contusions (p. 1071) 32 3. for patients with mild to moderate head injuries: a) for those with an abnormal initial CT, the CT scan is usually repeated prior to discharge b) stable patients with mild head injury and normal initial CT do not require follow-up CT Urgent follow-up CT: performed for neurological deterioration (loss of ≥ 2 points on the GCS, devel- opment of hemiparesis or new pupillary asymmetry), persistent vomiting, worsening H/A, seizures or unexplained rise in intracranial pressure (ICP) in patients with an ICP monitor. 60.5.5 Spine films 1. cervical spine: must be cleared radiographically from the cranio-cervical junction down through and including the C7–1 junction. Spinal injury precautions (cervical collar…) are continued until the C-spine is cleared. The steps in obtaining adequate films are outlined in Spine injuries, Radio- graphic evaluation and initial C-spine immobilization (p. 1141) 2. thoracic and lumbosacral LS-spine films should be obtained based on physical findings and on mechanism of injury (rarely for isolated TBI, especially in a patient who can tell you if they have spine tenderness on palpation); see Spine injuries, Radiographic evaluation and initial C-spine immobilization (p. 1141) 60.5.6 Skull X-rays Practice guideline: Skull X-rays (SXR) in evaluating mTBI Level II20: skull X-rays (SXR) are not recommended for evaluating mTBI A skull fracture increases the probability of a surgical intracranial injury (ICI) (in a comatose patient it is a 20-fold increase, in a conscious patient it is a 400-fold increase33,34). However, significant ICI can occur with a normal skull X-ray (SXR) (SXR was normal in 75% of minor head injury patients found to have intracranial lesions on CT, attesting to the insensitivity of SXRs35). SXRs aﬀect manage- ment of only 0.4–2% of patients in most reports.36 A skull X-ray (SXR) may be helpful in the following: 1. if a CT scan cannot be obtained, an SXR may identify significant findings such as pineal shift, pneumocephalus, air-fluid levels in the air sinuses, skull fracture (depressed or linear)… (how- ever, sensitivity for detecting ICI is very low) 2. with penetrating injuries: helps by visualization of radio-opaque objects 60.5.7 MRI scans in trauma Usually not appropriate for acute head injuries. This is due to longer acquisition time, less access to patients during study, increased diﬃculty in supporting patients (requires special non-magnetic ventilators, cannot use most IV pumps…), and MRI is less sensitive than CT for detecting acute blood.37 There were no surgical lesions demonstrated on MRI that were not evident on CT in one 60 study.38 There may be some additional benefit in combining CT with an MRI performed directly in the emergency department.39 MRI may be helpful later after the patient is stabilized, e.g., to evaluate brainstem injuries, small white matter changes,40 e.g., punctate hemorrhages in the corpus callosum seen in diﬀuse axonal injury (p. 1026)… Spinal MRI is indicated in patients with spinal cord injuries. Rapid sequence MRI may be useful for follow-up in pediatrics to minimize radiation exposure. https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:46 1012 Head Trauma 60.5.8 Arteriogram in trauma Cerebral arteriogram (p. 1096): useful with non missile penetrating trauma. 60.6 E/R management for minor or moderate head injury 60.6.1 Indications for admission to the hospital vs. observation at home ▶ Patients who may be discharged with observation at home. Patients with mild TBI (GCS = 14- 15) who meet criteria in ▶ Table 60.9 may be managed with observation at home with written head-injury discharge instructions, e.g., as illustrated in ▶ Table 60.10. For those not meeting discharge criteria, see sample admitting orders (p. 1012). Table 60.9 Criteria for observation at home 1. head CT scan not indicated (see indications (p. 1006)), or CT scan normal if indicated41 2. initial GCS ≥ 14 3. patient is now neurologically intact (amnesia for the event is acceptable) 4. there is a responsible, sober adult that can observe the patient 5. patient has reasonable access to return to the hospital E/R if needed 6. no “complicating” circumstances (e.g., no suspicion of domestic violence, including child abuse) Table 60.10 Sample discharge home instructions for head injuries Seek medical attention for any of the following: 1. a change in level of consciousness (including difficulty in awakening) 2. abnormal behavior 3. increased headache 4. slurred speech 5. weakness or loss of feeling in an arm or leg 6. persistent vomiting 7. enlargement of one or both pupils (the black round part in the middle of the eye) that does not get smaller when a bright light is shined on it 8. seizures (also known as convulsions or fits) 9. significant increase in swelling at injury site Do not take sedatives or pain medication stronger than acetaminophen (paracetamol in some countries) for 48 hours. Do not take aspirin or other anti-inflammatory medications because of interference with platelet function and theoretical increased risk of bleeding 60.6.2 Admitting orders for minor head injury (GCS ≥ 14) 1. activity: BR with HOB elevated 30–45° 2. neuro checks q 2 hrs (q 1 hr if more concerned; consider ICU for these patients). Contact physi- cian for neurologic deterioration 3. NPO until alert; then clear liquids, advance as tolerated 4. isotonic IVF (e.g., NS + 20 mEq KCl/L) run at maintenance (p. 1050): ≈ 100 cc/hr for average size adult (peds: 2000 cc/m2/d). Note: the concept of “running the patient dry” is obsolete 5. mild analgesics: acetaminophen (PO, or PR if NPO), codeine or tramadol if necessary 6. anti-emetic: give infrequently to avoid excessive sedation, avoid phenothiazine anti-emetics (which lower the seizure threshold); e.g., use trimethobenzamide (Tigan®) 200 mg IM q 8 hrs PRN for adults 60.6.3 Admitting orders for moderate head injury (GCS 9–13) 1. orders as for minor head injury (see above) except patient is kept NPO in case surgical interven- 60 tion is needed (including ICP monitor) 2. for GCS = 9–12 admit to ICU. For GCS = 13, admit to ICU if CT shows any significant abnormality (hemorrhagic contusions unless very small, rim subdural…) 3. patients with normal or near-normal CTs should improve within hours. Any patient who fails to reach a GCS of 14–15 within 12 hrs should have a repeat CT at that time42 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:46 Head Trauma – General Information, Grading, Initial Management 1013 60.7 Patients with associated severe systemic injuries 60.7.1 Intra-abdominal injuries Diagnostic peritoneal lavage (DPL) looking for bloody fluid or FAST (focused abdominal sonogram for trauma) are often used by trauma surgeons to assess for intra-abdominal hemorrhage. If negative and the patient is hemodynamically stable, the patient should be taken for cranial CT (with DPL—if the initial fluid is not bloody, the remainder of the lavage fluid may be collected for quantitative analysis as the head CT is being done). Patients with grossly positive DPL or positive FAST and/or hemodynamic instability may need to be rushed to the O.R. for emergent laparotomy by trauma surgeons without benefit of cerebral CT. Neurosurgical management is diﬃcult in these patients, and must be individualized. These guide- lines are oﬀered: ✖ CAUTION: many patients with severe trauma may be in DIC (either due to systemic injuries, or directly related to severe head injury possibly because the brain is rich in thromboplastin43). Operat- ing on patients in DIC is usually disastrous (p. 175). At the least, check a PT/INR/PTT 1. if GCS > 8 (which implies at least localizing) a) operative neurosurgical intervention is probably not required b) utilize good neuroanesthesia techniques (elevate head of bed, judicious administration of IV fluids, avoiding prophylactic hyperventilation…) c) obtain a head CT scan immediately post-op 2. if patient has focal neurologic deficit, an exploratory burr hole should be placed in the O.R. simulta- neously with the treatment of other injuries. Placement is guided by the pre-op deficit (p.1014) 3. if there is severe head injury (GCS ≤ 8) without localizing signs, or if initial burr hole is negative, or if there is no pre-op neuro exam, then a) measure the ICP: insert a ventriculostomy catheter (if the lateral ventricle cannot be entered after 3 passes, it may be completely compressed or it may be displaced, and an intraparenchy- mal fiberoptic monitor or subarachnoid bolt should be used) normal ICP: unlikely that a surgical lesion exists. Manage ICP medically and, if an IVC was inserted, with CSF drainage elevated ICP (≥ 2 mm Hg): inject 3–4 cc of air into ventricles through IVC, then obtain port- able intraoperative AP skull X-ray (intraoperative pneumoencephalogram) to determine if there is any midline shift. If there is mass eﬀect with ≥ 5 mm of midline shift, explore surgi- cally44 with burr hole(s) on the side opposite the direction of shift. If no mass eﬀect, intra- cranial hypertension is managed medically and with CSF drainage b) routine use of exploratory burr holes for children with GCS = 3 has been found not to be justified45 60.7.2 Fat embolism syndrome General information Most often seen after a long bone fracture (usually femoral, but may include clavicular, tibial, and even isolated skull fracture). Although almost all patients have pulmonary fat emboli at autopsy, the syndrome is usually mild or subclinical, only ≈ 10–20% of cases are severe, and the fulminant form leading to multiple organ failure is rare. Clinical findings usually appear within 12–72 hrs of injury, and do not always include the complete classic clinical triad of: acute respiratory failure (including hypoxemia, tachypnea, dyspnea) with diﬀuse pulmonary infil- trates (usually seen as bilateral fluﬀy infiltrates). May be the only manifestation of fat emboli in up to 75% of cases global neurologic dysfunction: may include confusion (PaO2 usually not low enough to account for these changes46), lethargy, seizures petechial rash: seen ≈ 24–72 hrs after the fracture, usually over thorax Other possible findings include: pyrexia 60 retinal fat emboli There is no specific test for fat embolism syndrome (FES). The following have been proposed, but have poor sensitivity and specificity: fat globules in the urine (positive in ≈ one–third47) and serum, serum lipase activity. In cases of unexplained neurologic or pulmonary abnormalities, it may be pos- sible to diagnose FES if on bronchoalveolar lavage48 > 5% of cells in the washings staining for neutral https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:46 1014 Head Trauma fat with red oil 0. Nonspecific tests include ABG (findings: hypoxemia, hypocarbia from hyperventi- lation, respiratory alkalosis). Treatment Pulmonary support with oxygen, and mechanical ventilation if necessary including use of PEEP. The use of steroids is controversial. Ethyl alcohol (to decrease serum lipase activity) and heparin have not been shown to be of benefit. Early operative fixation of long bone fractures may reduce the inci- dence of FES.49 Outcome Usually related more to the underlying injuries. Although FES itself is usually compatible with good recovery, 10% mortality is usually quoted. 60.7.3 Indirect optic nerve injury General information ≈ 5% of head trauma patients manifest an associated injury to some portion of the visual system. Approximately 0.5–1.5% of head trauma patients will sustain indirect injury (as opposed to penetrating trauma) to the optic nerve, most often from an ipsilateral blow to the head (usually frontal, occasionally temporal, rarely occipital).19 The optic nerve may be divided into 4 segments: intraocular (1 mm in length), intraorbital (25–30 mm), intracanalicular (10 mm), and intracranial (10 mm). The intracanalicu- lar segment is the most common one damaged with closed head injuries. Funduscopic abnormalities visible on initial exam indicates anterior injuries (injury to the intraocular segment (optic disc) or the 10–15 mm of the intraorbital segment immediately behind the globe where the central retinal artery is contained within the optic nerve), whereas posterior injuries (occurring posterior to this but anterior to the chiasm) take 4–8 weeks to show signs of disc pallor and loss of the retinal nerve fiber layer. Treatment See reference.19 No prospective study has been carried out. Optic nerve decompression has been advocated for indirect optic nerve injury; however, the results are not clearly better than expectant management with the exception that documented delayed visual loss appears to be a strong indication for surgery. Transethmoidal is the accepted route, and is usually done within 1–3 weeks from the trauma.50 The use of “megadose steroids” may be appropriate as an adjunct to diagnosis and treatment. 60.7.4 Posttraumatic hypopituitarism Trauma is a rare cause of hypopituitarism. It may follow closed head injury (with or without basilar skull fracture) or penetrating trauma.51 In 20 cases in the literature52 all had deficient growth hor- mone and gonadotropin, 95% had corticotropin deficiency, 85% had reduced TSH, 63% had elevated PRL. Only 40% had transient or permanent DI. 60.8 Exploratory burr holes 60.8.1 General information In a trauma patient, the clinical triad of altered mental status, unilateral pupillary dilatation with loss of light reflex, and contralateral hemiparesis is most often due to upper brainstem compression by uncal transtentorial herniation which, in the majority of trauma cases, is due to an extraaxial intracra- nial hematoma. Furthermore, the prognosis of patients with traumatic herniation is poor. Outcome may possibly be improved slightly by increasing the rapidity with which decompression is under- 60 taken; however, an upper limit of salvageability is probably still only ≈ 20% satisfactory outcome. Burr holes are primarily a diagnostic tool, as bleeding cannot be controlled and most acute hema- tomas are too congealed to be removed through a burr hole. However, if the burr hole is positive, it is possible that modest decompression may be performed, and then the definitive craniotomy can be undertaken incorporating the burr hole(s). With widespread availability of quickly accessible CT scanning, exploratory burr holes are infre- quently indicated. https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:46 Head Trauma – General Information, Grading, Initial Management 1015 60.8.2 Indications 1. clinical criteria: based on deteriorating neurologic exam. Indications in E/R (rare): patient dying of rapid transtentorial herniation (see below) or brainstem compression that does not improve or stabilize with mannitol and hyperventilation.53 a) indicators of transtentorial herniation/brainstem compression: sudden drop in Glasgow Coma Scale (GCS) score one pupil fixes and dilates paralysis or decerebration develops (usually contralateral to blown pupil) b) recommended situations where criteria should be applied: neurologically stable patient undergoes witnessed deterioration as described above awake patient undergoes same process in transport, and changes are well documented by competent medical or paramedical personnel 2. other criteria a) some patients needing emergent surgery for systemic injuries (e.g., positive peritoneal lavage + hemodynamic instability) where there is not time for a brain CT (p. 1013) 60.8.3 Management Controversial. The following should serve only as guidelines: 1. if patient fits the above criteria (emergent operation for systemic injuries or deterioration with failure to improve with mannitol and hyperventilation), and CT scan cannot be performed and interpreted immediately, then treatment should not wait for CT scan a) in general, if the O.R. can be immediately available, burr holes are preferably done there (equipped to handle craniotomy, better lighting and sterility, dedicated scrub nurse…), espe- cially in older patients (> 30 yrs) not involved in MVAs (see below). This may more rapidly diagnose and treat extraaxial hematomas in herniating patients, although no diﬀerence in outcome has been proven b) if delay in getting to the O.R. is foreseen, emergency burr holes in the E/R should be performed 2. placement of burr hole(s) as outlined under Technique below 60.8.4 Technique Position Shoulder roll, head turned with side to be explored up. Three pin skull-fixation used if concern about possible aneurysm or AVM (to allow for retractors and increased stability) or if additional stability is desired (e.g., with unstable cervical fractures); otherwise a horse-shoe head-holder suﬃces and saves time and makes it easier to turn the head to access to the other side if needed. Choice of side for initial burr hole Start with a temporal burr hole (see below) on the side: 1. ipsilateral to a blown pupil. This will be on the correct side in > 85% of epidurals54 and other extra-axial mass lesions55 2. if both pupils are dilated, use the side of the first dilating pupil (if known) 3. if pupils are equal, or it is not known which side dilated first, place on side of obvious external trauma 4. if no localizing clues, place hole on left side (to evaluate and decompress the dominant hemisphere) Approach Burr holes are placed along a path that can be connected to form a “trauma flap” if a craniotomy becomes necessary (▶ Fig. 60.3). The “trauma flap” is so-called because it provides wide access to most of the cerebral convexity permitting complete evacuation of acute blood clot and control of most bleeding. 60 First outline the trauma flap with a skin marker: 1. start at the zygomatic arch < 1 cm anterior to the tragus (spares the branch of the facial nerve to the frontalis muscle and spares the anterior branch of the superficial temporal artery (STA)) 2. proceed superiorly and then curve posteriorly at the level of top of the pinna 3. 4–6 cm behind the pinna it is taken superiorly 4. 1–2 cm ipsilateral to the midline (sagittal suture) curve anteriorly to end behind the hairline https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:46 1016 Head Trauma Burr hole locations temporal burr hole (1 in ▶ Fig. 60.3) ○ over middle cranial fossa typically on side of dilated pupil (if there is one) just superior to the zygomatic arch. Provides access to middle fossa (the most common site of epidural hematoma) and usually allows access to most convexity subdural hematomas, as well as proximity to mid- dle meningeal artery in region of pterion ○ if no epidural hematoma, the dura is opened if it has bluish discoloration (suggests subdural hematoma (SDH)) or if there is a strong suspicion of a mass lesion on that side if completely negative, usually perform temporal burr hole on contralateral side in the same loca- tion (not shown) if negative and if a CT cannot now be done and the OR immediately available from there, proceed to ○ ipsilateral frontal burr hole (2 in ▶ Fig. 60.3), if negative proceed to ○ parietal region (3 in ▶ Fig. 60.3), if negative proceed to ○ posterior fossa (4 in ▶ Fig. 60.3) zygomatic arch 1 cm 4 1 3 2 "Trauma flap" Location of burr holes Fig. 60.3 Exploratory burr hole placement illustrating the technique to place the burr holes (blue circles) along an imaginary skin incision (broken line) that could be converted to a “trauma flap” - excluding burr hole 4 (adapted55,56). Literature In 100 trauma patients undergoing transtentorial herniation or brainstem compression as outlined above,55 exploratory burr holes (bilateral temporal, frontal, and parietal, done in the O.R.) were pos- itive in 56%. Lower rates in younger patients (< 30 yrs) and those in MVAs (as opposed to falls or assaults). SDH was the most common extraaxial mass lesion (alone and unilateral in 70%, bilateral in 11%, and in combination with EDH or ICH in > 9%). When burr holes were positive, the first burr hole was on the correct side 86% of the time when placed as suggested above. Six patients had significant extraaxial hematomas missed with explora- tory burr holes (mostly due to incomplete burr hole exploration). Only 3 patients had the above neu- 60 rologic findings as a result of intraparenchymal hematomas. Outcome Mean follow-up: 11 mos (range: 1–37). 70 of the 100 patients died. No morbidity or mortality was directly attributable to the burr holes. Four patients with good outcome and 4 with moderate dis- ability had positive burr holes. https://ebooksmedicine.net/neurosurgery-book

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