5 Head Injury and ICU



10.1055/b-0039-171767

5 Head Injury and ICU



5.1 Head Injury



5.1.1 Definitions (Table 5.1)




























Concussion


Definition


Immediate and transient alteration in brain function including mental status and level of consciousness


Differences from mild traumatic brain injury (TBI)




  • Imaging studies are normal



  • Onset of symptoms is immediate (in mild TBI may be hours after trauma)


Contusion




  • “Bruise” of the brain



  • Associated with multiple microhemorrhages, vascular disruption and perifocal edema


Coup/countercoup injury


Location of brain injury may be the same as impact (coup) or opposite to impact (countercoup)


Malignant cerebral edema




  • Rapid hyperemia with loss of autoregulation after trauma resulting in severe brain swelling



  • Edema of second-impact injury



  • Very high mortality


Diffuse axonal injury (DAI)




  • Mechanism of injury: acceleration/deceleration injury



  • MRI/CT findings: hemorrhagic foci in corpus callosum and brain stem primarily



  • Histopathology: microscopic axonal damage



  • Possible presentation: posttraumatic coma for greater than 6 h without mass lesions or ischemia



5.1.2 Glasgow Coma Scale (GCS)


1 (Table 5.2)














































Score

BEST eye opening

BEST verbal

BEST motor in ANY limb

6




Spontaneous movement, following commands


5



Oriented, conversant

Localizes pain


4


Spontaneously

Confused

Withdrawal to pain


3


To sound

Inappropriate words

Flexion posturing: decorticate


2


To pressure/pain

Inappropriate sounds

Extension posturing: decerebrate


1


None

None

None



5.1.3 TBI Classification Based on GCS Score (Table 5.3)
























Classification

GCS score

Minor


15


Mild


13–14


Moderate


9–12


Severe


3–8



5.1.4 Cerebral Edema (Table 5.4a)























































Type

Cellular level

Blood–brain barrier

Location

Causes

Comments

Cytotoxic


Intra

Intact

Gray and white matter


  • Posttraumatic



  • Hypothermia



  • Intoxication

Not steroid responsive


Vasogenic


Extra

Disrupted

White matter


  • Tumors



  • Inflammation



  • High-altitude edemaa


Steroid responsive


Delayed ischemic


Extra

Disrupted

Gray and white matter


  • Post SAH or stroke



  • Toxin-mediated

May be a type of vasogenic edema


Interstitial


(Hydrocephalic)


Extra

Intact

White matter

Hydrocephalus


  • Transependymal CSF flow



  • Responds to CSF reduction


Osmotic


Intra + extra

Intact

Gray and white matter

Reduced plasma oncotic pressure




  • Hyponatremia



  • SIADH



High-altitude cerebral edema (Table 5.4b)





















Occurs with climbs above 2,000 meters in 50% of people


Symptoms


Ranging from headaches to paralysis and coma


Cause


Relative hypoxia


Treatment




  • Immediate descent



  • Oxygen, steroids


Prevention




  • Gradual ascent over 2–4 d



  • Avoidance of alcohol and hypnotics



Concussion

2 – 5 (Table 5.4c)

















Epidemiology




  • Most common TBI (6 per 1,000/y)



  • Most common in young male adults


Characteristics




  • Mechanisms of injury: direct OR indirect head trauma



  • Symptoms:




    • ±Short loss of consciousness (LOC)



    • Physical, cognitive, and emotional symptoms



  • GCS 13–15



  • Imaging: normal!!


Indications for CT/MRI




  • Age > 65 y



  • Coagulopathy



  • Symptoms:




    • Severe headache, vomiting



    • Seizures



  • GCS < 15



  • Focal or worsening neurological examination



Second impact syndrome (Table 5.4d)






















Definition


Second injury while still symptomatic from first


Epidemiology


Rare condition primarily in athletes


Causes/Mechanisms




  • Loss of autoregulation



  • Malignant edema from vascular engorgement and increased cerebral blood flow (CBF)


Presentation




  • “Walks off field” after second injury



  • Collapses within 1–5 min, coma, death


Mortality


50–100%



5.1.5 Herniation Syndromes (Table 5.5a)






























Name (alternate name)

Description

Subfalcine (cingulate)




  • Definition: lateral displacement of cingulum underneath falx cerebri



  • Can lead to compression of anterior cerebral artery (ACA) branches


Transtentorial (central)




  • Definition: downward displacement of cerebrum (typical stage-by-stage progression; see Table 5.5b)



  • Eye movement difficulty


Uncal (lateral transtentorial)




  • Definition: mesial temporal lobe compressed against ridge of the tentorium notch at the level of mesencephalon → causing midline shift resulting in anisocoria (typical “blown pupil”)



  • Most common


Cerebellar (foramen magnum)




  • Definition: compression of medulla from cerebellar tonsils



  • Presentation: fulminant heart rate and blood pressure (BP) changes; tetraparesis


External




  • Definition: herniation through a skull defect



  • Causes: posttraumatic, postsurgical


Upward




  • Usually iatrogenic



  • Mechanisms: extensive CSF drainage from ventriculostomy in the presence of posterior fossa mass



Stages of central herniation (Table 5.5b)









































Stage

Level of consciousness

Posture

Eyes

Cardiopulmonary system



  1. Diencephalic stage


Confused and drowsy


Constricted pupils


Gaze palsies




  • 3. Mesencephalic stage


Unconscious

Decorticate posturing

Dilated pupils

Hyperventilation




  • 4. Pontine stage


Unconscious

Decerebrate posturing

Dilated pupils

Irregular breathing




  • 5. Medullary stage


Unconscious

Flaccid




  • Loss of homeostatic control



  • Cheyne–Stokes breathing



  • Apnea and arrest



5.1.6 Brain Death (Table 5.6)




























Definition of death


(Uniform Determination of Death Act 1981 and Affirmation 2010)




  • Irreversible cessation of circulatory and respiratory functions


    OR



  • Irreversible cessation of all functions of the entire brain and brainstem (brain death)


Brain death examination criteria




  • Core temperature > 36°C (96.8°F)



  • Systolic BP (SBP) ≥ 100 mm Hg



  • No drugs that could influence examination, blood alcohol < 0.08%


Reflexes




  • Fixed pupils, no pupillary reaction to light



  • No corneal reflex (touching cornea with gauze or Q-tip)



  • Absent vestibulo-ocular reflex: no eye movement with ice water into external ear canal and head of bed (HOB) elevated to 30 degrees



  • Absent oculocephalic reflex (Doll’s eyes): head turning does not cause contralateral eye deviation



  • No gag reflex (test by pulling on endotracheal tube [ET] tube)



  • No cough reflex (test with bronchial suctioning)



  • No response to deep central pain



  • Failed apnea challenge: no respirations with pCO2 > 60 mm Hg


Ancillary tests (may vary between countries and states)


Electroencephalogram (EEG)


No electrical activity for 30 min


Cerebral angiography


Absence of CBF at carotid bifurcation or circle of Willis


Cerebral radionuclide angiogram


No radionuclide uptake in the brain parenchyma



5.1.7 Cerebral Blood Flow (Table 5.7a)























Values of CBF (ml/100 g of tissue/min)


Normal values




  • Average global CBF: 50



  • Average CBF in gray matter: 67–80



  • Average CBF in white matter: 18–25


Thresholds




  • 30: minimum CBF for normal neuronal function



  • 20–30: neuronal dysfunction, EEG slowing



  • 10–20: reversible neuronal dysfunction if CBF is restored, suppressed EEG



  • <10: irreversible neuronal dysfunction—cell death


Formulas/relationship with other parameters


CPP = MAP – ICP


  • CPP: cerebral perfusion pressure



  • MAP: mean arterial pressure



  • ICP: intracranial pressure


CBF = CPP/CVR

CVR: cerebrovascular resistance (CVR is mainly dependent on the diameter of the arterioles, meaning when the smooth muscle of their wall contracts→ ↓ diameter → ↑CVR → ↓ CBF and vice versa)



Factors regulating CBF (Table 5.7b)

























Flow–metabolism coupling





  • Definition:




    • ↑ Metabolism (seizure, hyperthermia) leads to ↑ CBF



    • ↓ Metabolism (anesthesia, sedation, hypothermia) leads to a ↓ to CBF



  • Mediators: via regional metabolic and neurogenic factors



  • Response rate: very fast (≈1 s)


Cerebral autoregulation




  • Definition:




    • Between CPP values 50 and 150 mm Hg, autoregulation works and cerebral arterioles can maintain stable CBF regardless of CPP fluctuations via changes in CVR (↑CPP → ↑CVR,↓ CPP → ↓CVR)



    • When CPP < 50, ↓CPP → ↓CBF (linearly) → ischemia



    • When CPP > 150, ↑CPP → ↑CBF (linearly) → ↑CBV (cerebral blood volume) → ↑ICP → edema/disruption of blood–brain barrier



  • Mediator: myogenic reflexes of smooth muscle in wall of arterioles and neurogenic factors



  • Response rate: slower than flow–metabolism coupling


PaCO2, PaO2 (arterial carbon dioxide and oxygen tension)


PaCO2




  • For PaCO2 20–80 mm Hg, CO2 has a linear relationship with CBF:




    • ↑PaCO2 (hypercapnia) → ↓CVR → ↑CBF



    • ↓PaCO2 (hypocapnia) → ↑CVR → ↓CBF



  • CO2 is a very potent vasodilator



  • Hyperventilation (↓PaCO2) can be used as a short-term measure for ↓CBF and thus ↓ICP


PaO2




  • For PaO2 > 60 mm Hg, oxygen has almost no effect on CBF



  • For PaO2 < 60 mm Hg, ↓PaO2 →↓CVR → ↑CBF



  • The oxygen effect on CBF is not as significant as that of CO2



5.1.8 Intracranial Pressure (Table 5.8a)
























ICP




  • Definition: the pressure within intracranial space relative to atmospheric pressure



  • Normal values: 8–15 mm Hg


Intracranial volume


The intracranial volume (Vtotal) within intact skull is fixed.


Vtotal = Vbrain + Vblood + VCSF = constant




  • Vbrain ≈ 1,400 mL (80%)



  • Vblood ≈ 150 mL (10%)



  • VCSF ≈ 150 mL (10%)


Monro–Kellie doctrine


An increase in the volume of one of the intracranial contents requires an equal reduction in the volume of the other intracranial contents, so that ICP within the fixed skull remains constant


Pressure–volume curve




  • Zone A (high compliance vs. low elastance): compensatory mechanisms (blood, CSF) are intact → large changes in volume cause little or no change in ICP



  • Zone B (↓compliance, ↑elastance): compensatory mechanisms progressively decrease → for the same change in volume, the ICP starts to increase more



  • Zone C (decompensation point, almost no compliance vs. high elastance): after a threshold, small increase in volume causes exponential increase in ICP → effects, if not treated: ischemia, herniation




  • Compliance = ΔV/ΔP



  • Elastance = ΔP/ΔV (differential change in pressure per unit volume)



  • Buffering mechanisms: CSF displacement into lumbar subarachnoid spaces, ↑venous outflow, ↓CBF and CBV



Management algorithm of increased ICP (Table 5.8b)
Level of evidence: Level I: good-quality randomized controlled trial (RCT) = high{H}, Level II—moderate-/poor-quality RCT OR good-quality cohort = medium [M], Level III: moderate-/poor-quality RCT or cohort OR moderate-/poor-quality case-control OR case series, databases, registries = low [L].


5.1.9 Admission and Discharge Management Algorithm for TBI


9 (Table. 5.9)


























Category

Criteria

Management

Low risk




  1. Asymptomatic



  2. Nonprogressive headache



  3. Dizziness



  4. Scalp hematoma or wound



  5. No LOC

Observation at home with written head injury instructions


Moderate risk


Any of the following:




  1. Age < 2 y



  2. Mechanism of injury:




    • Multiple trauma



    • Suspected child abuse



    • Unreliable or inadequate history



    • Alcohol/drug intoxication



  3. Types of head injury:




    • Serious facial injury



    • Significant subgaleal swelling



    • Possible penetrating skull injury OR depressed fracture



    • Signs of skull base fracture



  4. Symptoms:




    • Alteration/LOC on or after injury



    • Posttraumatic amnesia



    • Progressive headache



    • Vomiting



    • Posttraumatic seizure

Get noncontrast head CT:




  1. If CT reveals findings of TBI →in-hospital observation



  2. If CT is normal →discharge only if:




    • Patient is asymptomatic (except amnesia)



    • GCS ≥ 14



    • No domestic abuse



    • Patient has access to hospital



    • Responsible competent adult can stay with patient at home


High risk




  1. Penetrating injury/depressed skull fracture



  2. Decreased OR decreasing level of consciousness not due to other causes (drugs, alcohol, postictal, metabolic, etc.)



  3. Focal neurological deficit


  1. STAT noncontrast head CT



  2. Admission to ICU



5.1.10 Monitors Used in Traumatic Brain Injury



ICP monitors (Table 5.10a )








































Type of ICP monitor


Risk of hemorrhage


Bacterial colonization or infection


Malfunction


Comments


Intraventricular catheter (EVD)


1%

15%

5%


  • Preferred method!!



  • Most accurate



  • Most reliable



  • Least expensive



  • Allows CSF drainage



  • May be difficult to place


Intraparenchymal monitor


2%

15%

20%

Drift over time


Subarachnoid bolt


0

5%

15%

Lumen can occlude at high ICP and show false readings


Subdural sensor


0

5%

10%



















Indications for ICP monitor placement


Salvageable patient with GCS 3–8 and either:




  1. Abnormal CT


  • Hematoma



  • Contusions



  • Swelling



  • Herniation



  • Compressed basal cisterns




  • b. Normal CT + 2 of the following:


  • Age > 40 y



  • Uni- or bilateral motor posturing



  • SBP < 90 mm Hg

















ICP values

Normal ICP values




  • Preterm infants: 0–3 mm Hg



  • Term infants: 1.5–6 mm Hg



  • Children: 3–7 mm Hg



  • Adults: 10–15 mm Hg


Treatment threshold




  • Children: 20 mm Hg



  • Adults: 22 mm Hg



CBF monitor (Table 5.10b)






















Devices


Laser Doppler flow


  • Continuous



  • Non-invasive



  • Only regional


Thermal diffusion flowmetry probe

Invasive bedside monitor using thermal diffusion flowmetry probe inserted into white matter


CBF values


Normal values


  • Gray matter: 67–80 mL/100 g/min



  • White matter: 18–25 mL/100 g/min


Abnormal values


  • < 15 mL: may indicated vasospasm or ischemia



  • < 10 mL: may indicate infarction



Microdialysis probe (Table 5.10c)













Device




  • Invasive bedside monitor



  • Probe inserted into white matter, connected to micro-pump



  • Obtains extracellular fluid micro-samples


Measured substances




  • Glucose → ↓ extracellular glucose associated with ↑ mortality



  • Lactate → may ↑ in SJVO2 (jugular venous oxygen saturation) desaturation



  • Pyruvate



  • Lactate/pyruvate ratio



5.1.11 ICP Waveforms (Table 5.11)




































Name

Interpretation

Waveform

Characteristics

A wave


Physiologic

A-wave with 3 peaks:




  • P1: percussion wave = arterial pulsation



  • P2: tidal wave = intracranial compliance



  • P3: dicrotic wave = aortic valve closure


Physiologic condition: P1 > P2 > P3


Pathological condition: P2 > P1 indicates noncompliant brain = ↑ICP


Lundberg’s A waves


Pathologic: indicative of neurological deterioration and possible herniation

Plateau waves: ICP ≥ 50 mm Hg for 5–20 min


Lundberg’s B waves


Pathologic: probably related to change in vascular tone (vasospasm) and failing intracranial compensation

Oscillations at frequency 1–2/min


ICP 20–30 mm Hg


Lundberg’s C waves


Has been documented in healthy adults


Significance unknown

Oscillations 4–8/min


ICP >20 mm Hg



5.2 Traumatic Hemorrhagic Brain Injuries



5.2.1 Traumatic Intracerebral Hemorrhage (TICH)



TICH (AKA hemorrhagic contusions) (Table 5.12a)



































Epidemiology




  • Common (13–35% of severe TBI) 10



  • More common in temporal lobe, frontal lobes (however, they occur anywhere)


Mechanism


Sudden deceleration with resultant impact of brain on skull in coup/contracoup fashion 11


Presentation


Variable (from no level of consciousness alteration to coma)


CT appearance




  • Areas of increased density



  • Areas of heterogeneous density due to hemorrhage, infarction /necrosis, edema


Management (level III) 10


(!! no firm surgical criteria have been established)

Nonsurgical


Recommendations (indications):




  • No evidence of neurological compromise



  • Controlled ICP



  • No significant mass effect on serial CT scans


Close observation with: ICP monitoring (see Table 5.10a) + serial CTs


Surgical


Recommendations (indications)


  • Clinical: progressive neurological deterioration referable to lesion



  • ICP monitoring: medically refractory intracranial hypertension with large TICH lesion(S)



  • CT findings:




    • mass effect



    • volume > 50 mL



  • GCS 6–8 + all of the following CT findings:




    • Volume > 20 mL



    • Frontal OR temporal location



    • Midline shift > 5 mm and/or cisternal compression


Options


  • For diffuse medically refractory posttraumatic cerebral edema → bifrontal craniectomy within 48 h from injury



  • For diffuse medically refractory parenchymal injury → decompression:




    • Decompressive craniectomy



    • Subtemporal resection



    • Temporal lobectomy


Outcome 10


Evidence suggests, but does not prove, that outcome is poor in patients with progressive neurological deterioration, medically refractory intracranial hypertension, and mass effect on CT, who are not treated surgically



Delayed Traumatic Intracerebral Hemorrhage (DTICH) (Table 5.12b)




























Definition 12


Appearance of TICH (usually within 72 h of head trauma) in areas of the brain that were normal in appearance or nearly so on the initial CT scan


Epidemiology


3.3–7.4% in patients with moderate to severe TBI


Mechanism


Primary TICH progresses (microhematomas coalesce)


Factors 10 , 12


Coagulation abnormalities


Decompressive surgery for other intracranial hemorrhages


Secondary systemic insults


Dysautoregulation


Presentation


Patients are doing well initially after the injury and suddenly deteriorate (GCS < 8; most occur within 72 h)


CT appearance


Identical with TICH


Management


Treatment identical to primary TICH but higher mortality (50–75%)



5.2.2 Epidural Hematomas



Acute epidural hematoma (AEDH) (Table 5.13a)






































Definition


Bleeding occurs between: inner table of skull—dura


Epidemiology 11 , 13 , 14




  • 20% of severe TBIs



  • 10.6% of admissions for TBI



  • Usually male



  • Usually young (mean age: 20–30 y; rare < 2 y old or > 60 y old)



  • Usually laterally over hemispheres (70%; however, they occur anywhere)


Source of bleeding




  • Arterial: 85% (usually middle meningeal artery after temporoparietal skull fracture) → symptoms present soon after injury



  • Venous: 15% (middle meningeal vein, diploic veins, sinus) → symptoms present hours/days after injury, more benign


Presentation




  • Lucid interval 11 , 15 (<10–27%; definition: brief LOC just after head injury → transient complete recovery → followed by sudden neurological deterioration, hemiparesis, anisocoria, coma, death)



  • No posttraumatic LOC 60%


CT appearance 11




  • Classic appearance: uniformly high-density biconvex lesion adjacent to skull (84%)



  • However, in 10% it is crescent shaped (differential diagnosis [DDx] from subdural hematoma [SDH])



  • Does not cross sutures → confined (vs. SDH)



  • May cross the falx (vs. SDH)



  • Usually associated with fracture of overlying skull



  • Associated underlying acute subdural hematoma (ASDH) in 20% → rule out (R/O) intraoperatively


Management (level III) 13


Nonsurgical


GCS > 8 without focal deficit + all of the following CT findings




  • Volume < 30 mL



  • Thickness < 15 mm



  • Midline shift < 5 mm


Close observation + serial CTs


Surgical


Recommendations (indications)




  • Volume >30 mL regardless GCS score



  • Hematoma evacuation as soon as possible for AEDH in coma (GCS < 9) + anisocoria


Technique




  • Craniotomy: hematoma evacuation



  • R/O underlying ASDH



  • Place multiple tack-up sutures + central tenting suture


Mortality 14




  • With optimal treatment: 10% (better outcome than with all other traumatic hemorrhagic brain injuries; factors affecting mortality rate: pre-op motor response, pupillary asymmetry, presence of other intracranial pathology)



  • Overall: 20–55% (increased mortality usually due to delay of diagnosis [Dx] + surgery)



Delayed Epidural Hematoma (DEDH)

11 (Table 5.13b)























Definition


An EDH not present on the initial CT


Epidemiology


10% of EDH


Risk factors




  • Skull fracture (most common)



  • Coagulopathies



  • Rapid lowering of ICP (with medicines or surgery)



  • Rapid shock correction


CT appearance


Identical with AEDH


Management


Treatment identical to AEDH



5.2.3 Subdural Hematomas



ASDH (traumatic) (Table 5.14a)






































Definition


Hematoma is located between: dura and arachnoid layer (< 48 h from injury)


Epidemiology 16




  • 12–29% of severe TBI patients (more common than EDH)



  • Mechanism of injury: in younger patients, mainly due to motor vehicle accident (MVA) vs. in older patients mainly due to falls



  • Location: usually lateral hemispheric, but also interhemispheric, along tentorium, posterior cranial fossa



  • Delayed SDH (0.5% of operated ASDH) = SDH not present on initial CT (same treatment [Tx] as ASDH) 11


Source of bleeding 11




  • Subdural accumulation of blood around/from brain laceration (burst lobe) → more severe primary brain injury (usually) without lucid interval (usually)



  • Rupture of bridging or cortical veins due to brain acceleration–deceleration →less severe primary brain injury (usually) with lucid interval (usually)


Presentation 17




  • GCS < 8 (37–80%)



  • Lucid interval(may be present)



  • Worse vs. EDH


CT appearance 11




  • High-density crescentic lesion adjacent to skull



  • Associated brain edema and underlying brain injury (more often vs. EDH)



  • DDx from EDH: ASDH is less uniform, more diffuse, crescentic in shape


Management (level III) 17


Nonsurgical




  • All patients not fulfilling the surgical criteria should be closely observed with: intensive monitoring + serial CTs



  • Place ICP monitor in all SDH patients in coma (GCS < 9)


Small interhemispheric SDH: observe; surgery only for patients with neurological deterioration (high risk due to superior sagittal sinus, risk of venous infarct)


Surgical


Recommendations (indications)


Surgery ASAP for:


a. CT criteria regardless of GCS (any one of the following criteria):




  • Thickness > 10 mm



  • Midline shift > 5 mm


b. CT criteria (thickness < 10 mm + midline shift < 5 mm) + comatose patient (GCS < 9) → operate ASAP if any of the following criteria is fulfilled:




  • ↓GCS by 2 point between injury and admission and/or



  • Pupils: asymmetric OR fixed dilated and/or



  • ICP > 20 mm Hg


Caution: due to the association of ASDH with TICH, take into consideration the recommendations for management of both lesions


Technique




  1. Large craniotomy



  2. Hematoma evacuation




    • If severe brain swelling, consider:




      • Duraplasty



      • Leave bone flap off


Mortality 11




  • Overall mortality:




    • 50–90% (high mortality mainly due to underlying brain parenchymal injury; much worse than EDH)



    • Lower when surgery occurs < 4 h after injury 18



  • Factors for poor outcome: ↓GCS of admission, ↑age, postop ↑ICP, associated TICH 14



Spontaneous SDH

11 , 19 (Table 5.14b)























Source of bleeding


Depending on cause:




  • Bleeding site is usually arterial (cortical MCA branch in area of Sylvian fissure) a



  • Venous (from bridging vein rupture)


Risk factors/causes




  • Hypertension



  • Intracranial hypotension (spinal tap)



  • Coagulopathies (including iatrogenic)



  • Substance abuse



  • Vascular malformations (arteriovenous malformation [AVM], aneurysm)



  • Ginkgo biloba extract



  • Infection



  • Tumor


aMinor trauma: rarely a seemingly harmless head trauma or even a whiplash neck injury without direct head injury can be the cause particularly in the presence of pre-existing sylvian arachnoid cyst


Presentation


Usual presentation: sudden severe headache (without history of trauma) → level of consciousness alterations + variable focal neurological deficits


CT appearance




  • SDH of different density (hyper-, iso-, hypodense) depending on elapsed time from initial bleeding



  • Consider CTA to R/O AVM or aneurysm


Management


Same as traumatic ASDH + treat/address underlying cause:




  • AVM, aneurysm: take into consideration/treat first—can complicate SDH removal



  • Intracranial hypotension: identify site of CSF leak in spine → blood patch



  • Coagulopathies → treat OR reverse if iatrogenic



  • Treat infection



  • Treat tumor



  • Stop substances



Chronic subdural hematoma (CSDH) (Table 5.14c)









































Definition 11


SDH of with low density in CT (around 2–3 wk since initial bleeding) → contains dark “motor oil,” which does not clot


Epidemiology 11




  • Typical age: usually in older patients (average age: 63) → with age brain volume ↓ → vs. subdural space↑



  • 20% bilateral


Mechanism 20 , 21


Initially small ASDH → causes inflammation → fibroblasts form neomembranes (about 4 d after injury) on both hematoma surfaces (cortical, dural) → angiogenesis in membranes bleeding → enzymatic fibrinolysis of blood clot → liquefaction of blood clot + fibrin degradation products inhibit hemostasis after rebleeding


Loss of balance between plasma effusion and/or rebleeding from neomembranes vs. fluid absorption


Risk factors




  • Trauma <50% (usually trauma is so minor, it cannot be recalled)



  • Alcohol abuse



  • Seizures



  • Coagulopathies



  • CSF shunts



  • Patients at risk of falls


Presentation 11




  • Very slow worsening of neurological status



  • Variable:




    • (20–30%) → incidental finding 14



    • Minor symptoms (headache, confusion, speech difficulties, walking difficulties) or transient ischemic attack (TIA) like symptoms



    • Major symptoms: alterations of level of consciousness (even coma), hemiparesis, seizures


CT appearance




  • Low-density collection of crescentic shape over lateral surface of hemisphere (variable extent) ± diaphragms (see Table 5.14e)



  • Subacute SDH (4 d to 2–3 wk since initial bleeding) isodense → may be missed → look for midline shift, ask for enhanced CT


Management 11


Nonsurgical measures




  • Seizure prophylaxis



  • Treat coagulopathies (reversal if iatrogenic anticoagulation)



  • Steroids (controversial)


Surgical


Indications




  • Symptomatic CSDH



  • CT findings: thickness > 1 cm


Surgical options




  • Twist drill hole



  • Single burr hole



  • Two burr holes (recommended)



  • Craniotomy + excision of superficial CSDH membrane only (indications: multiloculated CSDH, persistent CSDH recurrences after above options have been used)


Placement of subdural drain for 24–48 h + patient flat in bed reduces rate of recurrence by 50% 22


Outcome of surgical management




  • Clinical improvement (>80% of patients) can be achieved by removal of >20% of CSDH 23



  • 90% resolution with one or two procedures (with twist drill hole + subdural drain)



  • CSDH recurrence in 10% (even with subdural drain left for 24–48 h)



  • 78% show residual fluid on post-op CT, which may take 6 mo to resolve



  • Overall surgical mortality: 0–8% 11 , 14

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May 11, 2020 | Posted by in NEUROSURGERY | Comments Off on 5 Head Injury and ICU

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