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Subdural Hematoma, Emergency Medicine

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Subdural Hematoma, Emergency Medicine

Basics

Description

Imaging is necessary in infants with persistent vomiting, new seizures, lethargy, irritability, bulging, or tense fontanels.

US can be used to visualize cerebral structures if fontanelles are patent.

Patients with chronic SDH often can be managed as outpatients in conjunction with neurosurgery, adequate home resources, and appropriate follow-up.

All patients need neurosurgical evaluation immediately.

  • Classification of subdural hematoma (SDH):Acute: Diagnosis within the 1st 3 daysSubacute: Diagnosis 3 days " “3 wkChronic: Diagnosis after 3 wk
  • CT description:Rarely crosses midlineDoes cross suture linesInner margins are often seen to be irregular.
  • Acute:Most commonly due to acceleration " “deceleration forces and less commonly from direct traumaSagittal movement of the head causes stretch of parasagittal bridging veins.Other bleeding sites include:Laceration of duraVenous sinus injuryCortical arteriesNontraumatic injuries: Intracerebral aneurysm rupture, arteriovenous malformation, coagulation disorder, arterial HTN, drug or alcohol abuse
  • Chronic:Encapsulated hematoma most likely caused by repeated small hemorrhages of bridging veins.
  • Acute: Diagnosis within the 1st 3 days
  • Subacute: Diagnosis 3 days " “3 wk
  • Chronic: Diagnosis after 3 wk
  • Rarely crosses midline
  • Does cross suture lines
  • Inner margins are often seen to be irregular.
  • Most commonly due to acceleration " “deceleration forces and less commonly from direct trauma
  • Sagittal movement of the head causes stretch of parasagittal bridging veins.
  • Other bleeding sites include:Laceration of duraVenous sinus injuryCortical arteriesNontraumatic injuries: Intracerebral aneurysm rupture, arteriovenous malformation, coagulation disorder, arterial HTN, drug or alcohol abuse
  • Laceration of dura
  • Venous sinus injury
  • Cortical arteries
  • Nontraumatic injuries: Intracerebral aneurysm rupture, arteriovenous malformation, coagulation disorder, arterial HTN, drug or alcohol abuse
  • Encapsulated hematoma most likely caused by repeated small hemorrhages of bridging veins.

Etiology

  • Acute:Most common type of intracranial hematoma (66 " “70%)Occurs most commonly at cerebral complexities > falx cerebri > tentorium cerebelliPeak incidence 15 " “24 yr, 2nd peak >75 yrRepresents 26 " “63% of blunt head injuryMotor vehicle crash (MVC) is most common cause overall.Falls and assault more commonly result in isolated SDH (72%) than do MVCs (24%).Elderly patients and those with seizure disorders are at increased risk.Mortality is related to presenting signs and symptoms as well as comorbidities:Mortality is 50% for age >70Less than 1/2 present as simple extra-axial collection (22% mortality rate) ’ ˆ Ό40% of patients will have complicated SDH: Parenchymal laceration or intracerebral hematoma (mortality rate >50%)3rd group associated with contusion (30% mortality rate with functional recovery of 20%)
  • Coagulopathy: INR >2 increases risk of bleed ƒ —2, INR >3 is associated with larger initial volume and increased expansion
  • Chronic:Most common in babies or elderly with atrophy:Associated with infarction in underlying brain
  • 75% of patients are >50
  • <50% have history of trauma
  • 50% are alcoholic
  • Epilepsy and shunting procedures
  • Most common type of intracranial hematoma (66 " “70%)
  • Occurs most commonly at cerebral complexities > falx cerebri > tentorium cerebelli
  • Peak incidence 15 " “24 yr, 2nd peak >75 yr
  • Represents 26 " “63% of blunt head injury
  • Motor vehicle crash (MVC) is most common cause overall.
  • Falls and assault more commonly result in isolated SDH (72%) than do MVCs (24%).
  • Elderly patients and those with seizure disorders are at increased risk.
  • Mortality is related to presenting signs and symptoms as well as comorbidities:Mortality is 50% for age >70Less than 1/2 present as simple extra-axial collection (22% mortality rate) ’ ˆ Ό40% of patients will have complicated SDH: Parenchymal laceration or intracerebral hematoma (mortality rate >50%)3rd group associated with contusion (30% mortality rate with functional recovery of 20%)
  • Mortality is 50% for age >70
  • Less than 1/2 present as simple extra-axial collection (22% mortality rate)
  • ’ ˆ Ό40% of patients will have complicated SDH: Parenchymal laceration or intracerebral hematoma (mortality rate >50%)
  • 3rd group associated with contusion (30% mortality rate with functional recovery of 20%)
  • Most common in babies or elderly with atrophy:Associated with infarction in underlying brain
  • Associated with infarction in underlying brain
  • May occur secondary to trauma at birth
  • Nonaccidental trauma more common

Diagnosis

Signs and Symptoms

  • Acute:1/5 have diagnosis discovered at autopsy.Most commonly misdiagnosed as intoxication or cerebrovascular accident (CVA)Headache and altered mental status:50% unconscious at discovery
  • Subacute/chronic:Headaches, nausea, vomiting, and seizures are frequent symptoms.Presentation varied:Fluctuating mental statusUnsteady gaitSlow progression of deficits
  • 1/5 have diagnosis discovered at autopsy.
  • Most commonly misdiagnosed as intoxication or cerebrovascular accident (CVA)
  • Headache and altered mental status:50% unconscious at discovery
  • 50% unconscious at discovery
  • Headaches, nausea, vomiting, and seizures are frequent symptoms.
  • Presentation varied:Fluctuating mental statusUnsteady gaitSlow progression of deficits
  • Fluctuating mental status
  • Unsteady gait
  • Slow progression of deficits
  • Acute:Headache and altered mental statusMost common clinical signs are hemiparesis or hemiplegia:Seen in 40 " “65%SDH opposite motor deficit in 60 " “85%Pupillary abnormality seen in 28 " “79%:SDH will be on same side of pupillary abnormality in 70 " “90%.Seizures may be seen in ’ ˆ Ό10% initially.Papilledema in <1/3
  • Chronic:Presentation is varied and mimics other diseases.
  • Headache and altered mental status
  • Most common clinical signs are hemiparesis or hemiplegia:Seen in 40 " “65%SDH opposite motor deficit in 60 " “85%
  • Pupillary abnormality seen in 28 " “79%:SDH will be on same side of pupillary abnormality in 70 " “90%.
  • Seizures may be seen in ’ ˆ Ό10% initially.
  • Papilledema in <1/3
  • Seen in 40 " “65%
  • SDH opposite motor deficit in 60 " “85%
  • SDH will be on same side of pupillary abnormality in 70 " “90%.
  • Presentation is varied and mimics other diseases.

Essential Workup

  • Mechanism of injury kinetics
  • Neurologic status: Baseline and at-scene
  • Complicating factors:Past medical history, medicationsAllergies, drug useRapid neurologic assessment:
  • Glasgow Coma scale ([GCS] after fluid resuscitation most important)
  • Brainstem reflexes:AnisocoriaPupillary light reflexCorneal, gag, oculocephalic/oculovestibularHead imaging
  • Past medical history, medications
  • Allergies, drug use
  • Rapid neurologic assessment:
  • Anisocoria
  • Pupillary light reflex
  • Corneal, gag, oculocephalic/oculovestibular
  • Head imaging

Diagnosis Tests & Interpretation

  • ABG, CBC, electrolytes with glucose, prothrombin time (PT), partial thromboplastin time (PTT)
  • Blood ethyl alcohol, drug screen
  • Head CT in coordination with other necessary trauma workup
  • Acute:Characteristic CT finding is crescent-shaped clot overlying hemispheric convexity.May have irregular medial border of hematomaMixed density of clot may represent active bleedingMost (60%) associated with other intracranial lesionsIntracranial volume of hematoma >2% predicts poor prognosis
  • Chronic:MRI is a better choice, as lesion may be isodense on CT from 2 " “3 wk.MRI volume in diffusion-weighted images correlates with Rankin disability score.CT may show hypodense lesion after 3 wk.Spinal radiographs
  • Characteristic CT finding is crescent-shaped clot overlying hemispheric convexity.
  • May have irregular medial border of hematoma
  • Mixed density of clot may represent active bleeding
  • Most (60%) associated with other intracranial lesions
  • Intracranial volume of hematoma >2% predicts poor prognosis
  • MRI is a better choice, as lesion may be isodense on CT from 2 " “3 wk.
  • MRI volume in diffusion-weighted images correlates with Rankin disability score.
  • CT may show hypodense lesion after 3 wk.
  • Spinal radiographs

Differential Diagnosis

  • Acute:Diffuse axonal injuryCerebral contusionIntracerebral bleedSubdural hygromaEpidural hematomaShaken baby/battered child syndrome
  • Chronic:Pseudotumor cerebriBrain tumorDementiaMeningitisCVA/transient ischemic attackCerebral atherosclerosisToxic, metabolic, respiratory, or circulatory causes
  • Diffuse axonal injury
  • Cerebral contusion
  • Intracerebral bleed
  • Subdural hygroma
  • Epidural hematoma
  • Shaken baby/battered child syndrome
  • Pseudotumor cerebri
  • Brain tumor
  • Dementia
  • Meningitis
  • CVA/transient ischemic attack
  • Cerebral atherosclerosis
  • Toxic, metabolic, respiratory, or circulatory causes

Treatment

Initial Stabilization/Therapy

  • Manage airway and resuscitate as indicated:Hypoxia is a strong predictor of outcome.Maintain SaO2 >95%.Rapid-sequence intubation (RSI) is indicated for GCS <9 or for evidence of increased intracranial pressure (ICP).RSI for PaCO2 >45, anisocoria, drop of GCS by 3, loss of gag reflex, C-spine injury
  • Routine hyperventilation is no longer recommended due to resultant diminished cerebral perfusion pressure.
  • Controlled ventilation to maintain PCO2 35 " “40 mm Hg:NS to maintain mean arterial pressure (MAP) 100 " “110 is necessary:A single episode of systolic BP <90 is associated with poor outcome.Spine precautionsElevate head of bed 20 " “30 ‚ ° (only after adequate fluid resuscitation to avoid resultant decrease in cerebral blood flow [CBF]).
  • Not considered helpful:SteroidsAntibiotic prophylaxisHyperventilation (unless herniation is imminent)Fluid restrictionCalcium channel blockersHypothermia not provenNaCl 3% not yet proven helpful
  • Hypoxia is a strong predictor of outcome.
  • Maintain SaO2 >95%.
  • Rapid-sequence intubation (RSI) is indicated for GCS <9 or for evidence of increased intracranial pressure (ICP).
  • RSI for PaCO2 >45, anisocoria, drop of GCS by 3, loss of gag reflex, C-spine injury
  • NS to maintain mean arterial pressure (MAP) 100 " “110 is necessary:A single episode of systolic BP <90 is associated with poor outcome.
  • Spine precautions
  • Elevate head of bed 20 " “30 ‚ ° (only after adequate fluid resuscitation to avoid resultant decrease in cerebral blood flow [CBF]).
  • A single episode of systolic BP <90 is associated with poor outcome.
  • Steroids
  • Antibiotic prophylaxis
  • Hyperventilation (unless herniation is imminent)
  • Fluid restriction
  • Calcium channel blockers
  • Hypothermia not proven
  • NaCl 3% not yet proven helpful

Ed Treatment/Procedures

  • Acute
  • Early neurosurgical intervention (<4 hr) in comatose patients shows reduced mortality:Burr holes may be used as temporizing measure in deteriorating patients.ICP monitoring is indicated for patients with abnormal CT who are intubated.Subdural evacuating port system has been shown to be equivalent to Burr hole for acute treatment of SDH
  • Nonoperative treatment may be indicated for small SDH:<20 mL of blood, <1 cm, midline shift <5 mm, no mass effect, no neurologic deficitThis requires frequent neurologic reassessment.10% go on to require operative intervention.
  • Maintain euvolemic state with isotonic fluids:Arterial line placement to monitor MAP, PO2, and PCO2Foley catheter to monitor I/O status
  • Control ICP:Prevent pain, posturing, and increased respiratory effort:Sedation with benzodiazepinesNeuromuscular blockade with vecuronium or rocuronium in intubated patientsEtomidate is a good induction agent.Mannitol may be used once euvolemic:Shown to increase MAP > cerebral perfusion pressure and CBF as well as decrease ICPKeep osmolality between 295 and 310.Use furosemide (Lasix) as an adjunct only if normovolemic.Treat HTN:Labetalol, nicardipine, or hydralazineTreat coagulopathyUse fresh frozen plasma 4+ unitsUse prothrombin complex concentrateTreat hyperglycemia if present:Associated with increased mortality in traumatic brain injuryTreat and prevent seizures:Diazepam and phenytoin (Dilantin), levetiracetam: Prophylactic anticonvulsants not indicated
  • Burr holes may be used as temporizing measure in deteriorating patients.
  • ICP monitoring is indicated for patients with abnormal CT who are intubated.
  • Subdural evacuating port system has been shown to be equivalent to Burr hole for acute treatment of SDH
  • <20 mL of blood, <1 cm, midline shift <5 mm, no mass effect, no neurologic deficit
  • This requires frequent neurologic reassessment.
  • 10% go on to require operative intervention.
  • Arterial line placement to monitor MAP, PO2, and PCO2
  • Foley catheter to monitor I/O status
  • Prevent pain, posturing, and increased respiratory effort:Sedation with benzodiazepinesNeuromuscular blockade with vecuronium or rocuronium in intubated patientsEtomidate is a good induction agent.
  • Mannitol may be used once euvolemic:Shown to increase MAP > cerebral perfusion pressure and CBF as well as decrease ICP
  • Keep osmolality between 295 and 310.
  • Use furosemide (Lasix) as an adjunct only if normovolemic.
  • Treat HTN:Labetalol, nicardipine, or hydralazine
  • Treat coagulopathy
  • Use fresh frozen plasma 4+ units
  • Use prothrombin complex concentrate
  • Treat hyperglycemia if present:Associated with increased mortality in traumatic brain injury
  • Treat and prevent seizures:Diazepam and phenytoin (Dilantin), levetiracetam: Prophylactic anticonvulsants not indicated
  • Sedation with benzodiazepines
  • Neuromuscular blockade with vecuronium or rocuronium in intubated patients
  • Etomidate is a good induction agent.
  • Shown to increase MAP > cerebral perfusion pressure and CBF as well as decrease ICP
  • Labetalol, nicardipine, or hydralazine
  • Associated with increased mortality in traumatic brain injury
  • Diazepam and phenytoin (Dilantin), levetiracetam: Prophylactic anticonvulsants not indicated

Medication

  • Diazepam: 5 " “10 mg (peds: 0.2 " “0.3 mg/kg) IV/IM q10 " “15min PRN; max. 30 mg (peds: 10 mg)
  • Dilantin: Adults and peds: Load 18 mg/kg at 25 " “50 mg/min
  • Etomidate: 0.3 mg/kg IV for induction of RSI
  • Fentanyl: 2 " “4 Ž Όg/kg
  • Hydralazine: 10 " “20 mg (peds: 0.1 " “0.5 mg/kg IV) q2 " “4h PRN
  • Labetalol: 20 mg IV bolus, then 40 " “80 mg q10min; max. 300 mg; follow with IV continuous infusion 0.5 " “2 mg/min; (peds: 0.4 " “1 mg/kg/h IV continuous infusion; max. 3 mg/kg/h)
  • Lasix: Adults and peds: 0.5 mg/kg IV
  • Levetiracetam: 1,500 mg PO/IV q12h
  • Lidocaine: As preinduction agent, 1.5 mg/kg IV
  • Mannitol: Adults and peds: 0.25 " “0.5 g/kg IV q4h
  • Midazolam: 1 " “2 mg (peds: 0.15 mg/kg IV ƒ — 1) IV q10min PRN
  • Nicardipine: 5 " “15 mg/h IV continuous infusion (peds: Safety not established)
  • Pentobarbital: 1 " “5 mg IV q6h
  • Prothrombin complex concentrate: 50 U/kg IV
  • Rocuronium: 1 mg/kg for induction
  • Thiopental: As induction agent, 20 mg/kg IV

Follow-Up

Disposition

  • Acute SDH patients should be admitted to the operating room or ICU by the neurosurgical service.
  • Subacute subdurals should be admitted to a monitored setting.

Pearls and Pitfalls

  • GCS on admission
  • Time to treatment
  • Pupil abnormalities
  • CT volume of hematoma and presence of midline shift
  • Midline shift > hematoma volume

Additional Reading

  • Beslow ‚ LA, Licht ‚ DJ, Smith ‚ SE, et al. Predictors of outcome in childhood intracerebral hemorrhage: A prospective consecutive cohort study. Stroke. 2010;41(2):313 " “318.
  • Chittiboina ‚ P, Cuellar-Saenz ‚ H, Notarianni ‚ C, et al. Head and spinal cord injury: Diagnosis and management. Neurol Clin. 2012;30(1):241 " “276, ix.
  • Huh ‚ JW, Raghupathi ‚ R. New concepts in treatment of pediatric traumatic brain injury. Anesthesiol Clin. 2009;27(2):213 " “240.
  • Krupa ‚ M. Chronic subdural hematoma: A review of the literature. Part 2. Ann Acad Med Stetin. 2009;55(3):13 " “19.
  • Kubal ‚ WS. Updated imaging of traumatic brain injury. Radiol Clin North Am. 2012;50:15 " “41.
  • Zhu ‚ GW, Wang ‚ F, Liu ‚ WG. Classification and prediction of outcome in traumatic brain injury based on computed tomographic imaging. J Int Med Res. 2009;37(4):983 " “995.

Codes

ICD9

  • 432.1 Subdural hemorrhage
  • 767.0 Subdural and cerebral hemorrhage
  • 852.20 Subdural hemorrhage following injury without mention of open intracranial wound, unspecified state of consciousness

ICD10

  • I62.00 Nontraumatic subdural hemorrhage, unspecified
  • P10.0 Subdural hemorrhage due to birth injury
  • S06.5X0A Traum subdr hem w/o loss of consciousness, init
  • P52.8 Other intracranial (nontraumatic) hemorrhages of newborn
  • I62.01 Nontraumatic acute subdural hemorrhage
  • I62.02 Nontraumatic subacute subdural hemorrhage
  • I62.03 Nontraumatic chronic subdural hemorrhage
  • I62.0 Nontraumatic subdural hemorrhage

SNOMED

  • 95453001 subdural intracranial hematoma (disorder)
  • 262952002 Traumatic intracranial subdural hematoma (disorder)
  • 281864001 Non-traumatic intracranial subdural hematoma (disorder)
  • 206191000 Local subdural hematoma due to birth trauma (disorder)
  • 304831001 Chronic intracranial subdural hematoma (disorder)