CASE

An 86-year-old female with past medical history of atrial fibrillation and coronary artery disease on apixaban and clopidogrel presents as a trauma activation after a mechanical fall from standing at her nursing facility.  She does not remember the fall, but her nurse reports she tripped over her walker, fell and struck her head.  She did not lose consciousness. 

In the ED, her vitals are BP: 195/90, HR: 65, RR: 12, SpO2 95% on room air. 

Her physical exam is significant for GCS 14 (E4V3M6), alert and oriented to self only, an ecchymosis to her left forehead with scattered ecchymoses on her arms and shins. 

Non-contrast CT of the brain shows a 10mm left frontal and parietal subdural hematoma without midline shift.

DIAGNOSIS

Traumatic Subdural Hematoma

DISCUSSION

Traumatic brain injury (TBI) is a significant cause of death and disability worldwide.  The highest rates occur in older adults; in 2013, more than 1 in 50 Americans 75 years or older had an ED visit, hospitalization, or death related to a TBI [2]. Although many older patients have low mechanism injuries, they are still at increased risk of developing intracranial hemorrhage (ICH), particularly when they are taking anticoagulant medications.  The American College of Emergency Physicians recommends considering head CT in all patients over 65 years old who present with even a mild TBI, and recommend a head CT in all patients older than 60 with TBI and loss of consciousness [3]. It is important to recognize and treat this diagnosis quickly as the initial medical management of these patients in the ED can have a significant impact on their neurologic outcomes.

Which came first, the bleed or the fall?

Sometimes it isn’t clear whether trauma caused the ICH or if the patient had a spontaneous ICH then fell.  It can be important to distinguish between these to determine if there is an underlying process that must be addressed.  The location of the bleed can give us a hint to it’s etiology.  The table below describes the most common locations for different types of bleeds.

If the location of the bleed does not suggest a traumatic cause, it is important to investigate possible causes of a spontaneous bleed, usually with a CTA brain [4].  Common causes include: hypertension, vascular malformation, coagulation problem, cerebral amyloid angiopathy, neoplasm, aneurysm, drugs, hemorrhagic conversion, or dural venous sinus thrombosis [5,6].  Management of spontaneous ICH is outside the scope of this discussion, but there are differences in terms of blood pressure goals and potential interventions needed.

Medical Management

The early resuscitation and medical management of patients presenting with TBI can have a significant impact on their neurologic outcome as well as their morbidity and mortality.  A single occurrence of hypotension or hypoxia in a severely brain injured patient can increase the risk of mortality by 150% [7].

Resuscitation should have the goal of maintaining cerebral oxygenation and perfusion with focus on correcting the following:

Blood Pressure:

For traumatic ICH the goal is to avoid hypotension and maintain SBP >100 mmHg in patients age 50-69 years old and >110 mmHg in age >70. 

There is no agreed upon upper limit of blood pressure for TBI, but it is vitally important to avoid hypotension [8,9].  Our institution uses a systolic blood pressure goal of <160 mmHg in TBI. There are different blood pressure goals in non-traumatic ICH which are outside the scope of this discussion. Before starting an anti-hypertensive medication, it is important to first control the patient’s pain, anxiety, and nausea.  If additional blood pressure control is needed, first line medications are labetalol as an IV push or infusion, or a nicardipine infusion [5].  

Airway/Breathing:

Patients should remain normoxic and normocapnic.  Prophylactic hyperventilation is not recommended as this can cause further brain injury by restricting cerebral blood flow.  Intubation should be considered for airway protection if the patient’s mental status is significantly depressed (usually GCS <8) [9,11].

Intracranial Pressure (ICP):

ICP monitoring (with a bolt or EVD) should be considered in patients with GCS <8 with structural damage on CT, patients with high risk of progression, or patients who are intubated, having clinical deterioration, or requiring urgent surgery [9].   

Treatments for reducing ICP include elevating the head of the bed to 30 degrees, maintaining adequate analgesia and sedation and preventing vomiting with anti-emetics.  Steroids should NOT be used to reduce ICP in TBI [5].  Patients showing signs or symptoms of increased ICP (including change in mental status, pupil irregularities, focal neuro deficits, or decerebrate or decorticate posturing) should be treated with mannitol or hypertonic saline.  EVD’s can also be used to drain CSF and decrease ICP [8].

Glucose:

Blood glucose should be maintained at 100-180 mg/dL. Hyperglycemia can cause edema, neuronal apoptosis, and destruction of the blood brain barrier [9,12].

Temperature:

Hyperthermia is known to worsen outcomes in TBI. Antipyretics and external cooling devices should be used to maintain normothermia [8]. 

Seizure Prophylaxis:

Up to 12% of all patients with TBI develop early post traumatic seizures (PTS), most of these happen in the first 48 hours.  Although early PTS is not a predictor of future epilepsy, it is important to prevent seizures because they cause hypoxia, hypercarbia, and increased ICP which cause secondary brain injury. Patients should be started on prophylactic anti-epileptic medication for the first 7 days.  Phenytoin is officially recommended by the Brain Trauma Foundation, but levetiracetam is commonly used as it has a preferable side effect profile [8,13].

Anticoagulation reversal:

Patients on anticoagulation, particularly warfarin, are at higher risk of progression of TBI [14].  Current recommendations are that these medications should be reversed per the guidelines listed below [15].

Reversal of anti-platelet medications (aspirin and P2Y12 inhibitors such as clopidogrel) is more controversial.  These may be reversed with platelet transfusion, but that carries significant risk including transfusion-related acute lung injury (TRALI), thrombosis, disseminated intravascular coagulation (DIC), and transfusion reactions. The current available data does not show a clear benefit to transfusion and some studies have shown possible harm [15].  The official recommendation from the Neurocritical Care Society is to NOT transfuse platelets for patients on antiplatelet agents unless they are undergoing a neurosurgical procedure [15]. DDAVP (0.4 mcg/kg dose IV) may be used for reversal of aspirin and clopidogrel, but is not effective for ticagrelor [15].

CASE RESOLUTION

The patient was given 4F-PCC for the reversal of abixaban, DDAVP to reverse the clopidogrel, levetiracetam for seizure prophylaxis, acetaminophen for pain, and ondansetron for nausea.  Her repeat blood pressure was 155/95, she maintained an SpO2 of 96% on 2L NC and her neuro exam remained unchanged. Her 6 hour repeat CT brain did not show any increase in the size of the hematoma and she was admitted to the neurosurgery floor.  

TAKE-AWAYS

• Resuscitation of patients with TBI is important and has a significant impact on morbidity and mortality

• Management should focus on maintaining normal blood pressure, adequate oxygenation, normal ventilation, normal ICP, glucose, normothermia, and seizure prophylaxis

• Reverse anticoagulation medications.

• Only reverse anti-platelet medications with platelets if the patient will be undergoing a neurosurgical procedure. DDAVP can be considered for the reversal of aspirin or clopidogrel.

  
  

AUTHOR: Hannah Chason, MD is a third year emergency medicine resident at Brown University/Rhode Island Hospital

FACULTY REVIEWER: Nicholas Asselin, DO is an attending physician for Brown Emergency Medicine

REFERENCES

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