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Phase 3 - Part 2 - Question 8 - First Consult

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Phase 3 - Part 2 - Question 8 - First Consult Powered By Docstoc
					Diagnosis
Summary Approach
An emergency head CT scan without contrast is imperative. It will usually reveal the presence of fresh
hemorrhage in the subdural space.

Clinical Presentation

Symptoms
       Confusion or lethargy
       Focal neurologic symptoms such as numbness
       Headache
       Dizziness
       Nausea or vomiting
       Ataxia
       Rarely, a patient may be asymptomatic

Signs
       Impaired level of consciousness
       Focal neurologic deficit, depending on location: a parietal acute subdural hematoma will
        result in contralateral hemiparesis or hemiplegia; blood over the dominant fronto-temporal
        lobes affects speech, causing aphasia
       Bradycardia and hypertension (Cushing response) may indicate raised intracranial pressure
        but are unreliable signs
       Seizures
       Unilateral pupillary dilation: a late sign indicating uncal herniation. If the raised intracranial
        pressure is not relieved rapidly, the patient may develop fixed dilated pupils bilaterally due to
        progressive brain herniation, followed by brain death
       Evidence of head trauma on physical examination

Examination
Complete neurologic exam:
       Mental status: assess level of consciousness. The internationally accepted standard
        measurement of consciousness is the Glasgow coma scale (GCS): points are assessed based
        on eye opening, best verbal response, and best motor response; scores range from 3 to 15
             Eye opening score: 4, eyes open; 3, eyes open to speech; 2, eyes open in response to
                pain; 1, no eye opening
             Best verbal response score: 5, alert and oriented; 4, confused; 3, responds with
                inappropriate words; 2, makes incomprehensible sounds; 1, no verbal response
             Best motor response score: 6, obeys commands; 5, localizes pain; 4, responds to pain
                with normal flexion/withdrawal; 3, responds to pain with abnormal flexion; 2,
                extends in response to pain; 1, no response to pain
       Cranial nerve: pupil asymmetry or other signs of oculomotor palsy can be a sign of
        herniation. Papilledema is not seen with acute subdural hematoma
       Motor: focal weakness or coordination deficit may be seen
       Sensory deficit is not likely to be the only focal sign
      Tendon reflexes are often asymmetric in patients with focal motor deficit. Plantar response
       may be extensor (Babinski response)
      Coordination and gait: limb or gait ataxia, or both, is common in patients with subdural
       hematoma
      Speech: the presence of blood overlying the dominant fronto-temporal lobes affects speech,
       causing aphasia

General:
      Chest: patients at risk for subdural hematoma may also be at risk for chest injury
       including pneumothorax, rib fracture, and sternal fracture
      Abdomen: evaluate for blunt trauma to spleen, gastrointestinal and urinary tracts
      Spine: examination of the entire spine, particularly the cervical spine to determine
       whether there is spinal column damage associated with the subdural hematoma

Questions to ask
      How did you sustain the injury? Patients with acute subdural hematoma have usually
       sustained a severe head injury, usually caused by a high-velocity road traffic accident,
       a fall from a height, an assault, or a sporting injury
      Are you taking blood thinners? Patients on oral anticoagulants and antithrombotic
       agents have an increased risk
      Are you taking any medication? Patients who are on anticoagulants are more likely to
       develop acute subdural hematomas and intracerebral hematomas following a
       relatively minor head injury. Rarely, aneurysm or arteriovenous malformation rupture
       can be a trigger
      Do you have a tendency to fall? Patients with ataxia from neurologic disorders have
       an increased risk

Diagnostic testing

      The investigation of choice is a noncontrast CT scan of the brain. Fresh blood
       layering between the dura and brain will appear bright, although small, early bleeding
       may be subtle
      Plain X-ray films of the cervical spine should be taken to evaluate for cervical spine
       fracture in conjunction with severe head injury
      Other investigations that should be performed include baseline hematologic studies,
       including complete blood count, routine biochemistry, and coagulation studies
      Plain skull X-ray films may help with evaluating for skull fractures
      Magnetic resonance imaging (MRI) is usually unnecessary for diagnosis, although
       once the patient is stable it may help reveal associated parenchymal brain lesions,
       such as edema and contusions, that are not seen well on CT scans
Treatment
Summary Approach

Goals
       The patient's condition must be stabilized using ABC principles
       The cervical spine must be protected by using a hard cervical collar, sandbags, and strapping
        until the cervical spine is cleared of injury
       Patients with a low Glasgow coma scale (GCS) (<7/15) probably need intubation and
        ventilation
       The patient must then be transferred rapidly to a specialized unit for further management.
        Neurosurgical treatment during the first 4h after injury may improve outcome, although this is
        controversial

Immediate action

       The patient should be stabilized using the ABC guidelines: ensure that there is a patent
        airway, that the patient is breathing, and that there is adequate circulation
       The cervical spine should be stabilized before transfer until investigations confirm that the
        patient has not sustained a cervical spine injury
       Patients whose GCS is less than 7/15 will probably need to be intubated and ventilated

Therapeutic Options

Summary of therapies
    The only medication that may be of value in the early management of acute subdural
     hematoma is mannitol. It can be given as a temporizing measure to reduce intracranial
     pressure until surgical treatment can be provided. Its effect will only last for a few hours. This
     is given only as an immediate life-saving maneuver, and specialists in neurosurgery,
     neurology, or trauma should be consulted prior to its use
    The use of hyperventilation is controversial given its potential to decrease intracranial blood
     flow. Hyperventilation of an intubated patient to a partial pressure of carbon dioxide (pCO2)
     of about 30mmHg can also be used to help decrease intracranial pressure temporarily. This is
     usually performed under the care of a neurosurgeon or in the intensive care unit
    Surgery (craniotomy for evacuation of acute subdural hematoma) is often required to remove
     the hematoma and decrease the intracranial pressure
    Patients undergoing anticoagulation therapy may not only be predisposed to acute subdural
     hematoma but are also at increased risk of complications from surgical drainage. Reversal of
     the coagulopathy should be performed as soon as possible. Protamine sulfate can be used to
     inactivate heparin. Warfarin therapy can be reversed with vitamin K and fresh frozen plasma
     (FFP). More recently, recombinant factor VIIa has been used for rapid reversal of warfarin-
     related coagulopathy. This agent may prove to be useful in cases where urgent surgical
     intervention is required
    Patients with subdural hematoma are at increased risk for seizures, so loading with phenytoin,
     valproate, or another intravenous anticonvulsant can be considered. The risk of seizures can
     persist, so many physicians continue anticonvulsant therapy for months after the injury.
     However, prophylactic use of anticonvulsants after head injury remains controversial
    The patient will require supportive care postoperatively and neurorehabilitation in the long
     term. This includes physical therapy, speech therapy, and occupational therapy
Order of therapies
      Mannitol
      Craniotomy for evacuation of acute subdural hematoma
      Physical therapy
      Occupational therapy

Efficacy of therapies
      Outcome in acute subdural hematoma remains poor in spite of speedier diagnosis and surgery.
       Mortality rates range from 36-90%. In a study of over 100 patients with acute subdural
       hematoma, the overall mortality rate was 66% and only 19% had a functional recovery
      The Glasgow Outcome Scale (GOS) is widely used to categorize outcome after severe head
       injury. Five categories exist: 1, death; 2, persistent vegetative state; 3, severe disability; 4,
       moderate disability; 5, good recovery. A GOS of 1-3 is considered a poor outcome; a GOS of
       4-5 is considered to be a favorable outcome
      Less than one-third of patients whose best initial GCS score is <8/15 have a favorable
       outcome

				
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