Surgery VERSUS cONCERVATIVE mANAGEMENT

Most SHs are managed surgically.

While there is little evidence for conservative management other than limited observational data, expert panel guidelines published in 2006 recommended nonoperative management in an intensive care unit with intracranial pressure monitoring for patients meeting the following criteria:

they are neurologically stable, have clot thickness <10 mm, midline shift <5 mm, no pupillary abnormalities, and no intracranial hypertension.7 SORⒸ

  • Observational studies in patients with SH suggest that surgery performed within 2 to 4 hours after the onset of neurological deterioration have mortality rates between 30% and 47%, as opposed to 80%°90% percent mortality with surgery delayed beyond 4 hours.7

  • Determine the Glasgow Coma Scale in patients with serious head trauma and consider airway protection in patients with a score less than 12.

  • Obtain an urgent noncontrast CT scan on any patient suspected of having an SH.

  • Blood studies should include1:

    • Complete blood count

    • Coagulation profile (important for patients on anticoagulants and with history of alcohol abuse)

    • Basic metabolic profile for electrolyte abnormalities

    • Type and screen/cross-match

  • If the noncontrast CT scan is nonrevealing, obtain a contrast CT or MRI, if available and no contraindications, particularly if the traumatic event occurred 2 to 3 days prior.

  • Emergently refer patients with an SH and deteriorating neurologic status or evidence of brain edema or midline shift to a hospital with neurosurgeons.

  • Consult a neurosurgeon expediently in patients with an SH and stable focal neurologic signs.

  • Avoid hypotension and hypoxia, as they are independent predictors of poor outcomes.1

  • Maintain pCO2 between 30 and 35 mm Hg with continuous mainstream or sidestream capnometry monitoring.

  • Medications may include1:

    • Anticonvulsants to prevent seizure-induced ischemia and surges in intracranial pressure.

    • Short-acting sedatives and paralytics only when necessary to facilitate ventilation or with elevated intracranial pressure.

    • Prothrombin complex concentrate, fresh frozen plasma, and/or platelets in patients with coagulopathies or receiving anticoagulant medications. Maintain prothrombin time within reference range and platelets above 100,000.

    • With herniation syndrome, administer mannitol 1 g/kg rapidly via IV push.

    • Avoid steroids, as they have been found ineffective in head-injury patients.

  • With traumatic injury, serial follow-up CT scans should be obtained during the first 36 hours following injury because of the high incidence of clot expansion during this period. Perform the first repeat scan within 6 to 8 hours of admission.7

  • Consider neurosurgical consultation in asymptomatic patients or those with only a headache and a small acute SH without brain edema or midline shift. These patients may be followed by serial CT scans without surgical treatment, but this should be done in consultation with experts in CT interpretation and management of SHs.7 SORⒸ

  • Evaluate any infant with an SH for child abuse or neglect.3 SORⒷ

 

 

subdural hematoma is due to tearing of a bridging vein by acceleration/deceleration forces. The bridging veins extend between the arachnoid mater and the dura mater and drain into the dural sinuses.

A subdural hematoma (SH) is a collection of blood between the dura and arachnoid membranes, but external to the brain.

SH may be acute or chronic. While most SHs are caused by trauma, they can occur at any age, most commonly in infants (abusive or unintentional head injury) and older adults due to cerebral atrophy with traction and rupture of bridging veins.

Rarely, SH may occur spontaneously, associated with a ruptured aneurysm, bleeding from intracranial tumors, or malignancy-induced coagulopathy.1

 Presentation varies widely in acute SH. While many patients are initially comatose, lucid intervals are reported in up to 38% of cases.1 Often, symptoms may be nonspecific, such as irritability or poor feeding in infants and confusion or headaches in adults.

 

The hematoma may present acutely or chronically.

Acute subdural hematomas are often associated with substantial underlying brain injuries, including brain contusions and diffuse axonal injury (DAI).

 

Image result for subdural hematoma

Tearing of a bridging vein can also lead to a chronic subdural hematoma. Chronic subdural hematomas are more commonly found in elderly or alcoholic patients, who have some degree of brain atrophy. The atrophying brain puts extra tension on the bridging veins and makes them more susceptible to tearing. From a clinical standpoint, it is important to note that chronic subdural hematomas are often the result of trivial or forgotten head trauma. Over the course of a few weeks the subdural hematoma undergoes organization and becomes encased by a fibrovascular membrane composed of granulation tissue. As organization proceeds, very small new blood vessels grow into the blood clot. These thin-walled vessels are prone to rupture, leading to additional hemorrhage and enlargement of the subdural hematoma. Chronic subdural hematomas are typically found over the convexities of the cerebral hemispheres, may be bilateral, and may act as mass lesions.

 

The hematoma acts as an enlarging mass lesion and may lead to brain shifts and herniation.

 

 

Content 9

 

Content 4

Content 3

Content 11

A 34-year-old driver was hit from behind at approximately 25 mph. He hit his head, but did not lose consciousness and did not seek care. Approximately 12 hours later, he developed a headache and confusion, and was taken to the emergency department by a family member. He was found to have an acute subdural hematoma.

Image not available.

CT scan of an acute subdural hematoma (arrow) seen as a hyperdense clot with an irregular border. There is a midline shift from the mass effect of the accumulated blood. (Courtesy of Kasper DL, Braunwald E, Fauci, AS, Hauser SL, Longo DL, Jameson JL. Harrison's Principles of Internal Medicine, 16th ed. New York, NY: McGraw-Hill; 2005:2450.)

He was hospitalized, and a neurosurgeon was consulted for surgical management.

Content 2

Content 3

 

Update as of

USMLE Reviewer (Subscription Required)