7.1 Intracerebral Hemorrhages

Intracerebral hemorrhage (ICH) has been a topic of significant research in the past several decades and includes multiple etiologies, including uncontrolled hypertension, amyloid angiopathy, anticoagulant use, cerebrovascular disease, tumors, migraines, and invasive procedures. Bleeding is usually short lived and is tamponaded by anatomical and physiological means; however, it is associated with a 30-day morbidity and mortality of 60% and 30%, respectively. ¹ Elevated blood pressure, defined as a systolic blood pressure (SBP) greater than 140 mm Hg, is seen in 75% of patients with acute ICH, and strict control of blood pressure is paramount in prevention of delayed rebleeding. ²

The ICH score described by Hemphil in 2001 offers a good predictive factor for the 30-day mortality (► Table 7.1). ³ Any delayed rebleeding may result in increased clot size and increased ICH score and, as a result, in a significant increase in estimated mortality.

To decrease the risk of delayed nontraumatic intracranial hemorrhage from head injury during the first hour to 24 hours, large spikes in SBP or any blood pressure greater than 140 mm Hg systolic must be prevented. Helping to prevent delayed nontraumatic intracranial hemorrhage would also include avoiding the use of hypotonic fluid and preventing hyperthermia.

7.2 Treatment Guidelines for Spontaneous ICH

Many attempts to classify surgical indications for evacuation of ICH have been and continue to be studied. ⁴ The International Surgical Trial in Intracerebral Hematoma (STICH) looked at the outcome of 1,033 patients (from 83 centers in 27 countries) treated with early surgery (open craniotomy) versus initial conservative treatment. ⁵ Ultimately, the STICH trial showed no significant difference between early surgical treatment and nonsurgical treatment groups as a whole. However, there was a subset of the early surgical group that seemed to have a better outcome than conservatively treated patients. These patients had supratentoral ICH that came within 1 cm of the surface. Therefore, the STICH II trail was performed, which looked at early surgery (within 48 hours) versus initial conservative treatment, specifically for patients with ICH with a volume of 10–100 mL, within 1 cm of surface, without intraventricular hemorrhage (IVH) and a GCS motor score of 5–6 and a GCS eye-opening score of ≥ 2. ⁶ The results showed there was no increase in death or disability at 6 months between groups, and there was a small benefit in overall survival.

Clearly there is a subset of patients that benefit from evacuation of hematoma. To that end the MISTIE and MISTIE-II trials (Minimally Invasive Surgery Plus Recombinant Tissue Type Plasminogen Activator for Intracerebral Hemorrhage) looked to employ a minimally invasive approach to clot evacuation in hopes to decrease the clot size and perihematomal edema (PHE) more effectively than medical treatment alone. ⁷ , ⁸ Currently the MISTIE III trial is under way and has completed enrollment. MISTIE III will determine if the reduction in PHE and clot size results in improved neurologic outcome.

IVH, often accompanying ICH, is associated with increased 30-day mortality based on ICH score. ³ IVH can result in obstructive hydrocephalus and depressed mental status and often requires placement of an external ventricular drain (EVD) for cerebrospinal fluid (CSF) diversion. The tedious task of ensuring continued drainage of sanguineous CSF requires continued flushing, a replacement of EVD. Additionally, drainage of CSF with normalized ICH doesn’t reverse the neurologic deficits likely due to toxicity of blood product. ⁹ , ¹⁰ The CLEAR IVH trial published in 2011 established that administration of intrathecal recombinant tissue plasminogen activator (rtPA) has an acceptable safety profile and has a dose-dependent response, with improved resolution of IVH compared to placebo. ¹¹ CLEAR III study results came out in February 2016. Injecting low-dose tPA into ventricles after intraventricular hemorrhage did not significantly improve the primary endpoint of a good functional outcome. However, the treatment was associated with a 10% reduction in mortality without increasing the number of patients left in a vegetative state or requiring nursing home care. From subgroup analysis, it was also evident that the intervention had the best results in patients who had the most blood evacuated. In those who had bigger clots with more than 20 mL of blood evacuated, there was a significant 10% increase in the number of patients achieving a good functional outcome.

At our institution we have developed a standardized protocol for patients presenting with ICH to both prevent delayed interval increase in ICH and support maximal recovery of neurologic function (► Fig. 7.3).

The treatment for acute ICH after neurological evaluation is as follows:

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  Immediate blood pressure reduction to SBP < 140 mm Hg (unless elevated creatinine/blood urea nitrogen [Cr/BUN] after control to indicate renal hypoperfusion).

  
  
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  Immediate reversal of coagulopathy.

  
  
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  Keep oxygenation in non-chronic obstructive pulmonary disease [COPD] patient ≥ 98%.

  
  
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  Start normal saline intravenous fluid.

  
  
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  Elevate the head to 30–45 degrees (if trauma suspected then reverse Trendelenburg).

  
  
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  Computed tomographic angiography/magnetic resonance angiography (CTA/MRA) to evaluate for vascular abnormality if the patient is less than 65 years old, or region of bleed is suspicious for aneurysm or arteriovenous malformation (AVM) bleed.

  
  
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  If the GCS score is ≤ 8, use EVD placement for intracranial pressure monitoring.

The general guidelines for evacuation of an ICH are as follows:

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  GCS score 5 to 13 or deterioration of 2 GCS points.

  
  
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  Volume greater than 30 mL.

  
  
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  No brainstem involvement, no active myocardial infarction (MI).

7.3 Protocol for Bedside Drainage of Intracerebral Hemorrhage

The criteria in ► Fig. 7.3 should be met before proceeding with bedside intraclot drain placement.

The following supplies are needed:

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  Cranial access kit.

  
  
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  Trauma-style ventricular catheter.

  
  
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  10 or 12 Fr Frazier suction tip and suction tubing.

  
  
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  Sterile gown/gloves/drape.

  
  
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  Local anesthetic.

7.4 Protocol for Intrathecal rtPA Administration for Intraventricular Hemorrhage

Place the EVD using the standard method. Prior to administering intrathecal rtPA ensure the CTA is negative for aneurysm or AVM. Ensure that SBP is kept strictly < 130 mm Hg before, during, and after clamping. If blood pressure is labile, use nicardipine or an equivalent during and after clamping to keep SBP < 140 mm Hg. First remove 3 mL of CSF from the EVD and administer 2 mg of intrathecal rtPA mixed in 3 mL of sterile saline or water via EVD. Keep EVD clamped for 1 hour or as long as the patient can tolerate without sustained elevated intracranial pressures. Open the EVD and place level at 6 mm Hg above the external auditory canal. Obtain a repeat CT head scan within 12 hours of administration of the first dose of rtPA. If the scan is negative for new hemorrhage proceed with administration of rtPA every 12 hours using the same protocol as for the initial administration. Continue with rtPA administration until there is CT evidence of resolution of the IVH, especially within the fourth ventricle and CSF output becomes blood tinged to clear. Check the CT head scan at least after the first and eighth dose.

Case Example

A 48-year-old woman was found in her automobile in status epilepticus with generalized tonicoclonic seizures and a history of traveling cross-country for 1 month. Her past medical history and family medical history were negative except for a 6-week fast for religious reasons. She was intubated and sedated; seizure control was achieved via benzodiazepines. Initially, she had a GCS score of 7 T with mild (4/5) left-sided hemiparesis. A CT scan of the brain demonstrated a 1.3 cm intraparenchymal hematoma in the right parietal lobe with edematous changes associated with an infarct in the left parietal convexity (► Fig. 7.4).

A thrombus was directly visualized on CT in the superior sagittal sinus and the right transverse sinus and later confirmed on magnetic resonance imaging (MRI). The patient was diagnosed with venous sinus thrombosis secondary to severe dehydration with an associated intracranial hemorrhage and infarction. Aggressive rehydration and anticoagulation therapy with heparin were initiated. On reexamination of the patient 4 hours after beginning the heparin protocol, the patient had improved and was observed to have a GCS score of 11 T with residual left hemiparesis but moving all extremities. The patient was weaned to extubation and continued to become more alert. Thirty-six hours status postheparinization, the patient was noted to have a flaccid left side, although with a GCS score of 15. An emergent CT scan of the brain demonstrated a rebleed into the original intraparenchymal hemorrhage in the right parietal convexity, now measuring 3 cm, with worsening edema bilaterally (► Fig. 7.5). The heparin protocol was halted, and aggressive rehydration continued as the primary treatment. The patient’s left hemiplegia gradually improved over the course of her hospital stay into a hemiparesis, and she was discharged to a rehabilitation center.

7.5 Delayed Traumatic Intracerebral Hemorrhage

Delayed hemorrhages previously discovered via angiography were considered relatively rare, yet with the advent of CT scanning, the ease of diagnosis and follow-up has increased, as well as the incidence. Etiologies are both posttraumatic and nontraumatic. The following section reviews the pathogenesis, diagnosis, management, and outcome of these lesions using three case examples. In most cases delayed hemorrhages can be prevented by following the same criteria for ICH:

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  Immediate blood pressure reduction to SBP < 140 mm Hg (unless elevated Cr/BUN after control to indicate renal hypoperfusion).

  
  
• 
  

  Immediate reversal of coagulopathy.

  
  
• 
  

  Keep oxygenation in non-COPD patients ≥ 98%.

  
  
• 
  

  Start normal saline intravenous fluid.

  
  
• 
  

  Elevate the head to 30–45 degrees (if trauma suspected then reverse Trendelenburg).

  
  
• 
  

  CTA/MRA to evaluate for vascular abnormality if the patient is less than 65 years old or the hematoma is suspicious for an aneurysm or AVM-associated bleed.

  
  
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  If the GCS score is ≤ 8, use EVD placement for intracranial pressure monitoring.

In 1891 Bollinger described delayed traumatic intracranial hemorrhages (DTICHs) as traumatische Spät-Apoplexie (“traumatic apoplectic event”) events using three criteria ¹² :

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   An apoplectic event preceded by a traumatic history.

   
   
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   A relatively symptom-free period followed by a neurologic decline.

   
   
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   The lack of preexisting vascular pathology.

Duret and other researchers expanded on Bollinger’s work by delineating the stages of DTICH. ¹³ , ¹⁴ In the early 1900s, continued research led to theories of pathogenesis for DTICH, which we will discuss. Today, improved imaging has increased detection and diagnosis of DTICH, which was previously limited to operative and autopsy findings and has enhanced our understanding of the disease. DTICH can be divided into epidural, subdural, and intracerebral hemorrhages.