A 64-year-old woman with a history of hypertension and hyperlipidemia presents with sudden onset headache and stupor. She is taken by ambulance to a nearby emergency department (ED); en route she is given 2 mg midazolam because of seizure-like activity. In the ED, the patient is minimally responsive to pain with a flaccid right arm and increased tone in her lower extremities and is subsequently intubated. Noncontrast head computed tomography (CT) demonstrates hyperdensity in the sylvian fissure and basilar cisterns and intraventricular hemorrhage (IVH). Her third and lateral ventricles are notably dilated. She is diagnosed with subarachnoid hemorrhage (SAH) with IVH and early hydrocephalus and is transferred to the neurologic intensive care unit (NeuroICU) for further management.
On arrival to the NeuroICU she is examined with no sedation and is found to not follow commands. Her pupils are symmetrically reactive, and she moves her left side purposefully but is flaccid in her right upper extremity. Vital signs are heart rate, 90 bpm; respiratory rate, 18 breaths per minute; temperature, 37.4°C (99.4°F); and blood pressure, 120/73 mm Hg (Figure 22-1).
Does this patient need an external ventricular drain (EVD)? What are the indications for EVD placement?
This patient’s presentation is consistent with Hunt and Hess (HH) grade IV and Fisher grade 3 SAH (see Chapter 1 for information on SAH grading). Radiographic evidence of acute hydrocephalus along with neurologic decline (failure to follow commands) call for emergent placement of an external ventricular drain (EVD) to alleviate intracranial hypertension. EVDs serve three primary functions in SAH: to monitor intracranial pressure (ICP), to drain cerebrospinal fluid (CSF) for treatment of hydrocephalus, and/or to acutely reduce ICP. EVD placement is therefore indicated when a patient is thought to have symptomatic hydrocephalus and/or elevated ICP based on neurologic examination and radiographic findings.
Ventriculostomy is considered standard-of-care for treating SAH-associated hydrocephalus and has been shown to improve both short- and long-term outcomes.1,2 However, there is no standard, evidence-based guideline for EVD placement in patients with SAH. Although the Glasgow Coma Scale score (eg, ≤ 12)3,4 and HH grade (eg, ≥ III)5 have been used to establish an objective threshold for ventriculostomy, the procedure should be generally considered in patients who demonstrate clinical or radiologic deterioration or have an unreliable neurologic examination. Patients who present comatose or severely lethargic are typically considered for emergent ventriculostomy (Figure 22-2).6,7 Minimal improvement in neurologic status despite normalization of the ICP in these patients may point to other etiologies such as seizure, medication effect, or metabolic derangement and prompts immediate investigation. Improvement in HH grade following ventriculostomy placement in patients scoring poor grade (IV and V) has been shown to predict more favorable long-term outcomes.2 As for those with fluctuating levels of consciousness, the impact of ventriculostomy on outcome remains unclear, and therefore, careful risk-benefit analysis is warranted.3 Figure 22-3 outlines our institutional ICP management protocol for patients admitted to the NeuroICU with aneurysmal SAH (aSAH).
Figure 22-3.
Algorithm for the management of subarachnoid hemorrhage–associated hydrocephalus. External ventricular drain (EVD) challenge is generally initiated within 1 week of EVD placement. Ventriculoperitoneal (VP) shunting is appropriate for patients with persistent hydrocephalus. ICP, intracranial pressure; SAH, subarachnoid hemorrhage.
Similarly, EVD placement is recommended in a variety of other neurologic conditions causing symptomatic acute hydrocephalus related to either noncommunicating or communicating hydrocephalus or evidence of elevated ICP.1 Common causes of obstructive or noncommunicating hydrocephalus include posterior fossa tumors, IVH, and intraventricular cysts or tumors. Communicating hydrocephalus may be seen in the setting of SAH, IVH, meningitis, and other pathologies. Elevated ICP without significant hydrocephalus is commonly caused by closed-head trauma.8 In the setting of posterior fossa mass lesions, a risk of upward transtentorial herniation exists with supratentorial CSF drainage.9 Though rarely reported, this risk should be considered when deciding to place an EVD for posterior fossa lesions; rapid removal of large quantities of CSF should be especially avoided in this clinical setting. Normalization of ICP with EVDs can prevent secondary cortical injury, improve neurologic status, and enhance operative exposure during surgery.10–13 Of note, normal ICP ranges for adults and young children are considered < 10 to 15 mm Hg and 3 to 7 mm Hg, respectively.8
Another indication for EVD placement is to aid wound healing in the postoperative neurosurgical patient. Those who undergo operations of the posterior fossa, for example, via a suboccipital or a far lateral approach, are at particularly high risk for a postoperative CSF leak through their incision. Therefore, the neurosurgeon often leaves an EVD in the patient for several days postoperatively, which allows for drainage of CSF through the EVD and alleviation of CSF pressure on the fresh incision. Once the incision has begun to heal and there is no evidence of CSF leak, the EVD can be removed.8
EVDs and ICP monitors have also been widely used in traumatic brain injury (TBI) though controversy remains regarding their indications and benefit to reducing mortality. In patients with radiographic hydrocephalus and coma or stupor, an EVD should be placed to determine if hydrocephalus is the cause of the patient’s poor mental status and to manage increased ICP if present. The decision to place an EVD for the routine management of elevated ICP in severe TBI is less clear. Patients with severe TBI may present with significant cerebral edema and collapsed ventricles, making placement of an EVD technically challenging. Management of elevated ICP using imaging and clinical exam or intraparenchymal ICP monitoring in TBI was compared in a large randomized controlled trial in that found no difference in long-term mortality between groups.14 Retrospective series have found significant mortality benefits from ICP monitoring in severe TBI and in select cases its use may be beneficial.15,16
The EVD is placed by making a frontal incision and single burr hole in the skull, so that the catheter can be passed through the frontal lobe and into the lateral ventricle, with the goal of placing the catheter tip at the foramen of Monro. The nondominant frontal lobe is preferred as an entry point because it minimizes the risk of symptomatic brain injury in the event of a procedural complication such as subdural, epidural, or intraparenchymal hemorrhage.8 The burr hole entry point should be in the mid-pupillary line and 2 to 3 cm anterior to the coronal suture. This entry site avoids the sagittal sinus and its tributaries as well as the primary motor cortex, which is usually located 4 to 5 cm behind the coronal suture. This well-known entry point is called Kocher’s point and is typically located 11 to 12 cm posterior to the nasion in the anteroposterior (A-P) direction and 2 to 3 cm lateral to midline (Figure 22-4). Although a right-sided (nondominant frontal lobe) placement is preferred, the EVD may be placed through the left side if the surgeon needs to avoid a lesion or hemorrhage in the right frontal lobe or lateral ventricle. In trauma patients, the surgeon may prefer to pass the EVD through the injured frontal lobe in order to minimize risk to normal parenchyma. When Kocher’s point is used as an entry point, the trajectory of the EVD pass through the parenchyma should be toward the medial canthus of the ipsilateral eye in a medial-lateral direction and the ipsilateral tragus in an A-P direction. This trajectory is usually achieved if the EVD is aimed exactly perpendicular to the skull surrounding the burr hole. Depending on the size of the lateral ventricles, the surgeon may pass the catheter 4 to 5 cm into the parenchyma before feeling a “pop” sensation that indicates entry into the lateral ventricle, with a return of CSF through the catheter. In order to advance the catheter tip to the foramen of Monro, the EVD is usually “soft passed” (advancing the catheter without the stylet) to a total of 6.5 to 7.0 cm from the outer table of the skull. The catheter is then tunneled a short distance under the scalp, in a direction that avoids a potential future shunt pathway (generally posteromedially).
Rates of EVD catheter misplacement ranged from 10% to 13% in large single-center series.17–20 Hemorrhage rates from EVD placement as high as 27% to 41% in individual large prospective and retrospective studies have also been reported in the literature.21,22 Despite these high figures, the mean hemorrhage rate from EVDs for any indication was 8.4% in one recent meta-analysis, though of those only 0.7% of hemorrhages were symptomatic.19 Therefore, a routine postplacement computed tomography (CT) scan is recommended to ensure correct placement and rule out hemorrhagic complications. In the event that hemorrhage is seen on a postprocedure CT scan, serial follow-up scans should be performed until bleed stability is confirmed.
EVDs can be placed either in the operating room (OR) or at the bedside using local anesthesia and/or conscious sedation.22–24 The OR provides a more sterile, controlled environment where acute complications can be efficiently managed. However, waiting for an OR may delay treatment when emergency EVD placement is necessary. Furthermore, transporting critically ill patients to the OR may simply be unsafe. Although EVD placement in an ICU setting may increase the risk of severe infection, there are no conclusive data to determine how the environment of EVD placement affects the overall complication rate and outcome.23,25,26
EVDs have traditionally been placed by neurosurgeons to ensure that the person who places the device can also manage procedure-associated complications, such as subdural or intracerebral hemorrhage. Recently, an increasing number of EVDs and ICP monitors have been placed by non-neurosurgeons, including neurointensivists, nurse practitioners, physician assistants, trauma surgeons, and general surgeons.27–29 The impact of EVD placement by non-neurosurgeons on procedural success, complication rates, and outcomes has yet to be determined. Nevertheless, the increasing trend toward non-neurosurgeon EVD and ICP monitor placement, if proven equally safe and effective, may provide patients with more expeditious care in select, resource-poor environments.
Although an EVD is thought to offer the most accurate ICP measurements, the surgeon may be unable to place an EVD in patients with collapsed ventricles, slit ventricles, or significant mass effect.8 In such cases, ICP can be monitored via placement of a fiberoptic parenchymal ICP bolt. If a parenchymal ICP monitor is placed and the team believes intracranial CSF volume is contributing to critically elevated ICP, a spinal drain may be placed in patients with communicating hydrocephalus. Additionally, the placement of a spinal drain has also been used to prevent the development of delayed cerebral ischemia.30 In effect, a parenchymal ICP bolt in conjunction with a spinal drain can serve the same functions as an EVD.31 Although intraparenchymal monitors are easily placed and can be disconnected during patient transport without the need for recalibration, they cannot accurately detect pressure alterations in deeper parts of the brain.31,32 The devices are also associated with mechanical failure, fragility, and monitor malfunction.
EVD catheters are available from a number of manufacturers; however, the important distinctions of clinical relevance include catheter diameter and antibiotic impregnation (see below). Standard catheters with internal diameters ranging from 1.3 to 1.5 mm have been widely studied and are well-suited for the majority of indications. In patients presenting with significant IVH, we prefer to place larger bore “trauma” catheters with an internal diameter of 2.6 mm and large fenestrations. The larger diameter and fenestrations allow small clots to flow more freely and prevent EVD occlusion. A theoretical risk of increased hemorrhage rates from the placement of larger diameter catheters exists; however, no studies confirm such an association. The radiographic appearance of standard and “trauma” catheters is shown in Figure 22-5.
Figure 22-5.
Standard external ventricular drain (EVD) catheters (left) are most commonly placed with internal diameters of 1.3 to 1.5 mm. A “trauma” catheter (right) has a larger internal diameter of 2.6 mm with larger fenestrations and may be used in the setting of intraventricular hemorrhage to theoretically prevent EVD obstruction.
Prior to receiving an external ventriculostomy, the 64-year-old patient undergoes CT angiography, which reveals a 13 × 5 × 5-mm left middle cerebral artery bifurcation aneurysm (Figure 22-6).
EVD placement has been suggested to increase the risk of rebleeding in patients with aSAH.3,33,34 An abrupt drop in ICP and resultant increase in the transmural pressure on the aneurysm are thought to cause the rebleeding.35 However, elevated risk of rebleeding in patients with aSAH after EVD placement remains controversial, and no study to date has conclusively established a causal relationship.36–38 Of note, patients requiring an EVD tend to present with worse HH grade, which in turn is associated with independent risk factors for rebleeding, such as larger aneurysm and dense SAH. Furthermore, conflicting results may be attributed to the failure to account for the following confounding variables: clinical grade, aneurysm treatment timing, duration of EVD placement during which the aneurysm remained untreated, and the interval between onset of SAH and EVD placement.37,39 In the absence of conclusive data, the presence of an aneurysm should not be a contraindication for EVD placement in the setting of SAH-associated hydrocephalus.7 Nevertheless, ICP should be normalized gradually to minimize the theoretical risk of rebleeding.
After the EVD is placed, the head of the patient’s bed should be elevated to 30°, with the patient’s neck in a neutral position to reduce ICP and increase venous return. The EVD CSF collection system is fixed to a pole next to the bed, with leveling such that zero is set at the height of the external auditory meatus (Figure 22-7).8 The drainage port is then fixed at a desired level above or below this zero reference. In patients SAH with unsecured aneurysms, we typically set the drainage port at 20 cm of H2O to prevent overdrainage and the creation of untoward transmural pressure, which may precipitate rebleeding. Postoperatively, once the aneurysm has been protected with clipping or coiling, we typically lower the EVD drainage level and titrate based on the patient’s clinical status and the degree of radiographic hydrocephalus. An alternative approach is to use intermittent drainage of CSF at predefined ICP thresholds (eg, ICP > 10 mm Hg for 5 minutes), which has been shown to decrease rate of EVD nonpatency with equivalent outcomes.40 Overdrainage should be avoided as it may lead to subdural hemorrhage and in rare cases herniation.
In the setting of a posterior fossa tumor, EVDs are often placed intraoperatively.8 CSF is drained to affect brain relaxation, which may be beneficial during the craniotomy and dural opening. During the postoperative period, the EVD may be initially set at a low height (eg, 5-10 cm H2O) and is progressively elevated over a 2- to 3-day period.
What are the most common infectious complications associated with EVDs? Should prophylactic antibiotic be used? What about antibiotic-coated catheters?
Soft tissue infection and ventriculitis are the most common ventriculostomy-related infections.19,41,42 Less common are intraparenchymal abscesses, subdural empyema, and osteomyelitis. Steroid use and duration of catheter placement are known risk factors for EVD-associated infection,43 and there have been no conclusive studies regarding the effects of systemic infection on the risk of neurologic infection.