16 Intraventricular Hemorrhage

16.1 Introduction

Endoscopic treatment of cerebral hemorrhage is not a novelty. Auer in 1985 was the first to describe an endoscopic approach to the treatment of an intracerebral hemorrhage with ventricular extension.1,2 The technique was initially met with mild enthusiasm, which subsequently turned into pessimism when the endoscopic technique proved to be hardly reproducible. Therefore, this approach, with few exceptions, was abandoned.3,4,5,6 However, experience reveals that a significant difference in success rate may be associated with the nature and the site of the lesion being treated.7,8,9,10,11 There is a substantial difference between the dense, hardened clots that form most intraparenchymal hematomas and the fragile, gelatinous intraventricular clots. Although attempts with various devices and techniques for intraparenchymal hematoma removal proved frustrating, even the 1-mm operating channel of a flexible endoscope may prove sufficient to rapidly clear and decompress the entire ventricular system of blood clots. Once it was proven that the early and nearly complete removal of intraventricular hemorrhage (IVH) was possible with endoscopic surgery, it became popular thanks to advances in and mastery of the technique and the improvement of the technology.3,4,11,12,13,14,15 We have to admit that complete removal of IVH is nearly impossible to achieve: the learning curve requires almost 20 procedures and mastering of the endoscopic anatomy of all the ventricular structures. Rather than engage in the time-consuming aspiration of clots from the lateral ventricles, we suggest, as indispensable, to decompress the third and fourth ventricles to reestablish the patency of cerebrospinal fluid (CSF) flow.

16.2 Pathophysiology

IVHs can be classified as primary or secondary. Primary IVHs are confined to the ventricular system and immediate parenchymal ependymal lining, originating from intraventricular sources or a lesion in contact with the ventricular wall. Secondary IVHs originate as an extension of an intraparenchymal or subarachnoid hemorrhage into the ventricular system. About 30% of IVHs are primary and 70% are secondary.16,17 Frequent causes of primary IVH include head trauma; insertion or removal of a ventricular catheter (i.e., surgical trauma); intraventricular vascular malformation; germinal matrix hemorrhage, aneurysm, or tumor; hypertension and/or bleeding diatheses. A large variety of other rare etiologies such as Moyamoya disease have been reported, and primary IVH may also be “spontaneous.”16 Because many conditions may cause an intracerebral hematoma or subarachnoid hemorrhage, secondary IVH also has a variety of etiologies. Most common among these are hypertensive hemorrhage (e.g., of the basal ganglia), cerebral aneurysm, head trauma, arteriovenous malformation (AVM), vasculitis, coagulation disorder, hemorrhagic transformation of an ischemic infarct, and tumors. The estimates on the clinical impact and mortality of the disease ranges from 50 to 80%. The most common cause of IVH in adults is spontaneous intracranial hemorrhage (ICH),18 followed by subarachnoid hemorrhage (SAH).17 Incidence of IVH in intracerebral hemorrhage is about twice that in SAH. Approximately 10% of aneurysmal SAH and 40% of primary ICH experience IVH.15,17 At present medical management of ICH and IVH revolves around the control of intracranial pressure (ICP). Despite best medical management, mortality remains high with only 38 to 50% of patients surviving the first year.10,15,18 Even with best medical management, mortality is as high as 50%.10,18 These studies suggest that measures to control ICP through control of such factors as hydrocephalus have little effect.15 The fibrinolytic system of cerebrospinal fluid (CSF) is limited19; blood may remain for weeks after hemorrhage, and clots acutely obstruct ventricular CSF pathways, while delayed clot resolution obstructs extraventricular CSF pathways.20,21 When present, blood degradation products may continue to contribute to patients poor clinical status, being responsible for chronic shunt-dependent hydrocephalus in more than 30% of them.20,21,22

16.3 Clinical Features

Patients with primary or secondary intraventricular hemorrhage can present with a variety of symptoms, depending on the underlying cause and the ventricular extension of clots. The clinical scenarios may vary from alertness with headache, nausea, and vomiting, to changes in consciousness, including coma.

16.4 Diagnosis and Neuroimaging

Patients should immediately undergo a computed tomography (CT) scan, an angio-CT scan, and a digital subtraction angiography ( DSA ) or MRI when deemed necessary. Urgent bloodwork should be obtained with special focus on prothrombin time and liver and kidney function. Preoperative management includes identification and correction of coagulation disorders, prophylactic anticonvulsants, body temperature, and glycemia correction. Mean arterial pressure should be kept below 110 mm Hg, and systolic pressure below 150 mm Hg.

16.5 Treatment

Treatment depends on patient’s medical and clinical conditions. The underlying cause of ventricular hemorrhage is a key factor. Oral anticoagulant and dual antiplatelet therapy should be considered as a contraindication for early endoscopic treatment. Age over 75 years with poor neurologic status is a relative contraindication.

16.5.1 Indications for Surgery

If ventricular blood is an epiphenomenon of an intracerebral hemorrhage, it is important to decide whether the cerebral hematoma has priority of treatment and if the ventricular extension of clots may be better relieved by the use of external ventricular drainage rather than immediate endoscopic treatment. In general, our policy in these cases to treat patients surgically for hematoma removal if it is deemed priority and to place an external ventricular device (EVD) immediately. Patients are then monitored in the intensive care unit (ICU) and with serial CT scans; if a good clinical response is obtained in the early days after surgery, we reconsider endoscopic removal of clots in cases with massive ventricular hemorrhage and tetraventricular extension. If ventricular clots are secondary to aneurysm rupture or AVMs, we perform early surgery or coiling to secure the aneurysm and/or malformation.7 Then in selected cases (cases of Fisher 4 SAH with massive tetraventricular clots), we recommend early endoscopic hematoma evacuation on patients with a relatively good prognosis, usually patients with a Glasgow Coma Scale of 6 or higher. The goal of hematoma evacuation is to decrease intracranial hypertension and prevent further neurological deterioration. In preterm infants with germinal matrix hemorrhage, the use of a flexible endoscopic exploration allows extraction of clots and ventricular lavage as well as an endoscopic third ventriculostomy and other procedures. The ideal timing is 3 to 4 weeks after the bleeding.

16.5.2 Operative Nuances

Two types of flexible endoscopes can be used with an external diameter of either 2.5 or 3.9 mm and an operative length of 53 cm. Internal diameter of the working channel is 1.2 mm (Fig. 16.1). The entire working channel per se is used as a suction cannula. Access is precoronal by 12-mm bur holes placed bilaterally. Lateral-ventricle cannulation is achieved with a semirigid peel-away introducer catheter and systolic blood pressure is kept at 120 mm Hg (Fig. 16.2). In the presence of ventricular vascular malformations, the approach from that side is avoided.7 Once the endoscope reaches the inundated ventricle, an energetic intermittent manual aspiration is started with a rigid syringe connected to the working channel of the endoscope (Fig. 16.3, Video 16.1). This action breaks down the clot and allows an initial visual orientation within the ventricle. Aspiration is alternated with irrigation with lactated Ringer’s solution at body temperature and is promptly stopped when the whitish color of the ventricular walls appears. Once the choroidal plexus and the foramen of Monro are identified, the endoscope is advanced into the third ventricle preferably on the right-sided bur hole, and the procedure is repeated (Video 16.1). Clot aspiration in the third ventricle paves the way to the aqueduct and to the fourth ventricle, where the cerebral aqueduct procedure is carefully performed because the endoscope fills the entire diameter of the aqueduct and potentially dangerous local hypertension might easily be caused by excessive irrigation with lactated Ringer’s solution. Finally, the endoscope is flexed toward the occipital horn and is withdrawn back into the lateral ventricle and the trigonus to clean the clots from these sections (Figs. 16.4, Fig. 16.5, and Fig. 16.6).23 At the end of the procedure, a monolateral or bilateral ventriculostomy is performed in all patients by placing a catheter for both intracranial pressure (ICP) monitoring and drainage (with a constant gradient of 15 mm Hg). The external ventricular diversion is generally kept open for 2 to 3 days, and then weaned off. A postoperative CT scan is mandatory to rule out complications such as rehemorrhage. Some authors suggest routinely performing ETV, although it is unclear whether it can prevent communicating hydrocephalus. It seems that ETV might support the resolution of obstructive hydrocephalus, but we have not been shown to prevent communicating hydrocephalus when there is incomplete removal of blood clots from the lateral and third ventricles, which is a possible worsening factor in those cases.20,21,24