Complications Specific to Pleural Type of CSF Shunt

Fig. 15.1

Drawing showing the pleural step of a VPL shunt technique. A small transverse skin incision is made in the third to the fifth anterior intercostal space, and the distal catheter of the shunt is passed to the thoracic incision through the subcutaneous tissue. The pectoralis major and the intercostal muscles are split to expose the pleura. Care is taken to avoid the costal nerve, according to the rib anatomy (n nerve, a artery, v vein)

Alternatively, the transdiaphragmatic route was reported by Rengachary in [42], as a substitute path to the peritoneum through the pleural cavity. We do not have experience with this route.

From a historical perspective, the VPL was initially described by Heile in [15]. An initial attempt to drain CSF into the thoracic duct and pleural cavity was reported by Ingraham and Sears [18]. Later, a series of VPL by Ransohoff in 1954 [40] and 1963 [41], Fein and Rovit [8], Venes (1979) [45] and Hoffmann (1983) [19] gave support to this option. Nonetheless, some reports on complications of VPL shunting have obscured the benefits of its use in daily clinical practice.

Although reported early, the first up to standard series of VPL shunting in the management of hydrocephalus was reported by Ransohoff in 1954. He pointed out that the procedure was relatively simple and that the pleural surfaces tended to absorb CSF well. Pleural effusions were not a significant problem in the initial six patients that he reported.

Nixon in 1962 [37] indicated that many surgeons had encountered problems, particularly pleural effusions, with VPL shunts and recommended the use of valves to avoid that complication, with good results in three patients.

The series of Jones et al. included, from 1969 to 1979, an initial series of 29 children, and later, from 1979 to 1982, a further series of 52 other patients received VPL shunts.

In 1979, Venes and Shaw described their technique for insertion of a pleural shunt, using a trocar to pass the tube to the pleural cavity. They mentioned a 10–20 % risk of a pneumothorax following VPL shunt insertion.

Further serial cases were reported by Hoffman et al. [16], giving support to this option, although not exempted from complications.

Megison and Benzel [33] have carried out a retrospective study of 88 pleural shunting procedures. There was a 7 % complication rate related to the use of the pleural space as the shunt finishing point. Complications at the pleural end included shunt obstruction, either functional or structural; pleural effusion; pneumothorax; and other technical problems. There were no deaths associated with shunt dysfunction or other complications. VPL shunting for hydrocephalus, when used with appropriate precautions and with careful patient selection, is a viable alternative for the treatment of adult hydrocephalus. Although the complications that are unique to this procedure are pneumothorax and pleural effusion, they were encountered infrequently in this series. The authors concluded that VPL shunting may be indicated when other routes are not available.

Piatt [39] reported that the survival of simple ventriculopleural shunts in his series was not significantly different from that of simple ventriculoperitoneal shunts in patients of comparable age with a comparable recent shunt revision history.

Table 15.1 shows the listed cases of reported complications in the literature, including cases from our personal series.

Table 15.1

Associated complications in the pleura related to hydrocephalus and to pleural shunts	Reference
Tension pneumothorax	[16]
Tension hydrothorax	[2]
Tension hydrothorax related to subdural-pleural shunt	[6]
Recurrent pleural effusion	[33]
Empyema	[19]
Disconnection	[39]
Migration	[20]
Dislodged/coiling	[34]
Pleural adhesions	[45]
Peritoneal effusion	[47]
Costal neuritis	Personal series
Cerebrospinal fluid galactorrhea	[35]
Hydrothorax related to ventriculoperitoneal shunt	[13]
Pleurisy with clear liquid due to ventriculoatrial shunt	[10]
Infarction pneumonia due to ventriculoatrial shunt	[44]
Cardiac tamponade and heart failure	[50]
Fibrothorax child	[49]
Glial tumor metastases	[46]
Fibrothorax adult	[22]

From here, we will discuss the possible complications that we may find with this technique.

15.2 Pneumothorax and Subcutaneous Emphysema

A pneumothorax (pl. pneumothoraces) is an abnormal collection of air or gas in the pleural space that separates the lung from the chest wall and which may interfere with normal breathing. Pneumothorax is also defined as the presence of any air inside the chest, and it can be made during the procedure of inserting the catheter through the thorax wall to the pleural cavity (Fig. 15.2). Subcutaneous emphysema develops when the air migrates into the subcutaneous space. It may also be found in the physical examination of patients with serious pulmonary disease.

Fig. 15.2

Schematic drawing showing a pneumothorax or presence of any air inside the chest

Usually the surgical technique employs either a thoracoscopic approach [26] or, usually, an intercostal incision to introduce the catheter inside the thorax. This latter technique may predispose for the development of a pneumothorax.

15.2.1 Prevention

Prevention is related to anesthesia events. Continuous feedback within the surgical and anesthetist team is essential. General anesthesia with orotracheal intubation, with no attempts to spontaneous breathing in order to avoid cough, avoiding nitrous oxide and providing hand ventilation to deflate the lung when the surgeon enters the parietal pleura are anesthetic management details for preventing complications such as pneumothorax and subcutaneous emphysema [14].

A positive pressure sustained ventilation administered by the anesthesiologist is used during approximation of the previously spread muscles with a single absorbable stitch. This minimizes the retention of air in the pleural space [33].

In general, no purse-string suture is needed at the pleural entry site [31, 38].

15.2.2 Identification

Physical exploration reveals crepitus at palpation, if there is associated subcutaneous emphysema, and thoracic auscultation shows decreased breath sounds. Chest radiograph is the standard procedure for the diagnosis of pneumothorax. It should be upright and preferably in the posteroanterior projection. If the patient cannot be upright, a lateral decubitus view with the suspect side positioned up may be helpful. Radiographs obtained in exhalation may accentuate the pneumothorax, but most of the thoracic surgeons have not found this technique useful enough in most clinical situations to warrant the double radiographic exposure. In general, the percentage of collapse is underestimated with the X-ray chest. It is feasible to find air in the subcutaneous space at X-ray when subcutaneous emphysema appears.

Computed tomography of the lungs gives an excellent evaluation of pneumothorax, but the cost-effectiveness of such a procedure must be questioned [28].

The physiologic consequences of a pneumothorax range from little, such as 10 % of collapse in a young person, to life-threatening, such as tension pneumothorax in an older patient with an already compromised cardiopulmonary function aggravated by mediastinal shift and compression of the contralateral lung [9].

15.2.3 Management

A small pneumothorax in a healthy patient can be observed and followed until its reabsorption. Supplying extra oxygen to such patients theoretically hastens the resolution of the pneumothorax, but the true cost-effectiveness of such treatment can be questioned. Kircher and Swartzel [23] estimated that 1.5 % of the air is reabsorbed over each 24-h period.

Simple aspiration is particularly useful in a smaller pneumothorax with a delayed diagnosis, when the passage of time suggests that the process will be self-limited.

Thoracocentesis is indicated when a wait and see conduct is not an option. A tube thoracostomy should be carried out for pneumothoraces over 30 % to hasten recovery or in cases of lesser degrees of lung collapse for those patients with symptoms of associated disorders, such as heart or chronic pulmonary disease. We prefer to insert tube thoracostomy of 24–28-F catheter directed toward the apex. Rarely, this iatrogenic pneumothorax requires a more aggressive surgical option, like videothoracoscopic approach or even thoracotomy. The complications of thoracocentesis include aggravation of pneumothorax, which may be seen in 3–20 % of patients, hemothorax, pulmonary edema, intrapulmonary hemorrhage, and hemoptysis. Other rare events are vagal inhibition, air embolism, subcutaneous emphysema, bronchopleural fistula, empyema, seeding of a needle tract with malignant cells, and puncture of the liver or spleen.

Subcutaneous emphysema is directly related to the pneumothorax and usually resolves itself when pneumothorax is resolved [9]. There is no need for a specific approach.

15.3 Pleural Effusions, Empyema, and Fibrothorax

The presence of a pleural collection of fluid observed on chest radiographs of patients with VPL shunting (Fig. 15.3a) should be of no concern in the absence of respiratory symptoms [21]. In our opinion [31], the finding of small hydrothoraces in otherwise asymptomatic patients indicates that the shunt is functioning. However, we consider that patients with VPL shunts must be regularly followed up in view of the reports on tension pleural effusions that can appear at any time, as a result of changes in the valve pressure or in the absorption capability of the pleural cavity [21, 25]. Still, the most frequent blunt complication of pleural shunts is symptomatic tension hydrothorax causing respiratory distress [2] (Fig. 15.4).

Fig. 15.3

(a, b) Pleural collection of fluid observed on the chest radiographs of patients with VPL shunting is shown in this schematic drawing. Fluid collection (single arrow) secondary to CSF drainage of a VPL shunt in the pleural space depicted in this thorax computed tomography. The distal catheter is in close relationship (double arrow)

Fig. 15.4

Schematic drawing showing a symptomatic tension hydrothorax causing respiratory distress

When pleural effusions are not resolved, fibrotic changes may develop. However, severe fibrotic change in the pleural cavity is an unusual complication of ventriculopleural shunts, and only two cases of a fibrothorax have been described [22, 49]. Although these cases do not warrant abandonment of the pleura as a potential site for CSF drainage, they raise awareness about this complication.

The development of fibrotic changes in the pleura is believed to be related to the chemical composition of CSF, an immune-related mechanism, or on the other hand, related to a low-grade infection. The length of time required to produce these severe changes appears to be quite variable. It is not clear whether the antisiphon devices will be able to prevent this complication, and a long-term follow-up of patients with these devices may help detect the development of fibrosis.

15.3.1 Prevention

Megison and Benzel [33] warned about the use of VPL shunting in adults with pulmonary disease. The ventilator reserve must be considered with particular care especially in meningomyelocele patients with kyphoscoliosis and in cases of Chiari malformation. In all these cases the burden of a pleural fluid effusion in an already-restricted ventilatory capacity might precipitate a frank respiratory failure [39].

Jones et al. [21] have achieved the use of an antisiphon device connected with the valve, with the aim of preventing the formation of clinically significant CSF pleural effusions. The authors reported that only 1 of 52 children developed a symptomatic hydrothorax that required conversion to a ventriculoperitoneal shunt

Nevertheless, the use of antisiphon devices in children frequently induces symptoms of underdrainage, owing to the narrow margins that these devices achieve for effectively controlling raised intracranial pressure [31].

Ventriculopleural shunts can be associated with debilitating scenarios, and caution should be exerted in their use in debilitated or immunocompromised patients, to avoid the occurrence of severe fibrotic changes in the pleural cavity with lung entrapment [22].

The general management consists of evaluation of pleural fluid and its drainage, supplemental oxygen, intravenous volume replacement, and the consideration of empiric antibiotics to cover coexistent infections. A comprehensive shunt evaluation with careful observation or revision of the ventriculopleural shunt is recommended. Removing the intrapleural shunt catheter must be considered, only if an infection has been demonstrated.

15.3.2 Identification and Specific Management

15.3.2.1 Pleural Effusion

Fluid collection in the pleural space decreases lung volume, increases intrathoracic pressure, and leads to irritation and chest pain (Fig. 15.3b). On examination, patients may demonstrate tachypnea, hypoxia, hypotension, dullness to percussion of the involved hemithorax, decreased chest wall expansion, and jugular venous distention.

Pleural fluid accumulates relatively slowly, allowing for the body to compensate with alterations in intravascular volume and reflex tachycardia [25].

Once a critical volume and pressure has been reached within the hemithorax, decreased venous return and hypotension ensues [48].

Pleural effusions develop due to the alterations in dynamics of net pleural fluid production and absorption. There are many possible mechanisms involved (Table 15.2). The mechanisms for accumulation of pleural effusions with ventriculopleural shunts remain speculative. The presence of a shunt catheter in the pleural space may produce local irritant effects, inducing a chronic subclinical inflammatory response, as supported by the predominant lymphocytosis in the pleural fluid. Inflammation leads to increased pleural fluid production and impaired lymphatic flow, causing pleural fluid accumulation and lung collapse. This further reduces the pleural surface area, resulting in a decrease in the net absorption of the pleural fluid. Continuous addition of cerebrospinal fluid compounds the problem, leading to rapid accumulation of large pleural effusions [2].

Table 15.2

Mechanisms of pleural effusions

Increased systemic hydrostatic pressure

Decreased oncotic pressure in the microcirculation

Increased pleural microcirculation permeability

Increased pulmonary interstitial fluid

Obstruction of lymphatic drainage

Flow of liquid from walls or other sources: peritoneum, retroperitoneum, cerebrospinal space, external catheters

Reduction of the negative pressure in the pleural space

Thoracic vascular rupture

Rupture of the thoracic duct

Beta-2-transferrin level has been used as a novel diagnostic strategy. A sample of fluid, drained via tube thoracostomy, was sent for beta-2-transferrin level. This desialated isoform of transferrin is almost exclusively found in the CSF with only minimal amounts present in cochlear perilymph and in the aqueous and vitreous humor of the eye. Multiple studies have validated the use of beta-2- transferrin as a specific marker for CSF leakage with sensitivity and specificity approaching 100 and 95 %, respectively. Furthermore, Huggins and Sahn [17] report the use of beta-2-transferrin to identify the presence of a CSF pleural effusion in an elderly patient with a duropleural fistula. According to the authors, beta-2- transferrin has never been previously utilized to identity CSF hydrothorax in children with VP shunts.

Increased densities on chest radiography are frequently attributed to parenchymal infiltrates when they actually represent pleural fluid. Free pleural fluid is best demonstrated with lateral decubitus chest radiography, ultrasonography, or computed tomographic scans. The presence of loculated pleural fluid is best demonstrated with ultrasonography [9].

Thoracocentesis with a needle aspiration of the pleural fluid under local anesthesia may be indicated. If the fluid appears benign, is not loculated, and can be removed totally or nearly so, thoracocentesis may be all that is necessary to control the disease process. Leukocyte count, Gram stain, cultures, cytological studies, and glucose and LDH levels of the fluid should be carried out. If negative, resolution usually occurs. If the fluid is positive by biochemical evaluation, staining, or culture, pleural effusion has turned to an empyema, and close chest tube drainage is required [30].

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