Medical Hardware Inside Software: CSF Shunts and Indwelling Devices in Children
Authors: Gary Schwartz, MD, FAAP, Assistant Professor of Emergency Medicine and Pediatrics; Assistant Director of the Pediatric Emergency Department, Vanderbilt University Medical Center, Nashville, TN.
Charles Seamens, MD, Assistant Professor, Department of Emergency Medicine, Vanderbilt University Medical Center, Nashville, TN.
Peer Reviewer: Steven G. Rothrock, MD, FACEP, Department of Emergency Medicine, Orlando Regional Medical Center & Arnold Palmer’s Hospital for Women and Children, Orlando, FL; Clinical Assistant Professor, Division of Emergency Medicine, University of Florida College of Medicine, Gainesville, FL.
Without question, technological advances in modern medicine have afforded critically ill children increased survival and improved outcomes from conditions that until recently had only dismal chances for any reasonable life expectancy or quality of life. Thousands of children every day are implanted with medical hardware such as cerebral spinal fluid shunts, central venous lines, and gastrostomy feeding devices. Unquestionably, these devices have prolonged and improved the quality of life for thousands of children. Unfortunately, accompanying the profound benefits of these new technologies are myriad complications and new risks to the "high-tech" child. For these reasons, emergency medical healthcare providers should be knowledgeable about the various medical hardware devices and their complications. These treatment modalities and the management of the most commonly associated complications are reviewed in this article.
The Editor
Hydrocephalus is not an uncommon pediatric disease, occurring in one of every 2,000 births.1 Each year neurosurgeons insert approximately 18,000 cerebral spinal fluid (CSF) shunts, making this the most common pediatric neurosurgical procedure.2-4 Unfortunately, shunt placement also has a very high complication rate; consequently, patients with CSF shunts are frequently brought to the ED with a wide spectrum of complaints. Because shunt problems are potentially life-threatening, any complaints consistent with a shunt malfunction should prompt emergent neurosurgical consultation.
The central nervous system is enclosed in a bony non-compliant structure and is composed of parenchyma, fluid, and vascular structures. Due to the noncompliance of the skull, any change in one of these components will require a compensatory change in the other components. Hydrocephalus occurs when the increased component is CSF. Cerebral spinal fluid is produced in the choroid plexus at a rate of 0.35 cc/min and flows through the ventricles into the spinal canal and subarachnoid space, where it is absorbed by the extensive venous plexus.5 Any disruption to this process results in hydrocephalus. Disruptions in CSF flow can be divided into three categories: increased production (e.g., choroid plexus tumor), obstruction of flow (e.g., congenital malformation or acquired process such as mass lesion or post infectious), or decreased absorption.
Shunt Function. Most patients with hydrocephalus need a CSF shunt.3 Medical modalities have had limited success in treating this condition regardless of the etiology. There are several types of CSF shunts, all of which are named according to where the CSF is drained. The most common type of shunt is the ventriculoperitoneal shunt, which drains into the peritoneal cavity. Much less commonly used is the ventriculoatrial shunt, which drains directly into the right atrium.6 This type of shunt used to be the most popular but is now infrequently used because of significant complications, such as endocarditis, thrombosis, and cardiac arrhythmias.7 Shunts that drain into the pleural space, ureter, or gallbladder are very rarely used.2
Regardless of the type of shunt used, the same basic design principles apply. The proximal tubing is inserted though a Burr hole in the occipital or frontal bones, and preferentially ends up in the anterior part of the lateral ventricle. This procedure is frequently performed using external landmarks, rather than direct visualization.3 Therefore, misplacement of the catheter tip is possible. The distal end of the tubing may have a preset 90° bend for insertion through the cranium to prevent kinking.8
The proximal tubing is usually attached to a valve system, which has both inlet and outlet valves separated by a chamber. There are several types of valves in use, each with unique features.8,9 Each valve system functions by releasing fluid after the preset pressure differential between the valves is reached. Unfortunately, pressure differences between the valves can be influenced by body position. When standing, the pressure difference can increase dramatically due to the low intra-abdominal pressure compared to the CNS pressure. This pressure differential can lead to overdrainage unless an antisiphon valve is installed.8,9
Some patients, especially those undergoing intraventricular chemotherapy, have a reservoir attached to the proximal catheter. The reservoir does not have a proximal valve. Therefore, medications injected into the reservoir can flow into the ventricle.
The distal tubing is connected to the outlet valve and tunneled under the skin to its final destination. The valve and tubing may be one piece or connected pieces.3,7 Since shunts are frequently placed in the newborn period, a large amount of extra distal tubing is inserted in order to allow for patient growth. Generally, the extra tubing does not appear to increase complications.3
Complications. Obstruction. Although CSF shunts are actually quite simple devices, complications do occur. The most common complication, which accounts for half of all shunt complications, is obstruction.3,10,11 Obstruction occurs most often in the proximal portion of the tubing (50%) during the first two years following shunt placement.11 In fact, obstruction in this area is most common immediately after insertion. Postoperative obstruction is usually due to debris, clots (from postoperative bleeding), or misplacement. Later on, obstruction is usually due to choroid plexus entrapment around the tubing, ependymal reaction, or immune reaction.3
The second place for obstruction to occur is at a valve. Malfunction due to manufacturing problems is very infrequent. More commonly, malfunction is due to cellular debris or infection. Again, immune complex-mediated malfunction may also play a role.3
Finally, malfunction may occur in the distal catheter, from pseudocyst formation at the tip, kinking, thrombosis, or occlusion of the tip with omentum.12 Distal obstruction is most common for shunts that have been in place for more than two years.11
Infection. Shunt infection is another frequent concern for patients with CSF shunts. Infections have an occurrence rate of approximately 5%.13,14 Half of the infections occur in the first two weeks and 75% in the first two months after shunt placement.6,15 Children less than 1 year of age are at highest risk.14
Infections are categorized as either wound or shunt infections. Wound infections are usually located over the site of the reservoir or in the abdominal wall in patients with VP shunts. These infections occur at the time of placement and manifest as a cellulitis with redness, warmth, and possible purulent discharge at the affected surgical site. Staphylococcal species are the most frequently cultured etiologic bacteria.6
The second type of infection involves the shunt itself. Infection at this site is also frequently acquired at the time of insertion. These infections are usually caused by a less virulent organism and significant signs of inflammation are often not present. The most commonly cultured organisms are Staphylococcus epidermidis (40-63%) and Staphylococcus aureus (20-27%).6,14,15 Gram-negative organisms are less commonly cultured and occur most frequently in patients with VP shunts (6-20%).15 Patients with gram-negative infections are usually more ill-appearing.16 It is also not uncommon to find mixed flora (10-15%).6,15 Mixed flora infections are often felt to be related to bowel perforation.6 Additionally, a higher risk of meningitis with traditional pathogens such as Pneumococcus, Haemophilus influenzae, and meningococcemia may exist for patients with shunts.6 Finally, infection rates are the same for VP and VA shunts, although infections in the latter may lead to other more serious complications. Some of these serious complications include sepsis, nephritis, endocarditis, and thromboembolic events.17,18
Overdrainage. Another complication that may be encountered is overdrainage of the CSF. This can cause the slit ventricle syndrome, which involves chronic overdrainage with collapse of the ventricles and transient obstruction of CSF flow.19 Symptoms may include headache, nausea, vomiting, lethargy, diplopia, and paresis of upward gaze.20 Symptoms are often alleviated when the patient lies down or lowers his or her head.20
Computerized tomography of the head will demonstrate small ventricles in 53-65% of patients with a shunt.21,22 Only a small fraction (11%) of patients with small ventricles will actually have the slit ventricle syndrome, and only a small number (6%) of these patients will need surgical treatment.21 Slit ventricle syndrome is less frequently seen now with the use of more sophisticated valves and antisiphon devices.
Other complications of shunts include migration of the distal tip of the peritoneal catheter, hernias, abdominal adhesions, volvulus, and bowel obstruction.12,23
Clinical Presentation. Headache, vomiting, and lethargy are classic symptoms of increased intracranial pressure. Any of these symptoms should prompt evaluation of the shunt because headache is present in only 13%, vomiting in only 26%, and lethargy in 40% of patients with shunt obstruction.24
Headache, lethargy, fever, and meningismus are classic symptoms of shunt infection. Unfortunately, these classic presentations are also infrequently seen. In studies of children with shunt infection diagnosed by CSF analysis, meningismus was only present in 20-29% of the cases. Other classic symptoms are also not common, with headache occurring in 5-14% and lethargy in 12% of patients.13,17 Fever is found most commonly and occurs in 73-95% of the patients.13,17,25
Patients may also present with complaints of both an obstructive and infectious process since one-third of obstructed patients also have a shunt infection.13 More common are nonspecific presentations such as fever without a source, poor feeding, and not acting right.15 This makes it difficult to tell which children have shunt malfunction. One study, which evaluated referral patterns of children with a shunt malfunction, found parents to be as good as general practitioners in identifying shunt malfunction.26 For this reason, a high level of suspicion for shunt malfunction should be maintained in children whose complaints cannot be explained by another process. This is especially true if the child is very young or the shunt has been recently revised or replaced. Due to the nonspecific complaints, the average delay from the onset of symptoms until shunt revision is 11.5 days.24
Patients with peritoneal shunts can present with shunt-related abdominal problems without neurologic complaints. These usually present with abdominal pain. Possible causes include peritonitis due to infection of the distal tubing, intestinal perforation, or volvulus.27,28
Diagnosis. Any child presenting with complaints that are suspicious for a shunt problem should be evaluated with a thorough history and physical examination. If shunt malfunction remains in the differential diagnosis afterward, further evaluation is required. Since other laboratory tests are of limited value, analysis of the CSF is necessary. It may be tempting to decide on whether to tap a shunt based on an abnormal peripheral white blood cell count, but in 25% of patients with documented shunt infection, the white blood cell count is normal.15
Evaluation of a shunt involves at least two sequential components: radiographic imaging and CSF evaluation.
Radiograph imaging starts with evaluation of ventricular size with cranial computed tomography (CT). Frequently these children do not have normal baseline ventricular size even with a normally functioning shunt. Therefore, comparison with a previous study is essential. Even with a CT scan unchanged from baseline, there is a chance early obstruction may be present (3-35%).26,29 Therefore, plain radiographs of the shunt valve and tubing are also needed to assess the continuity of the system and to rule out kinking of the tube.
After imaging studies, CSF analysis is necessary. A shunt tap is preferred to a lumbar puncture since the latter procedure will occasionally miss infections.30 Moreover, an LP is useless in the diagnosis of concurrent shunt obstruction, and both procedures have an exceptionally low risk of introducing an infection into the CSF.15
To perform a shunt tap, sterilely prepare the shunt site with betadine followed by alcohol. Insert a 23 gauge butterfly needle attached to a manometer into the valve chamber while occluding the outlet valve. By occluding the outlet, the manometer will reflect the ventricular pressure (opening pressure). Inability to obtain fluid will signify an occlusion proximal to the valve. After the pressure is recorded, the outlet is released and fluid drains into the distal catheter. Distal obstruction is present if the fluid will not drain from the manometer. Normal opening pressure is less than 5-10 cm (less than the valve’s preset opening pressure). All patients with a pressure over 20 cm have shunt obstruction and require urgent shunt revision. An opening pressure of 10-20 cm is indeterminate and may benefit from a radionuclide clearance study.31 Some neurosurgeons also recommend checking a drip interval, the time between drops of CSF as fluid is collected, and closing pressure.32
The CSF should be analyzed for cell count, culture, Gram’s stain, glucose, and protein. Organisms on Gram’s stain confirm the diagnosis of infection. Unfortunately, there is variability in the literature on the acceptable number of WBCs in the CSF obtained from a shunt. In one study, in non-infected shunt patients with shunt dysfunction, the median number of CSF WBCs was 18 cells/mm3, while in infected patients, it was 79 cells/mm3.6 There was a large overlap in each group since 47% of infected patients with a positive CSF culture had less than 20 WBCs.15 Interestingly, eosinophilia in the CSF has also been associated with shunt infection.33 CSF should also be analyzed for protein and glucose even though the glucose is normal in 80% of infected patients.25 If the CSF glucose is low, gram-negative organisms are more likely to be cultured.16 Even with normal CSF analysis, 17% of patients may have a positive culture.13 Tapping the shunt should be performed by the neurosurgeon since there is a small risk of infecting the hardware. More importantly, there can be difficulty in interpreting the CSF cell count and opening pressure.
Another test that is sometimes performed is pumping the shunt to check for obstruction. If the shunt cannot be pumped, a distal obstruction is presumed; the absence of filling following pumping indicates a proximal obstruction. Unfortunately, this test is of limited value, with only 20% sensitivity for identifying an obstruction.34
Treatment. Treatment of an obstructed shunt involves revision or replacement of the obstructed part. The timing of this will depend on the severity of the presenting symptoms. Children who are minimally symptomatic may have the procedure delayed for several hours. Children who have symptoms of increased pressure will need emergent relief with shunt revision.
If no neurosurgeon is available and emergent action is necessary, the physician can try several maneuvers to relieve the obstruction. For a distal obstruction, manually withdraw fluid from the reservoir by serial aspirations. The emergency healthcare provider should remove fluid slowly to prevent intracranial bleeding resulting from rapid fluid shifts. Cerebral spinal fluid should be removed until the manometer reading is less than 20 cm.35
A second method for relief of obstruction is to flush a small amount of saline through the distal tubing. Occlude the proximal valve prior to injection to unclog the distal end. The method for a proximal obstruction is similar, except as the fluid is flushed, the distal catheter is occluded, forcing proximal fluid flow.
If this does not relieve the obstruction and the patient is deteriorating emergently, intubate and hyperventilate while administering an osmotic diuretic such as mannitol.2 If these maneuvers do not help, an emergent ventricular puncture may be necessary. If time allows, consultation with a neurosurgeon should be obtained before the procedure is attempted. Restrain the child in a supine position. Shave the child’s hair and sterilely prep over the sagittal and coronal sutures. If the anterior fontanelle is open, a spinal needle is inserted 1 cm lateral to the sagittal suture along the coronal suture. If the suture is closed, the spinal needle is inserted 2-3 cm lateral to midline and just anterior to the coronal suture. If the skull cannot be penetrated by the spinal needle, use a bone marrow needle to make a hole in the skull. Insert and direct the spinal needle toward the inner canthus of the ipsilateral eye. The ventricle should be encountered by a depth of 5.5 cm or less. Remove fluid slowly until the pressure is less than 20 cm.36,37
Treatment for an infected shunt most often involves removal of the infected part, antibiotics, and externalization of the shunt. This is the most successful means to eradicate infection (96%).17,38 The antibiotic frequently chosen is vancomycin due to its excellent staphylococcal coverage. A third-generation cephalosporin or an aminoglycoside can also be administered to cover gram-negative organisms until CSF or blood cultures are available. The antibiotics should be administered intravenously or intraventricularly if CNS penetration of the chosen antibiotics is not sufficient. When the CSF is sterile, a new shunt is inserted.16,40 If the infected shunt is not removed and antibiotics alone are used, there is a higher risk of infection recurrence (23-50%).6,33 However, when the infectious agents are the more common meningitis pathogens such as Haemophilus influenzae, Pneumococcus, or Neiserria meningitidis, antibiotics alone may adequately clear the infection.39-41
Complications of Indwelling Venous Devices
More than 500,000 indwelling venous devices are inserted annually.42 Chronically ill children are surviving longer, and these lines often provide long-term access for any patient needing blood sampling, prolonged infusions (chemotherapy, crystalloids, and blood products), or hyperalimentation.42,43 More and more patients and their families care for these devices at home. These indwelling lines are available to ED staff to draw blood and administer medications, blood products, and IV fluids.44 While ED physicians are not usually responsible for placing these lines, they are often confronted with complications of these devices. Consequently, they should be familiar with the recognition and treatment of these complications.
Originally introduced by Broviac et al in 1979, these lines are now known by a variety of names such as Hickman, Broviac, and Groshong catheters. Each has slight differences in construction. As a group, they consist of a silastic catheter with one, two, or three lumens that is tunneled subcutaneously and inserted into the right atrium via subclavian approach.42,45 The subcutaneous portion of the catheter includes a Dacron cuff that becomes adherent to scar tissue (which may take 2-3 weeks), forming an internal anchor for the catheter and a barrier against ascending infection along the catheter from the skin surface.43,45-47 The external end separates into individual catheters for each lumen, each of which contains a reinforced sleeve with clamp and terminates in a disposable luer lock.42 A common exit point is the anterior chest wall.45 Broviac catheters are most often used in children and Hickman catheters in adults.48
There are a few important differences in construction of these devices. Hickman and Broviac catheters are open-ended and blood may back up into the catheter, causing clotting and obstruction. Therefore, a clamp is necessary when the catheter is not in use, and frequent heparin flushing is necessary to prevent clotting.43 Groshong catheters are similar to Hickman-type catheters with a few exceptions. First, the distal tip (residing in the superior vena cava) of the catheter is solid and blunt. Second, the lateral wall of the distal end has a pressure-sensitive two-way valve that eliminates the need for catheter clamping and frequent heparin flushes. Normal venous pressure results in the valve remaining closed with no backflow of blood into the catheter. External pressure exerted by the infusion of fluids opens the valve. Continued aspiration at the injection port also results in the valve opening and the ability to aspirate blood through the catheter. While this unique design precludes the use of heparin, Groshong catheters have to be flushed with saline every seven days.43,46 On the other hand, because of the design of the distal valve, Groshong catheter malfunction rates are 3-7 times higher than Hickman-type catheter rates.45 Finally, the proximal end of the catheter (external to the body) is removable for easier insertion and replacement without splicing.45
The Portacath is different in that it has a subcutaneous port with a silastic tube inserted into the right atrium via subclavian approach. The proximal end is a short segment tunneled subcutaneously that terminates in a titanium housing with a hard rubber dome. This infusion port will generally be found subcutaneously on the anterior chest wall. A recent variation on this theme is the forearm subcutaneous port. In these patients, the catheter enters a larger arm vein, either axillary or brachial.
Percutaneously inserted central catheters (PICC lines) are smaller silastic catheters inserted into the right atrium via an antecubital vein.44 These catheters are like the Hickman catheters in structure, and the proximal end is also outside the skin.
When accessing these catheters, rigorous sterile technique is mandatory.44 Hickman-like catheters and PICC lines can be accessed easily enough by removing the luer lock adapter on the end and by attaching a syringe or IV tubing directly to the catheter. Subcutaneous ports (Portacaths) need to be punctured with a noncoring needle (Huber needle, 19-22 gauge) for access. This needle has a deflected point and side opening to prevent coring or creating holes in the rubber dome.43 If standard (coring or hollow) needles are used to repeatedly access a subcutaneous port, there is the risk of creating a permanent, nonsealing hole in the rubber dome of the port, which might allow air embolization to occur. However, in a critical situation, any 18 or 21 gauge needle can be used. The dome of most ports is made of a hard rubber that is similar in consistency to a hockey puck. Therefore, the amount of force that is necessary to insert the needle through the dome is significant.44 The needle cannot be inserted too far, since it will contact the metal base of the port on deep insertion and a familiar "tick" will occur.42,44
Place an ice pack or a topical anesthetic such as EMLA cream to the area over the subcutaneous port prior to painful needle insertion attempts.43 An approximate 30-minute delay is necessary for EMLA cream to produce topical anesthesia. The needle can then be attached to either a syringe or IV tubing. This technique should allow approximately 2000 punctures.42 Hickman-like catheters and PICC lines can be used immediately after placement and confirmation of location by x-ray.49 Subcutaneous ports are usually not accessed for one or more days after placement.44 Showering and bathing are permitted for patients with healed incisions and no other complications.43
After access is achieved, one may phlebotomize by withdrawing 2-4 cc of the heparinized blood from the catheter, reclamping, and then using a separate syringe to remove the desired amount of blood. Coagulation tests are notoriously inaccurate when drawn through indwelling access devices, even when large amounts of blood are initially discarded.44
After blood is drawn, intravenous tubing may be connected directly to the external end of the catheter of the Huber needle. Since the internal diameter of the indwelling catheter will limit the rate of fluid administration, a larger-bore needle will not be advantageous.42 Flow rates without a positive pressure infusion pump can be achieved at 200-250 mL/h with smaller central venous catheters and up to 500 mL/h with larger catheters.45
To ensure patency, inject 1-5 mL of heparin (100 U/mL), clamp the line, and reposition the cap upon completion.44 An "antibiotic lock," a solution of antibiotics (vancomycin, amikacin, and minocycline) and heparin, may decrease the incidence of infectious complications, according to one study.50
Subcutaneous ports should be flushed as the needle is being withdrawn from the port. The portacath requires a heparinization flush after each infusion, and at least monthly, if not used more frequently.45
Hickman-type catheters and PICC lines should be flushed at least twice weekly with 5 mL heparinized saline. Daily flushing of these designs is not necessary and leads to an increased rate of infection. Groshong catheters need only be flushed once a week to insure patency.44 All of the currently used ports and catheters are safe for use in CT and MRI scanners provided they do not have a metal needle in place for access.44,51
Complications of indwelling vascular devices are common. They include occlusion, infection, thrombosis, and mechanical fracture of the catheter. (See Table 1.)
Occlusion. Indwelling venous catheters may become either partially or totally occluded during the course of use. Partial occlusion usually allows fluids to be readily infused into the device but without blood return.44 It has been estimated that 20% of long-term catheters will eventually fail to yield blood samples.51,52 Difficulty in drawing blood from a central venous catheter may be due to decreased vascular volume, catheter position or malfunction, and fibrin clot formation at the catheter tip.44 Several maneuvers can be helpful in obtaining a blood return from these devices when decreased vascular volume is suspected. First, place the patient in the Trendelenberg position to engorge the subclavian system. Patients who are markedly dehydrated may require IV fluid administration before blood return from the access can be demonstrated. Extending the arm on the side of the device above the head will sometimes permit blood return.44 Other maneuvers may be helpful, including turning the patient’s head, coughing, changing position, taking a deep breath, or performing a Valsalva maneuver.43,51 If occlusion occurs with a subcutaneous port, make certain that the Huber needle has fully penetrated the septum and is not occluded by the silicone dome. The port should be reaccessed to ensure correct placement of the needle.51 It is possible for the needle to be positioned in a subcutaneous pocket around the port. In this case, no blood will be able to be withdrawn, but flushing will be easy because the fluid is infusing into the pocket. To see if this is the case, infuse a small amount of fluid and watch for any swelling around the port or along the track of the catheter.43
Positioning of the catheter’s distal tip against a vessel wall or overzealous withdrawal on the syringe (excessive negative pressure) may be other causes of partial occlusion. Rapid infusion of fluid may help to reposition a catheter tip that is against a vessel wall.42,51 If not successful, a clot or precipitate should be suspected of occluding the catheter.47
Probably the most common cause of partial or total occlusion is formation of a fibrin clot at the tip of the catheter, which acts as a one-way valve. When aspiration occurs, the intimal surface of the vein or fibrin sheath is drawn into the tip, preventing blood from entering. The incidence of fibrin clot formation varies from weekly to yearly depending on the frequency of use and flushing of the device.43,44 An attempt may be made to aspirate a clot into a 10 mL syringe half filled with saline using a gentle push-pull motion. Since clots are unlikely to be aspirated through a needle, the syringe should be connected directly to the luer lock. If the catheter is still occluded after several attempts, a radiographic dye study should be performed to locate the site of the occlusion.47
Lack of blood return from one of these devices, however, is not an absolute contraindication to use. If the device has a long-term history of satisfactory use and a chest x-ray confirms the proper placement of the catheter tip in the superior vena cava, the device can be used for the infusion of fluids and medications even if no blood can be aspirated.42 When there is no blood return and resistance is felt to infusion of fluids, do not force the flush.43,46
If it is important that blood withdrawal is an integral part of the catheter’s function or the catheter is totally occluded, then thrombolytic infusion should be considered. The thrombolytics, urokinase and streptokinase, have been used successfully to reestablish catheter patency. Most practitioners prefer to use urokinase because it is associated with fewer anaphylactic reactions that seem to plague the use of streptokinase. These reactions are manifest by pruritis, fever, nausea, headache, and shock.53
The standard treatment for partial occlusion is a bolus of 0.5-1.0 mL of urokinase (5000 mcg/mL). The amount of time that the urokinase dwells in the access device is variable. The urokinase may be flushed out within 10 minutes or may be allowed to dwell for an hour or even overnight.42,44 In the systemic circulation, urokinase has a half-life of approximately 20 minutes.52 A urokinase flush successfully declots the line in up to 95% of cases.42 This process may usually be repeated once. Patients with central venous access systems that fail to respond to two trials of a urokinase bolus may be admitted for a continuous infusion of urokinase (100-200 units per kg of body weight per hour)47 until the catheter becomes patent.44,46,54 Alteplase (tPA) has been used when urokinase was not successful.52,53
Chemical precipitates may accumulate within the device, causing occlusion.55 The inner diameter of the catheter also influences the rate of occlusion, as particulate material is prone to deposit in catheters with smaller diameters.51 Precipitates are formed by poorly soluble intravenous fluid components or the interaction of incompatible solutions. Medications that are incompatible through multiple lumen catheters should not be infused because turbulence at the catheter tip permits mixture.42 Drugs that commonly result in a precipitate when infused incorrectly include calcium, diazepam, phenytoin, heparin, and TPN.52 Patency can be restored by improving the solubility of the precipitate; however, the decision of whether increasing or decreasing pH will improve the solubility of a precipitate is often difficult. In practice, if altering the pH one way does not result in restoring patency, it is reasonable to try to alter the pH in the opposite direction.53
Hydrochloric acid has been used to restore patency successfully to catheters obstructed by drug precipitates. To lower the pH of the precipitate, the catheter is instilled with 0.2-1.0 mL of 0.1% HCl using a tuberculin syringe over one hour.51 This small amount of HCl should not cause a metabolic acidosis.53 On the other hand, a common side effect of this technique is a febrile reaction, occurring in up to 42% of patients.46,52
Phenytoin precipitates are most difficult to resolve but have been cleared using sodium bicarbonate. Ethanol solutions have been used to clear lipid occlusions with success (take 3.5 mL of 98% dehydrated alcohol for injection and add 1.5 mL of sterile water to make 5 mL 70% ethyl alcohol).52,53 (See Figure 1.)
An uncommon condition, the "pinch-off" syndrome, may cause intermittent flush resistance and catheter compression and malfunction. It is recognized on chest x-ray as a narrowing of the catheter between the clavicle and first rib.56 When the patient is upright, the weight of the shoulder narrows the area and pinches off the catheter. Changing the shoulder position will temporarily relieve the obstruction of the catheter so that fluids can easily be infused.43 Compressed catheters are subject to shearing that can lead to catheter fracture and embolization of the tip.55 Since there is a risk of transection and embolization of the catheter, this condition is an indication for catheter removal.43 The time course of this process is variable but usually occurs within 3-6 months.55 Other causes of total occlusion include kinking and coiling of the catheter, which should be detected by x-ray.51
The incidence of catheter-related infection is reported to range from 4% to 60%. The wide variability is related to such factors as insertion techniques, routine maintenance, and the physical condition of the individual patient and the definition of infection.52 The presence of bacteria may be related to differing clinical scenarios from contamination to colonization to true infection.57
Risk Factors. Risk factors include age (< 1 year, > 60 years), altered host defense mechanisms, severity of underlying disease, remote infections, catheter type, catheter material, type of placement, and duration of use.57 Patients between 1 and 4 years of age have a greater risk of multiple septic complications.42 Infusate contamination has also been implicated in the pathogenesis of catheter-related septicemia.46,57
Catheter sepsis rates are very similar for single- and triple-lumen catheters, although there may be a trend to higher infection rates with triple lumen catheters.57 Antimicrobial agents can be chemically bonded to catheter surfaces and may decrease the incidence of catheter-related bacteremia.57,58
The insertion site may be dressed with sterile gauze or transparent film. Transparent dressings increase the risk of developing catheter-related infection.57,58 Chlorhexidine, rather than povidone-iodine and alcohol, is the preferred substance for skin disinfection with dressing changes. Topical antimicrobial agents confer only a modest benefit in protecting against catheter-related infection. If an ointment is to be used, the recommended agent is polymyxin/neomycin/bacitracin.57
Infections in vascular access devices take two forms, either local or systemic. Local infections occur at the site where the device exits the body and may be classified as exit-site infection or tunnel infection.
Exit-Site Infections. Exit-site infections are diagnosed by the appearance of erythema, tenderness, induration, and purulence at the exit site of the catheter.42 The exudate should be cultured when present. These local infections can be treated with stringent site care and either oral or intravenous antibiotics for 10-14 days. Since catheter removal is seldom necessary to clear these infections, it is reasonable to attempt a cure by treating with antibiotics without removing the catheter.46,52
Empiric therapy may be started with vancomycin since the majority of exit-site infections are due to coagulase-negative Staphylococcus. If the infection does not respond in a few days, the catheter should be removed.48 If the infection is due to Candida, the catheter should be removed before antifungal therapy is initiated.48 Unfortunately, this class of infection is unlikely to clear without removal.
Tunnel Infections. Catheter tunnel infections are more extensive than exit-site infections. These are diagnosed in the patient with fever and redness and tenderness along the subcutaneous tract. Pus is rarely expressed from the catheter and blood cultures are usually negative. These tunnel infections are most commonly caused by gram-positive organisms, which also routinely respond to vancomycin or amikacin/cefoxitin combination. However, there is a high rate of recurrence when antibiotics are stopped, and many physicians commonly remove devices with a tunnel infection without waiting for a clinical response to antibiotics.44,48,52
Line Sepsis. The other form of infection is device-related bacteremia or line sepsis. In the ED, this diagnosis is suspected after excluding other sources of fever. In device-related bacteremia, the vascular access device itself appears clinically normal. The diagnosis is often indirectly evaluated by quantitative blood cultures, drawn simultaneously via the device and via a peripheral site. If the blood from the catheter contains 5-15 times or more of the colonies than the peripheral blood, the presence of infection is confirmed.52,57 These infections most commonly involve gram-positive skin flora.42 A probable catheter-related septicemia is diagnosed when an organism is isolated from blood cultures and no other apparent source except the catheter. More confidence can be made in the diagnosis of catheter-related septicemia when the same organism is isolated from the exit site and blood or when the same organism is isolated from the catheter and a peripheral site. It may also be present when septicemia is refractory to antibiotic therapy but resolves when the catheter is removed.48,52
A more definitive method of diagnosis is to culture a segment of the catheter’s distal tip. However, this requires removal of the device and may represent only colonization of the catheter and not true infection.52,59 Culture of the tip is performed by rolling a 5 cm catheter segment across a blood agar plate in a defined reproducible manner.57 Staphylococci, streptococci, and diphtheroid organisms as well as Candida species are cultured most frequently from infected indwelling catheters. Staphylococcus epidermidis, a common skin organism, is the most frequently cultured organism.51,55,59 Gram-negative bacteria occur less frequently and may be associated with neutropenia.42,45 Fungal infections occur less frequently but are virulent. Children are common victims of fungal infections, and they often present with low-grade fever, bradycardia, thrombocytopenia, apnea, and a predominance of immature PMNs.42
Most often, the source of bacteremia is never established in the patient with a long-term catheter. Therapy of bacteremia is usually attempted with the catheter in place after at least the two sets of blood cultures have been obtained. Empiric therapy should be initiated with vancomycin and gentamycin. For patients with neutropenia, start a third-generation cephalosporin with antipseudomonal activity or an antipseudomonal penicillin.48
If the infection responds to antibiotic therapy, treatment should continued for 2-3 weeks. If no response is seen in 48-72 hours after initiation of antimicrobial coverage, the line should be pulled. The catheter should be removed immediately if either Pseudomonas or fungal species are isolated.48,53
The success rate of clinical response may be increased with the addition of a urokinase infusion to standard antibiotic regimens.44 A fibrin sheath can act as a nidus for reinfection by sequestering the organism to continually seed the circulation with each routine use.51 The rate of catheter-related septicemia leading to systemic sepsis is relatively low, occurring in less than 1% of individuals.57
Port Pocket Infections. Port pocket infections usually exhibit erythema, tenderness, and induration at the edge of the portal body.51 The port should not be accessed unless already in use. In this case, leave the needle in place for blood drawing and antibiotic infusion.46,52
If there is no evidence of skin necrosis over the reservoir, port pocket infections may initially be treated with two weeks of intravenous antibiotics without removal of the port. Purulent exudate in the subcutaneous space should be aspirated or drained.48 If there is skin necrosis present, the reservoir should be removed. Empiric antibiotic therapy may be started with vancomycin and an aminoglycoside or a third-generation cephalosporin.48
Other infectious complications include septic thrombophlebitis and endocarditis. Clinical manifestations of septic thrombophlebitis combine those of infection (fever and rigors) and those of thrombosis (an elevated jugular venous pulse, swelling of the arm, shoulder, neck and face) as well as an obstructed catheter. Reported causative organisms include S. viridans, S. epidermidis, S. aureus, K. pneumoniae, and E. coli. Diagnosis may be made by venography but is best made by a contrasted CT scan, which has the advantage of excluding other conditions that can compress blood vessels in the area.48
Catheter-related endocarditis presents in a fashion similar to endocarditis from other causes. However, the appearance of a new or changing cardiac murmur and peripheral stigmata of endocarditis are frequently absent. Chest x-ray may show multiple nodular densities in the pulmonary parenchyma suggestive of septic pulmonary embolization due to endocarditis on the tricuspid valve.48 Like other causes of endocarditis, diagnosis is usually made by echocardiography in addition to positive blood cultures. The catheter should be removed if either septic thrombophlebitis or endocarditis are suspected.48
PICC Line Complications. The most common complication of PICC lines is a sterile mechanical phlebitis, which is manifested by pain at the insertion site and up the arm, presence of a palpable venous cord, and reddening and swelling along the vein.43 Unfortunately, these physical findings are difficult to distinguish from a tunnel infection. This phlebitis is caused by a nonspecific inflammatory reaction to the catheter.55 The catheter can remain in place, and the patient is encouraged to use conservative measures such as warm compresses for 20 minutes throughout the day and to elevate the arm. If this condition does not resolve within 72 hours, the catheter should be removed.43
Another complication of PICC lines is bleeding that occurs at the insertion sites. Bleeding occurs most often the day after insertion. After this period, excessive bleeding is usually due to an underlying coagulopathy or excessive use of the arm.43
Only about 1 inch of catheter should be visible external to the insertion site.43 Extreme care must be taken when the dressing for a PICC line is removed since only tape holds the catheter in place. Consequently, it is very easy to inadvertently pull out several inches of the catheter.
On the other hand, PICC lines may also become "stuck" within the arm vein as a result of venospasm, which impedes withdrawal.55 If resistance is encountered as the catheter is withdrawn, do not apply excessive traction because the catheter could fracture. Instead, apply heat to the vein of the upper arm and flush the catheter with normal saline and try again. Other reasons for resistance include phlebitis, valve inflammation, and thrombosis.60
During removal of a PICC line, it may appear that only part of the catheter is removed. It is possible that the most internal part of the catheter has fractured and remained in the body. During insertion, the catheter is measured and cut to the appropriate length so that the tip lies either in the superior vena cava, subclavian, or axillary vein. This measurement should be recorded on insertion to allow verification that the catheter is intact when removed. The catheter length should be removed and compared with the length on insertion.43
Thrombosis. Factors that may predispose to subclavian vein thrombosis include catheter material composition, accelerated coagulation system, reduced flow in the venous system secondary to intrapulmonary or mediastinal disease, and possibly catheter size.61 Specific tumors such as adenocarcinoma of the lung seem to increase the risk for thrombus formation. Intrapulmonary disease, mediastinal disease, or hypercoagulability associated with malignancy also have been associated with increased risk for thrombus formation, catheter or not. Placement of the catheter tip deep into the right atrium can cause arrhythmias, and increase the chance for thrombosis.50 Left subclavian catheter placements have been associated with a significantly higher incidence of thrombus.51
The clinical presentation of thrombosis is generally insidious in evolution and is characterized by nonspecific pain on the chest wall, neck, or in the scapular area.61
Subclavian/axillary vein thrombosis may present with arm swelling while superior vena cava syndrome presents as face or neck swelling.61 In either case, these are not consistent findings.61 Since many patients will probably be aware of problems accessing their vascular devices, thrombosis is usually diagnosed before progression to the superior vena cava syndrome. However, thrombosis of the central vasculature may remain unrecognized until total venous obstruction occurs. Signs of venous obstruction include collateral circulation across the chest wall, distended neck veins, and edema in the supraclavicular areas.51 Clinical examination is usually satisfactory to consider the diagnosis; however, duplex sonography is the preferred method to confirm clinical findings. Venography will not only document clot in symptomatic patients but will show clot in 25% of asymptomatic patients.44
Pulmonary embolism is a most worrisome complication but a relatively unlikely event only associated with approximately 12% of the thromboses.44,61 Pulmonary embolism immediately following catheter flushing is unlikely.42
Patients with newly diagnosed thrombosis should be admitted. Venous thrombosis is treated with full anticoagulation.55 If no contraindications exist and chronic access is required, the catheter is left in place and a trial of thrombolytic therapy may be warranted. Streptokinase is often used but is more effective in the setting of acute occlusions, while line thrombosis is more subacute in progression.61 If lytic therapy fails or is contraindicated, long-term anticoagulation and/or device removal is required.43,44 The device should be removed if it is nonfunctional or if the thrombotic symptoms progress despite appropriate anticoagulation therapy.55,61
Vigilant flushing between drugs, routine flushing with urokinase, and the avoidance of incompatible infusions are the cornerstones to thrombosis prevention. Chronic oral warfarin has been helpful in preventing thrombosis.51
Fracture. Damage to the cannula in the form of small holes or tears can occur when the pressure inside the lumen becomes too high. Excessive pressures can occur when small syringes are used; larger syringes create lower pressures.62 Fractures of indwelling venous catheters are divided into fractures that occur intravenously, subcutaneously, and those that occur at the external end of Hickman-type catheters.
Pieces of catheter that break off in the venous system need to be retrieved emergently before they embolize to the arterial system. Fracture and embolism of the intravascular catheter tip is a rare but potentially lethal complication of indwelling access devices. Symptoms include the abrupt onset of dyspnea, palpitations, or atypical chest pain. Signs include hypoxia and atrial fibrillation. All of the catheter tips are radiopaque and can be visualized on routine chest x-ray.49 Many of these emboli can be removed nonsurgically depending on the exact location and size of the catheter fragment.44
Fractures that occur subcutaneously become manifest when the patient attempts to flush the catheter. Swelling and/or pain develops at some point in the subcutaneous tunnel when injection into the catheter is attempted. Almost invariably, these catheters must be removed. Repair cannot usually be accomplished.
Fractures of the external end of Hickman-type catheters are usually traumatic but may occur spontaneously. They are diagnosed by observing an obvious break in the catheter or leakage of fluid from a pinhole in the catheter when it is flushed.45 External fractures more than two inches from the exit may often be repaired in the ED with manufacturer-specific repair kits available for some but not all catheters.44,47,55
Other Complications. Additional complications of indwelling lines include mediastinitis, cardiac dysrhythmias, subcutaneous tunnel hematoma, and septic atrial thrombus.42 Local trauma to the intima may result in erosion of a catheter through the vessel wall with resultant hemorrhage. Gross mishandling of the external portion of the catheter can result in hemorrhage at the venous insertion site, the location of the Dacron cuff, or the skin exit point. Mishandling also increases the potential for air embolus.45 Although not common, retrograde perfusion into the cerebral circulation of parenteral solutions administered through indwelling catheters has been reported to cause neurologic complications such as stroke-like syndromes.
Port reservoirs may separate from the attached catheter and lead to extravasation of infused fluids manifest by a stinging or burning sensation at the infusion site.55 This usually results when the needle dislodges from the port. Other mechanisms of extravasation include catheter fracture resulting from compression, fibrin sheath formation, and slippage of port access needles from the reservoir.55 The degree of damage to the skin and subcutaneous tissues depends upon the type of drug extravasated, the duration of exposure, and site of extravasation.51
Air embolism may occur during catheter insertion, during infusions, or during catheter removal. Patients with low central venous pressures and those with compromised pulmonary function are at highest risk for this occasionally fatal complication.55
If the catheter has been placed into the right atrium, complications may include arrhythmias, endocardial damage, and risk of perforation and pericardial tamponade.63,64
Catheter migration into the jugular system may simply be monitored and is not a cause for catheter removal, although interventional radiographic techniques may be used to reposition the catheter.61
Physicians charged with caring for patients with central indwelling venous catheters should be aware of the common complications of these devices as well as their initial treatment.
Complications of Gastrostomy Tubes
Gastrostomy tubes, which are inserted into the stomach through the abdominal wall, allow the chronically ill, neurologically devastated patients with dysphagia to have their nutritional needs met. However, few studies have evaluated long-term complications of these tubes. The most common complications appear to be tube dislodgement or occlusion of the tube.65
If a tube comes out and needs replacement, it may simply be reinserted into the tract, provided firm adhesions are formed between the gastric and abdominal walls. When the tract has matured, it is usually safe to replace the tube. There is disagreement as to when the gastrocutaneous fistula tract has matured, ranging from seven days to three months.66,67 If the tube is inserted when adequate adhesions have not had a chance to form, there is a risk of inserting the tube into the peritoneal space as well as allowing leakage of gastric contents into the peritoneum, causing peritonitis. Air may leak through this tract as well, presenting as pneumoperitoneum, which is usually of no consequence. This must, however, be differentiated from a perforated viscous.68 Viscous lidocaine lubricant may decrease the discomfort of reinsertion of a tube.68 The common practice of replacing the tube and insufflating air while listening over the gastric area to confirm placement has resulted in a fatal air embolus in at least one case.74 Once a tube has been removed, the stoma will often close within 24-48 hours, but this may take up to 10-12 days.66
In the event that a regular PEG tube or button is not available, a Foley catheter may be inserted to keep the stoma open and allow tube feedings to continue.
Temporary short-term use of Foley catheters has minimal complications. There are two complications, however, to keep in mind with this technique: 1) rupture of the balloon, allowing the catheter to slip out; and 2) migration of the balloon, causing obstruction. The thin-walled balloon can tolerate the acid medium of the stomach for about three weeks. Gastrostomy tubes with balloons have been reported to cause gastric outlet obstruction or duodenal obstruction, usually presenting with abdominal pain and vomiting.70-72 Abdominal radiographs are diagnostic. The obstruction may be relieved by simply releasing the balloon.73 It is important to properly fix the tube to the abdominal wall (with sutures, if need be), so that the balloon is adherent to the gastric and abdominal wall and migration of the balloon is prevented.
To prevent clogged or occluded tubes, it is necessary to flush them with water after intermittent feedings or administration of medications. Crushed pills should be avoided (especially if they are sustained-release medications that depend on the pill matrix for their time-release characteristics) because they are a common cause of malocclusion.76
Leakage of gastric contents around the tube may be a manifestation of distal obstruction of the gastrostomy tube or simply of a stoma that is too large.70,71 If the former has been excluded, simply inserting a larger tube exacerbates the problem by enlarging the stoma even more. Sutures should be placed to tighten the orifice by physicians familiar with revision of stomal orifices.
Infections, such as superficial wound infections and cellulitis, may present as erythema and induration in the peristomal area or may progress to necrotizing fasciitis. This condition manifests as tender red streaks of the abdominal skin often associated with creptitus. Fever is invariably present, as well as systemic toxicity. It is usually caused by a mixture of aerobic and anaerobic bacteria. Necrotizing fasciitis requires emergent management with surgical debridement and intravenous antibiotics.66,71
Since complications may have subtle presentations, a water contrast radiologic study should be considered and used liberally to evaluate for extraluminal placement of gastrostomy tubes and such conditions as gastric obstruction, gastric ulcers, gastric perforations, fractured catheters, gastric torsions, intraperitoneal leak, tube migration, intussusception, intestinal obstruction, gastric fistulas, and obstruction of the catheter itself.75
Even though CSF shunts, indwelling venous catheters, and gastrostomy tubes are life-saving devices for children with complex medical conditions, they are associated with significant risks to the pediatric patient. As more of these medical devices are used to facilitate treatment in children, it is incumbent upon physicians to be familiar with the various devices, their functional mechanics, their indications, and the commonly associated complications as well as the treatment.
References
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Physician CME Questions
18. The most common problem related to a CSF shunt is:
A. infection.
B. obstruction.
C. fracture of the tubing.
D. valve dysfunction.
19. The most common organism causing CSF shunt infection is/are:
A. Staphylococcus epidermis.
B. Staphylococcus aureus.
C. Gram-negative organisms.
D. H. influenzae.
20. The most common presenting complaint of a child with a CSF shunt obstruction is:
A. headache.
B. vomiting.
C. lethargy.
D. irritability.
21. After a shunt is placed or revised, most infection will occur within:
A. less than six months.
B. 6-12 months.
C. 12-18 months.
D. more than 18 months.
22. Maneuvers to open an occluded line that is due to a blood clot include all of the following except:
A. urokinase bolus.
B. attempt to aspirate the clot.
C. continuous infusion of urokinase.
D. forcefully flushing the catheter to dislodge the clot.
23. Removal of an indwelling line is almost always necessary for:
A. exit-site infection.
B. tunnel infections.
C. bacteremia due to a line infection.
D. fever without a source on initial presentation.
24. Blood drawn from an indwelling line can be used for all of the following tests except:
A. CBC.
B. electrolytes.
C. coagulation tests.
D. type and screen.
25. Which of the following is true for gastrostomy button replacement?
A. A radiographic imaging study should be ordered whenever a replacement gastostomy tube is inserted.
B. A radiographic imaging study should be ordered only if a new gastrostomy tube is inserted into an immature tract.
C. Dislodged gastrostomy buttons do not need to be emergently replaced; instead they should be referred to a surgeon the following day.
D. A smaller gastrostomy button should never be inserted.
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