Handbook of Clinical Neurology, Vol. 119 (3rd series) Neurologic Aspects of Systemic Disease Part I Jose Biller and Jose M. Ferro, Editors © 2014 Elsevier B.V. All rights reserved
Chapter 4
Neurologic complications of cardiac tests and procedures CATHY SILA* Department of Neurology, Case Western Reserve University School of Medicine and Stroke and Cerebrovascular Center, University Hospitals—Case Medical Center, Cleveland, OH, USA
HISTORY Vascular access is the cornerstone of invasive cardiac monitoring and cardiac procedures. Crude methods of arterial blood pressure measurement were available by the late 1700s and by 1828, Jean-Louis Poiseuille had invented the mercury-filled manometer. This technology led to key experiments that were the foundation of Poiseuille’s Law, one of the most famous equations in hemodynamics (Poiseuille, 1828). By the end of World War II, catheters made of plastic and modern capacitance manometers enabled the first clinical use of a peripheral arterial line for continuous measurement of mean arterial pressure (Peterson et al., 1949). The first report of catheter access in the heart was performed in 1929 in a small hospital in Eberswald, Germany, by Werner Forssmann. During his surgical training, Forssmann advanced a percutaneous catheter into his own right atrium. Although his personal career was devastated by his selfexperimentation, he was awarded the 1956 Nobel Prize along with Cournand and Richards, for their application of his technique to image the cardiac chambers and valves. The first contrast visualization of the coronary arteries was performed by F. Mason Sones in 1958 via direct arterial exposure of the brachial artery, which became known as “the Sones technique” (Sones et al., 1959). Subsequent contributions in percutaneous arterial access by Sven-Ivar Seldinger, “the Seldinger technique,” introduction of the percutaneous femoral approach and development of specialized catheters by Melvin Judkins, and the introduction of coronary artery bypass graft surgery by Rene´ Favaloro, led to the development of coronary angiography which became the reference standard for assessing patients for coronary artery disease (Seldinger, 1953; Judkins, 1967; Favaloro, 1968). Many
contemporary cardiac tests and procedures require arterial or central venous access for diagnosis, monitoring, or therapeutics and although their safety has significantly improved due to protocols perfected over decades of use, their widespread use renders even the uncommon neurologic complication clinically relevant.
CLINICAL MANIFESTATIONS OF NEUROLOGIC COMPLICATIONS OF CARDIAC TESTS AND PROCEDURES Peripheral nervous system (PNS) complications Peripheral arterial catheters, or “A-lines,” are commonly used in critically ill patients for mean arterial pressure monitoring. In the setting of arterial pressure gradients resulting from local atherosclerotic stenosis or generalized vasoconstriction with shock, these central measurements are more accurate than peripheral blood pressure cuff monitoring. Arterial lines are typically placed in the radial or femoral artery but the brachial, axillary, and dorsalis pedis arteries can also be used. Arterial vascular access for diagnostic coronary angiography was initially performed by surgical exploration, or “cut down” of the brachial artery and insertion of catheters under direct visualization followed by surgical closure of the arteriotomy and skin. Although institutions and operators vary in their preference for accessing the left heart by the upper extremity brachial, radial, or axillary artery versus lower extremity femoral artery, direct surgical access has been largely replaced by percutaneous arterial access approaches. In addition, catheterization of the right heart is accomplished by percutaneous access of the femoral, internal jugular, or subclavian veins. The choice of
*Correspondence to: Cathy Sila, M.D., George M. Humphrey II, Professor of Neurology, 11100 Euclid Avenue HAN/5040, University Hospitals-Case Medical Center, Cleveland, OH, 44040, USA. Tel: þ1-216-844-8934, Fax: þ1-216-844-4785, E-mail: [email protected]
42
C. SILA
vascular site access varies by operator experience and preference but is also driven by the arterial size and anatomy required by the anticipated procedure. For diagnostic and therapeutic procedures requiring multiple changes of catheters, a vascular sheath is used which permits continuous vascular access. These range from 4–6 French for diagnostic catheterization procedures to as large as 24 French for interventional procedures, such as transcatheter valve replacement. The anatomic relationship of the peripheral nerves to their companion arteries and veins renders them vulnerable to injury. Adjacent peripheral nerves can be injured directly during line placement or indirectly from compression when swelling or hemorrhage produces a compartment syndrome.
PNS COMPLICATIONS OF RADIAL ARTERY CATHETERIZATION
The radial artery is the most frequently accessed site for the placement of an arterial pressure monitoring catheter in critically ill patients. The transradial approach for cardiac catheterization varies widely among operators, institutions, and countries and is used more frequently in Europe than the US. Technical expertise is required to overcome the difficulties in accessing and manipulating catheters through this smaller vessel; at 2 millimeters, the largest vascular sheath size is typically 6 French, which limits this technique primarily to diagnostic angiography. The risk of serious complications with radial artery access is less than 0.1%; this includes direct nerve injury or indirect nerve injury from compression due to hematoma or compartment syndrome (Wallach, 2004). The risk of a volar forearm compartment syndrome is increased with concomitant anticoagulation. When the pressure within the carpal tunnel is increased above 20–30 mmHg, the perfusion to the median nerve is impaired, presenting as acute pain and paresthesias followed by sensorimotor deficit. Prevention of nerve infarction requires prompt recognition and the performance of a fasciotomy and surgical release (Kokosis et al., 2010). A pre-existing carpal tunnel syndrome is a risk factor for symptomatic median nerve dysfunction following radial artery catheter placement and may be more common than typically recognized. In one prospective study of 151 patients undergoing radial artery catheter placement, symptoms of median nerve dysfunction were reported by 8/12 (67%) of those with prior carpal tunnel syndrome versus only 1/139 (0.7%) of those without prior symptoms (Martin et al., 1993).
PNS COMPLICATIONS OF BRACHIAL ARTERY CATHETERIZATION
The brachial artery is accessed for cardiac catheterization, particularly in patients with significant lower
extremity vascular disease or prior vascular surgery, and is also an alternate site for the placement of an arterial pressure monitoring catheter. The classic technique developed by Sones required surgical exposure which was complicated by a 1–2% risk of brachial artery thrombosis. Modern percutaneous access techniques have reduced the risk of serious complications with brachial artery access to 0.2–1.4%; this includes vascular complications, direct nerve injury and indirect nerve injury from compression due to hematoma and nerve infarction (Macon and Futrell, 1973). Concomitant anticoagulation therapy increases the risk of hematoma formation, particularly if the puncture was distal to the antecubital fossa and blood collects underneath the lacertus fibrosus (bicipital aponeurosis). The manifestations of median nerve involvement vary with the location of the nerve injury as the course of the median nerve varies with respect to the brachial artery. The median nerve runs lateral to the brachial artery within the upper arm and crosses anteriorly to the brachial artery within the antecubital fossa giving off the anterior interosseus branch and runs medial to the brachial artery within the forearm. Injuries to the median nerve in this region are often distinguished by concomitant involvement of the flexor pollicis longus. Although most nerve injuries improve with time, appreciable long-term disability with high median nerve injuries has been described (Kennedy et al., 1997).
PNS COMPLICATIONS OF AXILLARY ARTERY CATHETERIZATION
The axillary artery approach carries a higher complication rate so it is less frequently used than in prior decades. This approach remains essential when access with larger vascular sheaths is required in patients with severe lower extremity vascular disease. In one series of 320 axillary arteriograms, 9 (2.8%) sustained compression injuries of the median and ulnar nerves due to hematoma formation (Smith et al., 1989). The diagnosis may be difficult as the visual or palpable size of the hematoma may not correlate with the severity of the neurologic deficit and it may evolve up to 2 days postprocedure. Compartment syndrome within the medial brachial fascial compartment at the anterior axillary fold causes injury to the proximal median and ulnar nerves and spares the radial and musculocutaneous nerves due to their proximal exit.
PNS COMPLICATIONS OF FEMORAL ARTERY CATHETERIZATION
The femoral artery remains the primary access technique for interventional procedures requiring large vascular sheath access, cerebrovascular and peripheral vascular angiographic procedures, although in many
NEUROLOGIC COMPLICATIONS OF CARDIAC TESTS AND PROCEDURES institutions it has been replaced by other techniques for coronary angiography. The risk of injury to the femoral nerve or lumbar plexus ranges from 0.5% to 5.0% and is primarily due to retroperitoneal hemorrhage, but it can also be a complication of a femoral pseudoaneurysm or prolonged digital pressure for hemostasis. Risk factors for retroperitoneal hematoma following femoral catheterization from retrospective case series include the use of large-caliber vascular sheaths, multiple procedures, high femoral puncture, female gender, low body surface area, obesity, advanced age, peripheral vascular disease, chronic renal insufficiency, thrombocytopenia, and excessive anticoagulation (Kent et al., 1994). The retroperitoneal hematoma may result from the puncture site, laceration of an arterial branch, or a coagulopathy which may be independent of the procedure itself. Diagnosis requires a high index of suspicion as the clinical presentation may be subtle, without cutaneous ecchymosis or expanding mass, and herald as hypotension, tachycardia, diaphoresis, and worsening discomfort in the lower abdomen, groin, or back (Farouque et al., 2005). Injury to the femoral nerve typically occurs when the hematoma is within or near the iliopsoas muscle or when the hematoma tracks into the femoral canal and is further compressed by the inguinal ligament. Early symptoms include pain in the groin or hip with radiation into the anterior thigh, and compensatory hip flexion with increased pain upon attempts to extend the hip. Progressive focal deficits include paresthesias and sensory loss along the anterior thigh and medial leg, and weakness in the quadriceps, resulting in a lack of knee stabilization upon attempts to ambulate (Parmer et al., 2006). Early recognition of the symptoms, medical stabilization, and prompt reversal of coagulopathy is key in limiting neurologic morbidity. Patients who fail this approach should undergo angiography and assessment for possible endovascular treatment; persistent hemodynamic instability warrants urgent surgical intervention (Chan et al., 2008).
PNS COMPLICATIONS OF CENTRAL VENOUS CATHETERIZATION
Central venous line insertion into the subclavian or internal jugular veins can cause injuries to the vagus, recurrent laryngeal, or phrenic nerves (Martin-Hirsch and Newbegin, 1995). Injuries to the brachial plexus occur in 1–2%; the upper trunk is more often affected with internal jugular vein and lower trunk with subclavian vein catheterizations. Case reports cite multiple attempts at cannulation as a possible risk factor for nerve injury and ultrasound guidance has been recommended as a way to reduce the number of attempts.
43
PNS COMPLICATIONS OF TRANSESOPHAGEAL ECHOCARDIOGRAPHY
The most common complication of transesophageal echocardiography (TEE) is local trauma during placement, with serious perforation occurring in 0.1–0.2%. However, rare case reports of cerebral embolism, including two cases (0.0047%) from an aggregate database of 42 355 patients, resulted from periprocedural dislodgement of an intracardiac thrombus (Coˆte´ and Denault, 2008). Traumatic injury to the recurrent laryngeal nerve is a rare complication of TEE placement but a known complication of cardiac surgery with intraoperative TEE occurring in 4% of patients (Zwetsch et al., 2001). The causative role of the TEE is complicated by the fact that thermal injury to the recurrent laryngeal and phrenic nerves can also result from myocardial cooling techniques employing pericardial ice slush or cold saline (Hogue et al., 1995).
Central nervous system (CNS) complications CNS COMPLICATIONS OF CARDIAC CATHETERIZATION Cerebral embolism and ischemic stroke Ischemic stroke is the most common neurologic complication of diagnostic and therapeutic cardiac catheterization. The presumed mechanism is embolization of atherosclerotic plaque or thrombus dislodged during guiding catheter manipulation, platelet–fibrin thrombus that forms on the catheters, or air that arises during catheter flushing (Segal et al., 2001). Risk factors for stroke include advanced coronary artery disease or prior coronary revascularization, reduced ejection fraction, female gender, hypertension, diabetes, renal insufficiency, and prior stroke. Ischemic stroke complicates 0.08–0.17% of cardiac catheterization and catheterbased coronary interventions, 1–10% of endovascular balloon valvuloplasties, and 1–2% of atrial septal closures (Davis et al., 1979; Fuchs et al., 2002). In some series, 60% of events affecting the vertebrobasilar territory manifest as combinations of cortical blindness, hemianoptic visual field defects, intrinsic brainstem signs, confusion, and amnesia. Encephalopathy or seizures with temporal lobe ischemia are commonly misdiagnosed as a complication of sedative and analgesic medications, systemic hypotension, or large volumes of contrast material (Dawson and Fischer, 1977). The posterior circulation predominance of events has been postulated to be due to inadvertent catheterization of the vertebral artery, particularly when a retrograde radial or brachial artery approach is used (Kosmorsky et al., 1988). The carotid circulation accounts for 30–40% of focal deficits, consisting of combinations
44
C. SILA
of hemiparesis, hemisensory deficits, retinal ischemia, and dysphasia. Every catheterization laboratory should have a protocol for management of a periprocedural acute neurologic event. Although the outcome is good in about half the patients with resolution of deficits in 48 hours, disabling and fatal stroke can also occur. As the time of stroke symptom onset is known and baseline laboratories and clinical status are readily available, excellent results have been reported both with intravenous tissue plasminogen activator (tPA) or endovascular revascularization when utilizing the hospital’s acute stroke management team (Oezbek et al., 1995, Khatri et al., 2008). Transient cortical blindness following cardiac catheterization Another rare complication of cardiac catheterization is the syndrome of transient cortical blindness, reported in 0.01–0.05% (Zwicker and Sila, 2002). Transient cortical blindness also complicates other intra-arterial contrast procedures such as cerebral angiography and is attributed to a temporary disruption of the blood–brain barrier and cerebral dysautoregulation. The clinical manifestations include an acute, thunderclap, or subacute vascular headache with nausea and vomiting, and hypertension, in addition to the focal neurologic features of cortical blindness sometimes accompanied by amnesia, aphasia, and neglect. Neuroimaging features are similar to those seen in hypertensive encephalopathy, eclampsia, and the reversible cerebral vasoconstriction syndrome, with patchy enhancement involving the posterior cortex and white matter edema (see Fig. 4.1). The treatment is supportive with aggressive control of hypertension and calcium channel blocker therapy.
CNS COMPLICATIONS OF CENTRAL VENOUS ACCESS CATHETERS
Central venous access catheters, employed in critically ill patients to monitor central venous pressure and fluid balance and for the administration of cardioactive drugs, are more often complicated by venous air embolism, but in the presence of intracardiac or intrapulmonary shunting can rarely lead to cerebral air embolism. A literature review from 1975 to 1998 revealed 26 cases, 55% during unintentional catheter disconnection, 30% during removal, and 15% during insertion. An intracardiac or intrapulmonary shunt was identified in 60% of patients and overall mortality was 23% (Heckmann et al., 2000). The treatment of cerebral air embolism includes placing the patient immediately in the left lateral Trendelenberg position, aspirating the air, and administering 100% oxygen with transport to a facility where hyperbaric oxygen therapy can be performed,
Fig. 4.1. Following diagnostic cardiac catheterization, a 58year-old woman with a history of migraine developed a sudden throbbing headache, nausea, and vomiting with a left hemianopsia and left spatial inattention. She was treated with oral calcium channel blockers and her symptoms resolved over 2 days.
ideally within 6 hours of symptom onset, if there is not rapid improvement (Blanc et al., 2002). In addition, systemic anticoagulation has been recommended to prevent the intravascular thrombosis that results from the occlusive process (see Fig. 4.2). Placement of a central venous catheter in the internal jugular vein is complicated by inadvertant cannulation of the internal carotid artery in 6% of cases and 40% of these result in a hematoma. Causes of transient ischemic attack (TIA) and stroke include catheter-related embolization, vessel dissection, and hypoperfusion from compression by the hematoma or digital pressure to promote hemostasis.
CNS COMPLICATIONS OF THROMBOLYSIS FOR ACUTE MYOCARDIAL INFARCTION
Ischemic stroke complicates 1% of patients with acute myocardial infarction, especially those with advanced age, congestive heart failure, atrial fibrillation, and cardiac catheterization but the overall risk is cut in half if an intervention achieved successful reperfusion. The most feared risk of thrombolytic therapy for acute myocardial infarction is intracranial hemorrhage with its attendant morbidity and mortality. The risk of intracranial bleeding varies from 0.3% to 1% in recent trials with risk related to more aggressive dosing and combination antithrombotic therapies as well as advanced age and hypertension (Vaitkus et al., 1992). Multiple risk–benefit analyses indicate that the benefits for myocardial
NEUROLOGIC COMPLICATIONS OF CARDIAC TESTS AND PROCEDURES
45
Fig. 4.2. (A) and (B) Before and after windowing. During placement of an internal jugular venous catheter, a 42-year-old woman with a dilated cardiomyopathy unexpectedly started hyperventilating and the catheter tubing became briefly disconnected. Her speech suddenly became incomprehensible and then she developed a right hemiplegia and gaze deviation. Urgent noncontrast CT was unremarkable but adjustment of the window settings revealed air emboli in multiple left middle cerebral artery branches.
salvage and reduction in thromboembolic stroke still outweigh the risk for hemorrhagic stroke. In a systematic review of 244 intracranial hemorrhages complicating the GUSTO-1 trial, the patterns were diverse; although 46% were solitary and lobar in location, 30% also involved either the subdural or intraventricular space and many were bizarre with mottled appearances and blood–fluid levels suggesting multiple etiologic mechanisms (Gebel et al., 1998) (see Fig. 4.3). Most were recognized within 24 hours of thrombolytic therapy, many during the infusion. Neuropathologic studies have invariably demonstrated amyloid angiopathy, which is consistent with the increased risk with advanced age. Mortality was approximately 50% within the first week and was associated with earlier onset of symptoms, hemorrhage volume, and Glasgow Coma Scale score (Sloan et al., 1998).
LABORATORY INVESTIGATIONS Peripheral nervous complications are best addressed by electromyography including nerve conductions studies and needle electrode examination. Definitive studies require a delay of several weeks to allow for wallerian degeneration to be reflected in the needle examination but a baseline study can be useful in documenting preexisting nerve deficits to enhance interpretation of a subsequent study or if litigation is imminent. Although generally to be considered a low risk procedure, there are some important considerations pertinent to the cardiac or critically ill patient (Al-Shekhlee et al., 2003). Nerve conduction studies can result in electrical injuries in the intensive care unit setting or in patients with pacemakers or similar cardiac devices and the needle
Fig. 4.3. Within 2 hours of intravenous thrombolytic therapy for an acute myocardial infarction, an 81-year-old man became agitated and hypertensive then unresponsive with agonal respirations requiring intubation. Urgent CT imaging demonstrates a large multifocal hemorrhage with a blood–fluid level.
examination is invasive and can be associated with bleeding in the setting of antithrombotic therapies.
MANAGEMENT OFACUTE STROKE IN THE CARDIAC INTENSIVE CARE UNIT The diagnosis and management of an acute stroke in the setting of a cardiac procedure follows the same paradigm for acute stroke in other settings, although in the setting of the cardiac catheterization laboratory, stroke is almost exclusively ischemic in nature, and after
46
C. SILA
thrombolysis for acute myocardial infarction, intracranial bleeding should be the first consideration. A protocol should be in place in the cardiac catheterization laboratory in the event a complication should occur. In hospitals without neurointerventional services, the mainstay of treatment is intravenous tPA. Although heparin infusions can be reversed with protamine, glycoprotein IIb/IIIa inhibitors cannot, and the safety of tPA in their presence is unknown. In hospitals with neurointerventional capability and multipurpose catheterization laboratories, urgent neuroimaging to exclude an unlikely intracranial hemorrhage may not be necessary if one can proceed directly to angiographic documentation of an acute arterial occlusion relevant to the presenting neurologic deficit. Acute neurologic deterioration after thrombolysis for acute myocardial infarction should be presumed to be an intracranial hemorrhage until proven otherwise. All thrombolytic, antithrombotic, and antiplatelet therapies should be stopped immediately while the patient is stabilized and blood is drawn for coagulation studies including platelet count, prothrombin time (PT), and activated clotting time (ACT) or activated partial thromboplastin time (aPTT). Reversal of the coagulopathy should not be delayed by awaiting confirmation with urgent neuroimaging as the hemorrhage can expand rapidly within several hours.
CONCLUSIONS, FUTURE DIRECTIONS Although peripheral neurologic complications of catheter access procedures are uncommon, they can result in considerable neurologic disability. Proceduralists should be aware of the relevant anatomy and early signs of nerve injury so that prompt diagnosis and treatment can ensue. The diagnosis and management of acute stroke complicating cardiac tests and procedures follows the paradigm for acute stroke in other settings but antithrombotic therapies may limit appropriateness for intravenous tPA therapy but still be amenable to mechanical neurointerventional revascularization options. The ideal angiography suite of the future is patientcentric and multipurpose, coordinating diagnostic and therapeutic strategies for multivascular disease, allowing for multispecialty collaboration, and, in the event of a neurologic complication of a cardiac procedure, facilitating the various treating physicians to converge efficiently upon the patient.
REFERENCES Al-Shekhlee A, Shapiro BE, Preston DC (2003). Iatrogenic complications and risks of nerve conduction studies and needle electromyography. Muscle Nerve 27: 517–526. Blanc P, Boussuges A, Henriette K et al. (2002). Iatrogenic cerebral air embolism: importance of an early hyperbaric oxygenation. Intensive Care Med 28: 559–563.
Chan YC, Morales JP, Reidy JF et al. (2008). Management of spontaneous and iatrogenic retroperitoneal haemorrhage: conservative management, endovascular intervention or open surgery? Int J Clin Pract 62: 1604–1613. Coˆte´ G, Denault A (2008). Transesophageal echocardiographyrelated complications. Can J Anaesth 55: 622–647. Davis K, Kennedy JW, Kemp HGJ et al. (1979). Complications of coronary arteriography from the Collaborative Study of Coronary Artery Surgery (CASS). Circulation 59: 1105–1112. Dawson DM, Fischer EG (1977). Neurologic complications of cardiac catheterization. Neurology 27: 496–497. Farouque HM, Tremmel JA, Raissi Shabari F et al. (2005). Risk factors for the development of retroperitoneal hematoma after percutaneous coronary intervention in the era of glycoprotein IIb/IIIa inhibitors and vascular closure devices. J Am Coll Cardiol 45: 363–368. Favaloro RG (1968). Saphenous vein autograft replacement of severe segmental coronary artery occlusion: operative techniques. Ann Thorac Surg 5: 334–339. Fuchs S, Stabile E, Kinnaird TD et al. (2002). Stroke complicating percutaneous coronary interventions: incidence, predictors, and prognostic implications. Circulation 106: 86–91. Gebel J, Sila CA, Sloan MA et al. (1998). Thrombolysisrelated intracranial hemorrhage. a radiographic analysis of 244 cases from the GUSTO-I trial. Stroke 29: 563–569. Heckmann JG, Lang CJG, Kindler K et al. (2000). Neurologic manifestations of cerebral air embolism as a complication of central venous catheterization. Crit Care Med 28: 1621–1625. Hogue Jr CW, Lappas GD, Cresswell LL et al. (1995). Swallowing dysfunction after cardiac operations. Associated adverse outcomes and risk factors including intraoperative transesophageal echocardiography. J Thorac Cardiovasc Surg 110: 517–522. Judkins MP (1967). Selective coronary arteriography. A percutaneous transfemoral technique. Radiology 89: 815–824. Kennedy AM, Grocott M, Schwartz MS et al. (1997). Median nerve injury: an underrecognised complication of brachial artery catheterization? J Neurol Neurosurg Psychiatry 63: 542–546. Kent KC, Moscucci M, Mansour KA et al. (1994). Retroperitoneal hematoma after cardiac catheterization: prevalence, risk factors, and optimal management. J Vasc Surg 20: 905–913. Khatri P, Taylor RA, Palumbo V et al. (2008). The safety and efficacy of thrombolysis for strokes after cardiac catheterization. J Am Coll Cardiol 51: 906–911. Kokosis G, Blueschke G, Blanton M et al. (2010). Acute carpal tunnel syndrome secondary to iatrogenic hemorrhage: a case report. Hand 5: 1–3. Kosmorsky G, Hanson MR, Tomsak RL (1988). Neuroophthalmologic complications of cardiac catheterization. Neurology 38: 483–485. Macon WL, Futrell JW (1973). Median nerve neuropathy after percutaneous puncture of the brachial artery in patients receiving anticoagulants. N Eng J Med 288: 1396.
NEUROLOGIC COMPLICATIONS OF CARDIAC TESTS AND PROCEDURES Martin SD, Sharrock NE, Mineo R et al. (1993). Acute exacerbation of carpal tunnel syndrome after radial artery cannulation. J Hand Surg Am 18: 455–458. Martin-Hirsch DP, Newbegin CJ (1995). Right vocal cord paralysis as a result of central venous catheterization. J Laryngol Otol 109: 1107–1108. Oezbek C, Heisel A, Voelk M et al. (1995). Management of stroke complicating cardiac catheterization with recombinant tissuetype plasminogen activator. Am J Cardiol 76: 733–735. Parmer SS, Carpenter JP, Fairman RM et al. (2006). Femoral neuropathy following retroperitoneal hemorrhage: case series and review of the literature. Ann Vasc Surg 20: 536–540. Peterson LH, Dripps RD, Risman G (1949). A method for recording the arterial pressure pulse and blood pressure in man. Am Heart J 37: 771–782. Poiseuille JLM (1828). Recherches sur la Force du Coeur Aortique. The`se no.166. Didot, Paris. Segal AZ, Abernethy WB, Palacios IF et al. (2001). Stroke as a complication of cardiac catheterization: risk factors and clinical features. Neurology 56: 975–977. Seldinger SI (1953). Catheter replacement of the needle in percutaneous arteriography – a new technique. Acta Radiol 39: 368–376.
47
Sloan MA, Sila CA, Mahaffey KW et al. (1998). Prediction of 30-day mortality among patients with thrombolysis-related intracranial hemorrhage. Circulation 98: 1376–1382. Smith DC, Mitchell DA, Peterson GW et al. (1989). Medial brachial fascial compartment syndrome: anatomic basis of neuropathy after transaxillary arteriography. Radiology 173: 149–154. Sones MF, Shirey EK, Proudfit WL et al. (1959). Cine coronary angiography. Circulation 20: 773. Vaitkus PT, Berlin JA, Schwartz JS et al. (1992). Stroke complicating acute myocardial infarction – a meta-analysis of risk modification by anticoagulation and thrombolytic therapy. Arch Intern Med 152: 2020–2024. Wallach SG (2004). Cannulation injury of the radial artery: diagnosis and treatment algorithm. Am J Crit Care 13: 315–319. Zwetsch G, Filipovic M, Skarvan K et al. (2001). Transient recurrent laryngeal nerve palsy after failed placement of a transesophageal echocardiographic probe in an anesthetized patient. Anesth Analg 92: 1422–1423. Zwicker JC, Sila CA (2002). MRI findings in transient cortical blindness after cardiac catheterization. Catheter Cardiovasc Interv 57: 47–49.
Chapter 4
Neurologic complications of cardiac tests and procedures CATHY SILA* Department of Neurology, Case Western Reserve University School of Medicine and Stroke and Cerebrovascular Center, University Hospitals—Case Medical Center, Cleveland, OH, USA
HISTORY Vascular access is the cornerstone of invasive cardiac monitoring and cardiac procedures. Crude methods of arterial blood pressure measurement were available by the late 1700s and by 1828, Jean-Louis Poiseuille had invented the mercury-filled manometer. This technology led to key experiments that were the foundation of Poiseuille’s Law, one of the most famous equations in hemodynamics (Poiseuille, 1828). By the end of World War II, catheters made of plastic and modern capacitance manometers enabled the first clinical use of a peripheral arterial line for continuous measurement of mean arterial pressure (Peterson et al., 1949). The first report of catheter access in the heart was performed in 1929 in a small hospital in Eberswald, Germany, by Werner Forssmann. During his surgical training, Forssmann advanced a percutaneous catheter into his own right atrium. Although his personal career was devastated by his selfexperimentation, he was awarded the 1956 Nobel Prize along with Cournand and Richards, for their application of his technique to image the cardiac chambers and valves. The first contrast visualization of the coronary arteries was performed by F. Mason Sones in 1958 via direct arterial exposure of the brachial artery, which became known as “the Sones technique” (Sones et al., 1959). Subsequent contributions in percutaneous arterial access by Sven-Ivar Seldinger, “the Seldinger technique,” introduction of the percutaneous femoral approach and development of specialized catheters by Melvin Judkins, and the introduction of coronary artery bypass graft surgery by Rene´ Favaloro, led to the development of coronary angiography which became the reference standard for assessing patients for coronary artery disease (Seldinger, 1953; Judkins, 1967; Favaloro, 1968). Many
contemporary cardiac tests and procedures require arterial or central venous access for diagnosis, monitoring, or therapeutics and although their safety has significantly improved due to protocols perfected over decades of use, their widespread use renders even the uncommon neurologic complication clinically relevant.
CLINICAL MANIFESTATIONS OF NEUROLOGIC COMPLICATIONS OF CARDIAC TESTS AND PROCEDURES Peripheral nervous system (PNS) complications Peripheral arterial catheters, or “A-lines,” are commonly used in critically ill patients for mean arterial pressure monitoring. In the setting of arterial pressure gradients resulting from local atherosclerotic stenosis or generalized vasoconstriction with shock, these central measurements are more accurate than peripheral blood pressure cuff monitoring. Arterial lines are typically placed in the radial or femoral artery but the brachial, axillary, and dorsalis pedis arteries can also be used. Arterial vascular access for diagnostic coronary angiography was initially performed by surgical exploration, or “cut down” of the brachial artery and insertion of catheters under direct visualization followed by surgical closure of the arteriotomy and skin. Although institutions and operators vary in their preference for accessing the left heart by the upper extremity brachial, radial, or axillary artery versus lower extremity femoral artery, direct surgical access has been largely replaced by percutaneous arterial access approaches. In addition, catheterization of the right heart is accomplished by percutaneous access of the femoral, internal jugular, or subclavian veins. The choice of
*Correspondence to: Cathy Sila, M.D., George M. Humphrey II, Professor of Neurology, 11100 Euclid Avenue HAN/5040, University Hospitals-Case Medical Center, Cleveland, OH, 44040, USA. Tel: þ1-216-844-8934, Fax: þ1-216-844-4785, E-mail: [email protected]
42
C. SILA
vascular site access varies by operator experience and preference but is also driven by the arterial size and anatomy required by the anticipated procedure. For diagnostic and therapeutic procedures requiring multiple changes of catheters, a vascular sheath is used which permits continuous vascular access. These range from 4–6 French for diagnostic catheterization procedures to as large as 24 French for interventional procedures, such as transcatheter valve replacement. The anatomic relationship of the peripheral nerves to their companion arteries and veins renders them vulnerable to injury. Adjacent peripheral nerves can be injured directly during line placement or indirectly from compression when swelling or hemorrhage produces a compartment syndrome.
PNS COMPLICATIONS OF RADIAL ARTERY CATHETERIZATION
The radial artery is the most frequently accessed site for the placement of an arterial pressure monitoring catheter in critically ill patients. The transradial approach for cardiac catheterization varies widely among operators, institutions, and countries and is used more frequently in Europe than the US. Technical expertise is required to overcome the difficulties in accessing and manipulating catheters through this smaller vessel; at 2 millimeters, the largest vascular sheath size is typically 6 French, which limits this technique primarily to diagnostic angiography. The risk of serious complications with radial artery access is less than 0.1%; this includes direct nerve injury or indirect nerve injury from compression due to hematoma or compartment syndrome (Wallach, 2004). The risk of a volar forearm compartment syndrome is increased with concomitant anticoagulation. When the pressure within the carpal tunnel is increased above 20–30 mmHg, the perfusion to the median nerve is impaired, presenting as acute pain and paresthesias followed by sensorimotor deficit. Prevention of nerve infarction requires prompt recognition and the performance of a fasciotomy and surgical release (Kokosis et al., 2010). A pre-existing carpal tunnel syndrome is a risk factor for symptomatic median nerve dysfunction following radial artery catheter placement and may be more common than typically recognized. In one prospective study of 151 patients undergoing radial artery catheter placement, symptoms of median nerve dysfunction were reported by 8/12 (67%) of those with prior carpal tunnel syndrome versus only 1/139 (0.7%) of those without prior symptoms (Martin et al., 1993).
PNS COMPLICATIONS OF BRACHIAL ARTERY CATHETERIZATION
The brachial artery is accessed for cardiac catheterization, particularly in patients with significant lower
extremity vascular disease or prior vascular surgery, and is also an alternate site for the placement of an arterial pressure monitoring catheter. The classic technique developed by Sones required surgical exposure which was complicated by a 1–2% risk of brachial artery thrombosis. Modern percutaneous access techniques have reduced the risk of serious complications with brachial artery access to 0.2–1.4%; this includes vascular complications, direct nerve injury and indirect nerve injury from compression due to hematoma and nerve infarction (Macon and Futrell, 1973). Concomitant anticoagulation therapy increases the risk of hematoma formation, particularly if the puncture was distal to the antecubital fossa and blood collects underneath the lacertus fibrosus (bicipital aponeurosis). The manifestations of median nerve involvement vary with the location of the nerve injury as the course of the median nerve varies with respect to the brachial artery. The median nerve runs lateral to the brachial artery within the upper arm and crosses anteriorly to the brachial artery within the antecubital fossa giving off the anterior interosseus branch and runs medial to the brachial artery within the forearm. Injuries to the median nerve in this region are often distinguished by concomitant involvement of the flexor pollicis longus. Although most nerve injuries improve with time, appreciable long-term disability with high median nerve injuries has been described (Kennedy et al., 1997).
PNS COMPLICATIONS OF AXILLARY ARTERY CATHETERIZATION
The axillary artery approach carries a higher complication rate so it is less frequently used than in prior decades. This approach remains essential when access with larger vascular sheaths is required in patients with severe lower extremity vascular disease. In one series of 320 axillary arteriograms, 9 (2.8%) sustained compression injuries of the median and ulnar nerves due to hematoma formation (Smith et al., 1989). The diagnosis may be difficult as the visual or palpable size of the hematoma may not correlate with the severity of the neurologic deficit and it may evolve up to 2 days postprocedure. Compartment syndrome within the medial brachial fascial compartment at the anterior axillary fold causes injury to the proximal median and ulnar nerves and spares the radial and musculocutaneous nerves due to their proximal exit.
PNS COMPLICATIONS OF FEMORAL ARTERY CATHETERIZATION
The femoral artery remains the primary access technique for interventional procedures requiring large vascular sheath access, cerebrovascular and peripheral vascular angiographic procedures, although in many
NEUROLOGIC COMPLICATIONS OF CARDIAC TESTS AND PROCEDURES institutions it has been replaced by other techniques for coronary angiography. The risk of injury to the femoral nerve or lumbar plexus ranges from 0.5% to 5.0% and is primarily due to retroperitoneal hemorrhage, but it can also be a complication of a femoral pseudoaneurysm or prolonged digital pressure for hemostasis. Risk factors for retroperitoneal hematoma following femoral catheterization from retrospective case series include the use of large-caliber vascular sheaths, multiple procedures, high femoral puncture, female gender, low body surface area, obesity, advanced age, peripheral vascular disease, chronic renal insufficiency, thrombocytopenia, and excessive anticoagulation (Kent et al., 1994). The retroperitoneal hematoma may result from the puncture site, laceration of an arterial branch, or a coagulopathy which may be independent of the procedure itself. Diagnosis requires a high index of suspicion as the clinical presentation may be subtle, without cutaneous ecchymosis or expanding mass, and herald as hypotension, tachycardia, diaphoresis, and worsening discomfort in the lower abdomen, groin, or back (Farouque et al., 2005). Injury to the femoral nerve typically occurs when the hematoma is within or near the iliopsoas muscle or when the hematoma tracks into the femoral canal and is further compressed by the inguinal ligament. Early symptoms include pain in the groin or hip with radiation into the anterior thigh, and compensatory hip flexion with increased pain upon attempts to extend the hip. Progressive focal deficits include paresthesias and sensory loss along the anterior thigh and medial leg, and weakness in the quadriceps, resulting in a lack of knee stabilization upon attempts to ambulate (Parmer et al., 2006). Early recognition of the symptoms, medical stabilization, and prompt reversal of coagulopathy is key in limiting neurologic morbidity. Patients who fail this approach should undergo angiography and assessment for possible endovascular treatment; persistent hemodynamic instability warrants urgent surgical intervention (Chan et al., 2008).
PNS COMPLICATIONS OF CENTRAL VENOUS CATHETERIZATION
Central venous line insertion into the subclavian or internal jugular veins can cause injuries to the vagus, recurrent laryngeal, or phrenic nerves (Martin-Hirsch and Newbegin, 1995). Injuries to the brachial plexus occur in 1–2%; the upper trunk is more often affected with internal jugular vein and lower trunk with subclavian vein catheterizations. Case reports cite multiple attempts at cannulation as a possible risk factor for nerve injury and ultrasound guidance has been recommended as a way to reduce the number of attempts.
43
PNS COMPLICATIONS OF TRANSESOPHAGEAL ECHOCARDIOGRAPHY
The most common complication of transesophageal echocardiography (TEE) is local trauma during placement, with serious perforation occurring in 0.1–0.2%. However, rare case reports of cerebral embolism, including two cases (0.0047%) from an aggregate database of 42 355 patients, resulted from periprocedural dislodgement of an intracardiac thrombus (Coˆte´ and Denault, 2008). Traumatic injury to the recurrent laryngeal nerve is a rare complication of TEE placement but a known complication of cardiac surgery with intraoperative TEE occurring in 4% of patients (Zwetsch et al., 2001). The causative role of the TEE is complicated by the fact that thermal injury to the recurrent laryngeal and phrenic nerves can also result from myocardial cooling techniques employing pericardial ice slush or cold saline (Hogue et al., 1995).
Central nervous system (CNS) complications CNS COMPLICATIONS OF CARDIAC CATHETERIZATION Cerebral embolism and ischemic stroke Ischemic stroke is the most common neurologic complication of diagnostic and therapeutic cardiac catheterization. The presumed mechanism is embolization of atherosclerotic plaque or thrombus dislodged during guiding catheter manipulation, platelet–fibrin thrombus that forms on the catheters, or air that arises during catheter flushing (Segal et al., 2001). Risk factors for stroke include advanced coronary artery disease or prior coronary revascularization, reduced ejection fraction, female gender, hypertension, diabetes, renal insufficiency, and prior stroke. Ischemic stroke complicates 0.08–0.17% of cardiac catheterization and catheterbased coronary interventions, 1–10% of endovascular balloon valvuloplasties, and 1–2% of atrial septal closures (Davis et al., 1979; Fuchs et al., 2002). In some series, 60% of events affecting the vertebrobasilar territory manifest as combinations of cortical blindness, hemianoptic visual field defects, intrinsic brainstem signs, confusion, and amnesia. Encephalopathy or seizures with temporal lobe ischemia are commonly misdiagnosed as a complication of sedative and analgesic medications, systemic hypotension, or large volumes of contrast material (Dawson and Fischer, 1977). The posterior circulation predominance of events has been postulated to be due to inadvertent catheterization of the vertebral artery, particularly when a retrograde radial or brachial artery approach is used (Kosmorsky et al., 1988). The carotid circulation accounts for 30–40% of focal deficits, consisting of combinations
44
C. SILA
of hemiparesis, hemisensory deficits, retinal ischemia, and dysphasia. Every catheterization laboratory should have a protocol for management of a periprocedural acute neurologic event. Although the outcome is good in about half the patients with resolution of deficits in 48 hours, disabling and fatal stroke can also occur. As the time of stroke symptom onset is known and baseline laboratories and clinical status are readily available, excellent results have been reported both with intravenous tissue plasminogen activator (tPA) or endovascular revascularization when utilizing the hospital’s acute stroke management team (Oezbek et al., 1995, Khatri et al., 2008). Transient cortical blindness following cardiac catheterization Another rare complication of cardiac catheterization is the syndrome of transient cortical blindness, reported in 0.01–0.05% (Zwicker and Sila, 2002). Transient cortical blindness also complicates other intra-arterial contrast procedures such as cerebral angiography and is attributed to a temporary disruption of the blood–brain barrier and cerebral dysautoregulation. The clinical manifestations include an acute, thunderclap, or subacute vascular headache with nausea and vomiting, and hypertension, in addition to the focal neurologic features of cortical blindness sometimes accompanied by amnesia, aphasia, and neglect. Neuroimaging features are similar to those seen in hypertensive encephalopathy, eclampsia, and the reversible cerebral vasoconstriction syndrome, with patchy enhancement involving the posterior cortex and white matter edema (see Fig. 4.1). The treatment is supportive with aggressive control of hypertension and calcium channel blocker therapy.
CNS COMPLICATIONS OF CENTRAL VENOUS ACCESS CATHETERS
Central venous access catheters, employed in critically ill patients to monitor central venous pressure and fluid balance and for the administration of cardioactive drugs, are more often complicated by venous air embolism, but in the presence of intracardiac or intrapulmonary shunting can rarely lead to cerebral air embolism. A literature review from 1975 to 1998 revealed 26 cases, 55% during unintentional catheter disconnection, 30% during removal, and 15% during insertion. An intracardiac or intrapulmonary shunt was identified in 60% of patients and overall mortality was 23% (Heckmann et al., 2000). The treatment of cerebral air embolism includes placing the patient immediately in the left lateral Trendelenberg position, aspirating the air, and administering 100% oxygen with transport to a facility where hyperbaric oxygen therapy can be performed,
Fig. 4.1. Following diagnostic cardiac catheterization, a 58year-old woman with a history of migraine developed a sudden throbbing headache, nausea, and vomiting with a left hemianopsia and left spatial inattention. She was treated with oral calcium channel blockers and her symptoms resolved over 2 days.
ideally within 6 hours of symptom onset, if there is not rapid improvement (Blanc et al., 2002). In addition, systemic anticoagulation has been recommended to prevent the intravascular thrombosis that results from the occlusive process (see Fig. 4.2). Placement of a central venous catheter in the internal jugular vein is complicated by inadvertant cannulation of the internal carotid artery in 6% of cases and 40% of these result in a hematoma. Causes of transient ischemic attack (TIA) and stroke include catheter-related embolization, vessel dissection, and hypoperfusion from compression by the hematoma or digital pressure to promote hemostasis.
CNS COMPLICATIONS OF THROMBOLYSIS FOR ACUTE MYOCARDIAL INFARCTION
Ischemic stroke complicates 1% of patients with acute myocardial infarction, especially those with advanced age, congestive heart failure, atrial fibrillation, and cardiac catheterization but the overall risk is cut in half if an intervention achieved successful reperfusion. The most feared risk of thrombolytic therapy for acute myocardial infarction is intracranial hemorrhage with its attendant morbidity and mortality. The risk of intracranial bleeding varies from 0.3% to 1% in recent trials with risk related to more aggressive dosing and combination antithrombotic therapies as well as advanced age and hypertension (Vaitkus et al., 1992). Multiple risk–benefit analyses indicate that the benefits for myocardial
NEUROLOGIC COMPLICATIONS OF CARDIAC TESTS AND PROCEDURES
45
Fig. 4.2. (A) and (B) Before and after windowing. During placement of an internal jugular venous catheter, a 42-year-old woman with a dilated cardiomyopathy unexpectedly started hyperventilating and the catheter tubing became briefly disconnected. Her speech suddenly became incomprehensible and then she developed a right hemiplegia and gaze deviation. Urgent noncontrast CT was unremarkable but adjustment of the window settings revealed air emboli in multiple left middle cerebral artery branches.
salvage and reduction in thromboembolic stroke still outweigh the risk for hemorrhagic stroke. In a systematic review of 244 intracranial hemorrhages complicating the GUSTO-1 trial, the patterns were diverse; although 46% were solitary and lobar in location, 30% also involved either the subdural or intraventricular space and many were bizarre with mottled appearances and blood–fluid levels suggesting multiple etiologic mechanisms (Gebel et al., 1998) (see Fig. 4.3). Most were recognized within 24 hours of thrombolytic therapy, many during the infusion. Neuropathologic studies have invariably demonstrated amyloid angiopathy, which is consistent with the increased risk with advanced age. Mortality was approximately 50% within the first week and was associated with earlier onset of symptoms, hemorrhage volume, and Glasgow Coma Scale score (Sloan et al., 1998).
LABORATORY INVESTIGATIONS Peripheral nervous complications are best addressed by electromyography including nerve conductions studies and needle electrode examination. Definitive studies require a delay of several weeks to allow for wallerian degeneration to be reflected in the needle examination but a baseline study can be useful in documenting preexisting nerve deficits to enhance interpretation of a subsequent study or if litigation is imminent. Although generally to be considered a low risk procedure, there are some important considerations pertinent to the cardiac or critically ill patient (Al-Shekhlee et al., 2003). Nerve conduction studies can result in electrical injuries in the intensive care unit setting or in patients with pacemakers or similar cardiac devices and the needle
Fig. 4.3. Within 2 hours of intravenous thrombolytic therapy for an acute myocardial infarction, an 81-year-old man became agitated and hypertensive then unresponsive with agonal respirations requiring intubation. Urgent CT imaging demonstrates a large multifocal hemorrhage with a blood–fluid level.
examination is invasive and can be associated with bleeding in the setting of antithrombotic therapies.
MANAGEMENT OFACUTE STROKE IN THE CARDIAC INTENSIVE CARE UNIT The diagnosis and management of an acute stroke in the setting of a cardiac procedure follows the same paradigm for acute stroke in other settings, although in the setting of the cardiac catheterization laboratory, stroke is almost exclusively ischemic in nature, and after
46
C. SILA
thrombolysis for acute myocardial infarction, intracranial bleeding should be the first consideration. A protocol should be in place in the cardiac catheterization laboratory in the event a complication should occur. In hospitals without neurointerventional services, the mainstay of treatment is intravenous tPA. Although heparin infusions can be reversed with protamine, glycoprotein IIb/IIIa inhibitors cannot, and the safety of tPA in their presence is unknown. In hospitals with neurointerventional capability and multipurpose catheterization laboratories, urgent neuroimaging to exclude an unlikely intracranial hemorrhage may not be necessary if one can proceed directly to angiographic documentation of an acute arterial occlusion relevant to the presenting neurologic deficit. Acute neurologic deterioration after thrombolysis for acute myocardial infarction should be presumed to be an intracranial hemorrhage until proven otherwise. All thrombolytic, antithrombotic, and antiplatelet therapies should be stopped immediately while the patient is stabilized and blood is drawn for coagulation studies including platelet count, prothrombin time (PT), and activated clotting time (ACT) or activated partial thromboplastin time (aPTT). Reversal of the coagulopathy should not be delayed by awaiting confirmation with urgent neuroimaging as the hemorrhage can expand rapidly within several hours.
CONCLUSIONS, FUTURE DIRECTIONS Although peripheral neurologic complications of catheter access procedures are uncommon, they can result in considerable neurologic disability. Proceduralists should be aware of the relevant anatomy and early signs of nerve injury so that prompt diagnosis and treatment can ensue. The diagnosis and management of acute stroke complicating cardiac tests and procedures follows the paradigm for acute stroke in other settings but antithrombotic therapies may limit appropriateness for intravenous tPA therapy but still be amenable to mechanical neurointerventional revascularization options. The ideal angiography suite of the future is patientcentric and multipurpose, coordinating diagnostic and therapeutic strategies for multivascular disease, allowing for multispecialty collaboration, and, in the event of a neurologic complication of a cardiac procedure, facilitating the various treating physicians to converge efficiently upon the patient.
REFERENCES Al-Shekhlee A, Shapiro BE, Preston DC (2003). Iatrogenic complications and risks of nerve conduction studies and needle electromyography. Muscle Nerve 27: 517–526. Blanc P, Boussuges A, Henriette K et al. (2002). Iatrogenic cerebral air embolism: importance of an early hyperbaric oxygenation. Intensive Care Med 28: 559–563.
Chan YC, Morales JP, Reidy JF et al. (2008). Management of spontaneous and iatrogenic retroperitoneal haemorrhage: conservative management, endovascular intervention or open surgery? Int J Clin Pract 62: 1604–1613. Coˆte´ G, Denault A (2008). Transesophageal echocardiographyrelated complications. Can J Anaesth 55: 622–647. Davis K, Kennedy JW, Kemp HGJ et al. (1979). Complications of coronary arteriography from the Collaborative Study of Coronary Artery Surgery (CASS). Circulation 59: 1105–1112. Dawson DM, Fischer EG (1977). Neurologic complications of cardiac catheterization. Neurology 27: 496–497. Farouque HM, Tremmel JA, Raissi Shabari F et al. (2005). Risk factors for the development of retroperitoneal hematoma after percutaneous coronary intervention in the era of glycoprotein IIb/IIIa inhibitors and vascular closure devices. J Am Coll Cardiol 45: 363–368. Favaloro RG (1968). Saphenous vein autograft replacement of severe segmental coronary artery occlusion: operative techniques. Ann Thorac Surg 5: 334–339. Fuchs S, Stabile E, Kinnaird TD et al. (2002). Stroke complicating percutaneous coronary interventions: incidence, predictors, and prognostic implications. Circulation 106: 86–91. Gebel J, Sila CA, Sloan MA et al. (1998). Thrombolysisrelated intracranial hemorrhage. a radiographic analysis of 244 cases from the GUSTO-I trial. Stroke 29: 563–569. Heckmann JG, Lang CJG, Kindler K et al. (2000). Neurologic manifestations of cerebral air embolism as a complication of central venous catheterization. Crit Care Med 28: 1621–1625. Hogue Jr CW, Lappas GD, Cresswell LL et al. (1995). Swallowing dysfunction after cardiac operations. Associated adverse outcomes and risk factors including intraoperative transesophageal echocardiography. J Thorac Cardiovasc Surg 110: 517–522. Judkins MP (1967). Selective coronary arteriography. A percutaneous transfemoral technique. Radiology 89: 815–824. Kennedy AM, Grocott M, Schwartz MS et al. (1997). Median nerve injury: an underrecognised complication of brachial artery catheterization? J Neurol Neurosurg Psychiatry 63: 542–546. Kent KC, Moscucci M, Mansour KA et al. (1994). Retroperitoneal hematoma after cardiac catheterization: prevalence, risk factors, and optimal management. J Vasc Surg 20: 905–913. Khatri P, Taylor RA, Palumbo V et al. (2008). The safety and efficacy of thrombolysis for strokes after cardiac catheterization. J Am Coll Cardiol 51: 906–911. Kokosis G, Blueschke G, Blanton M et al. (2010). Acute carpal tunnel syndrome secondary to iatrogenic hemorrhage: a case report. Hand 5: 1–3. Kosmorsky G, Hanson MR, Tomsak RL (1988). Neuroophthalmologic complications of cardiac catheterization. Neurology 38: 483–485. Macon WL, Futrell JW (1973). Median nerve neuropathy after percutaneous puncture of the brachial artery in patients receiving anticoagulants. N Eng J Med 288: 1396.
NEUROLOGIC COMPLICATIONS OF CARDIAC TESTS AND PROCEDURES Martin SD, Sharrock NE, Mineo R et al. (1993). Acute exacerbation of carpal tunnel syndrome after radial artery cannulation. J Hand Surg Am 18: 455–458. Martin-Hirsch DP, Newbegin CJ (1995). Right vocal cord paralysis as a result of central venous catheterization. J Laryngol Otol 109: 1107–1108. Oezbek C, Heisel A, Voelk M et al. (1995). Management of stroke complicating cardiac catheterization with recombinant tissuetype plasminogen activator. Am J Cardiol 76: 733–735. Parmer SS, Carpenter JP, Fairman RM et al. (2006). Femoral neuropathy following retroperitoneal hemorrhage: case series and review of the literature. Ann Vasc Surg 20: 536–540. Peterson LH, Dripps RD, Risman G (1949). A method for recording the arterial pressure pulse and blood pressure in man. Am Heart J 37: 771–782. Poiseuille JLM (1828). Recherches sur la Force du Coeur Aortique. The`se no.166. Didot, Paris. Segal AZ, Abernethy WB, Palacios IF et al. (2001). Stroke as a complication of cardiac catheterization: risk factors and clinical features. Neurology 56: 975–977. Seldinger SI (1953). Catheter replacement of the needle in percutaneous arteriography – a new technique. Acta Radiol 39: 368–376.
47
Sloan MA, Sila CA, Mahaffey KW et al. (1998). Prediction of 30-day mortality among patients with thrombolysis-related intracranial hemorrhage. Circulation 98: 1376–1382. Smith DC, Mitchell DA, Peterson GW et al. (1989). Medial brachial fascial compartment syndrome: anatomic basis of neuropathy after transaxillary arteriography. Radiology 173: 149–154. Sones MF, Shirey EK, Proudfit WL et al. (1959). Cine coronary angiography. Circulation 20: 773. Vaitkus PT, Berlin JA, Schwartz JS et al. (1992). Stroke complicating acute myocardial infarction – a meta-analysis of risk modification by anticoagulation and thrombolytic therapy. Arch Intern Med 152: 2020–2024. Wallach SG (2004). Cannulation injury of the radial artery: diagnosis and treatment algorithm. Am J Crit Care 13: 315–319. Zwetsch G, Filipovic M, Skarvan K et al. (2001). Transient recurrent laryngeal nerve palsy after failed placement of a transesophageal echocardiographic probe in an anesthetized patient. Anesth Analg 92: 1422–1423. Zwicker JC, Sila CA (2002). MRI findings in transient cortical blindness after cardiac catheterization. Catheter Cardiovasc Interv 57: 47–49.
