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1 From the Department of Anesthesia, Kelowna General Hospital, Kelowna, British Columbia, Canada.
Address correspondence to: Dr. J. Anne Webster, Department of Anesthesia, Victoria General Hospital, One Hospital Way, Victoria, British Columbia V8Z 6R5, Canada. Phone: 250-727-4212; Fax: 250-721-9020; E-mail: jawebster{at}shaw.ca
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Clinical features: A 34-yr-old gravida 2, para 1 patient presented at 29 weeks gestation with dyspnea, orthopnea, chest pain, and cough. Investigations showed an anterior mediastinal mass due to Hodgkin’s disease. A course of vinblastine at 31 weeks gestation resulted in symptomatic improvement but at 34 weeks gestation she developed an acute cardiac tamponade for which pericardial window drainage was required. Additional help and equipment were assembled in case of cardiopulmonary deterioration. Intra-arterial pressure and continuous fetal monitoring were established and iv access was secured in both arms and the left foot. After awake fibreoptic intubation, spontaneous ventilation was maintained. Anesthesia consisted of local anesthetic infiltration of the anterior chest wall, supplemented with fentanyl, midazolam, and ketamine. The patient remained stable, was extubated fully awake, and then monitored in an intensive care area.
Conclusion: This patient presented with acute cardiac tamponade and an anterior mediastinal mass in late pregnancy, an unusual combination of challenges that requires a careful approach to anesthetic management.
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A second anesthesiologist, obstetrician, and pediatrician were recruited and equipment was assembled for rigid bronchoscopy and Cesarean delivery if necessary. The patient was given 30 mL of sodium citrate and brought to the operating room in the sitting position receiving oxygen by mask. Pulse oximetry, electrocardiography, and continuous fetal monitoring were initiated. In addition to an existing arm iv access site, large bore iv catheters were established in the opposite arm and left foot. An arterial pressure monitoring catheter was placed in the right radial artery under local anesthesia. Incremental doses of midazolam and fentanyl were given while topical anesthesia was applied to the airway. Airway anesthesia was accomplished with gargled, then expelled, topical 4% lidocaine, followed by 2% lidocaine spray applied to the pharynx and 3 mL 2% lidocaine administered subglottically through the fibreoptic bronchoscope. Awake fibreoptic intubation was followed by bronchoscopy, which revealed no obvious airway compression. End-tidal gas monitoring was instituted. Spontaneous ventilation was maintained with gentle assistance as necessary to control hypercapnia as seen on end-tidal gas measurements. Small doses of iv ketamine were titrated to achieve amnesia and analgesia in an anxious patient. The patient was placed gradually in a recumbent position with her head slightly elevated and her right side tilted down. The incision site was infiltrated with approximately 7 mL of 2% carbonated lidocaine. Sevoflurane (up to 1%) was used in response to movement and increased blood pressure to reduce the possibility of patient awareness. During the procedure 3 L of iv crystalloid solution were infused. When the surgeon opened the pericardium to drain 425 mL of sanguineous fluid, the systolic arterial pressure increased 10 to 15 mmHg. A total of 110 mg of ketamine, 3 mg of midazolam and 150 µg of fentanyl had been given by the completion of the surgery. No significant airway obstruction, hemodynamic decompensation, or fetal distress occurred. The patient was extubated when fully awake and was monitored in an intensive care area. Four days later labour was induced. Effective epidural analgesia was established early in labour to allow for rapid provision of regional anesthesia in the event of emergency Cesarean section. The patient proceeded to an uneventful vaginal delivery of a healthy female infant and resumed treatment for Hodgkin’s disease the following day.
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In cardiac tamponade, an increase in endogenous catecholamines causes increases in heart rate, contractility, and systemic vascular resistance. This compensates for impaired ventricular diastolic filling and the resultant decreases in stroke volume, blood pressure, and cardiac output.1–3 Right atrial or right ventricular collapse in the presence of a pericardial effusion on echocardiography confirms the diagnosis of tamponade.1 In the presence of tamponade, failure to maintain heart rate, contractility, and ventricular filling pressures may result in dramatic decreases in cardiac output, causing cardiovascular collapse.1 Since most general anesthetic agents cause myocardial depression and systemic vasodilation, and positive pressure ventilation decreases venous return, local anesthesia is recommended for relief of tamponade that is severe enough to cause hypotension.1,16,17 In less severe cases, several authors suggest the use of ketamine for analgesia or anesthesia because ketamine causes less respiratory depression and tends to support heart rate, contractility, and systemic vascular tone compared to other drugs.1,2,18 Spontaneous ventilation and intravascular volume expansion may help maintain and enhance venous return and hence help maintain and enhance ventricular filling pressures.1–3
An anterior mediastinal mass may cause sudden catastrophic obstruction of major airways or major vessels if general anesthesia is induced.4–15 These complications can occur even in patients who are asymptomatic while awake.6,7,12–14 Airway obstruction, which can occur at any stage of anesthesia,7,9,12,13,15 is the most common problem encountered.9 The causes of airway obstruction are several: the supine position allows the weight of the mass to lie directly over the major airways;13,15 anesthesia causes a decrease in chest wall13 and bronchial muscle tone thereby decreasing the tethering effect on airway diameter;4,12,15 loss of spontaneous ventilation decreases the airway dilating effect of negative intrathoracic pressure;4,12,15 and positive pressure ventilation paradoxically may worsen the obstruction by causing increased post-obstructive turbulence.15 Attempts to identify patients at risk of perioperative airway obstruction have used CT measurements of airway cross-sectional areas4,7,14 and flow volume loops.12,14 In children, Azizkhan et al. found a correlation between severity of symptoms and presence and degree of airway compression on CT scan. Based on his series of 50 children he suggested that a 35% or greater decrease in airway cross-sectional area indicated significant risk and that general anesthesia should be avoided in these patients.4 A flow volume loop, however, may reveal a decreased peak expiratory flow rate and a plateau shape to the expiratory limb of the loop, indicating significant intrathoracic airway obstruction,13 despite lack of CT evidence of airway narrowing.12,14 Neuman points this out and emphasizes the value of the flow volume loop as a dynamic measure of a dynamic process as opposed to a static measure as provided by CT scanning.12
By mechanisms similar to those for airway obstruction, general anesthesia in the presence of an anterior mediastinal mass can precipitate cardiac, superior vena cava, and pulmonary artery compression, although these problems are less common and less well characterized in the literature. Compression of major vessels can cause hypoxemia, hypotension, and cardiovascular collapse.6,9,13 Mass effects on major vessels may be evaluated by supine and upright echocardiography.5,6,8,12
Management of anesthesia in the presence of an anterior mediastinal mass is directed toward avoiding critical airway or major vessel obstruction. Lower limb iv access allows effective fluid and drug administration in the event of superior vena cava obstruction6,7,9,13 and continuous invasive arterial pressure monitoring facilitates prompt detection of cardiovascular compromise. Where possible, local, or regional anesthesia, provided the effect of vasodilation on venous return is considered, should be used.5,7,8,10,12–14,19 Ketamine is useful for sedation or anesthesia because it causes less respiratory depression and maintains chest wall and peripheral vascular tone better than most other agents.9,18,19 Spontaneous ventilation should be maintained as much as possible.4,5,12–15,19 If the site of airway compression identified on CT scan is relatively localized, it may be amenable to bypass with an endotracheal tube or rigid bronchoscope.4,7,9 Head up, lateral, or prone positioning can help shift the weight of the mass away from vital structures.4–6,9,13 In patients with significant CT, flow volume loop, or echocardiographic abnormalities, in whom general anesthesia is required, preoperative preparation for immediate cardiopulmonary bypass should be considered.4–7,9,12,13,20 If time permits, preoperative chemotherapy or radiotherapy may be used to shrink malignant anterior mediastinal masses to make anesthesia safer.9,13,15 However, this may seriously impair the ability to make an accurate tissue diagnosis if one has not been obtained.12,14,15
Since the patient was pregnant we intubated her awake to secure and protect her airway prior to obtunding the central nervous system with ketamine18 and sevoflurane. The positioning we used not only facilitated left anterior mini-thoracotomy, but shifted the uterus away from the inferior vena cava, allowing us to avoid compounding impaired venous return due to possible compression of the superior vena cava. In the event of cardiopulmonary deterioration or fetal distress, we were prepared for immediate Cesarean delivery to facilitate resuscitation of mother and infant.
In summary this patient presented with a symptomatic anterior mediastinal mass in late pregnancy and then developed acute cardiac tamponade requiring surgical drainage. Our approach of direct arterial pressure and fetal monitoring, use of lower limb iv access, awake intubation, partial head up and right lateral positioning, use of ketamine and local anesthesia, and maintenance of spontaneous ventilation was designed to minimize the potential adverse pathophysiologic consequences of anesthesia in the context of these three problems.
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Revision received June 11, 2003. Accepted for publication March 25, 2003.
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2 Lake CL. Anesthesia and pericardial disease. Anesth Analg 1983; 62: 431–43.
3 Stoelting RK, Dierdorf SF. Pericardial diseases. In: Stoelting RK, Dierdorf SF (Eds.). Anesthesia and Co-Existing Disease, 4th ed. New York: Churchill Livingston Inc.; 2002: 135–42.
4 Azizkhan RG, Dudgeon DL, Buck JR, et al. Life-threatening airway obstruction as a complication to the management of mediastinal masses in children. J Pediatr Surg 1985; 20: 816–22.[Medline]
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16 Breen PH, MacVay MA. Pericardial tamponade: a case for awake endotracheal intubation (Letter). Anesth Analg 1996; 83: 658.
17 Stanley TH, Weidauer HE. Anesthesia for the patient with cardiac tamponade. Anesth Analg 1973; 52: 110–4.
18 Stoelting RK. Nonbarbiturate induction drugs. In: Stoelting R (Ed.). Pharmacology and Physiology in Anesthetic Practice, 3rd ed. Philadelphia, Pennsylvania: Lippincott–Raven; 1999: 104–57.
19 Tinker TD, Crane DL. Safety of anesthesia for patients with anterior mediastinal masses: 1 (Letter). Anesthesiology 1990; 73: 1060.[Medline]
20 Chan YK, Ng KP, Chiu CL, Rajan G, Tan KC, Lim YC. Anesthetic management of a parturient with superior vena cava obstruction for cesarean section. Anesthesiology 2001; 94: 167–9.[Medline]
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