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Enhancing the safety of intraoperative RBC salvage
664
Pasterson IS, Klausner JM, Pugatch R, et al: Noncardiogenic pulmonary edema after abdominal aortic aneurysm surgery. Ann Surg 209:231236,1989 Because limb &hernia in experimental animals is associated with pulmonary dysfunction related to increases in leukocytes and thromboxane A,, the authors studied 20 humans undergoing abdominal aortic aneurysmectomy to determine the pulmonary vascular effects of aortic clamping. Increases in thromboxane A, could be temporally related to increased pulmonary artery pressures and resistance. Subse quently, pulmonary dysfunction, described as increased peak inspiratory pressure and physiologic shunt, was noted at 4 to 8 hours postoperatively. Interstitial pulmonary edema was noted on chest radiograph, but pulmonary artery wedge pressures were normal postoperatively. However, there are several problems with the study: (1) mean arterial pressure was not controlled during aortic clamping to the same extent in all patients, raising concern about left ventricular failure; (2) increases in peak inspiratory pressure postoperatively could be related to reduced neuromuscular blockade, postoperative ileus, or retroperitoneal bleeding; (3) to verify the cause and effect, an inhibitor of thromboxane could be administered and the protocol repeated; and (4) colloid osmotic pressure, an important factor in transpulmonary vascular exchange, was not measured.
Matthay MA, Wiener-Kronish JP: Respiratory management after cardiac surgery. Chest 954244341989 Although this review synthesizes little new information, it presents the effects of anesthesia, thoracic surgery, and cardiopulmonary bypass on pulmonary function in a clear, concise fashion. During general anesthesia, functional residual capacity decreases 20% due to alterations in the shape and motion of diaphragm and chest wall. General anesthesia is also associated with atelectasis, inhibition of hypoxic pulmonary vasoconstriction, and alterations of hypoxic/hypercarbic respiratory drives. After cardiac surgery, pulmonary dysfunction may result from atelectasis (possibly secondary to gastric distention, transient hemidiaphragm paresis, or left lower lobe retraction during surgery), pulmonary capillary leak syndrome (secondary to protamine reactions, interstitial pulmonary edema, complement/platelet activation, leukocytosis, inadequate blood supply to alveolar epithelium, microcirculatory damage secondary to the hyperkalemia of the cardioplegia solution), exacerbation of pre-existing pulmonary disease, and pulmonary edema, among other etiologies. Despite these possibilities, respiratory failure is relatively infrequent after cardiac surgery. The authors recommend early extubation of uncomplicated patients, and more prolonged mechanical ventilatory support for 12 to 18 hours for patients with ventricular dysfunction or chronic lung disease. Their recommendations for management of cardiac patients with pulmonary edema, chronic lung disease, or diaphragmatic dysfunction affirm earlier reports.
CAROL L. LAKE
Grover CJ, Parham CS: Role of thromboxane A, in the control of myocardial 0, supply/ consumption balance and severity of ischemia during pacing-induced ischemia. Circ Res 64:575582,1989 The thromboxane/prostaglandin endoperoxide recep tor antagonist SQ 29,548 was used to minimize ischemia caused by atria1 pacing of anesthetized, open-chest dogs with left anterior descending coronary artery constriction. Pacing alone did not cause ST segment elevation, but when combined with left anterior descending coronary artery stenosis, significant ST segment elevation resulted. Thromboxane, a potent vasoconstrictor and platelet-aggregating agent, is released during myocardial ischemia. In this study, in which regional myocardial blood flow was determined using radioactive microspheres and oxygen consumption by measuring oxygen saturation of venous blood from the ischemia region, SQ 29,548 increased flow and oxygen consumption to the ischemic area without altering oxygen supply/consumption balance. The amount of ST segment elevation at 40 and 70 minutes after administration of SQ 29,548 at a dose of 0.2 mg/kg plus 0.2 mg/kg/hr was significantly less than after saline placebo. These results may be caused by improved subendocardial tlow, although SQ 29,548 probably has other anti-ischemic effects.
Shaddy RE, Judd VE, McGough EC: Continuous intravenous phenylephrine infusion for treatment of hypoxemia spells in tetralogy of Fallot. J Pediatrics 114:468-470,1989 Hypercyanotic episodes in children with tetralogy result from right ventricular infundibular spasm, decreased systemic vascular resistance, and right-to-left shunting across a ventricular septal defect. Various therapies have been used during these episodes, including morphine, oxygen, kneecheat position, @-adrenergic blockade, and a-adrenergic agonists. This multipatient case report describes successful use of phenylephrine to terminate hypercyanotic episodes unresponsive to the other methods, including @blockade in two of the four patients. Doses of 5 pg/kg were used, but the degree of systemic hypertension produced was not determined. Because of its efficacy in the reported cases, the authors suggest that phenylephrine be used early in hypercyanotic episodes rather than being reserved for refractory events.
Bull BS, Bull MH: Enhancing the safety of intraoperative RBC salvage. J Trauma 29:320325,1989 Autotransfusion devices do not remove all cellular elements completely except for erythrocytes during salvage/ centrifugation/washing cycles. Under certain hydraulic conditions in the Latham bowl of the centrifuge, activated platelets and leukocytes may adhere to the side of the bowl rather than rising to form a buffy coat on the surface of the erythrocyte layer. Normally the buffy coat on top of the erythrocytes rises to overflow into the discard container. If the
LITERATURE REVIEW
platelet/leukocyte deposit is not washed out, it may undergo autodigestion, causing activation of platelets and leukocytes with release of procoagulant and leukotactic substances. Conditions favoring the development of the platelet/ leukocyte deposit include aspiration of partially clotted blood from the surgical field and saline dilution of blood during the washing process. Methods to modify formation of the platelet/leukocyte layer include use of citrate rather than heparin as the anticoagulant, observation of the buffy coat formation and appropriate slowing of the centrifuge to allow it to flow into the waste bag, and minimization of saline dilution of salvaged blood. Citrate, unlike heparin, interferes with platelet adhesion and can eliminate the platelet/leukocyte deposit.
Regel G, Sturm JA, Neumann C, et al: Occlusion of bronchopleural fistula after lung injury: A new treatment by bronchoscopy. J Trauma 29:223-226,1989 Fibrin glue adhesive successfully occluded bronchopleural fistulas (BPF) in five patients after blunt chest trauma, according to this report. The authors review the various modalities used to treat BPF and suggest that bronchoscopic occlusion is indicated for patients with severe respiratory dysfunction, lung infection, and loss of more than 40% of mean minute volume. Details of the bronchoscopic fibrin glue occlusion techniques are: (1) clearing of blood and secretions from bronchi in the injured area; (2) location of the leaking segment and its occlusion with a bronchoscopically guided balloon-tipped catheter; (3) inflation of the balloon and injection of fibrin glue through the catheter lumen into the bronchus beyond the balloon; and (4) withdrawal of the balloon catheter after 120 seconds and inspection of the site for air leakage. Despite the small number of patients treated, the method seems promising, particularly in critically ill patients.
Kirshner DL, Kirshner RL, Heggeness LM, et al: Spinal cord ischemia: An evaluation of pharmacologic agents in minimizing paraplegia after aortic occlusion. J Vast Surg 9305-308, 1989 Methods used to protect neural tissue from ischemia include hypothermia, oxygen free radical scavengers, and barbiturates. In this study, the authors evaluated the use of various solutions infused into a thoracic aortic segment during 40 minutes of ischemia induced by cross-clamping. During the study, the dogs were anesthetized with 1.5% halothane. Solutions tested included lactated Ringer’s (15 mL/kg at 4“C) infused at 300 mm Hg pressure, thiopental, 20 mg/kg, diluted to 50 mL in water, superoxide dismutase, 75,000 U, given one minute before declamping, and combinations of hypothermia, barbiturate, and superoxide dismutase. Only the animals receiving combination therapy with hypo thermia, barbiturate, and superoxide dismutase had significantly less neurologic impairment than the controls. How-
665
ever, there are several methodologic problems, including the failure to provide continuous hypothermia during aortic occlusion, the possibility of pressure effects because the thiopental was administered by hand-held syringe while the crystalloid was given under 300 mm Hg pressure, and only brief prerelease infusion of superoxide dismutase, a substance undergoing rapid renal clearance. Nevertheless, the results suggest the possibility that cord injury can be modified by decreasing its metabolic rate and reducing reperfusion injury.
Turpie AGG, Robinson JG, Doyle DJ, et al: Comparison of high-dose with low-dose subcutaneous heparin to prevent left ventricular mural thrombosis in patients with acute transmural anterior myocardial infarction. N Engl J Med 320:352-357,1989 In this double-blind randomized trial of two doses of subcutaneous heparin given as prophylaxis against left ventricular myocardial thrombosis, a dose of 12,500 U every 12 hours provided significantly better protection than a dose of only 500 units. Two-dimensional echocardiography was used to assess the presence of intraventricular thrombus in 221 patients 10 days after acute infarction. Heparin levels were determined by protamine titration midway between the doses. The incidence of ventricular thrombus was 11% in the high-dose compared to 32% in the low-dose group. Plasma heparin concentrations were also greater with the higher dose (0.18 + 0.017 U/mL v 0.01 f 0.005; PC .OOOl). Heparin concentrations also correlated with the occurrence of thrombus. There was a trend, though not statistically significant, toward reduction in the incidence of nonhemorrhagic stroke with high-dose heparin prophylaxis. The incidence of hemorrhagic complications, however, did not differ between the two groups. Although the use of heparin in acute myocardial infarction remains controversial, this study supports its use.
Klautz RJM, Ottenkamp J, Buis-Liem TN, et al: Anatomic correction for transposition of the great arteries: First follow-up (38 patients). Pediatric Cardiology lO:l-9,1989 The authors report their initial experience with the arterial switch procedure for transposition of the great arteries performed between 1983 and 1985. Operative mortality was 0.64%. Among the complications noted during longterm followup (6 to 35 months) were residual left-toright shunt and the presence of a right ventricular-topulmonary artery gradient. Left ventricular fractional shortening and end-diastolic dimensions were normal in all patients. Although only 1 of the 38 patients had aortic insufficiency, the aortic root diameter was increased in relation to body weight, suggesting a potential for development of aortic regurgitation. These results corroborate the excellent results noted by other investigators for patients with transposition of the great arteries corrected by arterial switching.
Pasterson IS, Klausner JM, Pugatch R, et al: Noncardiogenic pulmonary edema after abdominal aortic aneurysm surgery. Ann Surg 209:231236,1989 Because limb &hernia in experimental animals is associated with pulmonary dysfunction related to increases in leukocytes and thromboxane A,, the authors studied 20 humans undergoing abdominal aortic aneurysmectomy to determine the pulmonary vascular effects of aortic clamping. Increases in thromboxane A, could be temporally related to increased pulmonary artery pressures and resistance. Subse quently, pulmonary dysfunction, described as increased peak inspiratory pressure and physiologic shunt, was noted at 4 to 8 hours postoperatively. Interstitial pulmonary edema was noted on chest radiograph, but pulmonary artery wedge pressures were normal postoperatively. However, there are several problems with the study: (1) mean arterial pressure was not controlled during aortic clamping to the same extent in all patients, raising concern about left ventricular failure; (2) increases in peak inspiratory pressure postoperatively could be related to reduced neuromuscular blockade, postoperative ileus, or retroperitoneal bleeding; (3) to verify the cause and effect, an inhibitor of thromboxane could be administered and the protocol repeated; and (4) colloid osmotic pressure, an important factor in transpulmonary vascular exchange, was not measured.
Matthay MA, Wiener-Kronish JP: Respiratory management after cardiac surgery. Chest 954244341989 Although this review synthesizes little new information, it presents the effects of anesthesia, thoracic surgery, and cardiopulmonary bypass on pulmonary function in a clear, concise fashion. During general anesthesia, functional residual capacity decreases 20% due to alterations in the shape and motion of diaphragm and chest wall. General anesthesia is also associated with atelectasis, inhibition of hypoxic pulmonary vasoconstriction, and alterations of hypoxic/hypercarbic respiratory drives. After cardiac surgery, pulmonary dysfunction may result from atelectasis (possibly secondary to gastric distention, transient hemidiaphragm paresis, or left lower lobe retraction during surgery), pulmonary capillary leak syndrome (secondary to protamine reactions, interstitial pulmonary edema, complement/platelet activation, leukocytosis, inadequate blood supply to alveolar epithelium, microcirculatory damage secondary to the hyperkalemia of the cardioplegia solution), exacerbation of pre-existing pulmonary disease, and pulmonary edema, among other etiologies. Despite these possibilities, respiratory failure is relatively infrequent after cardiac surgery. The authors recommend early extubation of uncomplicated patients, and more prolonged mechanical ventilatory support for 12 to 18 hours for patients with ventricular dysfunction or chronic lung disease. Their recommendations for management of cardiac patients with pulmonary edema, chronic lung disease, or diaphragmatic dysfunction affirm earlier reports.
CAROL L. LAKE
Grover CJ, Parham CS: Role of thromboxane A, in the control of myocardial 0, supply/ consumption balance and severity of ischemia during pacing-induced ischemia. Circ Res 64:575582,1989 The thromboxane/prostaglandin endoperoxide recep tor antagonist SQ 29,548 was used to minimize ischemia caused by atria1 pacing of anesthetized, open-chest dogs with left anterior descending coronary artery constriction. Pacing alone did not cause ST segment elevation, but when combined with left anterior descending coronary artery stenosis, significant ST segment elevation resulted. Thromboxane, a potent vasoconstrictor and platelet-aggregating agent, is released during myocardial ischemia. In this study, in which regional myocardial blood flow was determined using radioactive microspheres and oxygen consumption by measuring oxygen saturation of venous blood from the ischemia region, SQ 29,548 increased flow and oxygen consumption to the ischemic area without altering oxygen supply/consumption balance. The amount of ST segment elevation at 40 and 70 minutes after administration of SQ 29,548 at a dose of 0.2 mg/kg plus 0.2 mg/kg/hr was significantly less than after saline placebo. These results may be caused by improved subendocardial tlow, although SQ 29,548 probably has other anti-ischemic effects.
Shaddy RE, Judd VE, McGough EC: Continuous intravenous phenylephrine infusion for treatment of hypoxemia spells in tetralogy of Fallot. J Pediatrics 114:468-470,1989 Hypercyanotic episodes in children with tetralogy result from right ventricular infundibular spasm, decreased systemic vascular resistance, and right-to-left shunting across a ventricular septal defect. Various therapies have been used during these episodes, including morphine, oxygen, kneecheat position, @-adrenergic blockade, and a-adrenergic agonists. This multipatient case report describes successful use of phenylephrine to terminate hypercyanotic episodes unresponsive to the other methods, including @blockade in two of the four patients. Doses of 5 pg/kg were used, but the degree of systemic hypertension produced was not determined. Because of its efficacy in the reported cases, the authors suggest that phenylephrine be used early in hypercyanotic episodes rather than being reserved for refractory events.
Bull BS, Bull MH: Enhancing the safety of intraoperative RBC salvage. J Trauma 29:320325,1989 Autotransfusion devices do not remove all cellular elements completely except for erythrocytes during salvage/ centrifugation/washing cycles. Under certain hydraulic conditions in the Latham bowl of the centrifuge, activated platelets and leukocytes may adhere to the side of the bowl rather than rising to form a buffy coat on the surface of the erythrocyte layer. Normally the buffy coat on top of the erythrocytes rises to overflow into the discard container. If the
LITERATURE REVIEW
platelet/leukocyte deposit is not washed out, it may undergo autodigestion, causing activation of platelets and leukocytes with release of procoagulant and leukotactic substances. Conditions favoring the development of the platelet/ leukocyte deposit include aspiration of partially clotted blood from the surgical field and saline dilution of blood during the washing process. Methods to modify formation of the platelet/leukocyte layer include use of citrate rather than heparin as the anticoagulant, observation of the buffy coat formation and appropriate slowing of the centrifuge to allow it to flow into the waste bag, and minimization of saline dilution of salvaged blood. Citrate, unlike heparin, interferes with platelet adhesion and can eliminate the platelet/leukocyte deposit.
Regel G, Sturm JA, Neumann C, et al: Occlusion of bronchopleural fistula after lung injury: A new treatment by bronchoscopy. J Trauma 29:223-226,1989 Fibrin glue adhesive successfully occluded bronchopleural fistulas (BPF) in five patients after blunt chest trauma, according to this report. The authors review the various modalities used to treat BPF and suggest that bronchoscopic occlusion is indicated for patients with severe respiratory dysfunction, lung infection, and loss of more than 40% of mean minute volume. Details of the bronchoscopic fibrin glue occlusion techniques are: (1) clearing of blood and secretions from bronchi in the injured area; (2) location of the leaking segment and its occlusion with a bronchoscopically guided balloon-tipped catheter; (3) inflation of the balloon and injection of fibrin glue through the catheter lumen into the bronchus beyond the balloon; and (4) withdrawal of the balloon catheter after 120 seconds and inspection of the site for air leakage. Despite the small number of patients treated, the method seems promising, particularly in critically ill patients.
Kirshner DL, Kirshner RL, Heggeness LM, et al: Spinal cord ischemia: An evaluation of pharmacologic agents in minimizing paraplegia after aortic occlusion. J Vast Surg 9305-308, 1989 Methods used to protect neural tissue from ischemia include hypothermia, oxygen free radical scavengers, and barbiturates. In this study, the authors evaluated the use of various solutions infused into a thoracic aortic segment during 40 minutes of ischemia induced by cross-clamping. During the study, the dogs were anesthetized with 1.5% halothane. Solutions tested included lactated Ringer’s (15 mL/kg at 4“C) infused at 300 mm Hg pressure, thiopental, 20 mg/kg, diluted to 50 mL in water, superoxide dismutase, 75,000 U, given one minute before declamping, and combinations of hypothermia, barbiturate, and superoxide dismutase. Only the animals receiving combination therapy with hypo thermia, barbiturate, and superoxide dismutase had significantly less neurologic impairment than the controls. How-
665
ever, there are several methodologic problems, including the failure to provide continuous hypothermia during aortic occlusion, the possibility of pressure effects because the thiopental was administered by hand-held syringe while the crystalloid was given under 300 mm Hg pressure, and only brief prerelease infusion of superoxide dismutase, a substance undergoing rapid renal clearance. Nevertheless, the results suggest the possibility that cord injury can be modified by decreasing its metabolic rate and reducing reperfusion injury.
Turpie AGG, Robinson JG, Doyle DJ, et al: Comparison of high-dose with low-dose subcutaneous heparin to prevent left ventricular mural thrombosis in patients with acute transmural anterior myocardial infarction. N Engl J Med 320:352-357,1989 In this double-blind randomized trial of two doses of subcutaneous heparin given as prophylaxis against left ventricular myocardial thrombosis, a dose of 12,500 U every 12 hours provided significantly better protection than a dose of only 500 units. Two-dimensional echocardiography was used to assess the presence of intraventricular thrombus in 221 patients 10 days after acute infarction. Heparin levels were determined by protamine titration midway between the doses. The incidence of ventricular thrombus was 11% in the high-dose compared to 32% in the low-dose group. Plasma heparin concentrations were also greater with the higher dose (0.18 + 0.017 U/mL v 0.01 f 0.005; PC .OOOl). Heparin concentrations also correlated with the occurrence of thrombus. There was a trend, though not statistically significant, toward reduction in the incidence of nonhemorrhagic stroke with high-dose heparin prophylaxis. The incidence of hemorrhagic complications, however, did not differ between the two groups. Although the use of heparin in acute myocardial infarction remains controversial, this study supports its use.
Klautz RJM, Ottenkamp J, Buis-Liem TN, et al: Anatomic correction for transposition of the great arteries: First follow-up (38 patients). Pediatric Cardiology lO:l-9,1989 The authors report their initial experience with the arterial switch procedure for transposition of the great arteries performed between 1983 and 1985. Operative mortality was 0.64%. Among the complications noted during longterm followup (6 to 35 months) were residual left-toright shunt and the presence of a right ventricular-topulmonary artery gradient. Left ventricular fractional shortening and end-diastolic dimensions were normal in all patients. Although only 1 of the 38 patients had aortic insufficiency, the aortic root diameter was increased in relation to body weight, suggesting a potential for development of aortic regurgitation. These results corroborate the excellent results noted by other investigators for patients with transposition of the great arteries corrected by arterial switching.