RSS-Feed abonnieren
DOI: 10.1055/s-2000-9640
Sepsis and Catecholamine Support are the Major Risk Factors for Critical Illness Polyneuropathy after Open Heart Surgery[1]
Publikationsverlauf
Publikationsdatum:
31. Dezember 2000 (online)
Background: Critical illness polyneuropathy (CIP) remains a problem after open heart surgery. Recently, we reported about a retrospectively performed study pointing out that sepsis, the application of higher amounts of catecholamines and intervention such as chronic venovenous hemodiafiltration may be involved in the onset of CIP. A prospectively performed study is presented in order to evaluate the significance of risk factors initially after open heart surgery. Methods: From June 1997 until September 1998, patients undergoing open heart surgery and being ventilated beyond 3 days were prospectively enrolled in the study and underwent a standard protocol of electromyographic investigation in order to determine CIP. Several items were recorded: amount of catecholamines, serum levels of urea, creatinine, albumine, and glucose. The duration of sepsis and chronic venovenous hemodiafiltration were reevaluated. Additionally the age, the left ventricular enddiastolic pressure prior to the operation, the time of ICU stay and the time of ventilatory support were compared. Results: Within the observation period, 37 adult patients could be enrolled in the study, whereas 12 patients did develop CIP and 7 patients did not. Patients developing CIP required significantly different amounts of epinephrine (0.17 ± 0.02 vs. 0.09 ± 0.01 mg/kg/day, p < 0.05, t-test) higher amounts of norepinephrine (0.06 ± 0.02 vs. 0.02 ± 0.01 mg/kg/day, p < 0.05, t-test), and lesser dosages of dobutamine (2.2 ± 0.5 vs. 4.9 ± 0.7, p < 0.05, t-test). After cardiac surgery, the plasma levels of urea was initially significantly elevated in patients developing CIP (127.4 ± 10.5 vs 97.3 ± 18.5, p < 0.05, t-test) Patients suffering from CIP stayed significantly longer in the ICU (40.3 ± 11.7 vs. 19.6 ± 11.3 days, p < 0.05 t-test) with an extended time of ventilator support. (769.6 ± 205.0 vs 295.0 ± 134.0 hours, p < 0.05, t-test). Patients of the CIP group were suffering significant longer from sepsis than patients without CIP. Conclusions: Sepsis and catecholamine support and an increased level of urea were associated with the development of CIP. The prevention of sepsis and a modulation of the catecholamine support in order to improve microcirculatory flow may reduce the onset of CIP in patients undergoing open heart surgery.
Key words:
Critical illness polyneuropathy - - Cardiac surgery - - Microcirculation - - Sepsis - - Catecholamine support - - Microcirculatory flow
1 This work was presented in part at the 28th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery, Dresden, February 24 to 27, 1999
References
- 1 Jones E L, Weintraub W S, Craver J M, Guyton R A, Cohen C. Coronary bypass surgery: Is the operation different today. J Thorac Cardiovasc Surg.. 1991; 101 108-15
- 2 Bolton C F, Young G B, Zochodne D W. The neurological complications of sepsis. Ann Neurol.. 1993; 33 94-100
- 3 Bolton C F, Laverty D A, Brown J D, Witt N J, Hahn A F, Sibbald W J. Critically ill polyneuropathy: electrophysiological studies and differentiation from Guillain-Barre'syndrome. J Neurot Neurosurg Psychiat.. 1986; 49 563-73
- 4 Hund E, Genzwürker H, Böhrer H, Jakob H, Thiele R, Hacke W. Predominant involvement of motor fibres in patients with critical illness polyneuropathy. Br J Anaesth.. 1996; 78 274-8
- 5 Bolton C F. Sepsis and the systemic inflammatory response syndrome: Neuromuscular manifestations. Crit Care Med.. 1996; 24 1408-16
- 6 Leijten F SS, de Weerd A W. Criticall illness polyneuropathy. A review of the literature, definition and pathophysiology. Clin Neurol Neurosurgery.. 1994; 96 10-9
- 7 Hund E-F, Fogel W, Krieger D, DeGeorgia M, Hacke W. Critical illness polyneuropathy: Clinical findings and outcome of a frequent cause of neuromuscular weaning failure. Crit Care Med.. 1996; 24 1328-33
- 8 Hund E-F. Neuromuscular complications in the ICU: the spectrum of critical illness-related conditions causing muscular weakness and weaning failure. J Neurol Sci.. 1996; 136 10-6
- 9 McLeod J G. Investigation of peripheral neuropathy. J Neurol Neurosurg Psych.. 1995; 58 274-83
- 10 Kimura J. Nerve conduction studies and electromyography and neurophysiologic recording. In: Saunders, ed. Peripheral Neuropathy. Philadelphia 1993: 597-644
- 11 Thiele R I, Jakob H, Hund E, Genzwuerker H, Herold U, Schweiger P, Hagl S. Critical illness polyneuropathy: a new iatrogenically induced syndrome after cardiac surgery?. Eur J Cardio-thorac Surg.. 1997; 12 826-35
- 12 Bone R C, Balk R A, Cerra F B. et al . Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Chest.. 1992; 101 1644-55
- 13 Waldhausen E, Keser G. Lähmungen durch Kohlenhydrate unter der Intensivtherapie. Anaesthesist.. 1991; 40 332-8
- 14 Waldhausen E, Mingers B, Lippers P, Keser G. Critical illness polyneuropathy due to parenteral nutrition. Intensive Care Med.. 1997; 23 922-3
- 15 Yawata Y, Craddock P, Hebbel R, Howe R, Silvis S, Jacob H. Hyperalimentation hypophosphatemia: hematologic-neurologic dysfunction due to ATP depletion. Clin Res.. 1973; 21 729
- 16 Spencer P S, Sabri M I, Schaumburg H H, Moore C L. Does a defect of energy metabolism in the nerve fiber underlie axonal degeneration in polyneuropathies?. Ann Neurology.. 1979; 5 501-7
- 17 Berek K, Margreiter J, Willeit J, Berek A, Schmutzhand E, Mutz N J. Polyneuropathies in critically all patients: a prospective evaluation. Intensive Care Med.. 1996; 22 849-55
- 18 Bolton C F, Young G B. Critical illness polyneuropathy due to parenteral nutrition. Intensive Care Med.. 1997; 23 924-5
- 19 Witt N J, Zochodne D W, Bolton C F. et al . Peripheral nerve function in sepsis and multiple organ failure. Chest.. 1991; 99 176-84
- 20 Weissman C. The metabolic response to stress: an overview and update. Anesthesiology.. 1990; 73 308-27
- 21 Wilmore D W. Catabolic illness. Strategies for enhancing recovery. N Engl J Med.. 1991; 325 695-702
- 22 Hoffmann J N, Hartl W H, Deppisch R, Faist E, Jochum M, Inthorn D. Hemofiltration in human sepsis: evidente for elimination of immunmodulatory substances. Kidney Int.. 1995; 48 1563-70
- 23 Bolton C F, Gilbert J J, Hahn A F, Sibbald W J. Polyneuropathy in critically ill patients. J Neurol Neurosurg Psychiat.. 1984; 47 1223-31
- 24 Bolton C F. Neuromuscular complications of sepsis. Intensive Care Med.. 1993; 19 58-63
- 25 Thijs L G, Schneider A J, Groeneveld A BJ. The haemodynamics of septic shock. Intensive Care Med.. 1990; 16 182-6
- 26 Bihari D, Smithies M, Gimson A, Tinker J. The effects of vasodilation with prostacyclin on oxygen delivery and uptake in critically ill patients. N Engl J Med.. 1987; 317 397-403
1 This work was presented in part at the 28th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery, Dresden, February 24 to 27, 1999
Dr. Rudolf I. Thiele
Institute of Plastination
Rathausstraße 18
69126 Heidelberg
Germany
Telefon: ++49-6221-331125
Fax: ++49-6221-331124
eMail: r.thiele@plastination.com