Anesth Analg 2004;98:872-873
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000106960.29644.69
LETTERS TO THE EDITOR
Vasopressin in Acute Brain Injury: A Note of Caution
Peter Bradley, MD,
Magdalena Hiler, MD, and
David Menon, MD
Department of Anaesthesia, University of Cambridge, Cambridge, United Kingdom
To the Editor:
While hypotension after acute brain injury is dangerous, we remain concerned that the use of vasopressin, as described by Yeh et al. (1), may contribute to cerebral ischemia.
Yeh et al. suggest that vasopressin may have vasodilatory actions in the brain. However, experimental studies are equivocal (2), and there are no data from human studies. While some patients with acute brain injury may need "second line" vasopressors, the possibility of cerebral vasoconstriction or reduction in blood flow remains a concern. Failure to exclude such side effects may result in potentiation of the secondary brain injury that we are trying to avoid. These observations are underlined by our recent experience with terlipressin, a vascular specific analog of vasopressin, in patients with acute brain injury and norepinephrine resistant hypotension. While terlipressin improved cerebral perfusion pressure and reduced norepinephrine requirements, it had no effect on intracranial pressure or middle cerebral artery flow velocities, measured using transcranial Doppler ultrasound. Until the safety of such agents is supported by formal clinical studies, we believe that their use in patients with acute brain injury should always be accompanied by monitors of cerebral blood flow and cerebrovascular adequacy such as transcranial Doppler ultrasound and jugular bulb oximetry.
References
- Yeh C-C, Wu C-T, Lu C-H et al. Early use of small-dose vasopressin for unstable hemodynamics in an acute brain injury patient refractory to catecholamine treatment: a case report. Anesth Analg 2003; 97: 577–9.[Abstract/Free Full Text]
- Faraci FM. Effects of endothelin and vasopressin on cerebral blood vessels. Am J Physiol Heart Circ Physiol 1989; 257: 799–803.
Response
Chun-Chang Yeh, MD,
Ching-Tang Wu, MD, and
Chih-Shung Wong, MD PhD
Department of Anesthesiology, Tri-Service General Hospital and National Defense Medical Center, Taipei, Taiwan, Republic of China
In Response:
We would like to thank Bradley et al. for their comments. We had demonstrated that employing a low-dose vasopressin infusion (0.01–0.04 IU/min) successfully restored patient’s hemodynamic stability and reduced the dose of catecholamines in an acute brain injury patient with catecholamine-resistant vasodilatory shock, neurogenic pulmonary edema, and myocardial dysfunction (1). In order to preserve cardiocirculatory homeostasis in patients who suffered advanced shock and pulmonary edema after fluid resuscitation, hyperventilation with PEEP and conventional high-dose vasopressors therapy, adding of low-dose of vasopressin can be an alternative therapy, in addition to catecholamines, for refractory vasodilatory shock, as many articles suggested (2,3). Currently, there are limited data on possible side effects of a continuous low-dose vasopressin therapy in vasodilatory shock. The effects of vasopressin in the brain vessels are a worthy issue to be investigated. As Dr. Bradley’s comments, both vasodilation and vasoconstriction had been reported that depended on the dosage and experimental conditions employed (4,5). From the clinical viewpoints, early establishment of adequate cerebral perfusion pressure (CPP) and stabilization of hemodynamics are important considerations in severe acute brain injury patients. Our report was consistent with Dr. Bradley’s clinical finding that terlipressin improved CPP and reduced norepinephrine requirements. In our case, no cerebral flow was measured by TCD. However, in our patient, we monitored the central venous pressure (CVP) during operation, after co-administration of low-dose vasopressin, dopamine and norepinephrine infusion were reduced markedly, mean artery pressure (MAP) rose, and there was no change in CVP; thus this means that CPP (MAP-CVP) was increased. Moreover, low-dose vasopressin has been demonstrated to cause pulmonary artery dilation, and thus decrease pulmonary artery pressure (PAP), in both humans and animals (6,7). A reduction of catecholamine dosage, after the adding of low-dose vasopressin infusion, may also contribute to the reduction of PAP, and thus improved the pulmonary edema of this patient.
We agree on the application of transcranial Doppler (TCD) ultrasound or jugular bulb oximetry to monitor cerebral blood flow in neurosurgical patient during vasopressin infusion. However, since it is difficult to use TCD during urgent craniectomy, we suggested using TCD in post-NICU care. Although there was no human data describing the effect of low-dose vasopressin in CPP, we are looking forward to seeing Bradley et al.’s investigation that may further support the use of vasopressin as a second line vasopressor in patients with severe acute brain injury accompanied by neurogenic pulmonary edema.
References
- Yeh CC, Wu CT, Lu CH, et al. Early use of small-dose vasopressin for unstable hemodynamics in an acute brain injury patient refractory to catecholamine treatment: a case report. Anesth Analg 2003; 97: 577–9.
- Dunser MW, Wenzel V, Mayr AJ, et al. Management of vasodilatory shock: defining the role of arginine vasopressin. Drugs 2003; 63: 237–56.[Web of Science][Medline]
- Dunser MW, Mayr AJ, Ulmer H, et al. Arginine vasopressin in advanced vasodilatory shock: a prospective, randomized, controlled study. Circulation 2003; 107: 2313–9.[Abstract/Free Full Text]
- Takayasu M, Kajita Y, Suzuki Y, et al. Oxyhemoglobin enhancement of vasopressin-induced constriction in rat cerebral arterioles. Life Sci 1995; 56: PL123–7.[Medline]
- Suzuki Y, Satoh S, Oyama H, et al. Vasopressin mediated vasodilation of cerebral arteries, J Auton Nerv Syst 1994; 49 (suppl): S129–32.
- Eichinger MR, Walker BR. Enhanced pulmonary arterial dilation to arginine vasopressin in chronically hypoxic rats. Am J Physiol 1994; 267: H2413–9.
- Wang HJ, Wong CS, Chiang CY, et al. Low-dose vasopressin infusion can be an alternative in treating patients with refractory septic shock combined with chronic pulmonary hypertension-case report. Acta Anaesthesiol Sin 2003; 41; 77–80.
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