Anesth Analg 2003;97:577-579
© 2003 International Anesthesia Research Society
NEUROSURGICAL ANESTHESIA
Early Use of Small-Dose Vasopressin for Unstable Hemodynamics in an Acute Brain Injury Patient Refractory to Catecholamine Treatment: A Case Report
Chun-Chang Yeh, MD,
Ching-Tang Wu, MD,
Chueng-He Lu, MD,
Chih-Ping Yang, MD, and
Chih-Shung Wong, MD PhD
Department of Anesthesiology, Tri-Service General Hospital and National Defense Medical Center, Taipei, Taiwan, Republic of China
Address correspondence and reprint requests to Dr. Chih-Shung Wong, Department of Anesthesiology, Tri-Service General Hospital and National Defense Medical Center, #325, Section 2, Chenggung Rd., Neihu 114, Taipei, Taiwan, Republic of China. Address e-mail to w82556{at}ndmctsgh.edu.tw
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Abstract
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IMPLICATIONS: Small-dose IV vasopressin infusion may be beneficial in acute brain injury patients with unstable hemodynamics who are refractory to fluid resuscitation and catecholamine vasopressors.
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Introduction
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Brain edema and increased intracranial pressure (ICP) are frequently encountered in acute brain injury patients. In addition, associated cardiac injury and neurogenic pulmonary edema may cause hypotension and hypoxemia, making the outcome worse. Reducing ICP and maintaining adequate perfusion of the brain and other major organs provides an opportunity for intervention before refractory hypoxia and hypotension develop (1). Vasopressors may increase neurogenic pulmonary edema and cause cardiac arrhythmias in acute brain injury patients with unstable hemodynamics (2). Vasopressin has been successfully used to reverse intractable hypotension in patients with vasodilatory shock (3), such as septic shock, postcardiotomy shock, and hemorrhagic shock. In this report, we describe a case with spontaneous cerebellar and subarachnoid hemorrhage complicated by pulmonary edema, myocardial dysfunction, and hypotension, which were refractory to fluid resuscitation and catecholamine vasopressors but improved by small-dose vasopressin infusion. The patient was transferred to the general ward 12 days after the operation.
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Case Report
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A 59-yr-old man was admitted to our emergency room. On admission, the Glasgow Coma Scale (GCS) score was 4 with stable hemodynamics. Sudden onset of cardiovascular collapse was noted and cardiopulmonary cerebral resuscitation (CPR) was performed immediately. On tracheal intubation, massive pinkish foaming sputum was noted, and the chest radiograph showed pulmonary edema. The brain computerized tomogram showed a huge hematoma in the left cerebellar hemisphere, together with subarachnoid hemorrhage over the posterior cranial fossa. Obliteration of the fourth ventricle and obstructive hydrocephalus of the rest of the ventricular system were also noted (Fig. 1). His GCS score became 2T. The electrocardiogram (ECG) revealed an inverted T wave in multiple leads suggesting myocardial ischemia. His laboratory data were within normal limits, except for a white blood cell count of 12,600/µL, a K+ concentration of 3.0 mmol/L, and a glucose concentration of 139 mg/dL. After endotracheal intubation, mechanical ventilation with 100% O2 was used, but the peripheral hemoglobin-oxygen saturation (SpO2) was approximately 75%–82%. IV glycerol was used to decrease the ICP. Cardiovascular support was given by IV fluid resuscitation (normal saline 1.5 L, colloid 500 mL) and dopamine infusion (5 µg · kg-1 · min-1). The dose of dopamine was progressively increased to 22.8 µg · kg-1 · min-1, and norepinephrine IV infusion was also administered (up to 6 µg/min) to maintain the mean arterial blood pressure (BP) around 80 mm Hg. The patient was sent to the operating room for emergent craniotomy and ventricular drainage.
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Figure 1. Brain computerized tomogram showing a huge hematoma in the left cerebellar hemisphere (leftward arrows), together with subarachnoid hemorrhage over the posterior cranial fossa, obliteration of the fourth ventricle, and obstructive hydrocephalus of the remainder of the ventricular system (upward arrows).
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Before anesthesia, the patient’s baseline BP was 108/55 mm Hg, HR 138 bpm, and SpO2 80%. General anesthesia was induced with IV fentanyl (50 µg) and thiopental (50 mg), and maintained with desflurane in 100% oxygen. Rocuronium was used for muscle relaxation. Monitoring included pulse oximetry, ECG, intraarterial BP (ABP), body temperature, central venous pressure, and capnography. Despite adequate fluid challenge and mechanical ventilatory support (tidal volume 8 mL/kg, positive end-expiratory pressure 6 cm H2O, end-tidal CO2 27–32 mm Hg), arterial blood gas analysis showed a PaO2 of 57–88 mm Hg and a PaCO2 of 63–66 mm Hg during the first 2 h, with an ABP of 105/55–68/40 mm Hg and HR of 130–145 bpm. An inverted T wave was observed in ECG lead II. In view of the poor response to the large dose of catecholamines (norepinephrine = 10.6 µg · kg-1 · min-1 and dopamine = 22.8 µg · kg-1 · min-1), IV vasopressin infusion (0.04 U/min) was added. The BP improved dramatically (ABP = 135/85–110/65 mm Hg) over the next 2 h, and oxygenation also improved (PaO2 of 238 mm Hg, under 100% O2). Moreover, the ECG returned to normal sinus rhythm, and no inverted T wave was observed. Dopamine and norepinephrine infusions were gradually tapered and discontinued before the patient was sent to the neurosurgical intensive care unit (NICU). Total blood loss was 2000 mL and total fluid replacement consisted of 1 L of blood, 2.5 L of crystalloid, and 0.5 L of colloid. The urine output was 1500 mL during the 4-h operation.
Twelve hours after arrival in the NICU, the cardiac output and mixed vein saturation were within the normal range without any increase in ICP. The patient’s hemodynamic data were also within normal limits. The pulmonary edema had also disappeared. The ECG revealed normal sinus rhythm without myocardial ischemic change. Urine output during the first 8 h in the NICU was 140–410 mL/h. A negative fluid balance of 2.2 L was observed in the first day after NICU admission, probably because of transient diabetes insipidus. Small-dose vasopressin infusion (0.01–0.04 IU/min) was discontinued 12 h after the operation. Twelve days later, the patient was transferred to a general ward with a GCS score of 6T and stable vital signs.
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Discussion
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Hypotension and hypoxemia are the most important factors that aggravate neurological injury and result in a poorer outcome after acute brain injury (4,5). The use of vasopressors to restore an increased BP is mandatory for maintaining adequate cerebral perfusion in intracranial hemorrhagic patients refractory to aggressive fluid resuscitation and controlled hyperventilation. Neurogenic pulmonary edema and associated myocardial dysfunction may occur as a result of a "sympathetic storm" in response to a rapid increase in ICP after cerebellar and subarachnoid hemorrhage (6). Endogenous vasopressin release is an important mechanism for vasoconstriction during the initial phase of hemorrhagic or septic shock, but prolonged hemorrhagic, septic, and other vasodilatory shock states may lead to a long-term reduction of blood vasopressin after the initial large concentration (7). The mechanisms of this endogenous vasopressin deficiency are autonomic dysfunction, depletion of neurohypophyseal and hypothalamic stores, negative feedback of endogenous vasopressin release, and the inhibitory effect of exogenous norepinephrine administration (7,8). In acute brain injury patients, particularly with prolonged hypotension during norepinephrine infusion, plasma vasopressin concentration may be severely decreased, and the early use of small-dose vasopressin infusion in severe brain injury patients with prolonged hypotension during operation may therefore be beneficial.
Vasopressin has been used mainly for the treatment of esophageal variceal hemorrhage and diabetes insipidus. Via vasopressin receptors, it constricts arterial blood vessels (9). However, it causes less vasoconstriction, or even induces vasodilation, in the lungs, heart, and other vital organs (8,10). Similarly, in the brain, different vessels respond to vasopressin with variable sensitivity, the circle of Willis being especially sensitive to the vasodilatory effect of vasopressin (11). Vasopressin was demonstrated to cause pulmonary vasodilation, and thus decrease pulmonary artery pressure, in both normal and hypoxic conditions in animals (12). Lindner et al. (13) found that vasopressin has a similar vasoconstrictive effect to epinephrine, thus improving myocardial and cerebral blood flow during CPR. It also provides an effective vasopressor effect in late-stage hemorrhagic shock patients, who are refractory to volume replacement and catecholamine treatment (14). Loeckinger et al. (15) also found that vasopressin infusion results in better gas exchange than epinephrine infusion in animals after CPR.
In our patient, fluid resuscitation and catecholamine infusion failed to restore his vital signs during the first two hours of operation. Dramatically, co-infusion of small-dose vasopressin with catecholamines improved the patient’s hemodynamics. This is probably because of the synergism of the vasoconstrictive effect of vasopressin and noradrenaline (16), as well as supplement of the vasopressin deficiency resulting from severe intracranial hemorrhage. The subsequent reduction of dopamine and norepinephrine infusion promoted pulmonary edema and myocardial dysfunction recovery.
This report provides evidence that early use of small-dose vasopressin infusion may stabilize deteriorating hemodynamics and also improve pulmonary and cardiac function in acute brain injury patients.
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References
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- Harukuni I, Kirsch JR, Bhardwaj A. Cerebral resuscitation: role of osmotherapy. J Anesth 2002; 16: 229–37.[Medline]
- Macmillan CSA, Grant IS, Andrews PJD. Pulmonary and cardiac sequelae of subarachnoid haemorrhage: time for active management? Intensive Care Med 2002; 28: 1012–23.[ISI][Medline]
- Landry DW, Oliver JA. The pathogenesis of vasodilatory shock. N Engl J Med 2001; 345: 588–95.[Free Full Text]
- Chesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993; 34: 216–22.[ISI][Medline]
- Pietropaoli JA, Rogers FB, Shackford SR, et al. The deleterious effects of intraoperative hypotension on outcome in patients with severe head injuries. J Trauma 1992; 33: 403–7.[ISI][Medline]
- Kolin A, Norris JW. Myocardial damage from acute cerebral lesions. Stroke 1984; 15: 990–3.[Abstract/Free Full Text]
- Forrest P. Vasopressin and shock. Anaesth Intensive Care 2001; 29: 463–72.[ISI][Medline]
- Holmes CL, Patel BM, Russell JA, Walley KR. Physiology of vasopressin relevant to management of septic shock. Chest 2001; 120: 989–1002.[Abstract/Free Full Text]
- Paradis NA. Epinephrine in cardiac arrest: a critical review. Ann Emerg Med 1990; 19: 1288–301.[ISI][Medline]
- Liard JF, Deriaz O, Schelling P, et al. Cardiac output distribution during vasopressin infusion or dehydration in conscious dogs. Am J Physiol 1982; 243: H663–9.
- Suzuki Y, Satoh S, Oyama H, et al. Regional differences in the vasodilator response to vasopressin in canine cerebral arteries in vivo. Stroke 1993; 24: 1049–54.[Abstract/Free Full Text]
- Eichinger MR, Walker BR. Enhanced pulmonary arterial dilation to arginine vasopressin in chronically hypoxic rats. Am J Physiol 1994; 267: H2413–9.
- Lindner KH, Prengel AW, Pfenninger EG, et al. Vasopressin improves vital organ blood flow during closed-chest CPR in pigs. Circulation 1995; 91: 215–21.[Abstract/Free Full Text]
- Morales D, Madigan J, Cullinane S, et al. Reversal by vasopressin of intractable hypotension in the late phase of hemorrhagic shock. Circulation 1999; 100: 226–9.[Abstract/Free Full Text]
- Loeckinger A, Kleinsasser A, Wenzel V, et al. Pulmonary gas exchange after cardiopulmonary resuscitation with either vasopressin or epinephrine. Crit Care Med 2002; 30: 2059–62.[ISI][Medline]
- Dunser MW, Mayr AJ, Ulmer H, et al. The effects of vasopressin on systemic hemodynamics in catecholamine-resistant septic and postcardiotomy shock: a retrospective analysis. Anesth Analg 2001; 93: 7–13.[Abstract/Free Full Text]
Accepted for publication March 20, 2003.
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Abstract
Introduction
