Vasodilatory Shock After Surgery for Aortic Valve Endocarditis: Use of Low-Dose Vasopressin
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- Lechner, E., Dickerson, H.A., Fraser, C.D. et al. Pediatr Cardiol (2004) 25: 558. doi:10.1007/s00246-003-0544-x
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This is the case report of a 13-year-old male who developed vasopressor-resistant hypotension after cardiac surgery for endocarditis. As norepinephrine resulted in aggravation of the preexisting ventricular arrhythmia, vasopressin was used to maintain blood pressure. The vasopressin continous infusion was started at 0.00002 units/kg/min and titrated up to 0.0003 U/kg/min. This low dose led to resolution of hypotension without causing side effects. As the appropriate indication and dose of vasopressin is not established, the cautious use of vasopressin in children is recommended.
KeywordsVasopressinVasodilatory shockEndocarditisCardiopulmonary bypass—children
Patients with staphylococcal endocarditis of the aortic or mitral valve are at high risk to develop complications such as severe congestive heart failure with unstable hemodynamic profile, perivalvular extension of the infection, or systemic embolization. When complications are recognized, treatment should be combined antibiotic therapy and surgery, as mortality rates among patients who have staphylococcal endocarditis involving the aortic valve and who were treated surgically range from 5% to 26% (compared with 51% of those treated with antibiotics alone [3, 5]).
Systemic vasodilation and severe hypotension can occur due to septic shock or from systemic inflammatory response after cardiopulmonary bypass. Vasopressin, a direct systemic vasoconstrictor and an antidiuretic hormone, has been used in high doses as a splanchnic vasoconstrictor in patients with variceal bleeding .
The successful therapy of vasodilatory shock secondary to sepsis or systemic inflammatory response syndrome after postcardiopulmonary bypass in adults with vasopressin has been reported previously [2, 4, 6, 8, 9, 10]. Data on the use of vasopressin in children with vasodilatory shock, however, are very limited, and indications and dosing have not been established [7, 10].
This case demonstrates the use of vasopressin in the treatment of vasodilatory shock after cardiac surgery in a child with Staphylococcus aureus endocarditis.
A 13-year-old previously healthy male without a known cardiac history presented with persistent fever and new heart murmur. Seven days prior to admission he had fevers up to 40°C. He complained of abdominal discomfort with vomiting, weakness, myalgias, and headache. A rapid Strep test on the third day of illness was negative, but white cell count and platelets were decreased. He received cephalexin for 2 days. On day five of illness a blood culture was drawn. The mother reported a minor injury from a splinter on the patient’s right foot, which had occurred 3 weeks prior to the onset of fever. On admission, he had a rash on his back, scattered petechiae and splinter hemorrhages on his palms, soles, fingers, and toes. In addition, he had a slightly inflamed healing abrasion on his right foot. A new grade 3/6 systolic and grade 3/6 diastolic murmur at the left sternal border and apex were ascultated. The pulses were bounding, and he had a palpable liver and spleen. Heart rate was 90 bpm, blood pressure 129/55 mmHg, and oxygen saturation was 98%.
Initial laboratory data revealed a white blood cell count of 15,460 cells/μL (79% segmented, 8% bands), a platelet count of 55,000 cells μL, a C-reactive protein of 25.7 mg/dL, and a mild coagulopathy with mildly elevated liver functions tests.
Chest X-ray demonstrated small bilateral pleural effusions and mild cardiomegaly. An echocardiogram revealed a bicuspid aortic valve with thickened leaflets, no aortic stenosis, and moderate aortic regurgitation. The aortic root was thickened and echogenic, consistent with an aortic root abscess. No discrete vegetations were seen. The left ventricle had normal dimensions and a systolic ventricular shortening fraction of 40%. An MRI of the brain done as part of the workup revealed multiple scattered areas of gliotic change and gyral swelling consistent with cerebral emboli. An abdominal ultrasound and computer tomography demonstrated an inhomogeneous lesion at the inferior splenic margin consistent with a splenic infarct or abscess.
Three separate blood cultures later were positive for methicillin-susceptible Stapylococcus aureus. Antibiotic therapy was initiated with vancomycin and gentamicin. This regimen was switched to nafcillin, rifampin, and gentamicin when the results of the resistance profile of the staphylococcos were available. Three days later an echocardiogram noted a new mobile vegetation on the anterior mitral leaflet without mitral regurgitation.
The patient underwent aortic root homograft replacement, mitral valve debridement with repair of the mitral annulus and aortic root with autologous pericardium, and closure of a patent foramen ovale. There was a cloudy, purulent-appearing pericardial effusion, out of which few white blood cells, but no organisms, were isolated. The operative course was uneventful. He came off bypass on dopamine at 5 μg/kg/min and nitroprusside at 0.5 μg/kg/min. As he had runs of ventricular tachycardia while coming off bypass, lidocaine was started at 20 μg/kg/min and increased to 40 μg/kg/min. The postoperative transesophageal echocardiogram revealed mild aortic valve regurgitation, no significant mitral valve regurgitation, and good biventricular systolic function.
Four hours postoperatively, he became hypotensive (systolic blood pressure < 80 mmHg, mean blood pressure < 40 mmHg). A fentanyl drip was used for sedation without any changes in dosage during this period. The patient was paralyzed with vecuronium bolus; the last bolus was given 2 h before the hypotension occurred. Nitroprusside was discontinued, dopamine was increased to 10 μg/kg/min, 500 mg of CaCl and 250 mL of albumin were administered, and norepinephrine was started at 0.05 μg/kg/min.
Low-dose continous infusions of vasopressin have been used recently in several trials in adults with vasodilatory shock secondary to sepsis or cardiac surgery [1, 6, 8, 9, 11]. It led to resolution of hypotension and reduction or withdrawal of catecholamine support, and it improved urine output without causing hyponatremia in adults. Sepsis and postcardiopulmonary bypass- induced severe vasodilation are associated with inappropriately low vasopressin plasma levels, so this vasopressin deficiency may contribute to the hypotension of vasodilatory shock [1, 6, 8, 10].
Summary of published articles on the use of vasopressin to treat vasodilatory shock
Reported side effects
Landry DW et al. , 1997
Argenziano M et al. , 1998
Vasodilation after CPB
Morales DLS et al. , 2000
Vasodilation after LVAD implantation
Limb ischemia with tissue necrosis and ischemic bowel
Patel BM et al. , 2002
Randomized controlled trial
Ryan DW et al. , 2002
Trials in children
Rosenzweig EB et al. , 1999
Vasodilatory shock after CPB
Liedel JL et al. , 2002
Peripherial ischemia without skin necrosis
No studies have been done to determine the appropriate dose of vasopressin in either adults or children. In adult studies and case reports the doses have ranged from 0.004 to 0.1 U/min (Table 1) [1, 6, 8, 9, 11]. Extrapolated from these adult data, the dose for children should range in between 0.00006 and 0.001 U/kg/min. In the two reported case series in children, vasopressin was used at a dose of 0.0003–0.008 U/kg/min for a mean of 71 ± 46 h. (Table 1) [7, 10]. In the 16 previously described children, no significant side effects were reported. Two patients had peripheral vasoconstriction without skin necrosis at a dose of > 0.007 U/kg/min . In the case of life-threatening gastrointestinal bleeding, a high-dose vasopressin infusion was used in children. At a rate of > 0.01 U/kg/min, it was associated with fluid overload, electrolyte abnormalities, and hypertension .
In all previous published studies in adults and in children, vasopressin was added to the existing therapy with traditional pressor agents.
In this case, the patient had a systemic inflammatory response with severe hypotension that was probably secondary to underlying staphylococcal sepsis and extended cardiopulmonary bypass. Administration of volume and high-dose dopamine had no effect on blood pressure; in addition, initiation of norepinephrine resulted in aggravation of the preexisting ventricular arrhythmia. Therefore, vasopressin was used as pressor agent to maintain blood pressure.
As the appropriate dose of vasopressin is not known, the vasopressin continuous infusion in this case was started at the very low dose of 0.00002 U/kg/min and slowly titrated up to 0.0003 U/kg/min to avoid side effects. Our major concern was not to induce splanchnic vasoconstriction in a patient with a history of possible splenic infarction. Therefore the initial dose was chosen from extrapolated adult data, which are lower than the reported doses used in children. During the vasopressin infusion, even at a very low dose, the blood pressure increased steadily. The patient was closely monitored and there were no clinical obvious signs of cutaneous, renal, or mesenteric ischemia. Vasopressin is a very potent drug with major side effects, and as its appropriate dose is not defined yet, it should be initiated at a low dose and slowly titrated, adjusted to effect, and not exceed an infusion rate of > 0.007 U/kg/min.
In selected patients with vasodilatory shock after cardiac surgery, vasopressin is an ideal agent compared to traditional pressor agents. Since indications, dosing, and duration of intravenous vasopressin therapy have not been established, its cautious use in children is recommended.