Intensive Care Med (2008) 34:1348–1349 DOI 10.1007/s00134-008-1014-y
Elena Caresta Paola Papoff Giovanna Bosco Angelica Bibiana Delogu Maria Edelvais Licheri Corrado Moretti
Torsade de pointes: an unknown complication of hypertensive encephalopathy Accepted: 13 January 2008 Published online: 5 February 2008 © Springer-Verlag 2008
CORRESPONDENCE
ECG showed a sinus rhythm with a ventricular rate of 58 bpm and a corrected QT interval (QTc) of 400 ms. Two-dimensional echocardiography showed mild left ventricular enlargement and moderate aortic and mitral valve regurgitation. Because these echocardiographic changes were the patient’s only manifestations compatible with acute rheumatic fever they were considered secondary to the severe systemic hypertension [2]. Thirty-six hours after admission, despite treatment with nitroprusside, the patient experienced an episode of marked agitation associated with a sudden increase in blood pressure (to 160/100 mmHg) and loss of consciousness. Central pulses were not palpable and the child was therefore resuscitated and mechanically ventilated. Electrocardiography (ECG) during the episode showed a typical tracing of TdP (Fig. 1a). TdP rapidly
resolved with bag and mask ventilation and a single dose of atropine; hence, no other medications were necessary. Blood gases and electrolytes at that time were normal. Cranial computed tomography (CT) excluded intracranial hemorrhage. Soon after the event and during the following hours QTc was markedly prolonged (580 ms; Fig. 1b) and premature ventricular beats were observed. Because of the persistent severe bradycardia (48 bpm) and ventricular ectopy, atrial pacing at 120 bpm was instituted via a transesophageal pacing catheter [3]. Serial ECG over the ensuing 3 days demonstrated a progressive reduction in the QTc interval associated with blood pressure normalization and no other conduction anomalies. No further runs of TdP developed, and antiarrhythmic medications were not required. The child was kept sedated and intubated for 72 h. Cardiac pacing
Sir: Torsade de pointes (TdP) is a distinctive form of ventricular tachycardia commonly associated with congenital or acquired long QT syndrome. The acquired form is usually secondary to the use of antiarrhythmic drugs or other noncardiac agents, although it can also be precipitated by electrolyte imbalance, heart disease, endocrine disorders, and any of several intracranial conditions [1]. We report here the unusual association of long QT syndrome and TdP with hypertensive encephalopathy in a 9-yearold child with poststreptococcal glomerulonephritis. The patient was referred to our pediatric intensive care unit because of hypertension (blood pressure: 198/130 mmHg), bradycardia, seizures and mental confusion. Magnetic resonance imaging (MRI) of the brain showed typical signs of posterior reversible encephalopathy. Laboratory tests suggested poststreptococcal glomerulonephritis (high ASO titers, low C3, normal C4, mild anemia, elevated blood urea nitrogen, decreased serum protein levels, hematuria, proteinuria). Treatment with nitroprusside and mannitol was therefore thus started to lower blood pressure by 20% a day and to relieve brain edema. On admission the child Fig. 1 a D2 lead showing torsade de pointes (paper speed 25 mm/s). b D2, V1 and V5 leads underwent complete heart screening. showing a QTc interval of 580 ms (paper speed 25 mm/s)
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was discontinued 48 h later (on day 4 after admission) when both heart rate and QTc returned to normal and the patientwas deemed no longer at risk of malignant ventricular arrhythmias. Nitroprusside infusion was stopped on day 2 and substituted with amlodipine and enalapril. The patient was discharged home after 17 days in a stable clinical condition. QTc at the time of discharge was 420 ms and echocardiography no longer disclosed signs of mitral and aortic regurgitation. Serial ECG and echocardiography over a 2-year follow-up period gave normal findings. Hypertensive encephalopathy is to our knowledge unique as a cause of polymorphic ventricular tachycardia associated with a prolonged QTc interval. Indeed, a literature search disclosed no other similar cases. Various intracranial conditions in-
cluding subarachnoid and intracranial hemorrhage, brainstem encephalitis and brain injury have been associated with ECG abnormalities, including QTc interval prolongation and life-threatening arrhythmias such as TdP [4–6]. Our case report describing a patient with TdP extends the known severe neurologic complications of hypertensive encephalopathy to cardiac disorders, including lifethreatening arrhythmias. We suggest that children with hypertensive encephalopathy undergo strict QTc interval monitoring and receive prompt antihypertensive therapy to prevent possible QTc prolongation. If the QTc is prolonged, then in addition to maintaining normal electrolytes, continuous rhythm monitoring is essential to detect ventricular ectopy and possible malignant ventricular arrhythmias.
References 1. Khan IA (2002) Clinical and therapeutic aspects of congenital and acquired long QT syndrome. Am J Med 112:58–66 2. Waller BF, Kishel JC, Roberts WC (1982) Severe aortic regurgitation from systemic hypertension. Chest 82:365–368 3. Villain E, Boudjemline Y, Bonnet D (2004) Emergency trans-oesophageal ventricular pacing in a child. Cardiol Young 14:333–334 4. De Keyser J, De Boel S, Ceulemans L, Ebinger G (1987) Torsade de pointes as a complication of brainstem encephalitis. Intensive Care Med 13:76–77 5. Ozdemir D, Ozdemir N, Unal N, Tektas S (2005) QTc dispersion in children with severe head trauma. Pediatr Emerg Care 21:658–661 6. Sen S, Stober T, Burger L, Anstatt T, Rettig G (1984) Recurrent torsade de pointes type ventricular tachycardia in intracranial hemorrhage. Intensive Care Med 10:263–264 E. Caresta · P. Papoff (u) · G. Bosco · M. E. Licheri · C. Moretti University of Rome “La Sapienza”, Department of Pediatrics, viale Regina Elena, 324, 00161 Rome, Italy e-mail:
[email protected] A. B. Delogu Catholic University, Department of Pediatrics, Rome, Italy
