Near-drowning continues to be a largely preventable tragedy frequenting emergency rooms across the country. After motor vehicle-related deaths, drowning is the second most common accident causing death in children.1,2 Several epidemiologic studies have examined the risk factors associated with near-drowning in the pediatric population including lack of supervision, trauma, alcohol, and seizures.3-7 Cardiac arrhythmias may be an important consideration for drowning survivors and their family when a plausible explanation is lacking. In this report, a boy whose near-drowning in a public pool was caused most likely by a ventricular tachyarrhythmia is described. After discovery of the probable cause of his near-drowning, several additional family members were identified as having inherited long QT syndrome (LQTS).
A previously healthy 10-year-old white boy was brought to the Emergency Room at Mayo Eugenio Litta Children's Hospital by emergency medical services in acute respiratory distress after being retrieved from the bottom of a public pool. History available at the time was limited and the duration of submersion was unknown. Reportedly, the near drowning victim was “racing” his younger brother. There was no suggestion of trauma and no past medical history of epilepsy. Paramedics were called, cardiopulmonary resuscitation was started, and the near drowning victim was defibrillated at poolside (Fig 1).
Arterial blood gas determination revealed a metabolic acidosis: pH 7.05, Paco2 47, HCO3 13, and −17 base deficit. The patient was paralyzed, sedated, intubated, and brought to the pediatric intensive care unit after cervical spine films and head computed tomography were negative. A chest x-ray demonstrated bilateral hazy infiltrates, areas of atelectasis, and right upper lobe collapse consistent with a significant acute lung injury. His condition gradually improved and he was dismissed without any neurologic impairment after being hospitalized for 27 days.
After he was stabilized, the cause of his near-drowning was sought. With the report of poolside defibrillation being performed, a 12-lead electrocardiogram (ECG) was obtained that demonstrated marked prolongation of the QT interval with a QTc = 0.56 sec1/2 (Fig 2). A preliminary diagnosis of LQTS was made. The plausibility of this diagnosis increased when he experienced a brief period of sustained ventricular tachycardia documented by electrocardiographic monitoring on hospital day 4 during sleep (Fig 3). Subsequently, the patient was started on propranolol, 2 mg/kg/day, and did not have further ventricular arrhythmias.
The family was then queried for a history of sudden deaths occurring before age 55, unexplained accidents, or fainting spells. Our near-drowning patient had reported to his mother that he had “blacked-out” once while walking home from school and once while playing baseball in the year preceding this event (Fig4 identified by arrow and IV-1). Further, a 30-year-old maternal aunt (III-4) revealed that she has “fainted too numerous times to count” since fourth grade (QTc = 0.49 sec1/2). In addition, the patient's maternal grandfather (II-2) has had several “falling episodes” accompanying emotional/anger outbursts (QTc = 0.52 sec1/2). Finally, a 50-year-old great uncle (II-5) had just experienced his first syncopal episode in a physician's office 1 month before this drowning. Baseline ECGs were obtained from family members suggesting that the near drowning subject is the proband of a large family with autosomal dominant LQTS (Fig 4). Of a four-generation kindred comprising 26 individuals, 5 including this patient have had syncope. Each symptomatic individual has a prolonged QT interval, QTc >0.46 sec.1/2 In addition, 8 other asymptomatic family members including the patient's mother (III-2) demonstrate QT prolongation.
Our patient demonstrates that cardiac arrhythmias, specifically those associated with the inherited LQTS, may be an important and possibly overlooked consideration during the historical assessment and evaluation of unexplained drownings. LQTS is manifested by prolongation of the QT interval (QTc >0.46 sec1/2), can present with syncope (30%), seizures (10%), and sudden death, and is estimated to occur in 1:10 000 to 1:15 000 individuals.8,9 Affected individuals are susceptible to polymorphic ventricular tachyarrhythmias, particularly torsades de pointes. There are two inherited forms of LQTS: autosomal recessive in Jervell and Lange-Nielsen syndrome, associated with sensorineural deafness, and autosomal dominant in Romano-Ward syndrome. To date, there are at least five different molecular genotypes responsible for autosomal dominant LQTS with four arising from defective cardiac ion channels.9
A search of the scientific literature adds one other case report and another citation of near-drowning as the initial presentation of LQTS.10,11 Harris et al10 reported a 6-year-old boy who had a “black-out” spell at a swimming pool but did not actually submerge. Nonetheless, he and his father had prolonged QT intervals. This particular family had been diagnosed with familial seizures affecting the father and two paternal uncles. In their review of 23 children with LQTS, Weintraub et al11 reported 1 child who presented as a near-drowning but was in normal sinus rhythm at the time of resuscitation.
Our patient represents the first believed documentation of the torsades de pointes arrhythmia on retrieval from a near-drowning and the first case of a near drowning victim serving to unmask a large family with LQTS. It is sobering that the family history of syncope remained hidden despite multiple previous medical encounters. Moreover, previous ECGs of 3 affected family members demonstrated the prolonged QT interval, but were overlooked. In one case, the prolonged QT interval was noted but its significance was dismissed. This underscores the importance of careful and thorough scrutiny of the ECG in evaluating prolongation of the QT interval.
The hallmark arrhythmia in LQTS, torsades de pointes, is often precipitated (60%) by some form of adrenergic arousal. Interestingly, swimming is a commonly cited precipitating activity for syncope (15%).12 The exact arrhythmogenic influence of swimming is not known. In a study evaluating different screening techniques to predict arrhythmogenesis during swimming and diving for children with known arrhythmias, 51 of 64 children with various arrhythmias developed significant arrhythmias while diving or swimming.13 In addition, nearly one third had significant tachyarrhythmias elicited by swimming. Realizing swimming can be an arrhythmogenic trigger again underscores the importance of considering cardiac causes in unexplained drownings.
It is important to recognize that postresuscitation hypoxic/ischemic cardiac dysfunction can cause transient QT prolongation and is not amenable to β-blocker therapy. We believe that inherited LQTS was responsible for our patient's near-drowning. Serial ECGs demonstrated sustained prolongation of the QTc, and he had a normal echocardiogram as well as a convincing past medical and family history. This case offers a perhaps overlooked addendum to the causes of near-drowning and underscores the importance of careful inquiry into long QT risk factors. It is not known how many unexplained drownings may be attributed to fatal ventricular arrhythmias arising from LQTS. Given the well known trigger association between swimming and syncope in confirmed cases of LQTS, it is likely that cases like this one are not unique.
In the absence of a clear identification as to the cause of drowning, we suggest that families be asked specifically for a history of sudden death, spells, “black-outs,” fainting, syncope, seizures not responsive to usual antiepileptic therapy, or any unexplained accidents occurring previously in the drowning victim or any related family members. Further, a 12-lead ECG should be obtained and the QT interval carefully examined in any unexplained near-drowning. If the history is suggestive but the ECG is borderline (QTc: 0.42–0.46 sec1/2), 24-hour ambulatory electrocardiographic monitoring or exercise ECG may be pursued. Finally, in the event of an unexplained, fatal drowning, similar historical information should be sought from the surviving family members. If a positive history is obtained, then an ECG should be obtained from members of the deceased victim's family. As evidenced by this child, an unexplained drowning (survived or fatal) may be the initial clue to revealing a family with the inherited LQTS.
- Received March 26, 1997.
- Accepted June 16, 1997.
Reprint requests to (M.J.A.) Department of Pediatrics and Adolescent Medicine, Mayo Eugenio Litta Children's Hospital, Mayo Foundation, Rochester, MN 55905.
Note. Primary caregivers could direct patients to the following Internet address: http://www.sads.org for more information. This address is for SADS (Sudden Arrhythmia Death Syndromes Foundation). This foundation provides information on long QT syndrome and other causes of sudden cardiac death.
- LQTS =
- long QT syndrome •
- ECG =
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- Pirie PL
- Kemp A,
- Sibert JR
- Quan L,
- Gore EJ,
- Wentz K,
- Allen J,
- Novack AH
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- Shen J,
- Li Z,
- Copyright © 1998 American Academy of Pediatrics