Case 2: An unusual cause of syncope

An 11-year-old girl presented to the emergency department with three brief episodes of syncope that day. Before each episode, the patient was standing and then felt weak and dizzy. Subsequently, she vomited once and experienced lower abdominal pain. She had no fever, diarrhea or dysuria. She denied visual or gait disturbances, weakness, paresthesia, chest pain or shortness of breath. There was a remote history of trauma one month previous when she fell approximately four feet off an unloading ski chairlift onto her abdomen. She was examined and medically cleared at the time. Her past medical history was unremarkable. Her menarche was one month earlier, and she denied being sexually active. She was on no medications. On physical examination in the emergency department, she appeared pale with slightly dry mucus membranes. She was alert with a supple neck. Her heart rate was 120 beats/min and her respiratory rate was 20 breaths/min. Her blood pressure was 110/60 mmHg and she was saturating 98% in room air. When she sat up, she felt dizzy and presyncopal. Her head and neck examination was normal. Her cardiorespiratory examination revealed a clear chest with no murmurs and normal peripheral pulses and perfusion. Her abdomen was soft with diffuse tenderness in the lower quadrants bilaterally. Her neurological examination was normal. Initial investigations revealed a white blood cell count of 14.3 × 109/L, hemoglobin of 101 g/L, and platelets of 274 × 109/L. The urine pregnancy test was negative. Liver function tests, renal function tests and amylase were normal. The chest x-ray and electrocardiogram were within normal limits. The patient was given a bolus of 20 mL/kg of normal saline and sent for an abdominal CT (computed tomography) scan where the diagnosis was made. When the hemoglobin was repeated 4 h later because of the CT scan findings, it had dropped to 81 g/L. Syncope during adolescence is usually a benign, isolated event. It is a fairly common presentation which usually warrants little or no investigation, and reassurance is often all that is required. Although, in some instances, as in this unusual case, syncope can have potentially life-threatening causes. An accurate history of the event, with attention to presyncopal signs and symptoms, and a thorough physical examination are often sufficient to separate out the more sinister problems. Further investigations, eg, chest x-ray, electrocardiogram and bloodwork done routinely, have a low yield. There were ‘red flags’ in this case (three episodes of syncope in one day, continued dizziness when sitting up and lower abdominal pain), which resulted in a more extensive work-up and tests not typically considered in the work-up of syncope (eg, pregnancy test, liver function, amylase and abdominal CT scan). True syncope is caused by any mechanism that causes a transient decrease in substrate delivery to the brain. Classification of the causes of syncope include: autonomic (which could be vasovagal), orthostatic (blood or fluid loss), reflex (breathholding, cough, micturition), cardiovascular (eg, arrythmias) or metabolic (eg, hypoglycemia). Other causes of transient and abrupt alteration in consciousness that should be considered in the differential diagnosis of syncope include neurological events (seizures, migraines) and hysterical causes (pseudoloss of consciousness). The above case illustrates orthostatic syncope caused by blood loss due to a delayed splenic laceration. In orthostatic or postural hypotension, there is a greater than 20 mmHg fall in systolic blood pressure when the patient's posture is changed from recumbant to erect. Other positive tests for orthostatic hypotension include an increase in heart rate by 20 beats/min or a feeling of dizziness when going from supine to any other position as in the above case. The incidence of recreational splenic injury in the paediatric population is low (5.6/year/1,000,000 children), with skiing being the most common cause. Other causes include snowboarding, hockey, football and bicycling. Teenagers (ages 12 to 14 years) appear to be at the highest risk. Abdominal injury may cause a splenic rupture and a secondary hemoperitoneum or a hematoma limited by the splenic capsule. Patients who have splenic injuries may present with either diffuse abdominal pain or localized tenderness in the left upper quadrant. Subphrenic blood may cause referred left shoulder pain (Kehr sign). Delayed splenic rupture after a subcapsular hematoma is still somewhat of a controversial diagnosis. Previous reports suggest a delayed rupture of the spleen, usually within days, in approximately 15% of cases. A delayed splenic rupture one month following trauma is exceedingly rare. Management of splenic injuries has evolved over the past three decades. The availability of noninvasive diagnostic CT scan and the morbidity of postsplenectomy sepsis syndrome have encouraged a nonoperative approach in many instances. Observation with or without blood transfusion (required in approximately 40% of cases) is usually a safe and effective therapeutic option. The decision to operate (splenectomy or splenorrhaphy) is based on several factors including hemodynamic status, hemoglobin of the patient and the grade of splenic injury. The above patient was managed nonoperatively and did not require a blood transfusion. Her lowest hemoglobin level was 71 g/L. She was discharged from the hospital in stable condition after seven days of observation with instructions of no physical activity for one month and follow-up at that time. Most children who faint have orthostatic syncope, vasovagal episodes or breathholding spells. Syncope occurs predominantly in teenage females, with a peak incidence between 15 to 19 years of age. The spleen is the most commonly injured intra-abdominal organ. Splenic injuries occur more often in children than in adults due to anatomical differences. A high index of suspicion for splenic injury is needed when a child presents with abdominal pain and a suitable mechanism of injury (eg, motor vehicle or bicycle accidents, falls). The case presentation should not exceed 200 words and should give the reader enough information to suspect the diagnosis without making it obvious. The discussion should not exceed 600 words and should be followed by a couple of ‘clinical pearls’. A maximum of two references may be included, if helpful. The submitted cases will undergo peer-review and revision at the discretion of the editors. Priority is given to cases illustrating an approach to common problems or important clinical clues to less common diagnoses that should not be missed. The Editorial Board hopes that this provides an opportunity for trainees and paediatricians practising outside of the teaching hospitals to share their clinical experiences and to publish in Paediatrics & Child Health. If you have a case to submit, contact Dr Friedman by e-mail at jeremy.friedman@sickkids.ca.

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