American Journal of Emergency Medicine (2005) 23, 223 – 224
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Correspondence Atrial septal defect: an important risk factor after trauma To the Editor, Asymptomatic patients with atrial septal defects (ASD) may be at increased risk of serious complications after trauma when right-to-left shunt and severe hypoxia occur acutely because of increased pulmonary artery pressure. A 21-year-old man, presented fully conscious with a fractured femur after a deceleration injury while driving at 60 mph. No clinical injuries or radiological abnormalities of the neck, chest, or abdomen were identified. Electrocardiogram showed sinus rhythm. Hematologic and biochemical tests were normal. On day 2, an intramedullary nail in the right femur was inserted. On day 3, the patient’s condition deteriorated. He was pale, with temperature 38.58C, blood pressure 85/45 mm Hg, and heart rate 140 beats per minute, and his jugular venous pressure was raised. Chest examination revealed a decrease in breath sounds at both lung bases and diminished heart sounds and pulse oximetry (Spo2) was 94% (Fio2 0.4). Arterial blood gas showed H+ 46 nmol d L 1, Paco2 5.5 kPa, Pao2 10.7 kPa, bicarbonate 21.7 mmol d L 1, and base excess 3.9 mmol d L 1. Chest x-ray showed a markedly enlarged heart (Fig. 1), and electrocardiogram showed low-voltage complexes with T-wave inversion in the chest leads and a new right bundle-branch block. Platelet count was 68 109 d L 1, hemoglobin 7.2 gd dL 1, and international normalized ratio 2.8. Fresh frozen plasma, platelets, and blood were transfused. Biochemistry tests showed urea 6.2 mmol d L 1, creatinine 192 lmol d L 1, K+ 5.9 mmol d L 1, creatinine kinase 2546 IU d L 1, markedly elevated alanine transferase 2246 IU d L 1(normal 5-40 IU d L 1), alkaline phosphatase 94 IU d L 1 (normal 40-110 IU d L 1), and total bilirubin 54 lmol d L 1 (normal b17 lmol d L 1). Meanwhile, oliguria ensued and later anuria. No myoglobinuria was detected. Transthoracic echocardiography showed large right atrium and ventricle, reduced right ventricular function, moderate tricuspid regurgitation and ASD 2 cm in size. A right-to-left flow and pulmonary artery dilatation were noted. No evidence of pericardial effusion was shown. 0735-6757/$ – see front matter D 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.ajem.2004.04.033
Major pulmonary embolus was excluded by computed tomography scan of the chest and pulmonary angiogram. Central and peripheral cyanosis ensued, and further deterioration in renal function and acidosis occurred. Tracheal intubation and ventilation became necessary. Continuous venovenous hemofiltration and hemodynamic support with inotropes and nebulized prostacyclin were started. Transoesophageal echocardiography (TOE) was performed, and 1.5- to 2-cm ASD was confirmed. Troponin I 8 ng d mL 1 (normal b0.5) was reported. During days 4 and 5, inotropes requirement decreased, but Fio2 remained high (0.8). Large bilateral pleural effusions were identified, and chest drains were inserted on both sides. An ultrasound of the abdomen showed an enlarged liver, but liver enzymes and bilirubin level decreased (alanine transferase 295 IU d L 1, alkaline phosphatase 90 IU d L 1, and bilirubin 32lmol d L 1). On days 6 and 7, Fio2 decreased (0.4), and inotropes were weaned. TOE showed a significant improvement in right ventricular function, with a huge right atrium. The ASD was smaller in size. Renal function was improving, and continuous venovenous hemofiltration was discontinued. During days 9 and 10, ventilatory support was weaned, and the trachea was extubated. Transthoracic echocardiogram reported an elevated right ventricular systolic pressure (50 mm Hg). Treatment with ramipril (angiotensin-converting enzyme inhibitor) was started. At 2 months’ cardiology clinic review, the patient was asymptomatic, and a transthoracic echocardiogram showed reasonable function of both ventricles and an ASD (smaller in size) was identified with left-to-right flow (no shunt reversal). The sequence of events pointed to the possibility of fat embolism and cardiac contusion. Cardiac tamponade is an important differential diagnosis after trauma and deceleration injuries particularly with a raised troponin I; however, elevated troponin I is not exclusive of myocardial contusion, and cardiac contusion is not necessarily related to the degree of thoracic trauma [1]. TOE offered an excellent diagnostic test [2] to exclude cardiac tamponade.
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Correspondence Cyanosis in this case could indicate Eisenmenger syndrome, but it could also be caused by unusual direction of tricuspid regurgitant flow (as shown by echocardiography) increasing the right-to-left shunt [8]. In conclusion, the presence of chronic ASD is an important risk factor after trauma that could precipitate complicated events. A high index of suspicion is essential to achieve a successful outcome.
References
Fig. 1
Chest x-ray (day 3) showing a markedly enlarged heart.
The patient fulfilled most of the major and minor criteria, as identified by Gurd and Wilson [3] for the diagnosis of fat embolism syndrome. Petechial rash was not seen, but retinal hemorrhages were identified. Although pathognomonic when present, petechial rash is not essential to diagnose fat embolism [4]. Compromised right ventricular function and pulmonary artery dilatation were shown by echocardiography [5], but major pulmonary embolus was excluded. The detection of ASD by echocardiography and TOE enlightened the pathological sequence of events highlighting the possibility of paradoxical embolisms. Foramen ovale is anatomically open in 25% of individuals but functionally closed by the higher pressure in the left atrium. Right-to-left shunt and subsequent paradoxical embolism may occur when pressure in the right atrium rises [6]. Complicated prognosis could result when larger emboli reach the systemic circulation [7]. In our patient, an acute right-to-left shunt was a result of the increase in the pulmonary pressure in the right side of the heart most likely as a consequence of fat embolism. The acute deterioration of liver function can be explained as a consequence of heart failure and an increased systemic back pressure.
[1] Girisgin AS, Cander B, Gederet YT, et al. The role of cTnI in the detection of etiological factors for cardiac contusion. Ulus Travma Derg 2002;8:82 - 5. [2] Weis RL, Brier JA, O’Connor W, Ross S, Brathwaite CM. The usefulness of transesophageal echocardiography in diagnosing cardiac contusions. Chest 1996;109(1):73 - 7. [3] Gurd AR, Wilson RI. The fat embolism syndrome. J Bone Joint Surg Br 1974;56B:408 - 16. [4] Mellor A, Soni N. Fat embolism. Anaesthesia 2001;56:145 - 54. [5] Goldhaber SZ. Echocardiography in the management of pulmonary embolism. Ann Intern Med 2002;136:691 - 700. [6] Muller LP, Seidel T, Wenda K, et al. Paradoxical embolism after femoral fracture. Unfallchirurg 1997;100:908 - 12. [7] Foritza AM, Rabinstein A, Kouch S, et al. Endovascular closure of a patent foramen ovale in the fat embolism syndrome: changes in the embolic patterns as detected by transcranial Doppler. Arch Neurol 2002;59:455 - 9. [8] Kowalski M, Hoffman P, Siudalska H, et al. Clinical and echocardiographic assessment of a right-to-left shunt across an atrial septal defect secondary to tricuspid regurgitation. Acta Cardiol 2001;56:233 - 7.
Sahir Rassam (Specialist Registrar)* Elizabeth Mathieson (Specialist Registrar) Les Gemmell (Consultant Anaesthetist) Department of Anaesthesia Wrexham Maelor Hospital Wrexham, LL13 7TD Wales, UK *Current Address: Anaesthetic Department University Hospital of Wales Heath Park, CF14 4XW Cardiff, UK E-mail address:
[email protected]
