A severe penetrating cardiac injury in the absence of cardiac tamponade

CASE

A 26-year old male sailor was involved in an altercation on board his ship 100 miles offshore. A 3-cm knife entry point was noted in the fourth intercostal space 6–7 cm to the left of the midline. He was transferred by air ambulance to the closest medical facility, a community hospital 45 min away.

INVESTIGATIONS AND MANAGEMENT

Upon arrival, eight hours after the incident, a large left-sided haemothorax was demonstrated on X-ray (Fig. 1A). A minimal pericardial effusion was also noted on CT. Chest drain insertion was followed by the immediate return of 1200 ml of blood. A loud systolic murmur was noted on auscultation. Transthoracic echocardiography (TTE) demonstrated significant mitral regurgitation (MR) and was suspicious for an anterior mitral leaflet prolapse. During this first TTE, no obvious ventricular septal defect (VSD) or pericardial effusion was visualized. The patient was urgently transferred to our cardiothoracic unit. Upon arrival, approximately 15 h after the injury, the patient was alert, tachycardic (heart rate of 90–100 beats per minute) and hypotensive (blood pressure of 100/60). His chest drain drained a further 800 ml. Haemoglobin and troponin I were 14.1 g/dl and 1000 (normal range = 0–14). A repeat bedside TTE to confirm the initial findings was performed revealing mild MR and a minimal pericardial effusion. Again, there was no evidence of VSD.

Figure 1:

Radiological Imaging. (A) Chest X-ray showing a large left-sided pleural effusion. (B) MRI of the brain demonstrated a large parietal watershed area infarct. (C) CT Thorax demonstrating a moderate left-sided pleural effusion/haemothorax and a VSD (arrow).

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The patient complained of a sudden onset of left arm weakness. A large right-sided parietal ischaemic infarct was demonstrated on MRI (Fig. 1B). A repeat CT revealed an increase in the volume of his left-sided haemothorax and a right-sided pleural effusion (Fig. 1C). In light of the high troponin and mechanism of injury, a third TTE was performed and showed marked anterior leaflet mitral valve prolapse with severe MR and a moderate muscular VSD with no pericardial effusion. Transoesophageal echocardiogram (TOE) revealed moderate to severe MR and a muscular VSD, which was also seen on the review of the repeat CT (Fig. 2A). The necessary mitral valve repair and VSD closure require full heparinization, which risks increasing the area of injury secondary to the cerebrovascular accident (CVA). Ten days after the CVA, a joint decision between cardiothoracic surgery, anaesthetics, neurology and cardiology determined that the patient could reasonably, safely undergo this procedure.

Figure 2:

Echocardiograms and intraoperative images. (A) Intraoperative image demonstrating the knife entry point in the free wall of the right ventricle; (B) Transthoracic echocardiogram demonstrating a VSD in the middle portion of the muscular part of the septum (demonstrated by the blue jet). (C) Transthoracic echocardiogram after VSD occlusion.

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Routine cardiopulmonary bypass via a median sternotomy and a transseptal approach was performed with mild hypothermia with cooling to 32°C and routine tubing for ascending aorta arterial and bicaval venous cannulation. Blood and cardioplegia were delivered via the antegrade and retrograde routes. The epicardial entry point was immediately visible on the free RV wall anteriorly (Fig. 2B). This point was already healed, thus suturing was not required. The mitral valve was repaired using a size 22 neochordae loop (W.L. Gore & Associates, AZ, USA). Attempted VSD closure was performed with a pledgeted prolene suture with a transtricuspid valve approach into the right ventricle. Bypass and cross-clamping time were 111 and 79 min, respectively. Postoperative TOE demonstrated a competent mitral valve, mild MR and an unchanged muscular VSD with a severe left to right shunt. His recovery was uneventful with no deterioration in his stroke symptoms. A subsequent percutaneous closure of his significant residual traumatic VSD was performed using an Amplatzer closure device (St. Jude Medical, MN, Fig. 2C). After 3 days in the cardiac intensive care unit, he was transferred to the ward. Upon discharge on postoperative day 21, only subtle residual arm motor impairment remained. He returned to his home country for recovery.

DISCUSSION

This case is notable due to the favourable outcome despite a concomitant CVA, a long delay from injury to appropriate medical treatment and the lack of pericardial tamponade in the presence of a penetrating cardiac wound deep enough to cause a muscular VSD and lacerate an anterior mitral leaflet primary chordae. Initially we thought the CVA was caused by prolonged hypotension on the ship; however, the injury was more focal (rather than in a watershed area as typically seen in cases of prolonged hypotension). Thus, the more likely aetiology was muscle or clot emboli caused by the knife. Data on the optimal timing of bypass surgery after CVA are limited. Thus, a multidisciplinary cooperation was required to determine the ideal time to minimize the risk of bleeding and re-infarction.

Cardiac stab injury is predominantly sustained by males, non-accidental and fatal [1, 2]. Mortality reported in large series approaches 60% [2, 3]. In the absence of pericardial tamponade, fatality rates are higher. In our case, the distances to the nearest hospital and to our trauma centre greatly increased the mortality risk. The pericardial effusion drained into the left pleural space, creating a haemothorax instead of a cardiac tamponade. Hypotension sealed the injured muscle of the right ventricle. Thus, no effusion, VSD or obvious injury was seen on initial echocardiography. The rising troponin levels and a marked systolic murmur indicated a high likelihood of myocardial injury leading to a further echocardiogram and re-evaluation of the CT thorax. This case highlights the importance of a high index of suspicion for cardiac injury based on the mechanism, even in the absence of pericardial tamponade.

ACKNOWLEDGEMENT

The authors would like to acknowledge Luther Keita, Department of Cardiothoracic Surgery, University College Hospital, Galway Ireland for his assistance with the images in the case report.

Conflict of interest: none declared.

REFERENCES