Saudi Journal of Anaesthesia

: 2017  |  Volume : 11  |  Issue : 2  |  Page : 239--241

Stroke complicating penetrating heart injury: Keys to the diagnostic workup and management

Ali Jendoubi1, Belgacem Bourguiba2, Ali Gaja3, Mohamed Houissa1,  
1 Department of Anaesthesia and Intensive Care, Charles Nicolle Hospital of Tunis, Faculty of Medicine, University of Tunis El Manar, Tunis, Tunisia
2 Department of Surgery, Charles Nicolle Hospital of Tunis, Faculty of Medicine, University of Tunis El Manar, Tunis, Tunisia
3 Department of Medical Imaging, Charles Nicolle Hospital of Tunis, Faculty of Medicine, University of Tunis El Manar, Tunis, Tunisia

Correspondence Address:
Ali Jendoubi
Department of Anaesthesia and Intensive Care, Faculty of Medicine, Charles Nicolle Hospital of Tunis, University of Tunis El Manar, Tunis

How to cite this article:
Jendoubi A, Bourguiba B, Gaja A, Houissa M. Stroke complicating penetrating heart injury: Keys to the diagnostic workup and management.Saudi J Anaesth 2017;11:239-241

How to cite this URL:
Jendoubi A, Bourguiba B, Gaja A, Houissa M. Stroke complicating penetrating heart injury: Keys to the diagnostic workup and management. Saudi J Anaesth [serial online] 2017 [cited 2023 Mar 28 ];11:239-241
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Full Text


Stroke is a rare but serious complication of penetrating heart injuries (PHIs).[1] This complication should be suspected in patients with focal neurologic signs.

A 28-year-old man was brought to the emergency department with a single stab wound to the left fourth intercostal space. He had no associated injuries. He was agitated with a blood pressure (BP) of 80/60 mmHg and a heart rate of 130 bpm. The external jugular veins were distended. Cardiac tamponade was highly suspected, rapid fluid resuscitation was initiated, and pericardiocentesis was immediately performed with aspiration of 75 ml of nonclotting blood. The patient was emergently transferred to the operating room where a left posterolateral thoracotomy was done. The effusion was evacuated. A laceration measuring 2 cm in length over the left ventricle was repaired.

Transient episode of asystole has occurred. He responded to internal cardiac massage and intravenous epinephrine, followed by initiation of the massive transfusion. A 32 French chest tube was left in the left pleural cavity and the chest was closed.

Postoperatively, the patient was admitted to the Intensive Care Unit. His BP was stabilized with 1 mg/h of norepinephrine and was extubated on the following day. A bedside transthoracic echocardiography (TTE) was performed on postoperative day 1 with normal left ventricular (LV) size and good ventricular wall function.

The patient was weaned off of vasopressors by postoperative day 2. However, the patient remained somnolent and developed right-sided hemiparesis and a partial visual field loss. Brain computed tomography (CT) scan showed the bilateral occipital and right frontal cortico-subcortical hypodensities [Figure 1]a and [Figure 1]b. Brain magnetic resonance imaging (MRI) performed shortly after the CT scan revealed the bilateral frontal and right occipital high-signal lesions in fluid-attenuated inversion recovery compatible with recent infarct on the diffusion-weighted imaging B1000 image [Figure 1]c and [Figure 1]d associated with the presence of microbleeds on T2-weighted image [Figure 1]e and [Figure 1]f. These imaging findings were suggestive of cardioembolism.{Figure 1}

Repeated TTE showed no abnormal findings. Transesophageal echocardiography found neither intracavitary thrombus nor patent foramen ovale. There was only a thin rim of pericardial effusion.

An emergency neurology consultation was called. Given the high suspicion of cardioembolic source of the stroke, it was decided to start careful anticoagulation therapy. The patient was discharged after 2 weeks of hospital stay. At last follow-up, we noted a significant neurofunctional improvement.

We propose through this case presentation to summarize the main causes of heart trauma-related sources of embolism and the current approaches for the diagnosis and management of this complication.

Etiologic aspects: The main sources of cardioembolism following PHIs are summarized in [Figure 2]{Figure 2}

The sudden onset of focal neurological sign following PHIs or persistent altered mental status despite adequate resuscitation should alert the clinician to the possibility of stroke. Echocardiography is the first-line examination.[2]

Cardiac thrombus: LV thrombus with systemic embolus has been described mainly following cardiac contusion or infarction, but this complication should also be considered after PHIs. The injury did produce a local thrombotic response causing thrombus formation.[3]

Posttraumatic myocardial infarction can be complicated by LV thrombus. TTE is the technique of choice. As has been mentioned in our case, small mural LV thrombi may still go undetected. Concerning the left atrial thrombus, it is often a late presentation of PHIs and could be associated with posttraumatic atrial fibrillation.

Traumatic ventricular septal defect (VSD): The incidence of VSD occurs in up to 4.5% of PHIs. VSDs are the most common secondary lesion encountered. It can be complicated by ischemic stroke.[4]Atrial fibrillation: Traumatic cardiac dysrhythmias usually developed within the first several hours or24–48 h after injury.Posttraumatic LV pseudoaneurysm: LV pseudoaneurysm, usually sequel to myocardial infarction, may rarely present after PHIs.[5]Paradoxical embolism: The other minor cardiac sources of embolism are the following: patent foramen ovale, atrial septal aneurysm, atrial septal defects, and aortocaval fistula. In these rare situations, clinical and echocardiographic periodic follow- up is mandatory.[5]Neuroimaging features: Neuroimaging studies, including CT and MRI, are the important diagnostic tools. As illustrated by our case, bihemispheric combined anterior and posterior circulation or bilateral or multilevel posterior infarcts are suggestive of cardioembolism. Hemorrhagic transformation of an ischemic infarct and early recanalization of an occluded intracranial vessel are suggestive of a cardiac origin of the stroke.Stroke complicating PHI is a preventable and treatable complication: Heparin anticoagulation followed by warfarin is the first-line treatment for most causes of cardioembolic stroke. Anticoagulation therapy affords substantial protection against early recurrent emboli. However, this benefit must be weighed against the risks of hemorrhage.[3]

Stroke is a relatively rare but well-documented complication of PHIs. Echocardiography is the cornerstone imaging modality for diagnosis of LV thrombi and other trauma-related sources of embolism. Anticoagulation therapy should be conducted carefully to prevent the first or recurrent stroke after PHIs with close clinical and neuroimaging monitoring.

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