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Saudi J Anaesth. 2017 Apr-Jun; 11(2): 239–241.
PMCID: PMC5389251

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

Sir,

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 [Figure1a1a and andb].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 [Figure1c1c and andd]d] associated with the presence of microbleeds on T2-weighted image [Figure [Figure1e1e and andf].f]. These imaging findings were suggestive of cardioembolism.

Figure 1
(a) Noncontrast computed tomography: Bilateral occipital cortico-subcortical hypodensities. (b) Noncontrast computed tomography: Right frontal cortico-subcortical hypodense area. (c) Axial fluid-attenuated inversion recovery image: bilateral frontal and ...

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
    Sources of embolic stroke complicating penetrating heart injury *late presentation; Blue boxes: the main causes. LV: left ventricle; LA: left atrium; PFO: patent foramen ovale; VSD: ventricular septal defect; RPA: right pulmonary artery; ACF: aortocaval ...
    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.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1. Bamous M, Abdessamad A, Tadili J, Kettani A, Faroudy M. Evaluation of penetrating cardiac stab wounds. Scand J Trauma Resusc Emerg Med. 2016;24:6. [PMC free article] [PubMed]
2. Pepi M, Evangelista A, Nihoyannopoulos P, Flachskampf FA, Athanassopoulos G, Colonna P, et al. Recommendations for echocardiography use in the diagnosis and management of cardiac sources of embolism: European Association of Echocardiography (EAE) Eur J Echocardiogr. 2010;11:461–76. [PubMed]
3. Dunne B, Tan D, Ihdayhid A, Xu XF, Edwards M, Merry C. Penetrating cardiac injury managed without surgery but with systemic heparinisation. Heart Lung Circ. 2015;24:e210–3. [PubMed]
4. De Bruin G, Pereira da Silva R. Stroke complicating traumatic ventricular septal defect. J Emerg Med. 2012;43:987–8. [PubMed]
5. Reddy D, Muckart DJ. Holes in the heart: An atlas of intracardiac injuries following penetrating trauma. Interact Cardiovasc Thorac Surg. 2014;19:56–63. [PubMed]

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