Salman Farooq

Prosthetic Aortic Valve Endocarditis with Left Main Coronary Artery Embolism: A Case Report and Review of the Literature.

Context: Coronary embolization is potentially a fatal sequela of endocarditis. Although the primary cause of acute coronary syndrome is atherosclerotic disease, it is imperative to consider septic embolism as an etiological factor. Case Report: Herein, we report a case of ventricular fibrillation and ST-segment depression myocardial infarction occurring in a patient who initially presented with fever and increased urinary frequency. Coronary angiography revealed new 99% occlusion of the left main coronary artery (LMCA). Transesophageal echocardiography showed bioprosthetic aortic valve with an abscess and vegetation. Histologic examination of the embolectomy specimen confirmed the presence of thrombus and Enterococcus faecalis bacteria. Subsequently, the patient was discharged to the skilled nursing facility in a stable condition where he completed 6 weeks of intravenous ampicillin. Conclusion: We present a rare case of LMCA embolism due to prosthetic valve endocarditis. The present report also highlights the diagnostic and therapeutic challenges associated with such patients.

Nonthrombotic Pulmonary Embolism: A Potential Complication of Polyacrylamide Hydrogel Cosmetic Injection

Context. Polyacrylamide hydrogel (PAAG) has gained importance as a synthetic soft tissue filling agent. It has been commonly employed by physicians in Europe for facial contouring and soft tissue augmentation. Previously, PAAG is considered nontoxic and well tolerated with a few mild procedural complications. Case Presentation. A 26-year-old female was hospitalized for dry cough, worsening dyspnea, and chest discomfort after 3 hours of multiple PAAG injections in buttocks. The patients condition deteriorated and rapidly advanced to acute respiratory failure. Therein, the diagnosis of nonthrombotic pulmonary embolism (NTPE) was established on standard set of investigations. She was intubated; corticosteroid and empiric antibiotic therapy was initiated resulting in improvement of her condition. Subsequently, extubation was done, and she was discharged from the hospital after an uneventful recovery. On 1-month follow-up, the patient had no previous symptoms. Conclusion. This report implicates clinicians to maintain a high index of suspicion for NTPE in patients presenting with respiratory symptoms following PAAG usage.

Characteristic Pulvinar Sign in Pseudo-α-galactosidase Deficiency Syndrome

Pseudo-α-galactosidase deficiency (PAGD) syndrome occurs when a mutation reduces measured enzyme activity in vitro, despite normal intracellular activity. White matter lesions have been reported infrequently in PAGD syndrome.1 Importantly, to our knowledge, no report mentions characteristic pulvinar hyperintensity on T1-weighted imaging in PAGD syndrome, a highly specific sign of Fabry disease in male patients.2,3 Although atrophy of selective brain areas occurs in a few cases, to our knowledge, no article reports diffuse cortical atrophy by imaging in Fabry disease or PAGD syndrome.1,4 We report a case of a woman in her 40s with a 3-year history of a complex progressive disorder with emotional lability, cognitive decline, generalized ataxia, and autonomic dysfunction. She denied paresthesias, dysesthesias, or loss of sensation. Metabolic testing showed reduced activity of α-galactosidase (0.056 U/L; normal range, 0.074-0.457 U/L). Autonomic testing demonstrated abnormal cardiac parasympathetic function (but no orthostatic hypotension) and a patchy decrease in sweat output on the quantitative sudomotor axon reflex test as well as a markedly abnormal thermoregulatory sweat test, with near complete global anhidrosis. Repeated magnetic resonance imaging (Figure) compared with one the prior year at an outside hospital showed unchanged global diffuse brain volume loss and bilateral mineralization of the pulvinar region of thalami (manifesting as hyperintensity in the pulvinar on T1-weighted imaging). Genetic testing showed the presence of the pseudo-α-galactosidase allele. Neuropsychological testing done in view of diffuse cortical atrophy showed mild neurocognitive and memory deficits (Table), and the patient was diagnosed with mild neurocognitive disorder. Magnetic resonance imaging of the entire spine showed no spinal cord lesions. Cerebrospinal fluid analysis showed elevated protein levels (95 mg/dL) but no pleocytosis (white blood cell counts: 0/μL; polymorphonucleocytes: 7%; lymphocytes: 83%; monocytes: 9%).

Acute visual loss in a patient with spinal cord injury

IntroductionPatients with spinal cord injury (SCI), especially those with injury at and above T6, are prone to transient episodes of hypertension induced by noxious triggers below the level of SCI, known as autonomic dysreflexia (AD). An uncommonly reported presentation of AD is posterior reversible encephalopathy syndrome (PRES).Case PresentationA 50-year-old male with the history of paraplegia from SCI presented with sepsis secondary to baclofen pump and urinary tract infections. On hospital day 4, he developed acute bilateral vision loss. The next morning he had a generalized-tonic-clonic seizure followed by cardiac arrest, with return of spontaneous circulation following resuscitation. Magnetic resonance imaging brain demonstrated multifocal areas of hyperintensity on T2 fluid-attenuated inversion recovery sequence, most pronounced in the occipital lobes. Systolic blood pressures (SBP) were under 180 mmHg throughout hospital stay but above his baseline (SBP 90 mmHg). PRES was diagnosed on the basis of clinical and radiologic evidence. With strict blood pressure (BP) control, there was resolution of visual abnormalities, headaches, encephalopathy, and seizures.DiscussionAlthough PRES has been most commonly described in malignant hypertension, it can be seen in patients with normotension or moderate hypertension who have low baseline BPs, such as patients with SCI. These patients are prone to AD due to imbalanced sympathetic outflow to vasculature below the level of injury caused by noxious stimulus. This results in massive regional vasoconstriction leading to an uncontrolled rise in BP above baseline. This episode of PRES could have been prevented by identifying patient’s risk, recognizing early signs and potential triggers of AD, and implementing aggressive treatment of the underlying noxious stimuli.

QRS fragmentation: its role in sherlocking the arrhythmogenic heart.

The electrocardiogram (ECG) is a commonly available basic diagnostic modality in in-patient, out-patient, and emergency departments. In patients with coronary artery disease (CAD), the presence of a fragmented QRS (f-QRS), which is an extra R wave (R′), notching of the single R wave, notching of the S wave in at least two contiguous leads on the 12-lead ECG, is associated with a myocardial scar from previous myocardial injury. Furthermore, the presence of f-QRS has been shown to be associated with adverse outcomes in CAD and non-CAD patients. In the present paper, we will solely focus on the usefulness and utilization of f-QRS in predicting ventricular tachyarrhythmia in many heart diseases, that is, ischemic cardiomyopathy, non-ischemic cardiomyopathy, hypertrophic obstructive cardiomyopathy, Brugada syndrome, and arrhythmogenic right ventricular cardiomyopathy. In the majority of such cases, ventricular tachyarrhythmia results in sudden cardiac death. Diagnosing them beforehand can lead to prevention and/or early treatment of these arrhythmias to prevent potential morbidity and mortality.