Posterior Reversible Encephalopathy Syndrome (PRES) is a neurological condition characterized by various clinical findings and imaging abnormalities. Patients can present with a myriad of symptoms ranging from headaches and confusion to seizures and focal neurologic deficits (hemiparesis, aphasia) [1][2][3]. We report a rare case of PRES induced by acute, malignant hypertension associated with alcohol withdrawal.A 58-year-old female with a history of hypertension and alcohol abuse was admitted to our critical care unit after she was found unresponsive at home, requiring intubation and sedation by paramedics. Of note, she had been discharged two days earlier following treatment for alcohol intoxication and acute kidney injury. Following that discharge, ramipril was stopped and she abstained from further alcohol use. Her blood pressure was 195/108 mmHg, pulse 102 bpm. She was normothermic with otherwise unremarkable neurologic, cardiac and pulmonary examinations, except for obtundation. Urinalysis, TSH, Ammonia, CT Thorax, urine toxicology, blood ethanol levels, CSF studies, and VBG were unremarkable. CT and CTA head showed subacute infarct within the right parietal lobe near the vertex. MRI brain revealed several hyperintense lesions in the posterior region of bilateral occipital lobes and along the watershed areas between the ACA and MCA territories, involving the subcortical white matter without restricted diffusion and apparent diffusion coefficient (ADC) findings suggestive of vasogenic edema, consistent with PRES. EEG showed frontal intermittent rhythmic delta activity (FIRDA); neurology was consulted and she was started on levetiracetam. Her blood pressure and encephalopathy improved following treatment of withdrawal with intravenous benzodiazepine. She was extubated later that day and was discharged at her baseline two days later on levetiracetam and ramipril. She followed with neurology, underwent repeat MRI showing interval resolution of occipital vasogenic edema and was weaned off of levetiracetam.There are two proposed mechanisms responsible for PRES that have been extensively discussed in literature: autoregulation/hyperperfusion and cerebral vasoconstriction/hypoperfusion theories.The autoregulation/hyperperfusion theory describes a failure in the ability of cerebral vessels to respond to variations in blood pressure [4]. With acute and significant elevations in blood pressure, exceeding the upper limit of autoregulation, animal studies have shown cerebral hyperperfusion due to arteriolar dilation, vasogenic edema, and vessel injury [5].The favoured cerebral vasoconstriction/hypoperfusion theory suggests that cerebral vasoconstriction in response to severe hypertension decreases blood flow to the brain leading to ischemia and subsequent hypoxia. Release and activation of endothelial factors in response to hypoxia promotes angiogenesis, increased membrane permeability, and breakdown of the blood-brain barrier causing vasogenic edema [4,5]. Findings that support this theory include the tendency of wate...

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Etoposide based combination chemotherapy is used with curative intent in patients with advanced testicular germ cell tumors. Common side effects involve nausea and vomiting (up to 43%), alopecia (up to 66%), leukopenia (up to 91%). Cardiovascular side effects are rare, and hypotension only occurs in 1%-2% of patients. Etoposide is not known to cause thyroid dysfunction. We observed a case of bradycardia and QTc interval shortening after introduction of etoposide based chemotherapy. Keywords: Chemotherapy; Leukopenia; Tumor Case ReportA 37-year-old male with stage IV mixed germ cell tumor of right testicle, with retroperitoneal lymphadenopathy and lung masses presented for cycle 2/4 of etoposide based chemotherapy and was found to be severely bradycardic with chest pain. Patient was not complaining of lightheadedness or dizziness. Vital signs were remarkable for blood pressure of 120/70 mmHg, pulse of 28 beats per minute, respiratory rate of 20 breaths per minute, saturating 100% on room air. Physical exam did not reveal any murmurs or gallops, but patient did have bradycardia. Comprehensive metabolic profile was within normal limits, and complete blood count was remarkable for chronic thrombocytopenia of 97.10 × 3 per µl. TSH level was 3.0 mIU/L and free T4 was 1 ng/dl [1,2]. Electrocardiogram showed sinus bradycardia with a rate of 28 beats per minute, without ischemic changes (Figure 1). Electrocardiogram prior to initiation of chemotherapy showed a sinus rhythm with a normal heart rate (Figure 2). Cardiac injury panel was not suggestive of ischemia. Chest X-ray and CT angiography of the thorax were also normal. The patient was treated with atropine on presentation and heart rate normalized transiently, but eventually became bradycardic again. Of note, the patient had episodic bradycardia following his first cycle of chemotherapy as well, and the electrocardiogram before the first cycle of chemotherapy showed heart rate was within normal range [3]. Nuclear stress test was also done and it did not suggest ischemic changes. Patient was discharged and advised to avoid β-blockers. On outpatient follow up, he was noted to have returned to normal sinus rhythm. Chemotherapy was resumed with cardiac monitoring.

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