Cocaine-Induced Toxic Leukoencephalopathy: A Case Report.

We present a case here where a 57-year-old South Asian male with disturbed mental status developed multifocal leukoencephalopathy, which we believe was caused by cocaine usage. Cocaine was detected in the urine toxicological sample. Non-acute CT head, with a follow-up brain MRI demonstrating hyperintensity of the T2 FLAIR signal corresponding to diffusion restriction throughout the whole supratentorial white matter, involving semiovale and subcortical U fibres in the occipital lobes as well as posterior frontal and parietal centrum. It was less likely that the patient had posterior reversible encephalopathy syndrome (PRES), which can potentially manifest similarly in a clinical and imaging context because there was no abrupt rise of blood pressure at presentation or during the patient's stay. Extensive examinations were conducted to exclude additional factors that may contribute to the patient's appearance, including autoimmune, vasculitis, and infectious diseases. Levamisole, a significant chemical that is frequently used to increase the volume of cocaine samples and has been linked to neuronal damage, should be examined in individuals who use cocaine and exhibit these kinds of clinical symptoms. The patient was prescribed 250 mg of methylprednisolone twice daily for five days after it was determined that cocaine-induced neuronal toxicity was the cause of his symptoms. Although no improvement was seen right away, over the course of the next few days, he did exhibit a gradual, albeit slight, improvement in his mental status while residing in the nursing home. It is crucial to comprehend the possible connection between cocaine usage, a commonly abused drug, and people exhibiting similar clinical symptoms. To have a better understanding of the pathophysiology and possible treatment approach, more research is necessary as there is now no recommended therapy regimen.

Acute Acalculous Cholecystitis due to primary acute Epstein-Barr virus infection treated with laparoscopic cholecystectomy; a case report.

INTRODUCTION: Epstein Barr virus (EBV) is a human herpes virus 4, transmitted through intimate contact between susceptible persons and asymptomatic EBV shedders. It usually presents with fever, pharyngitis and lymphadenopathy. Majority of individuals with primary EBV infection recover uneventfully. Acute Acalculous Cholecystitis (AAC) is usually seen in hospitalized and critically ill patients with major trauma, shock, severe sepsis, total parenteral nutrition and mechanical ventilation. CASE PRESENTATION: We report a 25-year- old woman presented with acute Epstein-Barr Virus (EBV)infection and hepatobiliary iminodiacetic acid (HIDA) scan confirmed presence of Acute Acalculous Cholecystitis (AAC). Conservative management was advised initially, but she had a laparoscopic cholecystectomy due to intolerable abdominal pain. CONCLUSION: AAC is a rare complication of acute EBV infection and it is usually managed conservatively, although our patient had laparoscopic cholecystectomy due to intolerable abdominal pain.

Exercise-induced acute compartment syndrome in a young man, occurring after a short race.

We describe a case of exercise-induced acute compartment syndrome (ACS) in a 23-year-old man who presented to his primary care physician 48 hours after he attempted to run a 5K race. He noticed searing pain in his left leg after the first half mile but had no other symptoms. He was referred to the emergency department and diagnosed with ACS, and a fasciotomy was done. A presentation of limb pain that is out of proportion to a known or suspected injury should prompt consideration of ACS. Early recognition and surgical management are essential to achieving the best possible outcome.

Acute reversible neurologic deficits due to ethyl chloride sniffing: a case report and review of literature.

Ethyl chloride (CH3CH2Cl) or chloroethane is a colorless volatile halogenated hydrocarbon gas found in many commercially available solvents, and it may be used as an inhalant of abuse. Neurologic toxicity has been reported, as well as deaths. We present a case of a 47-year-old HIV-positive man who presented with acute reversible neurologic deficits secondary to inhalational exposure to ethyl chloride. Laboratory studies and neuroimaging are nondiagnostic in ethyl chloride-induced neurotoxicity and thus requires a high index of clinical suspicion. The mainstay of treatment is supportive with withdrawal of the offending agent and observation for resolution of neurologic symptoms.

Bilateral Upper Extremity DVT in a 43-Year-Old Man: Is It Thoracic Outlet Syndrome?!

Recurrent deep venous thrombosis, involving bilateral upper extremities, is an extremely rare phenomenon. We are presenting a 43-year-old man who was diagnosed with left upper extremity deep vein thrombosis (UEDVT) and was treated with anticoagulation and surgical decompression in 2004. 9 years later, he presented with right arm swelling and was diagnosed with right UEDVT using US venous Doppler. Venogram showed compression of the subclavian vein by the first rib, diagnosing thoracic outlet syndrome (TOS). He was treated with anticoagulation and local venolysis and later by surgical decompression of the subclavian vein. Bilateral UEDVT, as mentioned above, is an extremely rare condition that is uncommonly caused by TOS. To our knowledge, we are reporting the first case of bilateral UEDVT due to TOS. Diagnosis usually starts with US venous Doppler to detect the thrombosis, followed by the gold standard venogram to locate the area of obstruction and lyse the thrombus if needed. The ultimate treatment for TOS remains surgical decompression of the vascular bundle at the thoracic outlet.

Pulmonary arterial hypertension secondary to ethanol sclerotherapy for renal artery embolization.

Pulmonary arterial hypertension (PAH) has been reported as a major complication to consider and promptly manage in the use of ethanol sclerotherapy. Most of the available data on the development of PAH is derived from the use of ethanol for embolization of arteriovenous malformation, but it has been rarely reported in its other fields of application. We describe a case of outpatient renal artery embolization using ethanol, in which respiratory failure develops secondary to PAH despite adhering to safe practice protocols. We highlight the importance of pulmonary arterial pressure monitoring and the treatment steps to follow in order to avoid irreversible fatal outcomes.