Wernicke encephalopathy (WE) is an acute neurological syndrome caused by thiamine (vitamin B1) deficiency. This disorder manifests as a triad of gait ataxia, confusion, and vision abnormalities. The absence of a full triad does not rule out WE. Because of its vague presentation, WE is commonly missed in patients with no history of alcohol abuse. Other risk factors for WE include bariatric surgery, hemodialysis, hyperemesis gravidarum, and malabsorption syndromes. WE is a clinical diagnosis that can be confirmed with an MRI of the brain as hyperintensities in the mammillary bodies, periaqueductal area, thalami, and hippocampus. If suspected in a patient, WE must be immediately treated with intravenous thiamine to prevent evolution into Korsakoff syndrome, coma, or death. Currently, there is no consensus in the medical community as to how much thiamine must be given and for how long. Therefore, there is a need for more research in the diagnosis and management of WE after bariatric surgery. Herein, we report a rare case of a 23-year-old female with a history of morbid obesity who developed WE two weeks after a laparoscopic sleeve gastrectomy.

Buried bumper syndrome (BBS) is a rare but severe complication of percutaneous endoscopic gastrostomy (PEG) tube feeding. Patients with BBS lose PEG tube patency and may experience peristomal pain, content leaks, or peritonitis. An early diagnosis can avert further complications. BBS is a clinical diagnosis, but an abdominal computerized tomography scan or upper endoscopy is needed to confirm the diagnosis. BBS is a long-term complication of PEG tube feeding, and cases of acute onset are scant in the literature. We report a unique case of a 65-year-old female with a history of stroke who developed BBS five weeks after PEG tube placement.

Calcium channel blockers (CCBs) are the most prescribed medications in clinical practice. These drugs treat many conditions, including migraine headaches, vasospasms, abnormal heart rhythms, and hypertension. This widespread use, however, has also been linked with the increased incidence of CCB toxicity cases. CCB toxicity may be from accidental ingestion or iatrogenic. Patients may show signs of cardiovascular toxicity such as hypotension, bradyarrhythmia, coma, or even death. The treatment includes discontinuing the offending medication, securing the airway, and raising blood pressure.Herein, we report a rare case of a 40-year-old male with a history of uncontrolled hypertension and advanced kidney disease who experienced iatrogenic cumulative calcium channel blocker toxicity while switching CCB classes due to a hypertensive emergency with concomitant atrial flutter. Although uncommon in clinical practice, iatrogenic CCB toxicity is possible and equally lethal. Clinicians must be cautious when initiating these drugs, switching between oral and intravenous formulations, or switching from one class to another to avoid overdoses.

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