IntroductionColonoscopy is a useful tool in modern medicine and is increasingly employed for both diagnostic and treatment purposes. However, bowel preparations can cause electrolyte imbalance, with the risk apparently related to the type of bowel cleansing solution used, the age of the patient and their comorbidities. Symptomatic hyponatremia, especially coma, is a rare complication of oral bowel preparation for colonoscopy and is thought to result from excessive antidiuretic hormone secretion.Case descriptionThe authors report the case of a 48-year-old man who developed symptomatic hyponatremia (coma) after bowel preparation with sodium picosulfate/magnesium oxide/citric acid prior to a colonoscopy. The patient was admitted to an intensive care unit where other causes of coma were excluded. The symptoms of hyponatremia rapidly resolved after sodium level correction with intravenous administration of hypertonic saline.DiscussionHyponatremic coma is an uncommon but serious complication of colonoscopy bowel preparation. Patients at risk (>65 years old, chronic kidney disease, heart failure, history of electrolyte problems, or taking thiazide diuretics, angiotensin-converting-enzyme inhibitors or antidepressants) should be closely monitored during bowel cleansing and macrogol-based solutions should preferably be used.LEARNING POINTSThe association between coma and hyponatremia should be kept in mind when patients undergo bowel preparation, especially if they have chronic kidney disease, heart failure, a history of electrolyte problems or are taking diuretics or antidepressants.Patients should be closely monitored (and their metabolic profile checked before bowel cleansing) and a low threshold maintained for investigation and treatment initiation in case of symptom development.Medications with the potential to cause fluid and electrolytes disturbances such as diuretics and antidepressants should be stopped or reduced in dose while the patient is undergoing bowel preparation.
Spontaneous bacterial peritonitis is a common and often serious complication of long standing ascites in the presence of advanced liver disease. We report a case of a 74-year-old woman with alcoholic cirrhosis admitted to our emergency department with a 1-week history of diffuse abdominal pain and increased abdominal perimeter. On physical examination, she had a significant abdominal distention and a positive fluid wave consistent with ascites. A diagnosis of spontaneous bacterial peritonitis was made and empiric therapy with ceftriaxone was started but the patient's condition worsened. Four days later Listeria monocytogenes was detected in peritoneal fluid culture and ampicillin was initiated according to in vitro sensibility test. The patient completed 14 days of treatment with clinical and laboratory improvement. Listeria is an uncommon cause of spontaneous bacterial peritonitis. Clinicians should be aware of the uncommon agents of spontaneous bacterial peritonitis, mainly when there is not a proper response to therapy.
Corticosteroids have become the cornerstone of therapy for many pathologies such as vasculitis. Steroid psychosis is a known complication of corticosteroids therapy, although infrequent. We describe a case of psychosis secondary to corticosteroids in a 69-year-old man with large-vessel vasculitis without previous history of psychiatric pathology. He was diagnosed with large-vessel vasculitis and the treatment started with prednisone 1 mg/kg/day. One week later, the patient presented with behavior change: emotional lability, disorientation and aggressiveness. The symptoms worsened for hallucinatory activity and cognitive deficit. After exclusion of other causes, the diagnosis of psychosis secondary to corticosteroids was assumed. It was decided to wean corticosteroids and start new therapy with methotrexate and tocilizumab and introduction of antipsychotic therapy. The patient had a good outcome with disease remission and had no further neuropsychiatric symptomatology. Systemic corticosteroids are widely used, sometimes with a low concern of its potential adverse effects. So it is important that physicians are aware of the potential for their adverse effects and the need to monitor disease activity and drug toxicity.
Inclusion body myositis (IBM) is a chronic inflammatory myopathy with a progressive course. It is more common in the later years of life and usually presents with limb weakness. We present the case of a patient who developed proximal weakness in the lower limbs and, four years later, facial asymmetry. Blood analysis revealed high lactate dehydrogenase and creatinine kinase values. The diagnosis was obtained through muscle biopsy which met the histological criteria for IBM. The patient started treatment with alemtuzumab, leading to stabilisation of the symptoms in two years.
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