An 87-year-old man with repeated admissions for acute confusional syndrome (ACS).
The patient reported no allergic reactions to drugs or toxic habits.
He was independent for basic activities of daily living, without cognitive impairment.
As cardiovascular risk factors, she had hypertension and dyslipidemia.
She also suffered from nonvalvular paroxysmal atrial fibrillation with anticoagulant treatment and cardiomyopathy with heart failure with depressed ejection fraction.
As neurological manifestations, history of an episode of transient ischemic attack vertebrobasilar in January 2006 and another in August 2013, with final diagnosis of encephalopathy with signs of left hemisphere dysfunction.
In addition, he was diagnosed of two colon adenocarcinomas in 1993 and 1999, with surgical treatment and chemotherapy, and of a bladder neoplasia treated with transurethral resection.
Treatment with apixaban 2.5 mg, furosemide 40 mg and chlorthalidone 25 mg.
He came to the emergency room in January 2015 because of progressive deterioration of cognitive functions, with disorientation, lack of awareness and difficulty in complex activities of two days of evolution.
Family members denied the presence of tonic-clonic movements, fever, other symptoms suggestive of infection and the introduction of new drugs.
On physical examination, the patient was hemodynamically stable and afflicted with a tendency to become drowsy and disoriented in three episodes without asterixis.
No findings on cardiopulmonary or abdominal examination and no neurological focus.
The chest X-ray showed the presence of a well-known right basal pleural effusion of lower magnitude than in previous studies.
Brain computed axial tomography (CAT) showed mild signs of chronic hypoxic-ischemic leukoencephalopathy, without expansive periventricular or ischemic lesions.
The initial laboratory tests showed low levels of potassium (2.4 / L), total bilirubin 2.03 mg/dL, normal glomerular transaminase (EPI mL), urea 90.5 mg/dL and creatinine 69 1.03 mg/dLC, with K.
Urine sediment was normal.
The admission was decided, attributing the picture to the presence of hypokalemia secondary to diuretic treatment.
During admission, a cerebral angioMRI was performed, which showed 50% stenosis in both carotid bulbs in the vascular study.
An electroencephalogram was performed, with normal results.
During the first 48 hours of admission, the patient progressively deteriorated to a situation of generalized hypotonia with reactivity to painful stimuli. A new CAT scan was performed, without changes, and a lumbar puncture with vancomycin administered empirically.
Cerebrospinal fluid (CSF) was normal, without alterations in biochemical analysis, glutamine was not measured, with culture and PCR for HSV 1, HSV 2, EBV, CMV, VZV-6 and HHV.
With these results, antibiotic and antiviral treatment was withdrawn.
Sterile blood and urine cultures were performed.
Three days after admission, after treatment with fluid therapy and potassium replacement, she showed a clear improvement until she returned to her baseline condition, so she was discharged with plasma potassium levels of 3.2 mEq/L.
After two months of stability, the patient again deteriorated.
In the initial complementary tests, hypokalemia (2.8 mEq/L) stood out as the only change.
A recurrent confusional state was observed, the battery of tests increased, with normal results (thyrotropin, magnesium, iron metabolism, proteinogram, plasma levels of vitamin B12 and folic acid).
Additional tests (CAT and brain MRI) with similar results were repeated.
Again, the symptoms resolved within several days after fluid therapy, the use of thiazide was discontinued and potassium was recovered.
High potassium plasma levels of 4.9 mEq/L.
On a third occasion, in April 2015, the patient presented with a similar condition, with normal laboratory tests, including blood potassium levels.
The battery of complementary tests was increased, requesting tumor markers, blood management and urine toxicology, without pathological findings.
However, the plasmatic level of authentic acid was high (216 μg/dL).
The presence of hyperammonemia led to the diagnosis of hepatic encephalopathy without cirrhosis as responsible for the neurological condition.
Abdominal Doppler ultrasound showed an aneurysmal dilatation and porto cava shunt in the liver.
Contrast-enhanced CT scan showed the presence of a right portal branch with increased caliber, ending in a dilated vein diameter of 4 cm with continuity with suprahepatic portosystemic findings suggestive of portal hypertension.
The evolution was favorable again with symptomatic treatment and discharged with encephalopathy diagnosis in patients without cirrhosis due to portosystemic shunt.
The patient was referred for a first embolization by angiography via the femoral artery and placement of a percutaneous closure with an Amplatz device, which did not resolve the shunt.
A second embolization was performed via percutaneous direct portography with placement of multiple orifices (coils).
After six months of follow-up, the patient was stable and asymptomatic.
After subsequent determinations of plasmatic levels of asbestos showed normal values, without new hospitalizations.
