A 76-year-old patient with a history of thalassemia minor, type 2 diabetes mellitus, adequately controlled with low doses of oral antidiabetics (HCV figures 1AC 6.8).
Cholecystectomy in youth and testicular hydrocele surgery
The patient was admitted for a 15-year history of syncope to disabling orthostatism, which had even functionally limited in recent years, to the point of preventing him from leaving the street.
It was partially studied for this reason in 1996.
In this study a complete paroxysmal AV block was found, which was initially interpreted as causing the symptoms, so a patient's VDD symptoms became manifest without complete remission.
It was decided to extend the study at the time, performing an Echocardiogram, which except for a mild hypertrophy of the left ventricle did not present other alterations, as well as an abdominal CT, which was normal.
Neurological examination was normal at that time.
The patient was discharged with the diagnosis of orthostatic syncopes idiop, initiating treatment with ethylephrine, beta-blocker and flu-like agents dio.
The patient, however, did not improve his symptoms, presenting syncopes to orthostatism almost daily, with frequent trauma, along with a state of presyncope maintained while the patient remained in the sitting position.
Because the symptoms were disabling, the patient was admitted to the hospital to complete the study and adjust the treatment.
In the anamnesis, the patient, in addition to syncopes, only reported nocturia 4-5 times a day, and diarrhea of 4-5 abundant watery stools, with no pathological products, weight loss of about ten years.
The anamnesis by organs and apparatuses was negative.
The physical examination revealed a significant fall in AT with sitting position in relation to decubitus, which went from values around the other AT intense feeling of Hg to values of 60/40 without any fall.
During these episodes, the patient did not present tachycardic consolidation with animation.
Physical examination showed only some behavioral disinhibition of the patient, not accompanied by signs of frontal release.
The rest of the neurological and general examination was normal.
The following complementary tests were performed for the patient's study: biochemistry: glucose 127; crea 1.16; total proteins 7; albumin8; calcium 9.9; phosphorus 2.9; potassium 8.76; cholesterol 125; triglycerides 174; sodium 140;
Blood count: white 6,740 (normal formula); seizures 4.34; Hb 9.7; MCV 68.7; platelets 169.000.
Hepatic profile: Normal.
Vitamin B12 925 and folic acid 16 levels.
Hormonal study: prolactin 10.4; FSH 9.2; LH 7.3; testosterone 277; cortisol night 9; cortisol basal 38; cortisol rhythm 76%; porphyrin total < 200; aldolase 3.
Electrophoretic spectrum: albumin 5; alpha1 3.3%; alpha2 15.3%; beta 13.7%; gamma 13.9%.
Blood in stools: negative.
Cranial TAC: The study shows signs of diffuse form in relation to the age of the patient without other relevant findings.
Colonoscopy: No lesions were observed in the visualized areas.
Biopsies were taken from the proximal descending colon to rule out macroscopic colitis.
Small diverticular orifices throughout the colon.
Colorectal mucosa biopsy: usual characteristics.
Specific staining for amyloid was performed and the results were negative.
Echocardiogram: hypertrophic left ventricle with systolic function low limits of normality with slight global hypokinesia.
Mild mitral regurgitation.
No amyloidosis data.
Arrhythmological study: Normal RVD with single functioning cable.
The stimulation frequency was reduced without obtaining its own ventricular rhythm (complete AV block with ventricular stimulation at 40 bpm).
Cold pressure test: TA with the patient in decubitus 112/68.
After 30" with ice hand: TA 108/56.
HIV seropositive:
Chest X-ray: No significant findings were found. Cardiac auscultation revealed no significant pelvic elevation; there were no significant lesions expected to occur in the supine position or sitting position: low baseline levels, without any occurrence of seizures.
Urine output was low.
Having established the normality of the complementary tests, the diagnosis of pure autonomic failure is ended, removing from the treatment the hypotensive drugs, keeping only ethylephrine and the patient fluently establishing a symptomatic improvement.
