A 27-year-old woman was admitted due to paresis of extremities, cramps and myalgias known for two months before, which worsened within 48 hours prior to consultation, until she was unable to walk.
She presented with edema of the eyelids and extremities from 15 years of age, initially premenstrual, later practically constant.
She reported no use of furosemide for one year (40-120 mg/day) increasing doses in the last two weeks; she also reported constipation treated with diet and natural medications.
She did not develop diarrhea; she ingested laxatives or other diuretics.
Physical strain: markedly deanimated; weight: 65 kg; height 1.68 mt, BMI: 23.0, heart rate (HR) 118 x' regular; blood pressure (BP) 105/63 mm' Hg.
Dry skin and mucous membranes; thyroid within normal limits; flat jugular veins in decubitus.
Pulmons without semiological alterations; heart: regular rhythm in two times without murmurs.
No edema; notorious hyporeflexia and paresis of lower limbs.
Laboratory at admission: Hb: 16.3 g/dl hematocrit: 46.9%, leukocytes: 17,100/mm3, ESR: 6l mm/h; blood glucose: 110 CK/MB 47; creatine
Plasma electrolytes: Na+ 135 mEq/1; K+ 2.0 mEq/1; Cl: 86.8 mEq/1.
Magnesaemia: 1.90 mg/dl (VN = 1.58 - 2.55).
Venous blood gas: pH 7.50, pC02 36 mmHg, HC03 29.5 mEq/1.
Troponin 0.02 ng/ml (VN = < 0.05); Uric N: 25 mg/dl; serum creatinine: 1.56 mg/dl; uricemia: 12.9 mg/dl; TSH: 5.024 gdl; proteinemia:
Urine: pH 5.0; proteins: traces; glucose (-); GR 6/ul (VN = < 15) Leukocytes 18/ul (VN = < 10).
Urocultiva: negative.
Twenty hours after admission, serum potassium was 2.50 mEq/1 and urinary electrolytes in an isolated sample: sodium 48 mEq/1, potassium 38.5 mEq/1 and chloride 73.7 mEq/1.
Figures 1 and 2 show the evolution of two electrode tracings (ECG).
Frequency-corrected QT space (Bazett's formula - mean of six determinations in D2, ECG at 25 mm/s) and depression ST segment, measured at 0.08 m sinus rhythm (1.57 mm / s).
The second ECG (43 h later) showed sinus rhythm, frequency 84 cpm, slight ST-segment depression of 1 mm in D2 and flattening of the T wave in aVF, V5 and V6.
No U wave was observed and QTc space was maintained within normal limits.
Nine ECGs at 5 and 26 days post discharge were normal.
1.
She received saline solution 0.9% (ev) with KCl (3 g/500 mi) and magnesium sulphate 25% (5 mi/ 500 mi).
Oral potassium was added (48 mEq/d) and diet (calculated by nutritional assessment) received only 37 mEq of potassium per day.
Table 1 illustrates the evolution of potassium, creatinine and potassium intake from admission to discharge.
The calculation of the latter represents the sum of the intravenous intakes, KCl tablets and the diet, punishing the latter for the lower intake mentioned.
On the second day, her hematocrit was 38.6%, and she recovered urine within 24 hours, without diarrhea or excessive sweating.
She was discharged on the fifth day, on a potassium-rich diet, KCl 8 mEq/d, oral magnesium 133 mg/d and paroxetine 20 mg/d.
1.
Forty-one days after admission, patients were studied on a controlled sodium-free diet, high potassium, and prescribed medications.
He said he didn't use diuretics.
His BP was 138 mmHg (debit), his HR was 64 x' regular.
Weight 71.0 kg Table 2 shows electrolytes, glomerular filtration rate and tubular sodium and potassium management, comparing them with those observed on the second day.
Plasma electrolytes were within normal limits, creatinine clearance 97.2 ml/min, urinary sodium excretion 214 mEq/d and potassium 80 mEq/d.
Epidermides of Na+ (FE+), K+ (FEK+) and Cl (FECl) were 1.1%, 12.9% and 1.71%, respectively.
1.
Forty-seven days after admission - denying diuretic intake - returned to control.
He continued therapy by eating a supposedly low-sodium and calorie diet.
She had added an oral contraceptive.
There was a recurrence of edema in hands and eyelids.
Weight: 70.1 kg, BP (debit): 112/90 mm Hg and regular HR 92 x'.
Mild oedema of the extremities was observed.
To investigate the response to changes in blood volume and distribution of body water was evaluated (dishabitation, fasting bioRP, aldosterona and plasma renin activity).
Searching for less common causes of edema, the simultaneous plasma prolactin level and insulin resistance were studied.
They demonstrated: plasma renin 5.0 ng/ml/h (VN = 1.3 - 4) and aldosterone 48.0 ng/dl (VN = 2.5 - 16), prolactin 11.2 ng/ml (VN = insulin 828).
Impeda institu bioeléctrica (Equipo Xitron 4200) P: 70,1 kg T 1,68 m.
BMI: 24.4 kg/mt2.
Total body water: 28.91 ± 0.01 1 = 41% of weight (Waking: 35.5 1 = 50.3% of weight).
Extrace-lular water: 13.84 ± 0.04 1 = 19.7% of weight (washed 16.2 1 = 23.1% of weight); intracellular water: 15.06 ± 0.03 1 = 21.3% of weight:
Finally, 99 days after admission, the patient continued to show edema, which we did not check; he maintained the medications.
Fasting was re-studied.
Weight: 71 kg BW: 119/ 84 mm Hg and HR: 64 cpm.
Senate: 118/82 mm Hg and 81 cpm.
Twelve mm Hg and FC: 94 cpm.
Its electrolytes were within normal limits of excreta + 138 mEq/ 1 K+ 4.2 mEq/1 Cl 106,3 mEq/1), sodium uricaemia was 4,1 mg/dl and -in isolated urine sample 0,1 %
Capillary permeability was evaluated using a simplified plethysmographic method.
A pressure cuff was inflated on the right arm up to 100 mm Hg (supradiastolic but infrasystolic level), remaining for 5 minutes, in order to produce venous occlusion and raise capillary pressure.
At the pressure minute, the displacement of liquid (water at room temperature) of the right hand was measured in a graduated specimen, comparing the displaced volume with that measured in biphasic conditions.
The compression of the brachial-quial artery did not cause an increase in hand volume, measured by volume displacement (baseline displaced volume read ml/volume displaced post compression: 100 mi).
