A 78-year-old woman was admitted with bacterial meningitis due to pneumococcus and confusional state.
Personal history: hypertension, asthma, ischemic heart disease and postoperative hypothyroidism.
Outpatient treatment with levothyroxine 100 μg/24h, valsartan 80 mg/24h, diltiazem 60 mg/8h, clopidogrel 75 mg/24h, budesonide 0.50 mg 1 inhalation/8h
Physical examination revealed fever of 38oC and temporo-spatial disorientation.
He had leukocytosis 20600 ul (> 11000 ul), INR: 1.3 (0.8-1.2), Cr: 0.86mg/dl (0.6-1.35 mg/dl), urea: 31mg/dl (10-50 mmol/dl).
An urgent brain computed tomography (CAT) ruled out acute pathology.
Lumbar puncture confirmed pneumococcal meningitis.
Treatment was initiated with 5% dextrose 1500 cc/day, 0.9% saline 1000 cc/day (40 mEq potassium chloride/24h), meropenem 2g/8h, dexamethasone 8 mg/8h and vancomycin 1g.
Treatment with dexamethasone 4mg/6h until the tenth day of admission, when it was discontinued without prior dose reduction, as well as fluid therapy.
On decimonovene day, a brain CT scan was repeated due to marked drowsiness and tendency to hypotension, with no pathological findings.
Analytical analysis showed Nap: 126mmol/l, Cr: 0.71 mg/dl, urea: 40 mg/dl, venous gas pH: 7.39 and Kp: 4.1 mmol/l.
She was diagnosed with syndrome of inappropriate antidiuretic hormone secretion (SIADH), starting fluid restriction at 1000cc/day and sodium chloride 2g/8h.
It did not improve with this treatment mmol/m, with Nap: 126 mmol/l, Nau: 79 mmol/l, Osmp: 253 mOsm/kg (275-290mOsm/kg), Osmu:
Clinically, the patient presented clinical euvolemia, bipsychia and disorientation.
There was a tendency to hypotension and hypoglycemia (stress: 60 mg/dl).
Baseline plasma cortisol was requested as part of the study of euvolemic hypoglycemic at 8.00 hours, with a result of 2.5 ug/dl (5-25 ug/dl), corticotropin hormone diagnosis-1.646 pg/ml (10: 2).
With the diagnosis of central AI due to sudden discontinuation of GC, treatment with oral hydroalteone 20mg/8h, initial Nap: 125mmol/l and 24-hour response: 134 mmol/l was initiated.
She was discharged after 48 hours with hydroalteone after normalization of hyponatremia and hyponatremia.
1.
Antidiuretic hormone-mediated hyponatremia (ADH) is common in hospitals.
Physiological stimuli such as nausea, pain, inadequate secretion of ADH or hypoisolism contribute.
SIADH is a discarding diagnosis and requires clinical euvolemia, with preserved thyroid and adrenal function2.
Treatment with chronic GC in supraphysiological doses inhibits the hypothalamic-pituitary-adrenal (HHA) axis, with risk of EA in case of inadequate interruption of treatment, this being one of the most frequent causes.
High doses of GC chronically decrease the synthesis of hypothalamic corticotropin-releasing factor (CRH) hypothalamic, losing its trophic and secretagogue effect on cortico3 cells.
In the absence of ACTH secretion, the fasciculoreticular adrenal area becomes infected.
However, the renin-angiotensin-aldosterone axis remains intact and, therefore, acid-base balance and renal potassium management.
Among the possible routes of administration of GC are oral, intravenous, ophthalmic, inhaled, rectal, transdermal, intramuscular or intra-articular, all of which should be considered.
In response to corticoids.olism, there is an increase in the synthesis and release of CRH and ADH in the parvocellular dorsomedial area of the hypothalamic paraventricular nucleus with the objective of stimulating secondary secretion of
The recovery process of the HPA axis is variable and can last weeks-months.
In this situation, excess ADH will result in an increase of aquoporins in the renal collecting tubule, not inhibiting its secretion in the presence of plasma hyposmolarity and risk of hyponatremia.
In the differential diagnosis in patients with hyponatremia after acute meningitis, cerebral salt-wasting syndrome, SIADH, hypothyroidism and central AI should be considered.
Elevated plasmatic levels and clinical euvolemia rule out cerebral salt-wasting syndrome.
Hypothyroidism must be very severe to produce hyponatremia and is an exceptional cause.
SIADH is a discard diagnosis, fundamental and frequently overlooked criterion.
The patient chronically used inhaled budesonide, which was suspended at the time of admission, being able to suppress the HPA axis at high doses when used chronically.
The discontinuation of inhaled GC has been described as a cause of acute central EA7.
Both aspects, previous chronic treatment with budesonide and high-dose dexamethasone treatment, marked the development of central AI.
Central AI presents nonspecific symptoms: asthenia, nausea, abdominal pain, hypotension or risk of hypoglycemia, among others.
A high clinical suspicion is essential for its diagnosis.
The clinical and analytical response to GC treatment in patients with central AI is spectacular.
Given the inhibition of vasopressin secretion and the consequent marked acuaresis, there is a risk of marked overcorrection of Nap during the first 24-48 hours of treatment.
This may be associated with an increased risk of developing osmotic myelinolysis, so it is the duty of the attending physician to prevent this condition by controlling the correction of natraemia.
The main message of this clinical case is to highlight the possibility of central EA in patients after treatment with prolonged GC, as well as SIADH is a discard diagnosis in patients with euvolemic hyponatremia.
