Profound Hyponatremia Research Articles

English

Rapid correction of hyponatraemia leads to serious neurological complications, like osmotic demyelination syndrome (ODS). In ODS, magnetic resonance imaging (MRI) often reveals features of pontine myelinolysis, that may occur in isolation or may, sometimes be associated with extrapontine myelinolysis. Isolated extrapontine myelinolysis is rare. We report the case of a 53-year-old lady brought to the emergency service with vomitings, and altered sensorium. She was found to have profound hyponatraemia (serum sodium 110 meq/L). Correction of hyponatremia was done with slow intravenous infusion of 3% sodium chloride. However, inadvertant, concomitant oral administration of salt led to overcorrection with serum sodium going upto 150 meq/L. She developed quadriplegia, depressed level of consciousness and respiratory failure and required ventilatory support. MRI brain showed features of isolated extrapontine myelinolysis.

Terlipressin-induced hyponatraemia

Terlipressin is a vasopressin (V1 receptor) agonist that causes splanchnic constriction and is used in the management of variceal bleeding. This case report demonstrates the profound hyponatraemia, sufficient to cause a fall in conscious level, developing following terlipressin administration for variceal gastrointestinal bleeding.

Acute Intermitent porphyria and early hematin treatment before confirming the diagnosis

The term porphyria refers to a heterogeneous group of metabolic diseases resulting from variable catalytic defects of the enzymes involved in the heme biosynthesis pathway. Acute intermittent porphyria (AIP) is an autosomal dominant disorder resulting from a partial deficiency of porphobilinogen (PBG) deaminase. A 21-year-old woman presented to us with the complaints of abdominal pain and vomiting. Her father and sister are diagnosed as acute intermittent porfiria. The laboratory findings showed profound hyponatremia, hypokalemia and high values of creatine kinase. AIP was suspected because of family history and clinic of patient. Our initial management consisted of continuous infusion of 10% glucose and 3% NaCI solution. We decided to start hematin treatment because of no clinical response with current therapy. After the hematin treatment she had regained consciousness, the abdominal pain subsided. The hyponatremia and elevation of creatine kinase was corrected. The analysis of PBG in 24-h urine confirmed the diagnosis of AIP.

Use of Desmopressin Acetate in Severe Hyponatremia in the Intensive Care Unit

Excessive correction of chronic and profound hyponatremia may result in central pontine myelinolysis and cause permanent brain damage. In the case of foreseeable or established hyponatremia overcorrection, slowing down the correction rate of sodium plasma levels (PNa) or reinducing mild hyponatremia may prevent this neurologic complication. This retrospective and observational study was performed with 20 consecutive patients admitted to two intensive care units for severe hyponatremia, defined by PNa <120 mmol/L and/or neurologic complications ascribable to hyponatremia and subsequently treated by desmopressin acetate (DDAVP) during correction of hyponatremia when the rate of correction was overtly or predictably excessive. The primary endpoint was the effectiveness of DDAVP on PNa control. DDAVP dramatically decreased the rate of PNa correction (median 0.81 mmol/L per hour [interquartile range, 0.46, 1.48] versus -0.02 mmol/L per hour [-0.16, 0.22] before and after DDAVP, respectively; P<0.001) along with a concurrent decrease in urine output (650 ml/h [214, 1200] versus 93.5 ml/h [43, 143]; P=0.003), and a rise in urine osmolarity (86 mmol/L [66, 180] versus 209 mmol/L [149, 318]; P=0.002). The maximal magnitude of PNa variations was also markedly reduced after DDAVP administration (11.5 mmol/L [8.25, 14.5] versus 5 mmol/L [4, 6.75]; P<0.001). No patient developed seizures after DDAVP or after subsequent relowering of PNa that occurred in 11 patients. Desmopressin acetate is effective in curbing the rise of PNa in patients admitted in the intensive care unit for severe hyponatremia, when the initial rate of correction is excessive.

Altered Mental Status in a Young, Healthy Female

A young previously healthy patient presented with fever and altered mental status. Her evaluation would eventually reveal a profound hyponatremia in the setting of a viral meningoencephalitis. This case report reviews the evaluation of hyponatremia and treatment options for syndrome of inappropriate antidiuretic hormone hypersecretion, her ultimate diagnosis.

Bilateral Scapular Fracture and Triceps Tendon Rupture After a Grand Mal Seizure: A Case Report.

We report a case of bilateral and simultaneous triceps tendon rupture and scapular fracture (Orthopaedic Trauma Association [OTA] classification 14-A3.2) after a single generalized tonic-clonic seizure. To the best of our knowledge, the current literature reports only three cases of bilateral complete triceps tendon rupture in hemodialysis patients1-3 and one case of bilateral partial triceps tendon rupture in an athlete4. Scapular fractures are most commonly caused by high-energy trauma, electric shock, or convulsions5-7, and there are several published cases of bilateral scapular fracture secondary to seizure activity6,8,9. Our case emphasizes the importance of recognizing renal osteodystrophy and secondary hyperparathyroidism as common underlying conditions leading to orthopaedic injuries. The patient was informed that data concerning the case would be submitted for publication, and he provided consent. A forty-two-year-old left-hand-dominant man was admitted to the intensive care unit with profound hyponatremia after a witnessed, single, generalized tonic-clonic seizure following a missed dialysis appointment. The chief symptom was bilateral upper-extremity weakness and limited shoulder motion, which occurred immediately after the seizure. Past medical history was notable for hypertension, gout, and polycystic kidney disease with chronic renal failure that required hemodialysis. Medication included 2000 mg of calcium acetate three times per day for hyperphosphatemia. One week prior to the seizure, the patient had hypocalcemia (calcium, 6.0 mg/dL) and hyperphosphatemia (phosphate, 8.9 mg/dL), and two weeks prior to the seizure, the parathyroid hormone level was 1900 pg/mL. The laboratory values on admission are listed in Table I; hyponatremia, hypocalcemia, and hyperphosphatemia were all present. View this table: TABLE I Vital Signs and Laboratory Values on Admission Radiographs and computed tomography (CT) of both shoulders (Figs. 1 and 2), with axial and coronal reconstructions, demonstrated comminuted fractures of the scapulae inferior to the glenoid (OTA …

Hyponatremic-Hypertensive Syndrome: Think of Unilateral Renal Artery Stenosis

Hyponatremic hypertensive syndrome (HHS) is an uncommon disorder, in which hypertension is associated with profound hyponatremia. It is mostly encountered in adults with unilateral renal artery stenosis. Although renovascular hypertension is one of the commonest causes for severe hypertension in children, HHS is rarely reported in childhood. The authors report a 9-y old boy with hypertensive emergency and severe hyponatremia due to unilateral renal artery stenosis who was successfully managed by vascular stenting of the affected vessel. Prompt recognition of this disorder can be life-saving and can subsequently lead to appropriate referral and treatment as in the present case.

Trouble de la marche révélant un syndrome de sécrétion inappropriée d’hormone antidiurétique associé à la prégabaline

Pregabalin, a molecule with similar structure of GABA neurotransmitter, initially developed as an antiepileptic, is now commonly used in the treatment of painful peripheral neuropathies. We report an 82-year-old man who presented with confusion, urinary incontinence and gait instability. He was receiving pregabalin for a left L5 radicular pain. Laboratory tests at admission revealed a profound hyponatremia (117 mmol/L) that was corrected by fluid restriction and pregabalin withdrawal. According to the patient and laboratory outcome, we established the diagnosis of inappropriate antidiuretic hormone secretion due to pregabalin. The test of Naranjo demonstrated a probable imputability of pregabalin.

1526P - Hyponatraemia as a Marker of Inferior Outcomes in Small Cell Lung Cancer (SCLC)

ABSTRACT Introduction Small cell lung cancer (SCLC) represents approximately 15% of all lung cancer diagnoses and is reducing in incidence. Hyponatremia is a common and debilitating electrolyte disorder, frequently documented in SCLC. Its occurrence is typically attributed to paraneoplastic syndrome- induced syndrome of inappropriate antidiuretic hormone hypersecretion (SIADH). The influence of hyponatremia on the survival of patients with lung cancer remains poorly understood. Aim: The aim of this retrospective study is to investigate clinical features and the prognostic value of hyponatremia in an unselected Irish patient population with small cell lung cancer (SCLC) with limited disease (LD) and extensive disease (ED). Method The data of patients diagnosed with SCLC in Beaumont hospital over a 3-year period was analysed retrospectively. Patients were identified from analysis of all lung cancers biopsies via the pathology department databank. Data was collected from clinical notes on identified patients including clinical performance status, serum sodium values, disease stage, chemotherapy regimens and response, radiotherapy, palliative care input and survival. Results 48 patients (22 male, 26 female) with a median age 64 yrs (range 41-87yrs), 29.17%(n = 14) with limited stage were identified. The standard chemotherapy was carboplatin–etoposide. 7 patients received 2nd line treatment with irinotecan. 16.6% patients did not receive chemotherapy (n = 8) due to poor performance status. Hyponatraemia (plasma sodium [P-Na] Conclusions Hyponatraemia is a common occurrence in patients with SCLC, and one of the most frequent paraneoplastic syndromes noted. Profound hyponatremia is associated with significantly shorter observed median survival and should be considered in generating treatment in patients with SCLC. Disclosure All authors have declared no conflicts of interest.

Diagnosis and management of hypoaldosteronism without hypoadrenocorticism in an alpaca

Primary hypoaldosteronism without concurrent hypoadrenocorticism was diagnosed in an 8-year-old female alpaca with acute onset of weakness progressing to recumbency within 6 hours after onset. Hematologic testing at admission revealed profound hyponatremia, hypochloremia, and acidemia with a normal blood potassium concentration. Further diagnostic testing, including an ACTH stimulation test, led to a diagnosis of hypoaldosteronism in conjunction with normal cortisol production. The hembra responded well to i.v. polyionic fluid therapy with sodium supplementation and was managed successfully long term with free access to saline (0.9% NaCl) solution in addition to water ad libitum. To our knowledge, this is the first reported case of hypoaldosteronism in an alpaca. Hypoaldosteronism should be considered in alpacas as a possible differential diagnosis for refractory hyponatremia or for hyponatremia in which an underlying etiology is not determined.

Stereoelectroencephalography in the presurgical evaluation of focal epilepsy in infancy and early childhood

The authors report on the use of stereoelectroencephalography (stereo-EEG) in the presurgical electroclinical evaluation of infants and very young children with focal drug-resistant epilepsy. Fifteen patients (9 girls and 6 boys, mean age 34.1 ± 7.3 months, range 21-45 months), potentially candidates to receive surgical treatment for their focal drug-resistant epilepsy, were evaluated using stereo-EEG recording for a detailed definition of the epileptogenic zone. Stereoelectroencephalography was indicated because neuroradiological (brain MRI) and video-EEG data failed to adequately localize the epileptogenic zone. Stereotactic placement of multicontact intracerebral electrodes was preceded by the acquisition of all pertinent anatomical information from structural and functional MRI and from brain angiography, enabling the accurate targeting of desired structures through avascular trajectories. Stereoelectroencephalography monitoring attempted to record habitual seizures; electrical stimulations were performed to induce seizures and for the functional mapping of eloquent areas. Stereoelectroencephalography-guided microsurgery, when indicated, pointed to removal of the epileptogenic zone and seizure control. Brain MRI revealed an anatomical lesion in 13 patients (lobar in 2 cases, multilobar or hemispheric in 11 cases) and was unremarkable in 2 patients. One patient underwent 2 stereo-EEG studies. The arrangement of the intracerebral electrodes was unilateral in all but 1 case. One patient died the day following electrode placement due to massive brain edema and profound hyponatremia of undetermined cause. In 8 cases intracerebral electrical stimulations allowed mapping of functionally critical areas; in 3 other cases that received purposeful placement of electrodes in presumably eloquent areas, no functional response was obtained. Of the 14 patients who completed stereo-EEG monitoring, 1 was excluded from surgery for multifocality of seizures and 13 underwent operations. Postoperatively, 2 patients exhibited an anticipated, permanent motor deficit, 3 experienced a transient motor deficit, and 2 experienced transient worsening of a preexisting motor deficit. Three patients developed a permanent homonymous hemianopia after posterior resections. Histological analysis revealed cortical malformations in 10 cases. Of the 10 patients with a postoperative follow-up of at least 12 months, 6 (60%) were seizure-free (Engel Class Ia), 2 (20%) experienced a significant reduction of seizures (Engel Class II), and 2 (20%) were unchanged (Engel Class IV). The present study indicates that stereo-EEG plays a prominent role in the presurgical evaluation of focal epilepsies also in the first years of life and that it may offer a surgical option in particularly complex cases that would have scarcely benefitted from further medical treatment. Results of stereo-EEG-guided resective surgery were excellent, with 80% of patients exhibiting a substantial improvement in seizures. In consideration of the potentially life-threatening risks of major intracranial surgery in this specific age group, the authors recommend reserving stereo-EEG evaluations for infants with realistic chances of benefiting from surgery.

Profound hyponatraemia following a tramadol overdose

Sir, Hyponatraemia is a common electrolyte disturbance associated with prolonged hospitalization and increased mortality. Among numerous aetiologies, tramadol is not routinely included in the list of causative medications. This case highlights an important biochemical side effect, and symptoms that may be easily overlooked without appropriate investigation. A 56-year-old man presented to hospital 12 h after an intentional overdose of 60 tramadol (50 mg) tablets and 20 co-dydramol (10/500) tablets. The past medical history included COPD, treated with spiriva and seretide inhalers. There was no other current or previous medication use. On examination, he was drowsy with pinpoint pupils and a respiratory rate of six breaths per minute. Blood pressure was 135/80 mmHg and heart rate 110 beats …

SIADH as a paraneoplastic syndrome of squamous cell carcinoma of the hypopharynx

Hypopharyngeal cancer is an uncommon malignancy, representing only 4.3% of head and neck cancers. It is usually found late in the course, accounting for its high five-year mortality. SIADH has been seen in other squamous cell cancers mainly of the lungs. We report a case of profound hyponatremia secondary to SIADH occurring in an elderly Vietnamese man in the setting of a large, well-differentiated squamous cell cancer of the hypopharynx. SIADH is a common occurrence in squamous cell cancer of the lung. It occurs in only 3% of head and neck tumors. The putative etiologies include direct carotid involvement by the tumor, carotid manipulation during operative dissection, and as a side effect of chemotherapy or radiation. In this case, SIADH preceded operative intervention and there was no carotid involvement of the tumor. SIADH is an uncommon occurrence in head and neck tumors despite majority of them being squamous cell cancers. Usual etiologies for SIADH in this setting include medication side effects and involvement or manipulation of the carotid artery. None of these factors were present in this case leading to the conclusion that SIADH was caused by the tumor itself.

Chapter 8. Hyperosmolar therapy

Chapter 8. Hyperosmolar therapy

Postprostatectomy seizures: A case report

A 75-year-old Caucasian male presented with generalized seizures half-hour post-transurethral resection of the prostate surgery. The intra-operative course was complicated by perforation of the posterior wall of the bladder neck during a difficult Foley catheter placement. This resulted in intraperitoneal extravasation of the glycine containing bladder irrigation fluid. An emergent laparotomy was performed, and 3.5-4 L of fluid was drained from the peritoneal cavity. Postoperative course was complicated by two seizures within a short interval. Patient developed profound hyponatremia (Na of 109 mEq/L). However, measured serum osmolality was normal (283 mOsm/kg). The serum osmolality remained relatively stable, indicating that the absorbed glycine and its metabolites remained osmotically active in the intravascular space (until they were dialyzed as mentioned later), making the hyponatremia less pernicious and an unlikely cause of patient's symptoms. The encephalopathy and seizures were ascribed to accumulation of toxic metabolites of glycine, especially ammonia (serum level -1261 mcmol/L). During a complicated postoperative period, patient developed oligo-anuric renal failure, and was started on slow low-efficiency dialysis for 8 hours resulting in rapid lowering of serum ammonia levels and glycine with reversal of encephalopathy including seizures. There was no recurrence of encephalopathy, seizures, or metabolic acidosis. Although rare, glycine toxicity may be life threatening. The pathophysiology, need for early detection and the role of early use of renal replacement therapy in acute glycine toxicity is discussed below.

Seizure and mental status change after surgery for pelvic organ prolapse

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a well-documented postoperative complication but infrequently seen after gynecologic procedures. Clinical presentation is often insidious, and neurologic sequelae may be severe, especially in women. We report the first published case of postoperative hyponatremia due to SIADH after vaginal reconstructive surgery. Our patient sustained a tonic-clonic seizure on postoperative day 2 in the setting of profound hyponatremia. Early detection and prompt treatment allowed her to achieve a complete recovery. Familiarity with uncommon complications of vaginal surgery is important. Prompt initiation of treatment can prevent potentially fatal consequences.

Transient pseudohypoaldosteronism masquerading as congenital adrenal hyperplasia

We report a six-week-old boy with genitourinary structural abnormalities who presented with profound hyponatraemia and hyperkalaemia due to transient type 1 pseudohypoaldosteronism (PHA) precipitated by a urinary tract infection (UTI), which responded rapidly to intravenous saline and antibiotics. In infants with structural abnormalities of the urinary tract, we wish to highlight the importance of recognizing type 1 PHA and its association with a UTI since prompt and appropriate treatment rapidly corrects the associated metabolic abnormalities. Conversely, the identification of type 1 PHA in an infant should precipitate a search for a UTI and structural abnormalities of the urinary tract.

Treating Profound Hyponatremia: A Strategy for Controlled Correction

An alcoholic patient presented with profound hyponatremia (serum sodium concentration, 96 mEq/L) caused by the combined effects of a thiazide diuretic, serotonin reuptake inhibitor, beer potomania, and hypovolemia. A computed tomographic scan of the brain was indistinguishable from one obtained 3 weeks earlier when he was normonatremic. Concurrent administration of 3% saline solution and desmopressin controlled the rate of correction to an average of 6 mEq/L daily and resulted in full neurologic recovery without evidence of osmotic demyelination. This case illustrates the value of controlled correction of profound hyponatremia.

A harmless high?

In March, 2010, a 15-year-old girl presented to our accident and emergency department with altered mental status, nausea, and vomiting. During the previous evening she had been out with friends, and had consumed a white powdery substance together with alcohol. On the day of admission she had become increasingly unwell, with symptoms that could not be attributed to a hangover and presented to us in the afternoon. Upon arrival, our patient was somnolent with a Glasgow Coma Score of 11 she opened her eyes in response to speech, uttered inappropriate words, and localised to pain. Blood pressure was 108/58 mm Hg; pulse rate was 54 beats per min; respiratory rate was 15 breaths per min; and ear-temperature was 36°C. Arterial blood gas analysis and 12-lead electrocardiogram were normal. There was no evidence of external injury, neck stiff ness, or localising neurological signs. Her pupils were dilated but reactive to light; there was no papilloedema. The remainder of the physical examination was normal. Brain CT scan was unremarkable; however, the cerebrospinal fl uid (CSF) opening pressure during lumbar puncture in the lateral decubitus position was raised at 350 mm of water. The CSF was otherwise normal with no signs of infection. Blood tests showed profound hyponatraemia at 118 mmol/L. Other relevant blood tests included: potassium, 4·5 mmol/L; bicarbonate, 23 mmol/L; urea, 3·3 mmol/L; creatinine, 46 umol/L; and blood glucose, 5·3 mmol/L. Serum osmolality was low at 256 mmol/kg, whereas urine osmolality was high at 742 mmol/kg. We suspected drug intoxication and did gas chromatography-mass spectroscopy of the patient’s urine; this was unequivocally positive for mephedrone metabolites, but was negative for opioids, methadone, barbiturates, cocaine, cannabinoids, alcohol, benzodiazepines, and amphetamines including ecstasy. Analysis of the white powder was consistent with mephedrone. A presumptive diagnosis of mephedrone-induced euvolaemic hypo-osmotic hyponatraemia with encephalopathy and

Profound hyponatremia in cirrhosis: a case report

IntroductionCirrhosis of the liver commonly leads to a state of chronic hypervolemic hyponatremia. Profound exacerbation of the hyponatremic state may occur in patients with decompensated cirrhosis in conjunction with acute stressors such as infection or binge alcohol ingestion.Case presentationA 47 year old man with a history of alcoholic cirrhosis presented to the hospital with symptomatic profound hyponatremia (serum sodium concentration of 105 meq/L) due to a recent infection and binge drinking. The patient was treated with antibiotics, diuretics and hypertonic saline and was placed on a fluid restricted diet. The serum sodium level corrected slowly over four days with symptomatic improvement occurring after two days. A brief discussion of the symptoms and treatment of acute and chronic hyponatremia in the setting of cirrhosis is included.ConclusionIn patients with cirrhosis, it is important to recognize the symptoms of hyponatremia, identify and treat any exacerbating conditions early in their course, and correct the serum sodium concentration slowly with frequent monitoring.