Hyponatremia in dogs and cats

Abstract

Objective: To review the pathophysiology, diagnostic approach, and treatment recommendations for hyponatremia in dogs and cats. Etiology: Hyponatremia almost always results from an increase in total body water (TBW), and not from loss of sodium. Abnormalities in antidiuretic hormone (ADH) are commonly part of the etiology of hyponatremia. Diagnosis: Diagnosis of hyponatremia focuses on the cause of the increase of TBW. Assessment of the patient's volume status and measurement of urine sodium concentration are important factors. Measurement or calculated estimation of plasma osmolality can also guide the assessment of hyponatremia.Therapy: Too rapid correction of serum sodium can precipitate osmotic demyelination syndrome.As a general rule, serum sodium concentration should be raised ≤10 mmol/L over 24 hours, but rapid increases in serum sodium are indicated if neurologic abnormalities are evident. Serum sodium can be increased using hypertonic saline, with dosing based on the patient's calculated sodium deficit. Treatment of the underlying cause of water ingestion or retention is also required to fully resolve hyponatremia. Prognosis:Mortality rates are significantly higher in dogs and cats with hyponatremia compared to those with normal serum sodium concentrations, even in patients with mild hypontremia (<5 mmol/L below the lower value of the reference interval). Hyponatremia is also associated with increased risk of death if present during specific disease states in dogs. K E Y W O R D Santidiuretic hormone, electrolyte, osmolality, sodium

The osmotic demyelination syndrome: the resilience of thalamic neurons is verified with transmission electron microscopy

“…[91][92][93][114][115][116][117][118][119][120][121] In other studies, where a rapid correction of chronic hyponatremia in rats recapitulates most of the human ODS histopathology, it was shown that myelin and oligodendrocyte losses occurred with neurons and axons sparing in specific brain regions such as cortical regions, hippocampus and basal ganglia associated with somatosensory relationship defects. 64,101,102 In this paradigm, following other similar studies, [72][73][74] the same murine model developed an astrocytopathy leading into oligodendrocytopathy with unambiguous demyelinating lesions in the thalamus, as shown in Figure 2a-d. Following hematoxylin and eriochrome cyanine R staining, parasagittal brain sections demonstrated a conspicuous loss of myelin of the white matter in several specific regions, such as the thalamus, colliculus, and pons.…”

“…One could also speculate that adjacent external zones of the damaged deteriorating regions with a blood-brain barrier remaining intact would assist with the less damaged and maintained astrocytes intercellular contacts with neurons and would facilitate in the structural and some functional resistance and reconstruction. 64,[71][72][73][74][101][102][103]109,110 In ODS, no blood-born cells or proteins have been spilled out like in other neurodegenerative defects (i.e. multiple sclerosis or other CNS vascular trauma associated pathologies) making the injurious region damaged free from other immune reactivity 112,113,133,273 and other eventual potent follow-up necrotic neural sequels.…”

“…237 Some salvage strategies, avoiding cell trauma toward neuron cell death seemed similar to. 238 The definition of ODS remained 72,73 because the main degradations occurred, caused by a disrupted osmotic gradient initiated in the vascular supply, transmitted injurious change signals to astrocytes that expanded into submitting oligodendrocytes into inadequate maintenance of the myelin 74,89 allowing some prompt but short-timed implication of the microgliocytes, properly 'trained' to then remove defective parts without creation of any other immunoreactive nerve tissue defects like in multiple sclerosis 111,239 as defined by the ODS condition [64][65][66][72][73][74]233 but where clarifications are still needed. 240 At ODS 48 h, myelin sheets have not all recovered and those repaired still contained disordered concentric layers due to intermembranous gaps and delicate smudge-like aspects.…”

“…62,63 Laboratory rats and dogs have traditionally been the species used in ODS research studies. [64][65][66][67] The development of genetically modified mouse models has hinted a way for the manipulation of genes or cells possibly relevant to the pathophysiology of ODS. Insofar, three other studies have tried to create rodent models of ODS.…”

A primary cilium in oligodendrocytes: a fine structure signal of repairs in thalamic Osmotic Demyelination Syndrome (ODS)

“…3,9,26 The high incidence noted in the recent years is probably caused by a more frequent magnetic resonance imaging (MRI) utilization for neurologic diagnostics in miscellaneous conditions. 8,14,[21][22][23][24][25][26][27][28][29][30] Found or induced in small mammals, 31,32 ODS research studies have been done with rats and dogs before mice. 4,[31][32][33][34][35][36][37][38][39][40][41] Future development of genetically modified mouse models may further clarify the pathophysiology of ODS, its associated disorders, as well as its resolution.…”