Serum osmolality

The clinician also needs to monitor body weight, serum osmolality, serum electrolytes, complete blood cell count, urinalysis, and cultures (if appropriate). With an urgent or emergency situation, evaluation of the volume status of the patient is the most important outcome. 

The client s osmolality serum level is assessed when administering mannitol, but this level does not evaluate the effectiveness of the medication. 

Garcia-Morales EJ, Cariappa R, Parvin CA. Osmole gap in neurosurgical-neurosurgical intensive care unit its normal value, calculation, and relationship with mannitol serum concentrations. Crit Care Med 2004 32(4) 986-991. 

The calculated serum osmolality helps determine deviations in TBW content. 

TBW depletion (often referred to as dehydration ) is typically a more gradual, chronic problem compared to ECF depletion. Because TBW depletion represents a loss of hypotonic fluid (proportionally more water is lost than sodium) from all body compartments, a primary disturbance of osmolality is usually seen. The signs and symptoms of TBW depletion include CNS disturbances (mental status changes, seizures, and coma), excessive thirst, dry mucous membranes, decreased skin turgor, elevated serum sodium, increased plasma osmolality, concentrated urine, and acute weight loss. Common causes of TBW depletion include insufficient oral intake, excessive insensible losses, diabetes insipidus, excessive osmotic diuresis, and impaired renal concentrating mechanisms. Long-term care residents are frequently admitted to the acute care hospital with TBW depletion secondary to lack of adequate oral intake, often with concurrent excessive insensible losses. 

Osmolality is a measure of the number of osmotically active particles per unit of solution, independent of the weight or nature of the particle. Equimolar concentrations of all substances in the undissociated state exert the same osmotic pressure. Although the normal serum osmolality is 280 to 300 mOsm/kg (280 to 300 mmol/kg), multiple scenarios exist where this value becomes markedly abnormal. The calculated serum osmolality helps determine deviations in TBW content. As such, it is often useful to calculate the serum osmolality as follows ... 

Serum creatinine, blood urea nitrogen, urinalysis, urine osmolality, specific gravity. 

Hyperglycemic hyperosmolar nonketotic syndrome Severe increase in serum glucose concentration without the production of ketones, leading to an increase in serum osmolality and symptoms... 

Osmolar gap The difference between the measured serum osmolality and the calculated serum osmolality. 

The potent antidiuretic hormone AVP orchestrates the regulation of free water absorption, body fluid osmolality, cell contraction, blood volume, and blood pressure through stimulation of three G-protein-coupled receptor subtypes Vi-vascular types a and b, V2-renal, and V3-pituitary. Increased AVP secretion is the trademark of several pathophysiological disorders, including heart failure, impaired renal function, liver cirrhosis, and SIADH. As a consequence, these patients experience excess water retention or inadequate free-water excretion, which results in the dilution of sodium concentrations, frequently manifesting as clinical hyponatremia (serum sodium concentration <135mmol/L). This electrolyte imbalance increases mortality rates by 60-fold. Selective antagonism of the AVP V2 receptor promotes water... 

Sugatt, R.H. 1980a. Effects of sublethal sodium dichromate exposure in freshwater on the salinity tolerance and serum osmolality of juvenile coho salmon Oncorhynchus kisutch, in seawater. Arch. Environ. Contam. Toxicol. 9 41-52. 

Depending on serum osmolality, hyponatremia is classified as isotonic, hypertonic, or hypotonic (Fig. 78-1). 

Prepare treatment medium containing various concentrations of test compound 19.7 ml of Eagle s medium (without serum) plus 300 pi of stock concentration of compound in a preferred solvent (e.g., water, ethanol, DMSO, etc.). The final concentration of solvent other than water should not exceed 1% v/v. Normally a range of 0-5000 pg ml-1 (final concentration) is covered. For a sparingly soluble compound, the highest concentration will be the lowest at which visible precipitation occurs. Similarly, if a compound has a marked effect on osmolality, concentrations should not be used that exceed 500 milliosmoles (mosm) per kg. In addition, a pH range of 6.5-7.5 should be maintained. 

Serum measurements of lithium, creatinine, electrolytes, and plasma osmolality... 

Urea concentration in the medulla plays an important role maintaining the high osmolarity of the medulla and in the concentration of urine. ADH secretion is regulated by serum osmolality and by volume status. A new class of drugs, the vaptans (see under Agents That Alter Water Excretion), are ADH antagonists. 

The calculated serum osmolality is dependent mainly on the serum sodium and glucose and the blood urea nitrogen and can be estimated from the following formula ... 

This calculated value is normally 280-290 mOsm/L. Ethanol and other alcohols may contribute significantly to the measured serum osmolality but, since they are not included in the calculation, cause an osmolar gap ... 

Table 58-2 lists the concentration and expected contribution to the serum osmolality in ethanol, methanol, ethylene glycol, and isopropanol poisonings. 

Hi) Osmolality. The majority of spoils drinks are formulated to be isotonic, i.e. to have an osmotic pressure matching that of blood serum. This is considered to optimise absorption from the intestine although, as stated earlier, water uptake is optimal with slightly hypotonic solutions. 

Blood serum osmolality varies slightly within the individual, and from person to person, but is generally taken to be 287 mOsm/kg. 

An 87-year-old woman received intra-articular betamethasone (Diprophos) 7 mg on three occasions for painful knee joints over 6 months. Six weeks after the last injection she developed diffuse pain and contractures in the legs, fatigue, nausea, abdominal pain, and weight loss of 6 kg. Both knee joints were tender but there was no effusion. Her serum sodium concentration was 123 mmol/1, serum osmolality 254 mosmol/kg, urine sodium 136 mmol/1, and urinary osmolality 373 mosmol/kg. The syndrome of inappropriate antidiuretic hormone secretion was diagnosed, but despite treatment she remained drowsy and hyponatremic. About a week later, she developed hypotension and symptoms of an acute abdomen. Further investigations showed that her basal cortisol concentration was low (36 nmol/1) but it increased to 481 nmol/1 after a short tetracosactide test, consistent with acute adrenal crisis. She recovered rapidly after treatment with oral hydrocortisone, but still required glucocorticoid substitution several months later. 

A 67-year-old man, who had taken amiodarone 200 mg/ day for 3 months, developed hyponatremia (serum sodium concentration 117 mmol/1) (27). He was also taking furosemide 20 mg/day, spironolactone 25 mg/ day, and lisinopril 40 mg/day. His urine osmolality was 740 mosmol/kg with a normal serum osmolality. Fluid restriction was ineffective, but when amiodarone was withdrawn the sodium rose to 136 mmol/1. 

A 62-year-old woman with paroxysmal atrial fibrillation who had taken amiodarone 300 mg/day had a serum sodium concentration of 120 mmol/1 with a normal serum potassium and a reduced serum osmolality (240 mmol/kg) the urinary sodium concentration was 141 mmol/1 and the urine osmolality 422 mmol/kg (25). There was no evident cause of inappropriate secretion of ADH and within 5 days of withdrawal of amiodarone the serum sodium concentration had risen to 133 mmol/ 1 and rose further to 143 mmol/1 14 days later. There was no rechallenge and no recurrence of hyponatremia during the next 6 months. Another case has been reported (28). 

A 76-year-old woman taking lisinopril 20 mg/day and metoprolol for hypertension developed headaches, nausea, and a tingling sensation in her arms. Her serum sodium was 109 mmol/1, with a serum osmolality of 225 mosm/kg, urine osmolality of 414 mosm/kg, and urine sodium of 122 mmol/1. She had taken diclofenac 75 mg/day for arthritic pain for 6 years and naproxen for about 1 month. Propoxyphene napsylate and paracetamol had then been substituted and zolpidem had been started. A diagnosis of SIADH was postulated and thyroid and adrenal causes were excluded. Lisinopril was withdrawn and fluid was restricted to 100 ml/day. The serum sodium gradually corrected to 143 mmol/1. 

A 34-year-old woman with a history of renal insufficiency induced by long-term use of cocaine developed respiratory failure and was intubated and sedated with intravenous lorazepam (65 mg, 313 mg, and 305 mg on 3 consecutive days). After 2 days she had a metabolic acidosis, with hyperlactatemia and hyperosmolality. Propylene glycol, a component of the lorazepam intravenous formulation, was considered as a potential source of the acidosis, as she had received more than 40 times the recommended amount over 72 hours. Withdrawal of lorazepam produced major improvements in lactic acid and serum osmolality. 

A 74-year-old man with rheumatoid arthritis developed nausea and headache 1.5 months after starting to take mizoribine. His serum sodium concentration fell to 118 mmol/1, but his urinary sodium excretion was normal and there was no hypotension or hemoconcentration. His serum antidiuretic hormone concentration was raised at 0.59 pg/ml in spite of a reduced serum osmolality to 254 mosm/kg. He had no organic disease likely to cause SIADH. Despite infusion of hypertonic saline, his serum sodium concentration did not return to normal. Shortly after mizoribine withdrawal, his serum sodium increased... 

---