The plasma osmolality and oncotic pressures in an organism can be used to determine the direction of fluid movement within the system, therefore, the relative concentration of ions and protein in the solvent. As a result, we can observe the results of the fluid movement, which can typically manifest as edema, dehydration, changes in blood pressure, seizures, and changes in intracranial pressure. Furthermore, disturbances in osmolality can be used as an indication for the use of intravenous fluids which can be used to quickly alter the plasma osmolality and oncotic pressures in the vascular system.
Osmolarity is the number of milliosmoles of solute per liter solution. This is different from osmolality (osm), which is the milliosmoles of solute per kilogram of solution.
Water flows from a compartment of low osmolality to a compartment with high osmolality. This can only occur if the membrane between the two compartments is permeable to water. An example of this is when comparing plasma osm and interstitial fluid osm. At the cellular level, we can compare the intracellular osm to the extracellular matrix. In this system, the phospholipid bilayer serves as the semipermeable membrane through which water can flow.
Osmolarity is the number of osmoles of solute per liter solution, which is different than osmolality, which is the osmoles of solute per kilogram of solution. Osmoles are different from moles in that it takes into account the dissociation of cations and anions in water.
If 1 kg of water gets added to 1 mole of NaCl salt, then we observe the salt separate into its ions. As a result, there will be 1 mol of Na and 1 mol of Cl. Restated, this means there are 2 osmoles of ions in 1 kg of water which results in a solution with an osmolality of 2osm/1kg.
Components that contribute to plasma osmolality:
Any solute in the plasma will contribute to the osmolality. Examples include proteins, ions, urea, and sugars. The relative osmoles of each are summed to give the total osmolality per 1 kg of plasma.
How to calculate plasma osmolality?
The Dorwart and Chalmers formula is widely used to estimate plasma osmolality. It utilizes the basic metabolic panel (BMP) to gain measured values of sodium, glucose, and blood urea nitrogen.
Serum Osmolality=1.86 (Na)+(Glucose)/18 +(BUN)/2.8+9
Water flows from a compartment of low osmolality to a compartment with high osmolality; this can only occur if the membrane in between the two compartments is permeable to water. An example of this is when comparing plasma osmolality and intracellular fluid osmolality.
For example, if a cell is in a relatively hyperosmolar solution, to reach homeostasis, fluid will diffuse out of the cell towards the highly concentrated environment. As a result, the cell will shrivel.
Posterior Pituitary/Renal Systems
Renin Angiotensin Aldosterone System (RAAS)
The RAAS system is crucial because it maintains extracellular volume, sodium concentration, and blood pressure. It does this by secreting a hormone called renin by the kidneys. Renin then circulates to the adrenal glands, and downstream effects occur. See mechanisms below for details.
The function of albumin in the serum is multifaceted. Albumin is a protein that can be utilized to carry lipid-soluble substances such as thyroid hormone, sex hormones, and triglycerides. It also serves a major role in contributing to the plasma oncotic pressure as it can comprise up to 50% of all circulating serum proteins. It has been used as an agent to expand intravascular volume and control both intracranial pressure and intraocular pressure.
Ions and glucose contribute to 95% of the osmotic pressure as they are the most abundant in the serum. Osmolality, and subsequently, osmotic pressure is not affected by the size or charge of the solutes but only the number of solutes.
The function of osmolality and oncotic pressure is to keep the ions suspended in solution at optimal concentrations which are set by the cells in the body, which helps create ion gradients leading to action potential generation, muscle contractions, and adequate glucose supply in the serum.
Posterior Pituitary/Renal Systems
Renin Angiotensin Aldosterone System (RAAS)
Macula densa cells are present in the wall of the distal convoluted tubule of the kidney; their primary function is to sense the concentration of sodium chloride in the filtrate. Only two physiologic scenarios exist:
Hypoosmolar Plasma: The pathologies decrease the osmolality of plasma
Psychogenic polydipsia: This is a psychiatric condition characterized as self-induced water intoxication. There are three phases to the disease process. First, there is a polyuria and polydipsia phase in which the patient is thirsty and has excessive urine output. The second phase appears as hyponatremia on blood as the kidney is unable to excrete all the water, which results in the hypo-osmolar plasma. The final phase consists of the sequelae from water intoxication and hyponatremia, which include delirium, ataxia, seizures, nausea, and vomiting. Death may result if the electrolyte abnormalities are not corrected promptly. Be aware central pontine myelinolysis as deadly sequelae of quick sodium correction.
Syndrome of inappropriate ADH (SIADH): This condition occurs when the human body produces and secretes an excessive amount of ADH via CNS tumors, lung cancers, and medications, resulting in the kidneys reabsorbing too much water and manifests as a dilutional hypo osmolar plasma and hypertension. Treatment can involve vasopressin receptor blocker such as tolvaptan, removing cancer, which is creating the ADH, remove the medications inducing SIADH, and therapy with hypertonic saline.
Nephrotic Syndrome: This general term serves to describe disease processes that result in proteinuria (over 3grams/day), accompanied by hypoalbuminemia, hypertriglyceridemia, and a hypercoagulable state. The characteristic proteinuria occurs when there is damage to glomerular basement membrane or podocyte foot processes, which result in a decreased plasma osmolality and oncotic pressure. Edema is frequently a presenting sign because there is not enough oncotic pressure to draw water into the vasculature from the extracellular matrix.
Liver Cirrhosis: The production of albumin takes place in the liver and is then secreted out of the hepatocytes and into the extravascular space and then returned to the blood via lymphatic drainage and being directly released into, a blood vessel, the space of Disse. When the liver incurs damage, it is unable to produce albumin and results in a hypoosmolar plasma.
Hyper Osmolar States:
Diabetes Insipidous (DI): This disease demonstrates excretion of a large volume of urine, which results in concentrated, hyperosmolar plasma (greater than 300mOsm/liter) and dilute, hypoosmolar urine (less than 300mOsm/liter). It can result from central damage to the neurons which are responsible for the creation of ADH. Examples of sources of damage include infarcts, germinomas, Langerhans histiocytosis, and sarcoidosis. Another cause for DI is end-organ resistance. Although there is ADH present, the patient will have a genetic mutation in the vasopressin receptors which render the hormone ineffective. 
Dehydration: see above.
There are many clinical implications of alterations to the plasma osmolar state and the oncotic pressure.
Clinicians can monitor the following:
Pathologies include (but are not limited to):
It is essential to consider all differential diagnoses; ultimately, further lab testing will be necessary to reach a diagnosis.
|||Kok B,Karvellas CJ, Management of Cerebral Edema in Acute Liver Failure. Seminars in respiratory and critical care medicine. 2017 Dec; [PubMed PMID: 29262439]|
|||Rasouli M, Basic concepts and practical equations on osmolality: Biochemical approach. Clinical biochemistry. 2016 Aug; [PubMed PMID: 27343561]|
|||Dorwart WV,Chalmers L, Comparison of methods for calculating serum osmolality form chemical concentrations, and the prognostic value of such calculations. Clinical chemistry. 1975 Feb; [PubMed PMID: 1112025]|
|||Gennari FJ, Current concepts. Serum osmolality. Uses and limitations. The New England journal of medicine. 1984 Jan 12; [PubMed PMID: 6361557]|
|||Valerio C,Theocharidou E,Davenport A,Agarwal B, Human albumin solution for patients with cirrhosis and acute on chronic liver failure: Beyond simple volume expansion. World journal of hepatology. 2016 Mar 8; [PubMed PMID: 26981172]|
|||Danziger J,Zeidel ML, Osmotic homeostasis. Clinical journal of the American Society of Nephrology : CJASN. 2015 May 7; [PubMed PMID: 25078421]|
|||Barajas L, Anatomy of the juxtaglomerular apparatus. The American journal of physiology. 1979 Nov; [PubMed PMID: 386808]|
|||SKIN TURGOR in dehydration. Nutrition reviews. 1957 Nov; [PubMed PMID: 13484138]|
|||Nigro N,Grossmann M,Chiang C,Inder WJ, Polyuria-polydipsia syndrome: a diagnostic challenge. Internal medicine journal. 2018 Mar; [PubMed PMID: 28967192]|
|||Bhatia MS,Goyal A,Saha R,Doval N, Psychogenic Polydipsia - Management Challenges. Shanghai archives of psychiatry. 2017 Jun 25; [PubMed PMID: 28904515]|
|||Peri A,Grohé C,Berardi R,Runkle I, SIADH: differential diagnosis and clinical management. Endocrine. 2017 Jan; [PubMed PMID: 27025948]|
|||Liebeskind DS, Nephrotic syndrome. Handbook of clinical neurology. 2014; [PubMed PMID: 24365309]|
|||Gatta A,Verardo A,Bolognesi M, Hypoalbuminemia. Internal and emergency medicine. 2012 Oct; [PubMed PMID: 23073857]|
|||Di Iorgi N,Napoli F,Allegri AE,Olivieri I,Bertelli E,Gallizia A,Rossi A,Maghnie M, Diabetes insipidus--diagnosis and management. Hormone research in paediatrics. 2012; [PubMed PMID: 22433947]|
|||Zhou WC,Zhang QB,Qiao L, Pathogenesis of liver cirrhosis. World journal of gastroenterology. 2014 Jun 21 [PubMed PMID: 24966602]|
|||Lee CS,Auld J, Heart Failure: A Primer. Critical care nursing clinics of North America. 2015 Dec [PubMed PMID: 26567488]|