The DDAVP clamp may be used to avoid this pitfall (next section). Tea-and-toast or beer potomania hyponatremia occur when low solute intake limits the ability of the kidneys to produce urine that maintains electrolyte homeostasis. Evaluate further for alternative or additional problems. ADH is primarily released in response to hyperosmolality–acting to reduce the amount of fluid excreted by the kidneys, thus retaining free water. Original episode written and produced by: Matthew Watto MD, FACP, Show Notes and CME questions by: Deb Gorth ScM, Cover Art and Infographic by: Edison Jyang, Hosts: Stuart Brigham MD; Matthew Watto MD, FACP; Paul Williams MD, FACP, Editor: Molly Heublein (written materials); Matthew Watto MD (audio), A novel, collaborative, POCUS fellowship training is available at the University of Pennsylvania for IM and FM graduates! 12 Cerebral edema can occur when acute (<48 hours) hyponatremia is not treated promptly and may cause increased intracranial pressure, seizures, coma, tentorial herniation, and death. . Interview season is in full swing and they’re actively accepting applications. A raised urea may suggest dehydration Her labs are notable for an elevated creatinine of 7.0. Even asymptomatic hyponatremia can still have clinical implications for older patients, it is associated with increased risk of falls and fractures (Kuo et al 2017). It is much easier to exceed this 2 L fluid consumption threshold. The differential diagnosis of hyponatremia with a high urine sodium and osmolality (as determined in this case) consists of diuretic use, primary or secondary adrenal insufficiency, cerebral salt wasting, salt-wasting nephropathy, and SIADH (1). Patients with symptomatic hyponatremia should be treated with hypertonic fluid (either 3% saline or hypertonic sodium bicarbonate). 3. MDCalc, These equations treat the body as a passive receptacle which receives IV fluid and does nothing with it. When this happens, your body's water levels rise, and your cells begin to swell. Contraindications to urea are as follows: Dosing and monitoring is outlined in the figure below (further discussion of aquaresis, This is an effective strategy for SIADH. Predictive equations will fail most spectacularly for patients with reversible hyponatremia. The cause of high protein should be investigated (ex: IVIG, lipid panel, or serum protein electrophoresis). This takes the patient's kidneys out of the equation, preventing the patient from auto-correcting. Aquaretics such as tolvaptan (vasopressin V2 receptor blocker) are particularly helpful in SIADH [48]. Out of stock at Walmart. Spot urine osmolality is only sometimes helpful because almost all cases of hyponatremia are associated with inappropriately concentrated urine. Salt tablets can relax fluid restriction by adding solute load. A 50-year old woman naive to the health care system presents to the ED with nausea, malaise, and decreased exercise tolerance for several weeks. If the hyponatremia is ADH independent, the spec grav (yes we’re cool) will be 1.005-1.010 [urine osmolality <100-200 mOsm/kg] for dilute urine or isosthenuric urine (a fancy way of saying a urine concentration neither more nor less dilute than protein-free plasma) indicating that the condition is likely caused by tea-and-toast, beer drinkers potomania, or primary polydipsia. Response to therapy will sometimes add diagnostic clarity, for example: Persistent, recurrent hyponatremia reflects an ongoing cause (e.g. Rate of correction for chronic low serum sodium is 5 mEq immediately, 10 mEq over the first day, and 8 mEq per day after that. History can also be a very useful tool; a diagnosis of heart failure, recent diarrhea, or history of certain medications can provide a clue to the pathology of hyponatremia. Dr. Topf’s book is $967 on Amazon. More information on the treatment of hyponatremia European Society of Endocrinology Clinical Practice Guidelines is Dr. Topf’s recommended resource. Pain (Salaami 2018), surgery (Cornforth 1998), positive pressure ventilation, asthma, medications (Liamis et al 2008), pneumonia (Don et al 2008), and head injury (Dozi et al 1982) can cause transient SIADH (Sterns 2015). @article{Hoek2009SevereHW, title={Severe hyponatremia with high urine sodium and osmolality. A urine sodium level less than 20 mmol/L is indicative of hypovolemia, whereas a level greater than 40 mmol/L is suggestive of the syndrome of inappropriate antidiuretic hormone secretion. (3) In reality, the urine electrolytes often aren't checked prior to administering fluid. The effect of 3% sodium on your patient's sodium can be calculated using this. (3) Monitor fluid balance, to make sure that the patient doesn't become volume overloaded or depleted. Dr. Topf has received honoraria from AstraZeneca and Cara Therapeutics. . Some individuals have a low sodium yet a high tonicity (. In SIADH urine sodium and urine osmolality are high for plasma osmolality. Low sodium with high osmolality is due to high levels of an additional osmolite, most likely glucose, drawing water into the blood. ADH dependent hyponatremia can either be hypervolemic (ex: heart failure, liver failure, or nephrotic syndrome), hypovolemic (ex: GI losses, renal losses, or bleeding), or euvolemic (SIADH, hypothyroid, or adrenal insufficiency). Overall, serum osmolality and urinary sodium measurements are integral to the diagnosis and management of hyponatremia. ). Even asymptomatic hyponatremia can still have clinical implications for older patients, it is associated with increased risk of falls and fractures (, Not all serum components cause movement of water; urea, ethanol, and other small nonpolar molecules that can freely cross the cell membrane and do not contribute to. Measuring the serum osmolality, urine sodium concentration and urine osmolality will help differentiate among the possible causes. Frequent doses of loop diuretic may cause frequent urination at night, interfering with sleep. Simply put, if you click on our Amazon.com links and buy something we earn a (very) small commission, yet you don’t pay any extra. Hypovolemic hyponatremia due to extra-renal volume loss. This will mimic nephrogenic diabetes insipidus. After 6-12 hours you may liberalize a bit. Failure to consider the osmotic effect of KCl is one driver of unexpected over-correction of hyponatremia. If you use the DDAVP clamp, be sure to restrict the patient's fluid intake. https://thecurbsiders.com/episode-list Original air date: July 17, 2017; Updated September 7, 2020. The patient has a urine sodium level of 200, urine potassium of 100, urine nitrogen of 20, and a urine glucose of 1. While a volume status exam would be a useful way to distinguish between these causes–with jugular venous pressure, orthostatics, peripheral edema, mucous membrane moisture, and skin turgor providing some information–, ). SSRI, anti seizure, sulfonylurea, or opioid medications can lead to SIADH mediated hyponatremia (Shepshelovich et al 2017 and Liamis et al 2008). The patient denied use of alcohol and illicit drugs. It provides an estimate of antidiuretic hormone (ADH) activity and can be used to evaluate the cause of hyponatraemia. Dr. Topf’s threshold for hospital admission hyponatremia is < 130 mEq/L. Euvolemic hyponatremia (SIADH, hypothyroidism, or adrenal insufficiency). The impact of oral potassium tablets on serum sodium can be estimated as above (if we approximate the total body water as roughly equal to 55% of the patient's weight). Thus, even though the kidney is “trying” to retain water, it's less able to achieve that. For patients with acute hyponatremia (definitely developing over <<48 hours), faster rates of sodium correction may be safe. The opinions expressed on this show are those of The Curbsiders and do not necessarily represent the views and opinions of their places of employment. Vasopressin or DDAVP (these don't technically stimulate ADH release, but rather directly stimulate ADH receptors. The “Seal Team 6” of hyponatremia is a “DDAVP clamp” performed in the ICU. Consider these calculations in the context of a diet that is 100 mOsm/day instead of the expected 600 mOsm/day, now the maximum amount of urine would be 2 L (100mOsm/day 50 mOsm/L = 2 L). This is the traditional therapy for hyponatremia. The dilute urine is evidence of its efforts; passing free water is its way of concentrating the extracellular fluid. The urine osmolality in ADH dependent hyponatremia is concentrated compared to serum, typically 300-800 mOsm/kg. You can help by adding to it. Normal sodium: 135-145. EMCrit is a trademark of Metasin LLC. AM cortisol and ACTH stimulation test abnormal? That can’t be correct for a paperback? using the urine specific gravity (spec grav if you want to sound cool) of the urine analysis (UA). Hyponatremia can cause anything from moderate symptoms like nausea and vomiting to severe symptoms like coma and death (Spasovski et al 2016). Urea will cause a pure water loss (aquaresis), so it will increase the sodium level with less volume loss. Always be sure to look for all potential reversible causes of SIADH (e.g. The limited urine production of acute kidney failure or end stage renal disease means that even smaller volumes of water ingestion are necessary to cause ADH independent hyponatremia. However, hyperglycemia is an indication that the body cannot effectively manage glucose, turning it into a component of tonicity. Topics covered include: true versus false hyponatremia, SIADH, tea and toast hyponatremia, beer potomania, safe rates of sodium correction, IV fluid choice, vaptans and more. For smaller patients, 1 or 1.5 ampules (50-75 ml) might be more appropriate (depending also on the clinical context and the urgency of increasing the sodium). Hypertonic bicarbonate is usually the fastest medication to obtain in an emergency. the patient has a urine osmolality > 150 mOsm/kg, they potentially have SIADH and because the body is retaining water, the patient may be fluid restricted, and not given any saline fluids. History can also be a very useful tool; a diagnosis of heart failure, recent diarrhea, or history of certain medications can provide a clue to the pathology of hyponatremia. Overall, urea is probably a 2nd or 3rd line agent here (and potentially inferior to lactulose). His book is free (it is linked on his website as well as the episode). Listeners can claim Free CE credit through VCU Health at http://curbsiders.vcuhealth.org/ (CME goes live at 0900 ET on the episode’s release date). fraternity hazing), Beer potomania (excessive beer intake with reduced solute intake), Elderly patients who eat a “tea-and-toast” diet, anorexia (low solute intake). While a volume status exam would be a useful way to distinguish between these causes–with jugular venous pressure, orthostatics, peripheral edema, mucous membrane moisture, and skin turgor providing some information–volume status exams are notoriously unreliable (Chung et al 1987). Hyponatremia due to heart failure is usually chronic and is not a life-threatening process. Summary: The etiology of hyponatremia is assessed based on urine osmolality and sodium. The first question to ask when a patient is found to have hypoosmolar-hyponatremia is: is this ADH dependent hyponatremia or is this ADH independent hyponatremia? This causes the body to suddenly excrete a lot of free water, thereby causing the sodium to rise. Tea-and-toast or beer potomania hyponatremia occur when low solute intake limits the ability of the kidneys to produce urine that maintains electrolyte homeostasis. More recently the TEMPO 3:4 trial found that tolvaptan slows the progression of autosomal dominant polycystic kidney disease (, More information on the treatment of hyponatremia, European Society of Endocrinology Clinical Practice Guidelines, Dr. Joel Topf’s Textbook. Premenopausal women (little extra space in cranium for brain to swell), Intracranial pathology (e.g. 50 mOsm/L = 2 L). With DDAVP, if the patient drinks too much they will lower their sodium. (1) Clinicians cannot reliably determine volume status at the bedside. TSH very elevated? Urinary osmolality corresponds to urine specific gravity in nondisease states. If the patient's sodium rises too quickly, don't give up (“well the patient's ok, they seem to have tolerated it”). The Curbsiders Internal Medicine Podcast. In SIADH, the excess of ADH results in water retention, but not solute retention. If there are no inputs, the sodium should stay roughly stable. Stuart was kind enough to remind us that axillary moisture is one of the best indicators of volume status, but for some reason, I keep forgetting to check my patients’ armpit sweat (. If urea is used, it should be closely monitored. Aiming for 6 mEq per day gives you a buffer; the guidelines are 0.5 meq/h, so if you aim for 6 mEq, and go a bit too fast, you still stay under the speed limit. Check cortisol to rule out adrenal insufficiency, which presents with hyperkalemia and salt wasting nephropathy (, ). Correction at rates >8-10 mM per day may cause osmotic demyelination syndrome (previously termed central pontine demyelination). In the United States, each hypertonic bicarbonate ampule generally contains 50 ml (as shown above). One of two things will happen at this point: (a) If the cause of hyponatremia has been eliminated (e.g. The best approach to chronic, asymptomatic hyponatremia could be to do nothing. Urine electrolytes and serum uric acid can provide additional information to distinguish between different etiologies of ADH dependent hyponatremia. No. Meanwhile, vaptans have a unique capacity to cause runaway water loss and overcorrection. This solute is subsequently excreted via urine, which can be concentrated in a range from 50 mmol/L to 1200 mmol/L. hours fluid restriction, urinary osmolality should be >850mmol/kg water • Urine sodium is useful for the differential diagnosis of hyponatraemia but must be interpreted with volume status and is difficult to interpret in those taking diuretics • Serum urea is a marker of extracellular fluid volume. Appropriate laboratory tests to help differentiate the hyponatremia include serum and urine electrolytes, serum and urine osmolality, and thyroid and adrenal hormones. The Curbsiders report no relevant financial disclosures. If the sodium has increased by <4 mM, then an additional round of hypertonic therapy may be needed (with a goal of increasing the sodium by ~4-6 mM total). After an overnight fast, the urine osmolality should be at least 3 times the serum osmolality ; After 12-14 hours of restricted fluid intake, urine osmolality should be > 850mOsm/Kg. Urine osmolality is primarily a test of urine concentrating ability and whether this is appropriate for the clinical state of the patient. Read the Clinical Chemistry Journal's November 2009 Clinical Case Study and student discussion. The following are 10 summary points to remember about this review article on hyponatremia in acute decompensated heart failure (ADHF): Hyponatremia (serum sodium ; 135 mEq/L) is present in about 20% of ADHF patients upon admission. ADH dramatically lowers water excretion → thus, water intake easily exceeds water output. It’s $$$ on Amazon, but g, Tartine (cookbook) by Elizabeth M. Prueitt, I Hate You, Don’t Leave Me by Hall Strauss, 8.0 Bit Techno- The Curbsiders Theme Song by Stuart Kent Brigham, Differentiate true and false hyponatremia, Recall the pathophysiology of true and false hyponatremia, Interpret blood and urine tests to identify the cause of hyponatremia, Recall the limitations of the volume status exam, List ADH dependent causes of hyponatremia, List ADH independent causes of hyponatremia, Explain the pathophysiology of beer drinker’s potomania and “tea and toast” hyponatremia, Use uric acid to differentiate SIADH from other causes of hyponatremia, Recall safe rates of correction for hyponatremia. Dr. Topf reminds us that a bowl of spaghetti is the same as a cup of water to a nephrologist–we are no longer eagerly awaiting an invitation to Dr. Topf’s Sunday night spaghetti dinners–because the carbohydrates are metabolized to water and CO2. At this point, they would require maintenance therapy for SIADH (e.g. Hypo-osmolality in euvolemic patients should cause excretion of a large volume of dilute urine (eg, osmolality < 100 mOsm/kg [< 100 mmol/kg]) and specific gravity < 1.003). The only decision to be made here is whether to give hypertonic therapy, explored in the next section: Dizziness, gait instability, tremor, multifocal myoclonus.
History Chapter 3 Class 8 Notes, Louis Early Jr Now, Mehndi For Kids, We Are Legion: The Story Of The Hacktivists Summary, Cauliflower Leaf Recipes, Azekah Daniel Drama List, Toyota Etios Liva Review Team-bhp,