2.0 ANCC CONTACT HOURS potomania: Drink in this atypical cause of By Mark McGraw, BSN, RN, CEN, CCRN, CTRN

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Copyright © 2012 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. IT WAS A TYPICAL MONDAY afternoon in the busy ED. I in- troduced myself to my next patient, Mr. H, a thin man in his mid-30s. After reviewing his vital signs, I asked how we could help him. As he sat there silently, his sister reported he’d been forgetful and shaky with periods of confusion for the past few days, but his condition had worsened today. “He’s always drunk...every day. This is nothing new!” She told me he’d been out of work because of abuse and dependence and had moved in with her a little over 6 months ago. The patient admitted to consuming at least thirty 12-oz

HOTO cans of beer (10.8 L) a day. P Caring for Mr. H taught me about an unusual but potentially TOCK S I fatal consequence of excessive beer consumption known as

4537/ beer potomania. This article describes this disorder and its OUG

D dangers, how to recognize it, and the critical, very specific

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Copyright © 2012 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. treatment needed to avoid serious The ED physician made a prelimi- • consumption of a large amount of complications, including osmotic nary diagnosis of dehydration and beer (usually more than fifteen 12-oz demyelination syndrome (ODS). See imbalance due to exces- or 5.4 L of beer) in a relatively Understanding the dangers of ODS for sive alcohol consumption and pre- short time.2-4 more information. scribed 2 L of 0.9% normal saline to Other general signs and symp- be administered I.V. Peripheral ve- toms, which are consistent with hy- More than meets the eye nous access was obtained, and blood ponatremia as well as acute alcohol On physical assessment, I found specimens were sent to the lab for intoxication, include the following: Mr. H to be underweight and visibly analysis. • peripheral edema and third spacing malnourished, with a BMI of 16. Within 20 minutes, the lab called • cerebral edema He had thin, frail arms and legs, with a critical test result. Mr. H’s • profuse diaphoresis sunken eyes, coarse brittle hair, and serum sodium level was 105 mEq/L • muscle cramping a kwashiorkor-like distended abdo- (normal 135 to 145 mEq/L). This • generalized weakness men. Although he was awake and critical sodium result triggered the • nausea and vomiting alert, he was disoriented to time. His lab to determine the serum osmolal- • changes in mentation or memory speech was clear most of the time, ity to help isolate the cause of the • restlessness and irritability but he occasionally slurred some hyponatremia, but the results weren’t • gait disturbances words, and he had bilateral upper available yet. • uncontrolled tremors (fine and extremity rest tremor. His lungs The patient reported eating noth- gross) were clear to auscultation, his heart ing and drinking only beer for the • seizures sounds were normal, and his abdo- past few days. His history and physi- • coma.5,6 men was soft but distended. Mr. H cal assessment findings, coupled stated he was worried because he with the critical lab result, indicated Potentially serious hadn’t urinated in 2 days. that his medical problem was more hyponatremia than just dehydration. When the lab Morbidity and mortality associated Understanding the called back with a serum osmolality with beer potomania depend on the dangers of ODS of 225 mOsm/kg (normal, 278 to severity of hyponatremia at admis- 300 mOsm/kg), additional lab work sion. From 10% to 35% of hospital- ODS occurs as a result of a rapid in- was ordered. ized patients are found to have some crease in osmolality, which can de- velop as a result of an overly aggres- Because the patient was unable to degree of hyponatremia, the most 7 sive increase in sodium levels during void, he was catheterized to obtain a common electrolyte abnormality. In treatment for hyponatremia. The rapid very dilute urine specimen with a a 2009 study of over 98,000 hospi- change leads to dysfunction of the specific gravity of less than 1.005 talized patients, even mild hypona- myelin-producing cells in the central (normal, 1.010 to 1.025), random tremia increased in-hospital, 1-year, nervous system. As these cells lose urine osmolality of 75 mOsm/kg and 5-year mortality.8 their functioning capabilities second- (normal, 50 to 1,200 mOsm/kg, Mortality is greater than 50% for ary to cellular injury, they lose the abil- with an average range of 500 to patients with who pres- ity to produce and maintain the my- 800 mOsm/kg), and random urine ent to the hospital with serum so- elin sheaths. This results in a loss of sodium of 16 mEq/L (no established dium levels less than 125 mEq/L.9 myelinated neurons within the ner- reference values).1 The patient was In a literature review of patients vous system.4,19,23 ODS may not manifest for 2 to 8 admitted to the ICU with the diagno- diagnosed with beer potomania, days following the initiation of treat- sis of beer potomania. 36% experienced complications ment for hyponatremia.4 The signs with treatment, 18% developed and symptoms, which can be irrevers- What’s beer potomania? some degree of ODS, and another ible or only partially reversible, include Beer potomania, an unusual cause of 18% died.4 paraparesis or quadriparesis, dyspha- hyponatremia, meets the following Most published case reviews of gia, dysarthria, behavioral disturbanc- diagnostic criteria:2 patients with beer potomania con- es, lethargy, confusion, disorientation, • severe hyponatremia (serum so- clude with a discussion of patients obtundation, and coma. Less common dium usually less than 110 mEq/L) left with a permanent neurologic signs include seizures. Some patients without any other obvious cause impairment, dying from too-rapid who are severely affected become • low serum osmolality correction of hyponatremia, or expe- “locked in”—despite being awake, they • can’t move or speak.19 history of long-standing protein riencing consequences related to malnutrition misdiagnosis.

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Copyright © 2012 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Understanding the disorder Serum sodium levels rising too The role of ADH The consumption of a large volume quickly, whether by rapid sodium ADH, which regulates the ability of the of beer, usually in conjunction with replacement or excessive diuresis kidneys to concentrate urine, is syn- history of poor dietary intake and with the loss of free water, places thesized by neurons in the hypothala- significant beer drinking, contributes added stress on the already over- mus and transported down their ax- to the pathophysiology of beer poto- stressed oligodendrocytes in the ons to the posterior pituitary gland mania. Beer is hypoosmolar: It’s central nervous system. Functioning and then released into the circulation. mostly water with a very low sodium as a neuron support network, oligo- One of the main stimuli for synthesis content (about 2 mEq/L), minimal dendrocytes produce and maintain and release of ADH is an increase in solutes, and no protein. As beer is protective and insulating myelin serum osmolality. ADH release is also absorbed, the osmoreceptors sense sheaths for neurons. Because they’re controlled by cardiovascular reflexes the increase in hypotonic fluids, highly sensitive to rapid fluctua- that respond to changes in BP or interpret this as a drop in serum tions in osmolality, the result can be blood volume. osmolality, and inhibit antidiuretic injury, dysfunction, and eventual Hypothalamus hormone (ADH) release. Osmolality necrosis of the oligodendrocytes.10 Osmoreceptors is a calculation of the ratio of body As myelin is lost, cellular signals and water to sodium and other solutes. electrical impulses are increasingly Normally as ADH levels drop, less disrupted. water is reabsorbed from the neph- The neurons and supportive cells rons and urine is produced. However, will initially adapt as extracellular ADH doesn’t work alone to produce concentrations of sodium and elec- urine; it’s the presence of trolytes are diluted by the retention Posterior and solutes that helps to pull fluid of free water, but the serum osmolal- pituitary gland into the nephron to be processed ity will continue to fall less than the for elimination. To produce 1 L of intracellular environment. Osmosis ADH maximally dilute urine, the kidneys will continue to move fluid into the require 50 to 60 mOsmol of solutes.3 cerebral cells in an ineffective effort The patient who’s chronically mal- to reach homeostasis. nourished or protein deficient As the fluid enters cells, they doesn’t have available solutes and swell, become dysfunctional, and will have a net retention of fluid eventually lyse when the volume is despite little or no ADH.3,4 See The too great for the cell walls to contain, role of ADH. resulting in cellular death. Urine: decreased flow and concentrated These solutes, normally obtained from the diet, include electrolytes, Diagnostic testing Source: Porth CM. Essentials of Pathophysiology: glucose, proteins, and other sub- There are no specific diagnostic Concepts of Altered Health States. 3rd ed. Philadelphia, PA: Wolters Kluwer Health/ 2 stances dissolved in the plasma. studies for beer potomania. In beer Lippincott Williams & Wilkins; 2011. Severe protein malnutrition, poor potomania, electrolyte studies dem- dietary intake, and lack of other onstrate hyponatremia, often with a more than likely be within normal sources of solutes cause the volume critically low serum sodium level. limits. of urine output to fall until the pa- Complete blood cell counts may As stated earlier, the lack of solutes tient becomes anuric (producing less show a dilutional drop in hemoglo- needed to produce even maximally than 100 mL of urine per day). The bin and hematocrit secondary to the dilute urine will cause a low urine patient can remain in this state until excessive fluid intake. The urine output. The urine specific gravity sufficient solutes are reintroduced to osmolality test will likely be less will be low because of the effect of produce a maximally dilute urine, than 100 mOsm/kg consistent with maximal dilution. The absence of when the urine output can become water intoxication as seen with beer solutes causes the urine to be hypo- severe and overwhelming.4,7 potomania.11 osmolar (less than 100 mOsmol/ As a result, intake in this patient of Unless the patient has an underly- kg).12 The low urinary osmolality is more than 5 L of water or the equiv- ing metabolic or organic disorder, rare and seen only with beer poto- alent of about 14 beers will cause an thyroid studies, liver panel, renal mania, primary , reset overall net fluid retention and hypo- function studies, and cortisol, glu- osmostat syndrome, or a very low natremia. cose, and catecholamine levels will dietary sodium intake.7,11,13 www.Nursing2012.com July l Nursing2012 l 27

Copyright © 2012 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Although the excretion of urinary Many treatment options sodium is partially dependent on Goals for patients with beer potoma- intake, it also reflects the ’s nia are to concentrating capacity. It may be low • slowly correct hyponatremia in conditions of volume overload • prevent neurologic disabilities and conditions affecting the heart, secondary to ODS thyroid, liver, and kidney.5 • prevent alcohol-related complica- tions such as alcohol withdrawal Look out for this clinical picture syndrome (AWS) or Wernicke Patients with beer potomania will encephalopathy. likely arrive for treatment several The many treatment options for hours to days following the onset of patients with beer potomania include symptoms. Many patients have signs both fluid restriction and infusion and symptoms consistent with acute Beer is hypoosmolar: It’s of various concentrations of saline, hyponatremia, hypervolemia, and diuretics, and hypotonic fluids with mostly water with a very 11,16,17 long-standing protein malnutrition. low sodium content, . The earliest clinical indicators of minimal solutes, and no Treatment parameters must be hyponatremia are vague neurologic protein. developed and implemented on a complaints. Their severity depends case-by-case basis to carefully bal- on how quickly sodium is decreasing anuric until sufficient amounts of ance the benefits with possible risks. and cerebral edema is developing. solutes have been restored. The This is challenging because underly- of acute hypo- sudden introduction of solutes or ing conditions may be masked by natremia include difficulty concen- other metabolites from snacking, the alcohol ingestion, which could trating, confusion, lethargy, agitation, drinking soda, or even taking impact treatment. Judiciously moni- headache, seizures, anorexia, nausea, certain prescription medications tor urine output and serum sodium and vomiting. The more severe the can cause a dangerous and over- levels and perform frequent neuro- signs and symptoms, the more severe whelming diuresis that will cause logic assessments as priority nursing the degree of hyponatremia.6,14 Many sodium levels to dramatically in- interventions. of the signs and symptoms of beer crease. Even patients without neu- When patients’ sodium is being potomania may be noted in those rologic manifestations should be actively replaced, treatment goals with acute . considered high risk and be kept should be to achieve a serum sodium To evaluate a significant change in N.P.O. for at least first 24 hours level increase of less than 6 mmol/L mental status, the healthcare pro- following admission. Meticulously in the first 24 hours, less than vider may need to rely heavily on a monitor serum sodium levels at 12 mmol/L in the first 48 hours, and comprehensive assessment and ac- least every 2 hours in the early less than 14 mmol/L in 72 hours to counts of patients’ activities and be- acute phase of treatment. prevent cerebral injury.18 These rec- havior. Patients with severe signs and Protein malnutrition causes many ommendations are lower than the symptoms of acute hyponatremia, physical assessment findings includ- previously held ideal of less than such as coma and respiratory arrest, ing brittle, coarse, and thick hair and 10 mmol/L in the first 24 hours and require very aggressive treatment to nails. Patients may look older than 18 mmol/L in 48 hours because prevent permanent neurologic dis- their chronologic age because their they’ve been associated with an ability or death. hair can be prematurely gray and even lower incidence of neurologic The lack of dietary protein, exces- dermal proteins that maintain skin complications.18 sive beer intake, and oliguria or tone may have degenerated. Their Patients with severe signs and anuria can lead to fluid overload, skin may be so fragile that it sepa- symptoms such as respiratory dis- including hypertension with bound- rates under pressure. The tongue tress, seizure, or coma require an ing pulses, dyspnea on exertion, may be atrophied and there may be acute increase in serum sodium level pulmonary crackles, and peripheral muscle wasting.15 by 1 to 2 mmol/L in the first 2 to edema. Third spacing occurs as the Protein malnutrition delays wound 3 hours, without exceeding the 24- loss of circulating plasma proteins healing, so any ecchymoses, abrasions, and 48-hour goals.18 lowers vascular oncotic pressure. and lacerations will be slow to heal. Achieving this small but life- These patients, despite being hy- Patients will also report a diminished saving spike in the serum sodium pervolemic, will remain oliguric or urine output. is the most important nursing

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Copyright © 2012 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. intervention to prevent long-term will be to developing signs and disability in these patients.18 The symptoms of AWS. Other factors quickest and most reliable method to consider include comorbidities, for acutely raising the serum sodium coagulopathies, and hepatic and level is to administer 50 to 100 mL pancreatic function. For more infor- of 4% hypertonic saline over 30 min- mation, see “Managing Alcohol utes and repeat once if severe symp- Withdrawal in Hospitalized Patients” toms haven’t improved.18 (April, Nursing2012). An asymptomatic patient may be more likely to develop ODS with Prompt recognition faster rates of correction as previ- and treatment ously recommended (10 mmol/L in Mr. H was managed with conserva- 24 hours) because his or her brain tive measures in the ICU. A central has adapted to a hyponatremic Lack of dietary venous access device was inserted. environment and isn’t displaying He was kept N.P.O. for 24 hours and 6 protein, excessive beer outward signs of distress. intake, and oliguria or voided less than 3 L during the first Patients should remain N.P.O. for anuria can lead to fluid 24 hours. The patient was later ad- at least 24 hours following admis- overload. vanced to a clear diet. sion. Remember that any additional About 14 hours after admission, fluids will only potentiate the pa- his sodium level increased to 112 tient’s condition by further diluting mEq/L. He received 100 mg thiamine, plasma. The reintroduction of sol- tion of desmopressin to the clinical followed shortly by an infusion of 2 utes, including sodium from I.V. flu- treatment plan. Desmopressin is D5W. His sodium level remained at ids, can precipitate an overwhelming synthetic ADH that acts at the level of 112 mEq/L for the remainder of the diuresis in extreme cases, approxi- the collecting tubules to increase wa- first 24 hours. mately 10 L within a few hours. ter absorption.22 When desmopressin He spent the next 6 days in the Keeping the patient N.P.O. and moni- is given intranasally, its antidiuretic hospital with blood draws every toring urine output are key nursing effect will begin within 15 to 30 min- 2 hours for the first 2 days, then interventions to help prevent an utes and peak within the hour. The slowly decreasing to every 4, then overwhelming diuresis that may in- duration of action ranges from 6 to every 8 hours. Nausea was controlled advertently cause sodium levels to 14 hours.23 This pharmacologic in- with around-the-clock doses of on- spike and increase patients’ risk of tervention will limit urine volume, dansetron, which was discontinued ODS.5,19 increase urine concentration, and on hospital day 2. At the end of day To prevent the serum sodium level increase free water retention. 2, the patient received multivitamins from rising too quickly, anticipate an The healthcare provider will con- and folic acid in his I.V. fluid. infusion of D5W to replace free water sider the results of a comprehensive Lorazepam was administered for in patients with a sustained urine assessment, including mental status, withdrawal signs and symptoms, output greater than 500 mL/hour.2,20 in combination with lab values including increasing tremors, anxiety,

D5W is rapidly metabolized and has when prescribing treatment. Follow and tactile hallucinations. On hospi- no osmotically active particles after institutional policies and proce- tal day 3, Mr. H had his first meal, it’s infused into the vascular com- dures; some facilities require ICU which was well tolerated. On day 4, partment; once the dextrose is me- monitoring. he was discharged from the ICU to a tabolized, only free water remains.21 progressive care bed. Multiple con- The infusion rate is based on the Be on alert for alcohol sults were arranged to help Mr. H hourly urine output; the replacement withdrawal deal with his chronic alcohol use ratio is 0.25 to 1 mL of D5W per mL The healthcare team should recog- and dependence. The patient was of urine due to be infused within the nize the potential for AWS in these subsequently discharged without following hour.2 Administer thiamine patients. Hospitalization will inter- any signs or symptoms of ODS on as prescribed to prevent Wernicke fere with their alcohol consumption; hospital day 6. encephalopathy. this should be taken into consider- If the patient’s serum sodium level ation during care planning. The Ready for a case? rises too quickly with the treatment more time that’s elapsed since their Your recognition of a patient with described above, anticipate the addi- last drink, the closer these patients beer potomania and understanding www.Nursing2012.com July l Nursing2012 l 29

Copyright © 2012 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. of the careful management needed lines 2007: expert panel recommendations. Am J 18. Sterns RH, Nigwekar SU, Hix JK. The treatment Med. 2007;120(11 suppl 1):S1-S21. of hyponatremia. Semin Nephrol. 2009;29(3):282-299. could prevent serious disabilities or 8. Craig S. Hyponatremia in emergency medicine. 19. Sterns RH. Overview of the treatment of hypo- death. Educate your colleagues and Medscape. 2010. http://emedicine.medscape.com/ natremia. UpToDate. 2010. http://www.uptodate. vulnerable patients about this little- article/767624-overview. com/contents/overview-of-the-treatment-of- ■ 9. Simon EE. Hyponatremia. Medscape. 2012. hyponatremia. known condition. http://emedicine.medscape.com/article/242166- 20. Sterns RH. Osmotic demyelination syndrome overview. and overly rapid correction of hyponatremia. Up- REFERENCES 10. Káradóttir R, Attwell D. Neurotransmitter ToDate. 2012. http://www.uptodate.com/contents/ receptors in the life and death of oligodendrocytes. osmotic-demyelination-syndrome-and-overly- 1. Fischbach F, Dunning MB III. A Manual of Labo- rapid-correction-of-hyponatremia. ratory and Diagnostic Tests. 8th ed. Philadelphia, PA: Neuroscience. 2007;145(4-5):1426-1438. Wolters Kluwer Health/Lippincott Williams & 11. Sanders LR. Water metabolism. In: McDermott 21. Alexander M, Corrigan A, Gorski L, Hankins J, Wilkins; 2009. MT, ed. Endocrine Secrets. 5th ed. Philadelphia, PA: Perucca R, eds. Infusion Nursing: An Evidence-Based Elsevier Mosby; 2009. Approach. 3rd ed. St. Louis, MO: Saunders/Elsevier; 2. Dickson RP, Luks AM. A 65-year-old man with 2010. severe hyponatremia and . Chest. 12. Sterns RH. Lunch with the expert: hyponatre- 2010;138(2):445-447. mia, beer potomania. Presented at the Second 22. Porth CM. Essentials of Pathophysiology: Concepts of Altered Health States. 3rd ed. Philadelphia, PA: 3. Liamis GL, Milionis HJ, Rizos EC, Siamopoulos International Course on Fluid, Electrolyte and Acid-Base Disorders in Clinical Practice, Parma, Wolters Kluwer Health/Lippincott Williams & KC, Elisaf MS. Mechanisms of hyponatremia in Wilkins; 2011. alcohol patients. Alcohol Alcohol. 2000;35(6):612- Italy, 2007. http://www.electrolytes.unipr.it/Lunch 616. Expert_Sterns_BeerPotomania_Hyponatremia.pdf. 23. Desmopressin: Drug Information. Micromedex Data Base. DRUGDEX System. (Version 5.1) [In- 4. Sanghvi SR, Kellerman PS, Nonovic L. Beer 13. Freda BJ, Davidson MB, Hall PM. Evaluation of hyponatermia: a little physiology goes a long way. tranet]. Greenwood Village, CO: Thomson Reuters; potomania: an unusual cause of hyponatremia at 2011. high risk of complications from rapid correction. Cleve Clin J Med. 2004;71(8):639-650. Am J Kidney Dis. 2007;50(4):673-680. 14. Craig S. Hyponatremia in emergency medicine 24. Musana AK, Yale SH. Central pontine myelin- clinical presentation. Medscape. 2010. http:// olysis: case series and review. WMJ. 2005;104(6): 5. Heideman RL, Heideman NH. Hyponatremia. 56-60. In: Abeloff MD, Armitage JO, Niederhuber JE, emedicine.medscape.com/article/767624-clinical# a0217. Kastan MB, McKenna WG, eds. Abeloff’s Clinical Mark McGraw is an RN III mobile intensive care nurse, Oncology. 4th ed. Philadelphia, PA: Churchill 15. Grover Z, Ee LC. Protein energy malnutrition. and trauma clinical leader in the ED of Christiana Livingstone/Elsevier; 2008. Pediatr Clin North Am. 2009;56(5):1055-1068. Hospital at Christiana Care Health System in Newark, Del. 6. Duggal AK, Yadav P, Agarwal AK, Rewari BB. 16. Rocha PN. Hyponatremia: basic concepts and Clinical approach to altered serum sodium levels. practical approach. J Bras Nefrol. 2011;33(2):248-260. The author and planners have disclosed that they J Indian Acad Clin Med. 2006;7(2):91-103. 17. Sterns RH, Hix JK, Silver S. Treating profound have no financial relationships related to this article. 7. Verbalis JG, Goldsmith SR, Greenberg A, Schrier hyponatremia: a strategy for controlled correction. RW, Sterns RH. Hyponatremia treatment guide- Am J Kidney Dis. 2010;56(4):774-779. DOI-10.1097/01.NURSE.0000415301.20409.4e

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