How Does Alcohol Affect Sodium Levels?

Drug Misuse and Addiction | National Institute on Drug Abuse Addiction is defined as a chronic, relapsing disorder characterized by compulsive drug seeking and use despite adverse consequences. It is considered a brain disorder, because it involves functional changes to brain circuits involved in reward, stress, and self-control.

• Those changes may last a long time after a person has stopped taking drugs.
• Addiction is a lot like other diseases, such as heart disease.
• Both disrupt the normal, healthy functioning of an organ in the body, both have serious harmful effects, and both are, in many cases, preventable and treatable.
• If left untreated, they can last a lifetime and may lead to death.

Modified with permission from Volkow et al.1993. Note: These PET scans compare the brain of an individual with a history of cocaine use disorder (middle and right) to the brain of an individual without a history of cocaine use (left). The person who has had a cocaine use disorder has lower levels of the D2 dopamine receptor (depicted in red) in the striatum one month (middle) and four months (right) after stopping cocaine use compared to the non-user.

Does drinking alcohol cause low sodium levels?

Beer Potomania—An Unusual Cause of Hyponatremia The first case of severe hyponatremia, since referred to as beer potomania, in a heavy beer drinker patient was reported in 1972. Electrolyte abnormalities are common findings in patients with a history of heavy alcohol use.

Excessive consumption of beer in particular, which has a low solute content (sodium concentration, 1.8 mEq/L and potassium concentration, 7.2 mEq/L), to the exclusion of other solute intake may result in severe hyponatremia. We report a case of severe hyponatremia that occurred in a patient who, owing to his underlying colon cancer, was drinking beer and ingesting little other food.

His hyponatremia improved with increased solute intake and, upon correction of his serum sodium, he had no subsequent neurologic sequelae. The first case of severe hyponatremia in a heavy beer drinker patient was reported in 1972 by Gwinup et al. This condition has since been referred to as beer potomania.

Electrolyte abnormalities are common findings in patients with a history of heavy alcohol use. In the study by Liamis et al, among hospitalized patients with history of chronic alcohol consumption, 17.3% had hyponatremia. The excessive consumption of beer in particular, which has a low solute content (sodium concentration, 1.8 mEq/L; potassium concentration, 7.2 mEq/L), to the exclusion of other solute intake may result in severe hyponatremia.

We report a case of severe hyponatremia that occurred in a patient who, owing to his underlying colon cancer, was drinking beer and ingesting little other food. His hyponatremia improved with increased solute intake and, upon correction of his serum sodium, he had no subsequent neurologic sequelae.

A Hispanic man, age 84 years, with history of chronic alcohol abuse and recently diagnosed stage IV sigmoid adenocarcinoma presented to the Emergency Department with nausea, weakness, decreased appetite, and abdominal pain for the past 3 to 4 days. The patient had been ingesting approximately 12 cans of beer daily in addition to his usual diet for the preceding 50 years, but during the week before his presentation, because of worsening abdominal pain, he was drinking his habitual quantities of beer but otherwise eating minimally.

On physical examination, his temperature was 37.1°C, blood pressure 142/81 mmHg, pulse rate 78 beats/min, without orthostatic changes, respiratory rate 18 breaths/min, and oxygen saturation 97% on room air. He was in no acute distress and did not appear intravascularly volume depleted.

His lungs were clear bilaterally, and his heart sounds were normal without murmurs. He had tenderness in the epigastric area without rebound tenderness, with normal bowel sounds and no organomegaly. He was oriented and coherent in conversation. His neurologic exam and deep tendon reflexes were normal. He had no tremors.

The patient’s laboratory data showed white blood cells 15.4 × 1000/mcL, hemoglobin 12.7 g/dL, platelets 347 × 1000/mcL, international normalized ratio 1.1, glucose 160 mg/dL, sodium 116 mEq/L, potassium 4.1 mEq/L, chloride 85 mEq/L, CO 2 19 mEq/L, blood urea nitrogen 6 mg/dL, creatinine 0.58 mg/dL, serum osmolality 250 mOsm/kg, uric acid 3 mg/dL, phosphorus 2.8 mg/dL, calcium 8.3 mg/dL, magnesium 1.1 mg/dL, alanine transaminase 20 U/L, aspartate transaminase 27 U/L, total bilirubin 0.8 mg/dL, thyroid stimulating hormone 2.19 mcIU/ml, albumin 2.8 g/dL, and cortisol 23.8 mcg/dL.

His urinalysis showed specific gravity 1.005, pH 6, negative leukocyte esterase, negative nitrite, white blood cells 0–2, red blood cells 0–3, urine sodium 35 mEq/L, urine chloride 37 mEq/L, urine potassium 11 mEq/L, urine creatinine 26 mg/dL, and urine osmolality 182 mOsm/kg. A computed tomography scan of his abdomen and pelvis with intravenous contrast revealed a new abscess adjacent to the previously seen sigmoid carcinoma with local lymphadenopathy and hepatic metastatic disease.

The patient received 1 L of 0.9% sodium chloride intravenously in the Emergency Department and was started on antibiotics for the sigmoid abscess. The surgical consultant did not recommend surgical intervention. He received intravenous thiamine and magnesium supplementation for his history of heavy alcohol drinking and hypomagnesemia.

1. He was encouraged to increase his oral intake with a normal diet as tolerated.
2. He subsequently underwent a brisk diuresis of approximately 1.8 L during the first 8 hours.
3. His intravenous fluid was promptly discontinued and the patient’s serum sodium was checked every 2 to 3 hours to monitor for overly rapid correction.

His serum sodium increased by 8 mEq/L in the first 24 hours and 14 mEq/L in the first 48 hours. His serum sodium remained between 130 mEq/L and 133 mEq/L throughout the remainder of his hospitalization. He was closely observed for any change in his neurologic status or signs and symptoms of acute alcohol withdrawal.

1. None appeared.
2. The most common electrolyte abnormality seen in clinical practice is hyponatremia, which is also found in up to 30% of hospitalized patients.
3. In the study by Liamis et al, hyponatremia was the third most common electrolyte abnormality detected in 127 hospitalized chronic alcoholic patients, with a prevalence of 17.3%.

Traditionally, the evaluation of hyponatremia begins with the determination of serum osmolality followed by a clinical assessment of volume status (see Sidebar: ). Most clinical hyponatremia is associated with a low serum osmolality.

How does drinking alcohol affect your sodium levels?

– Potomania causes a dangerously low sodium level in your blood, called hyponatremia. There are many different conditions that can cause low sodium levels. In potomania, it’s typically a combination of malnourishment and binge drinking over time. Sodium is an important nutrient that helps regulate the balance of water in your body.

1. Most people get enough sodium from their diet.
2. However, when someone stops eating, the levels of sodium in their blood can drop — especially when combined with excessive intake of fluids low in sodium.
3. This is common among people who misuse alcohol, some of whom get most of their calories from drinking beer and other alcoholic beverages.

Baseline serum sodium levels can also drop due to a recent illness affecting electrolyte levels, particularly when there’s vomiting or diarrhea. To work properly, your kidneys require a certain amount of sodium. Without it, they can’t clear excess fluids from your body.

1. That excess fluid builds up in your blood and causes your cells to swell.
2. Swelling in the brain causes the neurological symptoms of potomania.
3. Normally, when someone stops eating, their body breaks down fat and muscle to use as energy.
4. This provides the body with enough sodium to keep the kidneys working.

Drinking excessive quantities of water or beer, however, will dilute this sodium, making it ineffective. Learn about other effects of alcohol on your body.

Does alcohol cause hypo or hypernatremia?

Osmotic demyelination syndrome (ODS) includes central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM). CPM is classically described as the radiological manifestations of osmotic myelinolysis, and clinical symptoms range from subtle changes in cognitive functions to life-threatening autonomic and brainstem dysfunction and death, EPM develops in extrapontine sites through mechanisms similar to CPM but the cases of EPM have been reported rarely than those of CPM, CPM is most commonly observed in association with predisposing factors, such as chronic alcoholism, malnutrition, and rapid correction of hyponatremia, and therefore, sodium correction over 12 mEq/L/day is not recommended, Although ODS developing from the rapid correction of hyponatremia in chronic alcoholics has been examined widely, hypernatremic osmotic insult is relatively poorly described and remains unclear, The only one case that described the patient who was a chronic alcoholic and suffered from CPM and EPM without hyponatremia during alcohol withdrawal was reported. Here we report the case of osmotic demyelinolysis involved pontine and extrapontine associated with hypernatremia in a chronic alcoholic during alcohol withdrawal. A 56-year-old alcoholic man was transferred to the emergency room with a history of confusion, motor weakness, and gait disturbance for a few days. He had been drinking more than one bottle of soju every day for 30 years and stopped drinking 4 days ago. After he stopped drinking, the above symptoms occurred. His caloric food intake was poor, and he had consumed only alcohol in the preceding 15 days before quitting drinking. He already had alcoholic liver cirrhosis, Wernicke’s encephalopathy, and alcoholic dementia. The initial vital signs revealed a blood pressure (BP) of 110/68 mmHg, pulse of 88 bpm, respiratory rate of 20 breaths per minute, and temperature of 36.6°C. On initial neurological examination, the patient could answer only simple one-step obey commands, and he was only oriented to place. His pupils were isocoric and pupil light reflex was prompt. Other cranial nerve function tests did not show any abnormal findings. The Glasgow Coma Scale was 13/15 (eye scores, 4; verbal scores, 5; and motor scores, 4). Initial laboratory data revealed severe hypernatremia (serum sodium level, 164 mEq/L), hypokalemia (potassium level, 2.9 mEq/L), anemia (hemoglobin level, 6.9 g/dL), and abnormal liver function (aspartate transaminase level, 145 IU/L). Brain computed tomography (CT) was negative for acute hemorrhage or edema. He was admitted to the internal medicine department to focus on treatment for anemia, chronic obscure bleeding, electrolyte imbalance, and acute kidney injury (blood urea nitrogen /creatinine, 52.9/1.20). After 3 days, his mental status changed from drowsy to stupor, and he developed respiratory failure and was attached to a ventilator. Brain magnetic resonance imaging (MRI) showed high signal intensities symmetrically in the bilateral pons, basal ganglia, thalamus, and cerebral and cerebellar cortices on T2-weighted and fluid-attenuated inversion recovery (FLAIR) images. Diffusion-weighted imaging (DWI) showed marked hyperintense lesions corresponding to the areas of low signal intensity on quantitative apparent diffusion coefficient (ADC) images ( Fig.1 ). It was compatible with CPM and EPM. Finally, the patient died of complicated pneumonia with acute respiratory failure. CPM and EPM are the radiological manifestations of osmotic myelinolysis, affecting different brain regions. The radiological manifestations are confined to the pons in cases of CPM and to the extrapontine sites in cases of EPM. The lesions are mostly symmetrical. Frequently affected parts in ODS are the pons in CPM and the cerebellum, lateral geniculate body, external capsule, hippocampus, putamen, cerebral cortex, thalamus, and caudate nucleus and more infrequently, the claustrum, internal capsule, midbrain, and internal medullary lamella, in EPM, EPM is more commonly observed with hypernatremia, In particular, hippocampal involvement may be related to the high vulnerability of the hippocampus to the neurotoxic effects of osmotic derangement and general systemic stress, Associations between hyponatremic osmotic disturbances and cerebral lesions are well-studied. In 1979, Messert et al. reported on the concept of the grid theory, i.e., the basis pontis consists of grid fibers which are vulnerable to cerebral edema because of declined elasticity with tegmentum, which lacks the grid fibers, preservation. The worse edema of the grid, the worse strangulation of myelin sheaths and blood vessels leading to demyelination, necrosis, and death. This theory is supported by the sparing of the dorsal pons or pontine tegmentum. It has been increasingly recognized that EPM can occur in the setting of other osmotic challenges, such as glycemic state and end-stage renal disease regardless of serum sodium levels, According to a recent report, clinical symptoms do not correlate with age, the presence of comorbid conditions, initial serum Na + levels, serum osmolality, or the serum Na + correction rate, Apart from correction rates, the presence of additional metabolic derangements, such as serum K + levels and hyperglycemia, are considered to be independent risk factors for the development of ODS, Therefore, an increase in serum sodium, as well as potassium levels, should not exceed 12 mEq/L in the first 24 hours and 18 mEq/L in the first 48 hours, In addition, severe hypophosphatemia most likely also contributes to the development of EPM, In cases of hypernatremia, osmotic differences are subtle because of the rapid ionic and water shifts across the cell membrane with little effect on cell volume but a significant effect on decreased extracellular space volume, Blood-brain barrier (BBB) disruption occurs secondary to osmotic stress and is one of the leading factors in the pathogenesis of EPM, Compared with patients with no comorbid conditions, the presence of indirect central nervous system (CNS) comorbid conditions, such as alcoholism, especially alcohol withdrawal, malnutrition, diuretic use, burns, post-liver transplantation, and post-partum dehydration status, before hypernatremic challenge renders the brain more vulnerable to ODS with mildly elevated sodium levels, MRI is the imaging technique of choice for the diagnosis of ODS because it has a greater sensitivity for CPM than CT and a superior capacity for demonstrating EPM lesions. CPM is characterized by hyperintensity on T2-weighted, FLAIR, DWI imaging, and hypointensity on T1-weighted, ADC imaging, But EPM shows variable images, not characteristic or typical ones. In this case, brain MRI images corresponded with typical radiological findings of CPM and extrapontine lesions were showed the same results. One study reported that early DWI changes are a common finding in ODS but do not regularly precede the tissue changes that are detectable on conventional MRI sequences, With these radiologic findings, neurologic examinations, laboratory findings, and past history, we finally diagnosed ODS and could differentiate from other possible diseases. The prognosis of ODS varies. Early reports on CPM indicated approximately 100% mortality rate within 3 months following hospital admission, The most recent large series of 34 cases showed that only 2 patients died, 10 survived but were left dependent, 11 had some deficits but were independent, and 11 recovered completely, Pediatric patients have a better recovery rate, and the associated MRI lesions are more reversible, Younger patients had a worse outcome than older patients. Common electrolyte imbalance associated with chronic alcoholics is hypomagnesia, hyponatremia, hypocalcemia, and hypophosphatemia. Hyponatremia has been reported to be more common than hypernatremia. The mechanism of hyponatremia is below; the lowering of secretion of antidiuretic hormone (ADH) by alcohol cause excessive urination. However, the minimum of 50 to 60 mOsmol of solutes is necessary to dilute a maximum of 1 L urine. Drinking low alcohol concentration liquor, such as beer, may cause hyponatremia (beer potomania syndrome) because the relatively huge amount of free water is over-absorbed than that of excreted solutes. However, drinking high alcohol concentration liquor may cause volume depletion, resulting in hypernatremia. So, reset osmostat syndrome can be developed in chronic alcoholics, which is inappropriate natriuresis (> 40 mmol/L) despite serum hyponatremia. CPM can be commonly developed in chronic alcoholics. Malnutrition and hypokalemia have been suggested for predisposing factors, Previous reports have highlighted the importance of serum Na + correction in ODS associated with hyponatremia in chronic alcoholics, however, there have been very few case reports of ODS with hypernatremia. Especially during alcohol withdrawal, there was not reported case associated with hypernatremia. In our case, CPM and EPM were observed simultaneously after correction of hypernatremia, and it was assumed that chronic alcoholism and quitting drinking caused brain structural changes which are vulnerable to get an injury to change of serum sodium level. Therefore, this case suggests that ODS easily occurs, particularly in at-risk patients, such as known alcoholics who are still drinking or stops drinking within a few days, malnourished patients, and chronic patients with liver and kidney diseases, whether or not abnormal serum sodium level is present. ODS should be included in the differential diagnosis of patients who manifest with new psychotic symptoms during alcohol withdrawal. It is not difficult to distinguish ODS from Wernicke’s encephalopathy through determination of whether nystagmus is present, improvement with thiamine supplementation, or signal changes on MRI. Management of these conditions involves recognition of at-risk patients, careful electrolyte correction, prompt and exact diagnosis, and management of associated complications with early rehabilitation for functional recovery. Conflict of Interest: The authors have no potential conflicts of interest to disclose. Ismail FY, Szóllics A, Szólics M, Nagelkerke N, Ljubisavljevic M. Clinical semiology and neuroradiologic correlates of acute hypernatremic osmotic challenge in adults: a literature review. AJNR Am J Neuroradiol 2013;34:2225–2232. Förster A, Nölte I, Wenz H, Al-Zghloul M, Kerl HU, Brockmann C, et al. Value of diffusion-weighted imaging in central pontine and extrapontine myelinolysis. Neuroradiology 2013;55:49–56. Martin RJ. Central pontine and extrapontine myelinolysis: the osmotic demyelination syndromes. J Neurol Neurosurg Psychiatry 2004;75 Suppl 3:iii22–iii28. Kallakatta RN, Radhakrishnan A, Fayaz RK, Unnikrishnan JP, Kesavadas C, Sarma SP. Clinical and functional outcome and factors predicting prognosis in osmotic demyelination syndrome (central pontine and/or extrapontine myelinolysis) in 25 patients. J Neurol Neurosurg Psychiatry 2011;82:326–331. Messert B, Orrison WW, Hawkins MJ, Quaglieri CE. Central pontine myelinolysis. Considerations on etiology, diagnosis, and treatment. Neurology 1979;29:147–160. Tarakji AG, Tarakji AR, Shaheen U. Central pontine and extrapontine myelinolysis secondary to fast correction of severe hyponatremia and hypokalemia in an alcoholic patient. Int Urol Nephrol 2014;46:201–205. McCormick WF, Danneel CM. Central pontine myelinolysis. Arch Intern Med 1967;119:444–478. Menger H, Jörg J. Outcome of central pontine and extrapontine myelinolysis (n = 44). J Neurol 1999;246:700–705. Arieff AI. Central nervous system manifestations of disordered sodium metabolism. Clin Endocrinol Metab 1984;13:269–294. Elisaf M, Kalaitzidis R. Metabolic abnormalities in alcoholic patients: focus on acid base and electrolyte disorders. J Alcohol Drug Depend 2015;3:185.

How does alcohol cause Hypernatremia?

Acute ingestion of alcohol induces a water diuresis owing to suppression of circulating vasopressin levels, predisposing patients to dehydration and hypernatremia.

Why does beer lower sodium?

“Beer Potomania” – A Syndrome of Severe Hyponatremia with Unique Pathophysiology: Case Studies and Literature Review Beer potomania, a unique syndrome of hyponatremia, was first reported in 1972. It is described as the excessive intake of alcohol, particularly beer, together with poor dietary solute intake that leads to fatigue, dizziness, and muscular weakness.

The low solute content of beer, and suppressive effect of alcohol on proteolysis result in reduced solute delivery to the kidney. The presence of inadequate solute in the kidney eventually causes dilutional hyponatremia secondary to reduced clearance of excess fluid from the body. Early detection of hyponatremia due to beer potomania in the hospital is necessary to carefully manage the patient in order to avoid neurological consequences as this syndrome has unique pathophysiology.

We are reporting two cases, presenting to the emergency department with severe hyponatremia. After a detailed initial evaluation of the patients and labs for hyponatremia, a diagnosis of beer potomania was established in both cases. Considering the unique pathophysiology of beer potomania syndrome, the patients were closely monitored and treated appropriately to prevent any neurological sequelae.

Eywords: beer-potomania, severe hyponatremia, osmotic demyelination syndrome, alcoholic beer, potomania vs. siadh, serum sodium concentration, osmolar load, dilutional hyponatremia The unique syndrome of hyponatremia in heavy beer drinkers (consuming five or more drinks per day) was first reported by Gwinup, et al.

in 1972, Hyponatremia is a common electrolyte abnormality in hospitalized patients with a history of chronic alcoholism. As the study conducted by Liamis, et al. showed 17.3% of hospitalized chronic alcoholics have severe hyponatremia, However, it has been crucial to quickly diagnose beer potomania in a chronic alcoholic presenting with severe hyponatremia, due to other concomitant causes such as malnutrition, the use of diuretics or antipsychotics, congestive heart failure and cirrhosis.

Case 1 History and physical examination A 59-year-old male with past medical history significant for alcoholism, chronic obstructive pulmonary disease (COPD), grand-mal seizures, and mood disorder was brought to the emergency department (ED) following a seizure earlier in the day. The patient denied any fall, head trauma or loss of consciousness.

He had a significant history of alcohol abuse over the last 25 years, drinking nine to 10 cans of beer per day. As reported by the patient’s family, he had poor dietary habits and eats one meal in a day, three to four days per week. He has a 40-year history of smoking one pack a day.

The patient denied any intravenous drug abuse, recent travel, or any history of hepatitis. Review of home medications revealed that he takes Trazodone, Risperidone, and Phenytoin. He mentioned that he is compliant with his medications. He denied any excessive water intake, diarrhea, vomiting, cold or heat intolerance, and lower extremities swelling.

He also denied headache, cough, hemoptysis, chest pain, fever, night sweats or weight loss. Upon initial physical examination, the patient appeared malnourished, lethargic and in moderate respiratory distress. His vitals were as follows: blood pressure of 127/83 mmHg, heart rate of 110 beats per minute, respiratory rate of 20 breaths per minute, oxygen saturation of 85% on room air and had no fever.

His body mass index (BMI) was 16. His pupils were equal, round and reactive to light. He appeared euvolemic. Cardiac auscultation revealed regular rhythm without murmurs or gallops, and audible S1 and S2. He had wheezing, ronchi and generalized decreased breath sounds bilaterally on lung examination. He had tenderness in the epigastric region without rebound tenderness, with normal bowel movements and no organomegaly.

He was oriented to person and place, but not to time. On neurological examination, he appeared confused and deep tendon reflexes were unremarkable. He had no tremors or asterixis. His Glasgow score was 14. Hospital course and differential diagnosis His laboratory workup performed at the time of presentation in the ED is listed below (Table ).

1. Patient’s urine toxicology returned positive for cannabinoids and opioids.
2. A chest x-ray was unremarkable.
3. Echocardiogram of the heart showed mild ventricular hypertrophy with no diastolic dysfunction.
4. Computed tomography (CT) of the head without contrast, showed cerebral atrophy with no acute changes.

Biochemical and hematologic studies ordered at the time of initial presentation in the emergency department.

Test	Result	Reference
White blood cells (WBC)	7.3 x 10 3 µL	3.4-10.8 x 10 3 µL
Hemoglobin (Hb)	13.6 g/dL	12.6-17.7 g/dL
Hematocrit (Hct)	40.70%	37.5-51.0%
Platelet count	354 x 10 3 µL	150-379 x 10 3 µL
Serum sodium (Na)	118 mmol/L	134-144 mmol/L
Serum potassium (K)	4 mmol/L	3.5-5.2 mmol/L
Serum chloride (Cl)	90 mmol/L	96-106 mmol/L
Serum bicarbonate	27 mmol/L	18-29 mmol/L
Blood urea nitrogen (BUN)	4 mg/dL	6.0-24 mg/dL
Creatinine	0.56 mg/dL	0.6-1.2 mg/dL
Serum glucose	129 mg/dL	65-100 mg/dL
Serum calcium	9.2 mg/dL	8.7-10.2 mg/dL
Serum phosphate	3.2 mg/dL	2.5-4.5 mg/dL
Serum magnesium	2.1 mg/dL	1.7-2.2 mg/dL
Aspartate aminotransferase (AST)	76 IU/L	0.0-40 IU/L
Alanine aminotransferase (ALT)	35 IU/L	0.0-44 IU/L
Total protein	7.3 g/dL	6-8.3 g/dL
Albumin	2.9 g/dL	3.5-5.5 g/dL
Alkaline phosphatase (ALP)	99 IU/L	39-117 IU/L
Total bilirubin	1.4 mg/dL	0.0-1.2 mg/dL
Direct bilirubin	0.2 mg/dL	0.0-0.3 mg/dL
International normalized ratio (INR)	1	≤1.1
Serum uric acid	3.4 mg/dL	3.4-7.0 mg/dL
Thyroid-stimulating hormone (TSH)	1.12 µIU/mL	0.45-4.5 µIU/mL
Serum osmolarity	259 mOsm/kg	275-295 mOsm/kg
Urine specific gravity	1.043	1.003-1.030
Ketones in urine	Trace	Absent

Regular protocol for acute COPD exacerbation was followed, and patient oxygen saturation and partial pressure O2 returned to normal. Urinary sodium and osmolarity was not checked in the ED. The patient was administered intravenous 1 L of 0.9% sodium chloride in the ED, together with intravenous thiamine, folic acid, magnesium sulfate, multivitamins, and chlordiazepoxide.

Nephrology was consulted for hyponatremia of sodium 118 mmol/L and the patient was admitted to the medical unit. The patient’s poor nutritional status, being on Risperidone and significant history of alcoholism raised concern of dehydration, syndrome of inappropriate antidiuretic hormone (SIADH) and beer potomania, respectively.

The urine osmolality was 72 mOsm/kg H2O, and urine sodium was 19 mmol/L. Low urine osmolarity and low urine sodium levels excluded the SIADH and cerebral-wasting syndrome as the cause of this patient’s hyponatremia, The patient also denied drinking excessive water, which ruled out psychogenic polydipsia.

• Patient’s unremarkable physical examination, together with clear chest x-ray and no significant abnormality on echocardiogram, made it easier to rule out congestive heart failure.
• Considering the patient’s history (of chronic alcohol abuse and recent seizure), clinical presentation (of lethargy and malnourishment), lab values (of low serum osmolarity, urinary osmolarity, urinary sodium level), and absence of any other plausible explanation, directed us to establish the diagnosis of beer potomania syndrome,

In the next 16 hours following the administration of 1 L of 0.9% sodium chloride in the ED, the patient had a brisk diuresis of about 3 L. The patient’s sodium went up from 118 mmol/L to 129 mmol/L, an increase of 11 mmol/L in 16 hours. A one-liter bolus of 5% dextrose water (D5W) was given and then the patient was started on banana bag with base solution of D5W.

• With this fluid sodium level improved back to 127 mmol/L at 24 hours of admission.
• D5W infusion was adjusted every few hours according to change in serum sodium level to prevent rapid auto correction of serum sodium level which could lead to osmotic demyelination syndrome (ODS).
• Over the period of the next few days, the patient’s serum sodium levels stayed constant between 131 and 133 mmol/L.

The patient was feeling comparatively less lethargic and he did not develop any neurological sequelae. The serum sodium progression since admission in the ED until day five is shown below (Figure ). The patient was also educated on alcohol cessation and suggested to slowly increase his dietary food intake.

1. Serum sodium level (mmol/L) versus hospitalization time (hours).
2. Point A, shows serum sodium level of 118 mmol/L on admission, when patient was started on 0.9% sodium chloride, together with thiamine, magnesium sulfate and folic acid.
3. Point B, shows serum sodium level of 129 mmol/L at 16 hours after admission, when nephrology was consulted.0.9% sodium chloride was discontinued, a bolus of D5W was administered followed by D5W based banana bag.

Point C, shows serum sodium level of 127 mmol/L at 24 hours since admission. Point D, shows serum sodium level of 131 mmol/L at 48 hours. Point E, shows serum sodium level of 133 mmol/L at 72 hours, and point F shows serum sodium level of 131 mmol/L at 96 hours.

Case 2 History and physical examination A 60-year-old male presented to the emergency room with weakness and lack of appetite. It was accompanied with dizziness, but no loss of consciousness or trauma. The patient admitted drinking 12-20 cans of beer, 12 ounces each. He has been smoking two packs per day for the last 40 days.

The patient denied taking any medicine at home. He denied any excessive water intake, diarrhea, vomiting, cold or heat intolerance, and swelling. He also denied headache, cough, hemoptysis, chest pain, fever, night sweats or weight loss. Upon initial physical examination, the patient appeared malnourished, drowsy and unkempt.

1. His vitals were as follow: afebrile, blood pressure of 96/67 mmHg, heart rate of 103 beats per minute, respiratory rate of 15 breaths per minute, oxygen saturation of 96% on room air.
2. His BMI was 17.5.
3. His pupils were equal, round and reactive to light.
4. The patient appeared to have intravascular volume depletion with dry, pale skin and delayed capillary refill of about 4 seconds with low BP and tachycardia.

Cardiac auscultation revealed regular rhythm without murmurs or gallops and audible S1 and S2. On lung examination, there were no rales, wheezes or crackles appreciated. His bowel sounds were normal with no tenderness, organomegaly or distention. He had no jugular venous distention or peripheral edema.

He was oriented to person, place and time. On neurological examination, he appeared drowsy. Deep tendon reflexes were unremarkable. He had no tremors or asterixis. His Glasgow score was 15. Hospital course and differential diagnosis His biochemical and hematologic workup performed at the time of admission in the ED is listed below (Table ).

A chest x-ray was also done and it showed no signs of pulmonary edema or mediastinal mass. Echocardiogram of the heart was not performed. CT scan of the head without contrast showed no abnormalities. Biochemical and hematologic studies ordered at the time of initial presentation in the emergency department.

Test	Result	Reference
White blood cells (WBC)	9 x 10 3 µL	3.4-10.8 x 10 3 µL
Hemoglobin (Hb)	13.7 g/dL	12.6-17.7 g/dL
Hematocrit (Hct)	35.60%	37.5-51.0%
Platelet count	163 x 10 3 µL	150-379 x 10 3 µL
Serum sodium (Na)	106 mmol/L	134-144 mmol/L
Serum potassium (K)	4.6 mmol/L	3.5-5.2 mmol/L
Serum chloride (Cl)	74 mmol/L	96-106 mmol/L
Serum bicarbonate	24 mmol/L	18-29 mmol/L
Blood urea nitrogen (BUN)	9 mg/dL	6.0-24 mg/dL
Creatinine	0.4 mg/dL	0.6-1.2 mg/dL
Serum glucose	98 mg/dL	65-100 mg/dL
Serum calcium	7.9 mg/dL	8.7-10.2 mg/dL
Serum phosphate	3.7 mg/dL	2.5-4.5 mg/dL
Serum magnesium	1.9 mg/dL	1.7-2.2 mg/dL
Aspartate aminotransferase (AST)	43 IU/L	0.0-40 IU/L
Alanine aminotransferase (ALT)	69 IU/L	0.0-44 IU/L
Total protein	6.2 g/dL	6-8.3 g/dL
Albumin	2.7 g/dL	3.5-5.5 g/dL
Alkaline phosphatase (ALP)	123 IU/L	39-117 IU/L
Total bilirubin	0.9 mg/dL	0.0-1.2 mg/dL
Direct bilirubin	0.3 mg/dL	0.0-0.3 mg/dL
International normalized ratio (INR)	1	≤1.1
Serum uric acid	2.1 mg/dL	3.4-7.0 mg/dL
Thyroid-stimulating hormone (TSH)	1.13 µIU/mL	0.45-4.5 µIU/mL
Serum osmolarity	232 mOsm/kg	275-295 mOsm/kg
Urine random osmolality	159 mOsm/kg	300-900 mOsm/Kg of water
Urine specific gravity	1.012	1.00-1.030
Urine sodium	19 mmol/L	20-40 mmol/L

Considering the signs and symptoms of hypovolemia on physical examination, severe hyponatremia of 106 mmol/L and low-normal blood pressure, the patient was started on 0.9% sodium chloride-based banana bag in the emergency room. The patient also showed interest in food and had two big meals in the emergency room.

• A few hours after presentation, he had a brisk diuresis of unmeasured amount as he denied initially to have foley catheter.
• Within 16 hours of 0.9% sodium chloride-based banana bag fluid administration, the patient’s serum sodium jumped up to 119 mmol/L, an increase of 13 mmol/L.0.9% sodium chloride-based intravenous fluid was discontinued but the patient’s serum sodium level went up to 128 mmol/L in first 32 hours since his presentation.

Nephrology was consulted and the patient was moved to the medical unit. After admission to the medicine unit, the patient was started on adjusted amount of 5% dextrose water-based banana bag. Sodium level dropped to 121 mmol/L in the next 12 hours. The patient’s serum sodium level increased slowly over the next few days, as shown below (Figure ).

• After day five onwards, the patient’s serum sodium stayed between 132 and 134 mmol/L and the patient did not develop any neurological sequelae.
• Serum sodium level (mmol/L) versus hospitalization time (hours).
• Point A, shows serum sodium level of 106 mmol/L on admission, when patient was started on 0.9% sodium chloride, together with thiamine, magnesium sulfate, folic acid and chlordiazepoxide.

Point B, shows serum sodium level of 119 mmol/L at 16 hours after admission, 0.9% sodium chloride was discontinued. Point C, shows serum sodium level of 128 mmol/L at 36 hours since admission, nephrology was consulted at this point, 1 L bolus of D5W was given followed by D5W based banana bag.

Point D, shows serum sodium level of 121 at 48 hours. Point E, shows serum sodium level of 126 mmol/L at 64 hours. Point F, shows serum sodium level of 129 mmol/L at 86 hours. Point G, shows serum sodium level of 131 mmol/L at 96 hours. Point H, shows serum sodium level of 133 mmol/L at 112 hours. The initial presentation of the patient pointed towards the hypovolemic hyponatremia, however, low serum uric acid could not be explained by simple hypovolemic hyponatremia.

Given the patient’s low urine osmolarity and low serum uric acid, with poor oral intake and significant history of alcoholism raised the concern of beer potomania. Syndrome of Inappropriate ADH secretion (SIADH) and cerebral salt wasting syndrome were unlikely with low urine sodium and low urine osmolality.

• The initial rapid correction of hyponatremia with low serum uric acid level suggests that hyponatremia was contributed by both hypovolemic hyponatremia and beer potomania.
• Pathophysiology Understanding the pathophysiology is critical for the proper management of dilutional hyponatremia in a patient with beer potomania syndrome.

A person with normal renal function and normal dietary intake removes about 600-900 mOsm/day. With the maximal urinary dilation of 50 mOsm/L, a person can excrete about 20 L of water without becoming hyponatremic, allowing for broad range of water intake (reaching up to 20 L),

1. As free-water clearance in a person with normal diluting capacity is dependent on osmole excretion, a decrease in daily dietary osmole intake can have a vast decrease in the excretory capacity of the kidney.
2. Therefore, this decrease in daily dietary osmoles in even minute fluid excess can cause dilutional hyponatremia.

Beer potomania patients have a long-term history of beer intake, as well as a poor diet. Beer has trace amounts of sodium and almost negligible protein content. In addition, beer has some calories that prevent the muscular proteolysis resulting in a dramatic decrease in urea generation.

Thus, these patients have very low osmolar load as dietary protein breakdown is the main component of the osmolar load, as well as small amounts from sodium and potassium. In our two cases, patients with nine to 20, 12 oz cans of beer daily, their approximate osmole intake was 225-250 mOsm/L per day.

Assuming normal urinary dilation capability, any fluid intake more than 3-4 L will result in water retention and subsequently dilutional hyponatremia in these patients, In beer potomania patients, the ability to reabsorb free-water from the collecting tubules is decreased due to suppressed antidiuretic hormone,

This suppression of antidiuretic hormone explains a brisk diuresis in our patients following the administration of solute (0.9% sodium chloride, thiamine, magnesium sulfate, folic acid, multivitamins, chlordiazepoxide) in the emergency rooms as well as a sudden increase in the serum sodium level of these patients over the short period of time.

In the literature review performed by Sanghvi, et al.18% of the patients with beer potomania developed osmotic demyelination syndrome, Oligodendrocytes are myelinating cells of the central nervous system. They are extremely sensitive to sudden increases in serum sodium level, resulting in pontine or extrapontine demyelination.

• This process of demyelination is known as osmotic demyelination syndrome (ODS),
• ODS can result in dyspnea, dysphagia, dysarthria, and ataxia,
• Management guidelines After a detailed review of the literature and understanding the pathophysiology of beer potomania, Sanghvi, et al.
• Suggested the management guidelines to prevent a rapid increase in serum sodium level and development of ODS.

Their recommendations are listed below (Table ). Recommendations by Sanghvi, et al. for correction of hyponatremia in beer potomania.

Management Recommendations for Correction of Hyponatremia in Beer Potomania

Nothing by mouth except medications for 24 hours

No intravenous fluids unless symptomatic

Prescribe intravenous fluids in finite amounts if needed

Intensive care status

Check serum sodium every two hours

Goals – Serum sodium increase < 10 mEq/L in first 24 hours - Serum sodium increase < 18 mEq/L in first 48 hours

Reduce serum sodium levels if necessary

Give any intravenous medications in sugar solutions (5% dextrose in water)

If caloric intake is needed, use intravenous sugar solution (5% dextrose in water)

In this case study, we tried to highlight the importance of the early detection of beer potomania in an alcoholic patient, presenting with severe hyponatremia in the emergency department. This case study was also designed to illustrate the importance of understanding basic pathophysiology of beer potomania, for the successful management and prevention of any neurological sequelae.

This case study and our brief review of the literature are directed towards an improvement in the management of beer potomania. In addition, we also find the recommendations suggested by Sanghvi, et al. consistent with the relatively safe management of severe hyponatremia. The content published in Cureus is the result of clinical experience and/or research by independent individuals or organizations.

Low Sodium (Hyponatremia): Dangers, Symptoms, and Causes Explained By Dr.Berg

Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein. All content published within Cureus is intended only for educational, research and reference purposes. Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional.

Do not disregard or avoid professional medical advice due to content published within Cureus. The authors have declared that no competing interests exist. Consent was obtained by all participants in this study 1. Beer drinker’s hyponatremia. Inappropriate concentration of the urine during ingestion of beer.

Gwinup G, Chelvam R, Jabola R, et al. Calif Med.1972; 116 :78–81.2. Mechanisms of hyponatraemia in alcohol patients. Liamis GL, Milionis HJ, Rizos EC, et al. Alcohol Alcohol.2000; 35 :612–616.3. Cerebral salt-wasting syndrome and inappropriate antidiuretic hormone syndrome after subarachnoid hemorrhaging.

1. Nakajima H, Okada H, Hirose K, et al.
2. Intern Med.2017; 56 :677–680.4.
3. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction.
4. Sanghvi SR, Kellerman PS, Nanovic L.
5. Am J Kidney Dis.2007; 50 :673–680.5.
6. Beer potomania—An unusual cause of hyponatremia.
7. Ujubu DA, Khosraviani A.

Perm J.2015; 19 :74–76.6. “Beer potomania” in non-beer drinkers: effect of low dietary solute intake. Thaler SM, Teitelbaum I, Berl T. Am J Kidney Dis.1998; 31 :1028–1031.7. Impact of solute intake on urine flow and water excretion. Berl T. J Am Soc Nephrol.2008; 19 :1076–1078.8.

• Pontine and extrapontine myelinolysis: a neurologic disorder following rapid correction of hyponatremia.
• Arp BI, Laureno R.
• Medicine (Baltimore) 1993; 72 :359–373.9.
• Therapeutic relowering of the serum sodium in a patient after excessive correction of hyponatremia.
• Soupart A, Ngassa M, Decaux G.
• Clin Nephrol.1999; 51 :383–386.10.

Osmotic demyelination syndrome. Abbott R, Silber E, Felber J, et al. BMJ.2005; 331 :829–830. : “Beer Potomania” – A Syndrome of Severe Hyponatremia with Unique Pathophysiology: Case Studies and Literature Review

Does drinking more water increase sodium?

Based on the fact that about two thirds of our bodies are comprised of water, it may seem obvious that consuming water is important for our health. But a new study finds that by increasing plain water consumption, we can control our weight and reduce intakes of sugar, sodium and saturated fat. Share on Pinterest Drinking more water is associated with reduced intakes of sugar, sodium and saturated fat, researchers say. The study, published in the Journal of Human Nutrition and Dietetics, is led by Prof. Ruopeng An, from the University of Illinois.

1. Though most people meet their body’s fluid requirements by drinking plain water and other beverages, we also get some fluids through certain foods, such as soup broths, celery, tomatoes and melons.
2. To further investigate how increasing water intake can affect parameters of health, the researchers used a nationally representative sample of more than 18,300 adults in the US from the National Health and Nutrition Examination Survey (NHANES) 2005-2012.

The researchers asked participants to recall all foods and drinks they consumed on 2 days that were between 3-10 days apart. Prof. An then calculated the amount of plain water that each participant consumed as a percentage of daily dietary water intake from both foods and drinks.

Why do you need salt after drinking alcohol?

Do you ever get those hangovers that keep you in bed all day – sometimes even two days? Where even the idea of getting up and being productive is too much to consider? Splitting headaches and nausea so bad that even the thought of breakfast makes you want to puke? Where all you can do is reach for the tylenol, chug some water, and hope for the best? We’ve all been there before.

• And we don’t want to be there again.
• That’s why we’re here to breakdown the best, step-by-step method for preventing those nasty hangovers.
• With all the spammy hangover “cures” all over the web, it can be difficult to wade through what is and isn’t true in an industry that is oversaturated with bogus advice.

This bulletproof hangover prevention process is backed by science every step of the way. But this isn’t some one-step, easy-peasy, cure-all. The key to hangover success is prevention. And if you really want to prevent your hangover, you’ve got to start your preparation well in advance.

• Prevention.
• Is the only way to truly treat a hangover,” says Dr.
• Ed Boyer, a medical toxicologist at Boston’s Brigham and Women’s Hospital.
• You are 90% more likely to wake up hangover-free if you begin your hangover prevention strategy the day before.
• And if you wait until the next morning to start fighting that hangover, you are 100% too late.

Get started early. This step-by-step, hour-by-hour guide is full of evidence-based methods that will help you avoid the worst hangover symptoms and enjoy both your night out and the next morning. The Day Before You Go Out Step 1. Hydrate your body Drink a ton of water If you know that you are going to be drinking that evening, make sure to drink a ton of water throughout the day beforehand.

1. Alcohol is a diuretic which means that it causes the kidneys to send water straight to the bladder instead of retaining it in the body – AKA it makes you pee a lot.
2. This causes dehydration which may contribute to symptoms like thirst, headache, fatigue and dry mouth.
3. Head this off as much as possible by drinking a ton of water throughout the day before you go out to make sure you’re as hydrated as possible before you start drinking.

Two Hours Before You Go Out Step 2. Eat a fatty meal – Nourish yourself with healthy fats You’ve probably heard that you should never drink on an empty stomach. There’s some truth to that – but not all foods are created equally when it comes to hangover prevention.

Alcohol is not fat-soluble, so if you eat a fat-heavy meal before drinking, the fat in the meal will create a lining in your stomach that will significantly slow down the absorption of alcohol and help prevent a hangover the next morning. But keep in mind that a fatty meal doesn’t necessarily mean it has to be full of unhealthy saturated fats like a greasy burger (saturated fat should only make up 5-6% of your caloric intake, any more than that is bad for your heart and cardiovascular health).

There are plenty of healthy fats that will do the same thing. We recommend something healthy and plant-based like avocados, olive oil, or nuts like almonds or walnuts that will have the same hangover preventing effect without the cholesterol of a burger.

• As You Begin Drinking Step 3.
• Take an Over EZ – Use a hangover prevention vitamin or supplement Take one Over EZ capsule with your first drink of the night to effectively prevent many of the worst hangover symptoms.
• This all-natural supplement helps your body neutralize acetaldehyde, the main hangover-causing toxin, and flush it from your body quickly, effectively reducing your hangover symptoms.

First, Over EZ’s unique combination of Zinc, Magnesium, and the Amino Acid L-Cysteine safeguard your liver from damage sustained while drinking and work together to prevent and reduce hangover symptoms. Next, Over EZ’s combination of B-complex vitamins, minerals, and others ingredients including Chicory Root, Milk Thistle, Amla Extract, Chinese Date Extract, Grape Extract and Beet Juice restore the body’s natural balance and replenish necessary vitamins and nutrients in order to get you back to feeling your best.

1. As You Are Drinking Step 4.
2. Eep it light and don’t mix your drinks – Stay away from mixing spirits, distilled drinks and beer.
3. Pick your Poison wisely Some alcohols have a higher concentration of congeners, chemicals that contain impurities and can contribute to worsened hangover symptoms,
4. In general, lighter colored alcohols like vodka, gin, and white wine have lower concentrations of congeners than darker colored alcohols like whiskey, dark rum, and red wine.

If you want to head off a hangover, stick to lighter colored drinks throughout your night. If you want to play it safe, the best practice is to choose one beverage and stick to it. Make sure not to mix drinks as it increases the likelihood that you’ll lose track of what you’ve had, drink more, and drink faster without realizing it – AKA you’ll be a lot more hungover in the morning.

1. Step 5. Pace yourself & drink water – This isn’t a horse race.
2. Remember, it takes your body about one hour to process one alcoholic beverage.
3. If you drink faster than that you can almost guarantee that you’ll feel the effects the next morning.
4. Eep an eye on the clock and sip your drinks slowly in order to prevent some of the worst hangover symptoms.

And of course, always drink a glass of water between each alcoholic beverage. Step 6. Snack throughout the evening Eating while you drink is key to continuing to slow the absorption of alcoho l. Be sure to continue to eat throughout the night but avoid salty foods, they’ll only dehydrate you more.

• Something healthy but carb-heavy is always good – think whole wheat crackers & cheese or finger sandwiches.
• If you wan’t something to take with you, a couple granola bars or a bag of veggie chips should do the trick.
• Just don’t go too heavy on the fatty foods (burgers, chips, fried foods), they won’t help your stomach and you may wake up feeling queezy or sick.

At the End of the Night Step 7. Stop while you’re ahead There’s no need for that last shot. In order to avoid the worst of a hangover, skip that last drink. Instead, have a big glass of water before bed and get a good night’s sleep – both will help you wake up the next morning feeling refreshed.

• As Soon As You Wake Up the Next Morning Step 8: Don’t skip your routine There’s a reason we are creatures of habit.
• Your body actually rewards you when you wake up close to the same time everyday even if you got less sleep.
• In fact, keeping a regular routine can improve your health in a ton of different ways including lowering your stress levels, improving your eating habits, and allowing time for regular exercise.

You might want to sleep in after a night out but don’t hit that snooze button – your body will thank you for it later. Step 9. Don’t pound coffee. In fact, stay away from caffeine. One cup of coffee is ok, but don’t down the whole pot the next morning. Large doses of caffeine will dehydrate you even more than you already are.

Instead, grab a glass of water or orange juice. Orange juice is packed full of Vitamin C which, according to some studies, can help accelerate alcohol metabolism. Step 10. Drink lemon, sugar, salt water This is one of the easiest and healthiest ways to naturally fight a hangover. If you’re still feeling a little rough the next morning, mix up a concoction of water, lemon juice, and a couple pinches each of sugar and pink Himalayan salt.

This is essentially a homemade Oral Rehydration Solution (ORS), Alcohol drains your body of electrolytes but the salt and sugar help replenish these while the water hydrates you. Combine that with the high concentration of Vitamin C and citric acid in lemon juice and you’ll be feeling better and re-hydrated in no time.

1. An Hour or Two After Getting Up Step 10.
2. Make an omelette Eating anything will help fight that hangover, but eggs are a particularly good choice if you are feeling the effects of the previous evening.
3. Eggs contain high levels of cysteine, an amino acid that helps break down acetaldehyde, the root cause of hangovers.

Over EZ also contains an especially strong dose of the same hangover-fighting amino acid, so if you take an Over EZ the night before and eat some eggs the next morning, you’ll be feeling great in no time. As the Day Goes On Step 11: Exercise! Go for a run, lift some weights, hit the yoga studio – whatever your preferred workout is, do it.

1. Several studies have shown that exercising after a night out is one of the best ways to kick the remnants of a hangover.
2. Be sure you’re well hydrated before you begin because a hard workout will dehydrate you more, but your efforts will be rewarded with less brain fog, better memory/cognition, and increased endorphins.

You can have the best of both worlds. Have that drink with your buddies and make it to your morning workout the next day. Just follow these step-by-step, science-backed ways to prevent the worst hangovers and live your life compromise-free,

What electrolytes are lost when drinking alcohol?

Abstract – The present review summarizes the current knowledge on the multiple effects of alcohol overconsumption on the kidney function as well as on water, electrolyte and acid-base homeostasis. In contrast to the well known transitory diuretic effects, the overall long-term effect of chronic alcohol overconsumption is water and salt retention with expansion of extracellular volume.

Furthermore, depletion of magnesium, phosphate and calcium is also frequently found in alcohol-dependent patients. These electrolyte disturbances may be associated with the alcohol-induced hypoparathyroidism and parathyroid hormone resistance of the skeletal muscle as well as with the decrease of serum osteocalcin.

Metabolic acidosis with lower arterial blood pH and plasma bicarbonate concentrations was revealed in alcoholic patients upon admission and a significant correlation between chronic alcohol overconsumption and increased incidence of hyperuricemia and gout attacks was also reported.

1. Alcohol seems to have dual effects on the blood pressure.
2. Increased blood pressure was demonstrated in men above 80 g and in women above 40 g ethanol consumption daily.
3. In contrast, young adults consuming only 10 to 20 g per day had lower blood pressure than the abstinent group indicating a J-curve relationship.

This is in line with the lowered risk for coronary heart disease associated with regular consumption of small alcohol amounts. The mechanisms responsible for the association between alcohol overconsumption and postinfectious glomerulonephritis have not been elucidated yet.

Can drinking too much alcohol cause electrolyte imbalance?

Abstract – The acute effect of ethyl alcohol ingestion is to induce diuresis with excretion of free water and preservation of electrolytes. This occurs as the blood alcohol concentration is increasing and is due to the suppression by alcohol of the endogenous release of ADH.

1. During a steady blood alcohol concentration, alcohol acts as an antidiuretic, causing retention of water and electrolytes.
2. While at steady state, additional doses of alcohol will produce progressively smaller and eventually absent diuretic responses.
3. The chronic effect of alcohol is to promote isosmotic retention of water and electrolytes due to increased ADH levels.

Excess water and electrolytes are acutely excreted in response to additional alcohol ingestion. With the cessation of alcohol intake, this excess will be excreted over several days. Routine parenteral fluid administration to chronic and withdrawing alcoholics should be avoided.

What is a dangerously low sodium level?

What is hyponatremia? – Hyponatremia means that the sodium level in the blood is below normal. Your body needs sodium for fluid balance, blood pressure control, as well as the nerves and muscles. The normal blood sodium level is 135 to 145 milliequivalents/liter (mEq/L).

How long does it take to recover from low-sodium?

Intravenous Sodium Replacement – If you have severe hyponatremia, you may need sodium to be replaced with intravenous (IV) fluids. This is when fluids containing water, sodium, and other key electrolytes are delivered gradually by “drips” into a vein using a needle. The medical team will restore the sodium level over the course of several hours or days, depending on the severity of your condition.

Should I eat more salt if my sodium is low?

How much salt should we eat? – Our bodies need a small amount of salt for a variety of functions, such as the working of nerves and muscles. However, there is enough sodium present in all foods that a lack of sodium does not generally cause any problems in these areas.

It is rarely necessary to add extra salt to food. Salt levels are often included in the nutritional information on food packets. Salt is also called sodium chloride, and the figures given may be for salt or for sodium. The recommended maximum daily intake of sodium for a healthy adult is 2.4 g, which is equivalent to 6 g of salt.

This is about a level teaspoonful. Many food labels also use a traffic light system, in which high levels of salt may be indicated by a red label. Because of increased awareness of the problems of eating too much salt, average salt intake in the UK has fallen by 15% since 2001.

What are the warning signs of low sodium?

Low blood sodium (hyponatremia) occurs when you have an abnormally low amount of sodium in your blood or when you have too much water in your blood. Low blood sodium is common in older adults, especially those who are hospitalized or living in long-term care facilities.

1. Signs and symptoms of hyponatremia can include altered personality, lethargy and confusion.
2. Severe hyponatremia can cause seizures, coma and even death.
3. Hyponatremia is more common in older adults because they’re more likely to take medications or have medical conditions that put them at risk of the disorder.

These risk factors include:

• Drugs that make you urinate more (diuretics)
• Some types of antidepressants
• Carbamazepine, an anti-seizure medication
• Underactive thyroid or adrenal glands
• Decreased function of the kidneys, liver or heart
• Certain cancers, including lung cancer
• Certain illnesses, such as pneumonia or urinary tract infections, that can cause dehydration

Hyponatremia treatments may include changing a medication that affects your sodium level, treating the underlying disease, changing the amount of water you drink or changing the amount of salt in your diet.

Is beer good for low sodium?

Taking alcohol with a (large) pinch of salt: Understanding the osmoles in “beer potomania” and “starvation potomania” Department of Nephrology, Kaiser Permanente, 9961 Sierra Ave, Fontana, CA 92335, USA Find articles by : © Indian Journal of Nephrology This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Alcoholism is a major problem globally and beer drinking is on the rise. Many of the alcoholics sustain only on beer for days and do not get adequate solutes in the form of food. Similar situation can arise in cases of decreased food intake due to severe deliberate restriction or other factors like decreased appetite from cocaine.

In these cases, salt free liquid intake may still be adequate. Such situations are conducive to the development of hyponatremia. Some of the solutes in diet, such as salt and protein, act as osmoles in urine. In these conditions, understanding the role played by solutes in diet and osmoles in urine is of vital importance for appropriate treatment of hyponatremia.

• Eywords: Beer potomania, hyponatremia, osmoles, starvation potomania Alcoholism is a major issue globally.
• Alcohol consumption in USA is rising and in between 22% and 26% of US community hospital admissions are alcohol related.
• Continued drinking despite adverse consequences is considered alcohol use disorder and 9% of US adults meet these criteria.

In USA, according to National Institute on Alcohol Abuse and Alcoholism (NIAAA), 3 in 10 adults drink at levels that put them at risk for alcoholism, liver disease and other problems. A standard drink in USA is considered to contain about 14 g of absolute alcohol.

This amounts to one 12-ounce bottle or can of either beer or wine cooler, one 5-ounce glass of wine, or 1.5 ounces of 80-proof distilled spirits. Heavy or at risk drinking is considered when either daily or weekly limits are exceeded. According to NIAA those limits are 4 drinks/day or 14 drinks/week in men.

In women it is either 3 drinks/day or 7 drinks/week. The risks of alcoholism exist on a continuum spectrum. Nearly 4% of at-risk drinkers have alcohol dependence, which is a condition of craving and loss of control over drinking despite harm, with daily or near daily drinking.

• Besides many negative personal, social and health consequences, electrolyte disorders are a common finding in alcohol related hospital admissions, the most commonly encountered being hyponatremia.
• Various other mechanisms of hyponatremia in alcoholics have been described.
• These include hypovolemia, pseudohyponatremia from hypertriglyceridemia and cerebral salt wasting syndrome from alcohol induced cerebral atrophy.

Another scenario for development of hyponatremia involves excess water intake relative to solutes. Excessive chronic consumption of beer without adequate food intake can cause severe hyponatremia. It is called “beer potomania”, if laboratory values are mostly consistent with water intoxication and no other cause of hyponatremia is found.

1. Demanet et al,
2. First coined this entity in 1971 and since then it has been reported in the literature approximately 23 times.
3. Beer has a very low content of sodium and protein and no other major source of solutes or osmoles.
4. Some chronic severe alcoholics subsist solely on beer.
5. Many can drink more than 24 cans a day.

Because of this they have extremely little daily intake of solutes. Intake of water or solute free liquid, in excess, will not necessarily induce hyponatemia in an otherwise healthy patient with properly functioning kidney with normal diluting and concentrating capacity (for example, the absence of hydrochlorothiazide and arginine vasopressin respectively).

• Ingestion of adequate food containing solutes, some of which end up as urinary osmoles, allows excretion of ingested water in excess of 20 L/d.
• However, such a person may develop water intoxication leading to hyponatremia if the excretion of water is limited due to the lack of simultaneous ingestion of solutes, as explained below.

Urinary osmolar excretion is determined by dietary intake of solutes, predominantly sodium chloride (NaCl) and urea. Urinary urea comes from mostly ingested protein nitrogen in nitrogen balanced patients. An average 24-h American adult osmolar excretion is about 900 mOsm.

1. Of that, approximately 300 mOsm is contributed by urea, 300 mOsm by NaCl and rest by potassium, magnesium, calcium, phosphates, sulfates, bicarbonate, ammonia, uric acids, amino acids, and creatinine.
2. One level teaspoon of table salt contains approximately 6200 mg NaCl.
3. The ratio of Na is 40% in NaCl and ratio of Cl is 60% (molecular weight Na 23 and MW Cl 35.5).

Hence, there is approximately 2400 mg Na in a teaspoon of table salt. To convert Na and Cl in mg to mEq it is divided by the respective MW. Hence, 2400 mg Na (1 teaspoon) will give 104 mEq of Na. Using the same method of calculation, 1 teaspoon of salt will provide about 104 mEq Cl and hence a total of 208 mEq or mOsm of NaCl.

• The contribution that protein intake make on urinary osmoles cannot be calculated accurately.
• This also depends on the nitrogen balance in a person.
• Approximately 45-50 mOsm of urinary urea are contributed by 10 g of protein intake.
• Normal human renal physiology is such that amount of urine excretion is dependent on solutes in urine that act as osmoles.

In normal human urine osmolality can be as low as 50 mOsm/L; means that for every liter of urine excretion at least 50 mOsm would be required. Hence, the maximum volume of urine excretion/day can be calculated by dividing the total daily solute excretion by maximally diluted urine osmolality for that patient.

• Using an average of 900 mOsm, daily excretion will be 900/50, or 18 L/d urine volume.
• In other words, this person can drink 18 L water with no problems.
• Predominantly in heavy beer drinkers with no other food intake there will be very minimal solute intake.
• Beer does contain carbohydrates which prevent ketosis while drinking and hence generally ketones will not be acting as osmoles in these cases.

Without ketosis, 70 kg alcoholics will consume about 35 g of their own protein stores/day. That will provide about 170 mOsm from urea and other obligatory solutes from cellular catabolism will add about 75 mOsm to a total of about 245 mOsm. Consuming a 24 pack of 12-ounce beer cans/day with each about 14 mg Na will give 336 mg, which is 14 mOsm Na (336/23).

1. Similar 24 pack beer will give 2304 mg potassium which will provide 59 mOsm (2304/39).
2. So only about 73 mOsm will be added by daily alcohol, leading to total daily solute excretion of 318 mOsm (245 + 73).
3. However, the patient is still ingesting a volume of 8640 ml.
4. Taking out about 1000 ml for insensible loss will still leave roughly 7640 ml in the body.

The total 24 h urine volume will be about 6360 ml (318/50), leaving 1280 ml daily in extracellular space to cause water intoxication. This daily extra addition of water will lead to hyponatremia. On top of this, some of these beer drinkers may also have some non-osmotic secretion of antidiuretic hormone as a result of volume depletion from chronic gastrointestinal losses/diarrhea or nausea/vomiting.

• This will prevent urine osmolality to go as down as low as 50 mOsm.
• In fact in such patients maximal urine dilution may just be no lower than 100 mOsm.
• In above example the urine excretion will be cut in half to 3180 ml leaving about 3180 ml for water intoxication on daily basis.
• Also in these patients the measured serum osmolality from lab may not be low due to contribution of ethanol levels in blood.

Blood alcohol level in mg/dl has to be divided by 4.6 to convert to mOsm. Similarly urinary alcohol levels may mask urine hypo-osmolality, though urine Na will be low. Contribution of alcohol to urine osmolality can be calculated by multiplying serum alcohol levels by 1.4.

1. Though alcohol induces diuresis via antagonizing AVP, is well-known, but it is initiated by the increase in blood alcohol levels.
2. However it is not maintained for long even if high steady levels of alcohol maintained.
3. Hence, likely this does not help counter development of hyponatremia in chronic alcoholics.

Also in these cases the clinical state is such that although there is conducive situation for brisk diuresis due to suppressed AVP but no solutes that will maintain urine output. This causes the extra water to stay in body causing hyponatremia, oliguria and edema.

• However, these patients have brisk diuresis when solutes are introduced.
• Take an example of 1 L of 0.9% saline that has 308 mEq.
• With urine osmolality of 50 mOsm/L this 1 L will be excreted with 6 L of urine, or 5 extra L of free water.
• As an example if a 70 kg alcoholic man who has some extra body water, e.g.

about 5 L, total body water of about 45 L then his serum Na will go up by about 13 points (110 × 45/40) after 5 L of free water urine loss. This can cause more rapid than expected rise of serum Na.18% of patients with beer potomania developed osmotic demyelination syndrome (ODS).

In order to minimize risks of ODS, Sanghvi et al, have described a detailed approach to management of these hyponatremic patents, after admission. Rules of rate of rise of Na remain same as any other patients but these include intensive care units with frequent Na monitoring, cautious initiation of oral feeding with nothing per oral in the initial hours, intra venous fluids in limited amounts, use of D5W if needed to restrict rate of rise of Na.

Similar situation can also be observed in starvation and with deliberately restricted diets. Also in severe malnutrition and severe loss of appetite (as in cocaine abuse), where there is significant salt free liquid ingestion, as in alcoholics, “starvation potomania” can arise.

It is important to recognize such conditions because recovery depends highly on very cautious osmotic replenishment. Source of Support: Nil Conflict of Interest: None declared.1. Muller A. Alcohol consumption and community hospital admissions in the United States: A dynamic regression analysis, 1950-1992.

Addiction.1996; 91 :231–42.2.4th ed. Washington, DC: American Psychiatric Association; 2000. Diagnostic and Statistical Manual of Mental Disorders. text revision.3. Grant BF, Dawson DA, Stinson FS, Chou SP, Dufour MC, Pickering RP. The 12-month prevalence and trends in DSM-IV alcohol abuse and dependence: United States, 1991-1992 and 2001-2002.

Drug Alcohol Depend.2004; 74 :223–34.4. National Institute on Alcohol Abuse and Alcoholism. National Institute of Health. “Rethinking Drinking”. Available from:,5. Friedmann PD. Alcohol use in adults. N Engl J Med.2013; 368 :1655–6.6. Demanet JC, Bonnyns M, Bleiberg H, Stevens-Rocmans C. Coma due to water intoxication in beer drinkers.

Lancet.1971; 2 :1115–7.7. Campbell MC. Hyponatremia and central pontine myelinolysis as a result of beer potomania: A case report. Prim Care Companion J Clin Psychiatry.2010; 12 (4):ii. PCC.09100936.doi:10.4088/PCC.09l00936ecr. PubMed PMID:21085565; PubMed Central.

PMCID: PMC2983455.8. Blalock T, Gerron G, Quiter E, Rudman D. Role of diet in the management of vasopressin-responsive and -resistant diabetes insipidus. Am J Clin Nutr.1977; 30 :1070–6.9. Berl T. Impact of solute intake on urine flow and water excretion. J Am Soc Nephrol.2008; 19 :1076–8.10. Fenves AZ, Thomas S, Knochel JP.

Beer potomania: Two cases and review of the literature. Clin Nephrol.1996; 45 :61–4.11. Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: An unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis.2007; 50 :673–80.12.

• Eisenhofer G, Johnson RH.
• Effect of ethanol ingestion on plasma vasopressin and water balance in humans.
• Am J Physiol.1982; 242 :R522–7.13.
• Magner PO, Ethier JH, Kamel KS, Halperin ML.
• Interpretation of the urine osmolality: The role of ethanol and the rate of excretion of osmoles.
• Clin Invest Med.1991; 14 :355–8.14.

Eggleton MG. The diuretic action of alcohol in man. J Physiol.1942; 101 :172–91.15. Thaler SM, Teitelbaum I, Berl T. “Beer potomania” in non-beer drinkers: Effect of low dietary solute intake. Am J Kidney Dis.1998; 31 :1028–31. Articles from Indian Journal of Nephrology are provided here courtesy of Wolters Kluwer – Medknow Publications : Taking alcohol with a (large) pinch of salt: Understanding the osmoles in “beer potomania” and “starvation potomania”

How do you increase sodium in your blood?

Summary – In conclusion, maintaining the proper sodium balance in your body is essential for your overall health and well-being. If you have low sodium levels, incorporating more sodium-rich foods, consuming sports drinks or electrolyte solutions, and considering sodium supplements can help increase your sodium levels.

Does drinking alcohol deplete potassium?

Alcohol consumption historically has been found to reduce the amount of potassium excreted by the kidneys (e.g., Rubini et al.1955), although the body’s hydration state may help determine whether potassium excretion will increase or decrease in response to alcohol.

Why do you need salt after drinking alcohol?

Do you ever get those hangovers that keep you in bed all day – sometimes even two days? Where even the idea of getting up and being productive is too much to consider? Splitting headaches and nausea so bad that even the thought of breakfast makes you want to puke? Where all you can do is reach for the tylenol, chug some water, and hope for the best? We’ve all been there before.

And we don’t want to be there again. That’s why we’re here to breakdown the best, step-by-step method for preventing those nasty hangovers. With all the spammy hangover “cures” all over the web, it can be difficult to wade through what is and isn’t true in an industry that is oversaturated with bogus advice.

This bulletproof hangover prevention process is backed by science every step of the way. But this isn’t some one-step, easy-peasy, cure-all. The key to hangover success is prevention. And if you really want to prevent your hangover, you’ve got to start your preparation well in advance.

1. Prevention.
2. Is the only way to truly treat a hangover,” says Dr.
3. Ed Boyer, a medical toxicologist at Boston’s Brigham and Women’s Hospital.
4. You are 90% more likely to wake up hangover-free if you begin your hangover prevention strategy the day before.
5. And if you wait until the next morning to start fighting that hangover, you are 100% too late.

Get started early. This step-by-step, hour-by-hour guide is full of evidence-based methods that will help you avoid the worst hangover symptoms and enjoy both your night out and the next morning. The Day Before You Go Out Step 1. Hydrate your body Drink a ton of water If you know that you are going to be drinking that evening, make sure to drink a ton of water throughout the day beforehand.

• Alcohol is a diuretic which means that it causes the kidneys to send water straight to the bladder instead of retaining it in the body – AKA it makes you pee a lot.
• This causes dehydration which may contribute to symptoms like thirst, headache, fatigue and dry mouth.
• Head this off as much as possible by drinking a ton of water throughout the day before you go out to make sure you’re as hydrated as possible before you start drinking.

Two Hours Before You Go Out Step 2. Eat a fatty meal – Nourish yourself with healthy fats You’ve probably heard that you should never drink on an empty stomach. There’s some truth to that – but not all foods are created equally when it comes to hangover prevention.

• Alcohol is not fat-soluble, so if you eat a fat-heavy meal before drinking, the fat in the meal will create a lining in your stomach that will significantly slow down the absorption of alcohol and help prevent a hangover the next morning.
• But keep in mind that a fatty meal doesn’t necessarily mean it has to be full of unhealthy saturated fats like a greasy burger (saturated fat should only make up 5-6% of your caloric intake, any more than that is bad for your heart and cardiovascular health).

There are plenty of healthy fats that will do the same thing. We recommend something healthy and plant-based like avocados, olive oil, or nuts like almonds or walnuts that will have the same hangover preventing effect without the cholesterol of a burger.

As You Begin Drinking Step 3. Take an Over EZ – Use a hangover prevention vitamin or supplement Take one Over EZ capsule with your first drink of the night to effectively prevent many of the worst hangover symptoms. This all-natural supplement helps your body neutralize acetaldehyde, the main hangover-causing toxin, and flush it from your body quickly, effectively reducing your hangover symptoms.

First, Over EZ’s unique combination of Zinc, Magnesium, and the Amino Acid L-Cysteine safeguard your liver from damage sustained while drinking and work together to prevent and reduce hangover symptoms. Next, Over EZ’s combination of B-complex vitamins, minerals, and others ingredients including Chicory Root, Milk Thistle, Amla Extract, Chinese Date Extract, Grape Extract and Beet Juice restore the body’s natural balance and replenish necessary vitamins and nutrients in order to get you back to feeling your best.

As You Are Drinking Step 4. Keep it light and don’t mix your drinks – Stay away from mixing spirits, distilled drinks and beer. – Pick your Poison wisely Some alcohols have a higher concentration of congeners, chemicals that contain impurities and can contribute to worsened hangover symptoms, In general, lighter colored alcohols like vodka, gin, and white wine have lower concentrations of congeners than darker colored alcohols like whiskey, dark rum, and red wine.

If you want to head off a hangover, stick to lighter colored drinks throughout your night. If you want to play it safe, the best practice is to choose one beverage and stick to it. Make sure not to mix drinks as it increases the likelihood that you’ll lose track of what you’ve had, drink more, and drink faster without realizing it – AKA you’ll be a lot more hungover in the morning.

• Step 5. Pace yourself & drink water – This isn’t a horse race.
• Remember, it takes your body about one hour to process one alcoholic beverage.
• If you drink faster than that you can almost guarantee that you’ll feel the effects the next morning.
• Eep an eye on the clock and sip your drinks slowly in order to prevent some of the worst hangover symptoms.

And of course, always drink a glass of water between each alcoholic beverage. Step 6. Snack throughout the evening Eating while you drink is key to continuing to slow the absorption of alcoho l. Be sure to continue to eat throughout the night but avoid salty foods, they’ll only dehydrate you more.

Something healthy but carb-heavy is always good – think whole wheat crackers & cheese or finger sandwiches. If you wan’t something to take with you, a couple granola bars or a bag of veggie chips should do the trick. Just don’t go too heavy on the fatty foods (burgers, chips, fried foods), they won’t help your stomach and you may wake up feeling queezy or sick.

At the End of the Night Step 7. Stop while you’re ahead There’s no need for that last shot. In order to avoid the worst of a hangover, skip that last drink. Instead, have a big glass of water before bed and get a good night’s sleep – both will help you wake up the next morning feeling refreshed.

• As Soon As You Wake Up the Next Morning Step 8: Don’t skip your routine There’s a reason we are creatures of habit.
• Your body actually rewards you when you wake up close to the same time everyday even if you got less sleep.
• In fact, keeping a regular routine can improve your health in a ton of different ways including lowering your stress levels, improving your eating habits, and allowing time for regular exercise.

You might want to sleep in after a night out but don’t hit that snooze button – your body will thank you for it later. Step 9. Don’t pound coffee. In fact, stay away from caffeine. One cup of coffee is ok, but don’t down the whole pot the next morning. Large doses of caffeine will dehydrate you even more than you already are.

Instead, grab a glass of water or orange juice. Orange juice is packed full of Vitamin C which, according to some studies, can help accelerate alcohol metabolism. Step 10. Drink lemon, sugar, salt water This is one of the easiest and healthiest ways to naturally fight a hangover. If you’re still feeling a little rough the next morning, mix up a concoction of water, lemon juice, and a couple pinches each of sugar and pink Himalayan salt.

This is essentially a homemade Oral Rehydration Solution (ORS), Alcohol drains your body of electrolytes but the salt and sugar help replenish these while the water hydrates you. Combine that with the high concentration of Vitamin C and citric acid in lemon juice and you’ll be feeling better and re-hydrated in no time.

1. An Hour or Two After Getting Up Step 10.
2. Make an omelette Eating anything will help fight that hangover, but eggs are a particularly good choice if you are feeling the effects of the previous evening.
3. Eggs contain high levels of cysteine, an amino acid that helps break down acetaldehyde, the root cause of hangovers.

Over EZ also contains an especially strong dose of the same hangover-fighting amino acid, so if you take an Over EZ the night before and eat some eggs the next morning, you’ll be feeling great in no time. As the Day Goes On Step 11: Exercise! Go for a run, lift some weights, hit the yoga studio – whatever your preferred workout is, do it.

• Several studies have shown that exercising after a night out is one of the best ways to kick the remnants of a hangover.
• Be sure you’re well hydrated before you begin because a hard workout will dehydrate you more, but your efforts will be rewarded with less brain fog, better memory/cognition, and increased endorphins.

You can have the best of both worlds. Have that drink with your buddies and make it to your morning workout the next day. Just follow these step-by-step, science-backed ways to prevent the worst hangovers and live your life compromise-free,

How long does it take to recover from low sodium?

Intravenous Sodium Replacement – If you have severe hyponatremia, you may need sodium to be replaced with intravenous (IV) fluids. This is when fluids containing water, sodium, and other key electrolytes are delivered gradually by “drips” into a vein using a needle. The medical team will restore the sodium level over the course of several hours or days, depending on the severity of your condition.

Can low sodium be caused by not drinking enough water?

Your sodium levels may get too low if your body loses too much water and electrolytes. Hyponatremia may also be a symptom of certain medical conditions.

Can drinking too much alcohol cause electrolyte imbalance?

Abstract – The acute effect of ethyl alcohol ingestion is to induce diuresis with excretion of free water and preservation of electrolytes. This occurs as the blood alcohol concentration is increasing and is due to the suppression by alcohol of the endogenous release of ADH.

1. During a steady blood alcohol concentration, alcohol acts as an antidiuretic, causing retention of water and electrolytes.
2. While at steady state, additional doses of alcohol will produce progressively smaller and eventually absent diuretic responses.
3. The chronic effect of alcohol is to promote isosmotic retention of water and electrolytes due to increased ADH levels.

Excess water and electrolytes are acutely excreted in response to additional alcohol ingestion. With the cessation of alcohol intake, this excess will be excreted over several days. Routine parenteral fluid administration to chronic and withdrawing alcoholics should be avoided.