Severe metabolic derangement: a case of concomitant diabetic ketoacidosis and beer potomania

Abstract

Diabetic ketoacidosis (DKA) and hyponatraemia associated with beer potomania are severe diagnoses warranting intensive care level management. Our patient, a middle-aged man, with a history of chronic alcohol abuse and insulin non-compliance, presents with severe DKA and severe hyponatraemia. Correcting sodium and metabolic derangements in each disorder require significant attention to fluid and electrolyte levels. Combined they prove challenging and require an individualised approach to prevent the overcorrection of sodium. Furthermore, management of these conditions lends to the importance of understanding the pathophysiology behind their hormonal and osmotic basis.

Background

Diabetic ketoacidosis (DKA) and hyponatraemia associated with beer potomania are diseases of significant fluid and electrolyte derangement, which often require admission to the intensive care unit (ICU). DKA is often diagnosed quickly with routine laboratory studies and rapid initiation of therapy with intravenous fluid and insulin shortly after. Similarly, hyponatraemia can be diagnosed quickly with a metabolic profile; however, determining the underlying cause often delays treatment. The multiplicity of aetiologies makes a full diagnosis difficult and may also delay the initiation of treatment of other conditions. In this case, we will discuss the medical history of a patient who presents with significant hyponatraemia while also in a state of DKA and the care taken to avoid possible consequences, the most worrisome being central pontine myelinolysis.

Case presentation

A middle-aged man with a medical history of alcohol abuse, alcoholic steatosis, chronic pancreatitis, chronic hyponatraemia, insulin-dependent diabetes mellitus, osteomyelitis and medical non-compliance presents to the emergency department with chief reports of confusion, disequilibrium and nausea. He reports that prior to arrival, he had been drinking an average of 12 beers a day, eating poorly and had difficulty maintaining his daily function for the last few days. He also reports he was non-compliant with his insulin and oral medications for the last month.

In the emergency department, vital signs reflected rapid shallow breathing, moderate hypotension and tachycardia. The patient met sepsis criteria and had labs drawn including blood cultures. He was given a bolus of normal saline and subsequently initiated on broad spectrum antibiotics: cefepime and vancomycin. His initial metabolic profile reflected a blood glucose of 428 mg/dL, a corrected glucose sodium level of 110 mmol/L, bicarbonate of 9 mmol/L and an anion gap of >31. Given this profile, a venous blood gas and beta-hydroxybutyrate (BHB) level were drawn and showed a PH of 7.16 and 7.6 mmol/L, respectively, reflecting severe DKA. Alcohol was also noted to be elevated at 67.3 mg/dL. Sodium at our institute is measured through an indirect ion method with a Roche Cobas 6000 machine.

The patient was admitted to the ICU for management of acute encephalopathy and severe metabolic derangements. He was diagnosed with DKA, severe sepsis and hyponatraemia suspected to be due to beer potomania. Urine and serum studies showed a serum osmolality of 261 mOsm/kg, urine osmolality of 261 mOsm/kg and urine sodium under 20 mmol/L. Thyroid-stimulating hormone reflected a non-impaired function at 1.99 μIU/ml. Liver function testing reflected mild alcoholic hepatitis with aspartate aminotransferase of 162 U/L, alanine transaminase of 65 U/L and total bilirubin of 0.3 mg/dL.

The patient was initiated on a modified DKA protocol, which consisted of intravenous continuous insulin, lactated ringers at 100 mL/hour, and 20 units of insulin glargine nightly. Within 24 hours of admission, the corrected sodium increased to 113 mmol/L. The patient was then transitioned to dextrose 5% in free water at 100 mL/hour to slow the rate of sodium correction. A nutritional evaluation was also preformed, and the patient was found to have protein-calorie malnutrition and placed on a diabetic diet consisting of 60 g of carbs per meal and medical food supplementation with Boost protein drinks. Multivitamin therapy with high-dose thiamine was initiated as well.

After approximately 80 hours in ICU, the patient’s sodium had improved to 118 mmol/L and their DKA was fully resolved. He was transitioned from continuous insulin infusion to a basal-prandial regiment of insulin. During this time, blood cultures grew methicillin-sensitive staphylococcus aureus and antibiotics were switched to cefazolin.

The patient was then transferred from the ICU for continued care to the general medicine step down floor. Nephrology was now consulted to assist with persistent hyponatraemia, which remained low at 118–120 mmol/L. The patient was initiated on low-dose demeclocycline and furosemide for suspicion of concomitant syndrome of inappropriate antidiuretic hormone (SIADH)/SIAD. Fluid restrictions of 1500 mL/day were also put into place. After 1 week with this therapeutic management, the patient’s sodium improved into the 130 s. Liver function also during this time returned to normal levels.

For the remainder of his admission, the patient was maintained on this regiment and sodium levels remained within the low 130 s. Unfortunately, shortly prior to discharge, he developed worsening respiratory status and was diagnosed with bilateral pneumonia with parapneumonic effusions, which required expanded antibiotic therapy and pleural decortication. After recovery, the patient was discharged with demeclocycline 150 mg two times per day and furosemide 20 mg/day for 30 days.

Outcome and follow-up

The patient on follow-up maintained low normal sodium level while on his prescribed demeclocycline and furosemide therapy. After their discontinuation and a relapse back to significant alcohol consumption, his sodium returned to their previous level in the low 120 s.

Discussion

Our patient presented with multiple life-threatening metabolic derangements, including hyperglycaemic, acidosis and hyponatraemia. His history played a significant role in contributing to the determination of the cause of these conditions. His hyperglycaemic crisis fits well into the diagnosis of DKA. Factors that corroborated this diagnosis included his elevated blood sugar on admission along with evidence of ketosis and acidosis. The diagnosis of beer potomania was determined through his low sodium, history of heavy alcohol consumption and correction with solute-rich isotonic fluid.

DKA is defined by a combination of metabolic acidosis, increased total body ketones and hyperglycaemic.¹ The hallmark signs of DKA were noted in our patient: dehydration, encephalopathy, kussmaul breathing and gastroenterological upset.^{2 3} His metabolic panel and blood gas similarly met the common criterion including blood PH under 7.3, a glucose over 250 mg/dL, an anion gap over greater than 12 and bicarbonate under 18 mmol/L and evidence of ketosis such as BHB or urine ketones.^{2 4}

The development of DKA is often linked to many precipitating factors include infections, trauma, myocardial infarctions or iatrogenic causes such as non-compliance.^{1 2} In our patient, his infection and non-compliance acted as acute stressors leading to a worsening insulin-deficient state.³ This relative insulin deficiency could not compensate for the increase of counter-regulatory hormone such as cortisol, catecholamines and glucagon-causing ketoacid formation.⁴

However, alternative sources of ketosis do exist and were considered as possible differentials such as alcoholic ketoacidosis (AKA) and starvation ketosis. AKA is a condition that occurs in the setting of malnourishment and heavy alcohol consumption, causing production of ketone bodies due to alcohol’s impairment of both hepatic gluconeogenesis and lipolysis.^5–7 This ketoacidosis increases in severity as alcohol level begins to drop, but rarely causes severe metabolic acidosis of under a PH of 7.3.⁵ In starvation ketosis, the patient produces ketone bodies but have appropriate insulin levels and rarely develop clinically significant metabolic acidosis.⁵ Further, these disorders usually have low or normal glucose levels and respond well to nutrition and vitamin therapies, allowing for restoration of non-ketone metabolism.^{6 7}

In our patient’s case, their condition suggested DKA rather than AKA or other conditions. Their hyperglycaemic, uncontrolled diabetes, bacteraemia, severe acidosis and requirement for multiple days of continuous insulin therapy make other diagnosis unlikely. The patient was also on presentation heavily intoxicated and reported drinking immediately prior to admission. This makes the timing unlikely for AKA, which requires more time for alcohol levels to drop to produce ketone bodies.^{5 6}

Our patient’s second life-threatening metabolic abnormality was hyponatraemia. After correcting for his elevated glucose, his sodium remained extremely low at 110, leading us to suspect beer potomania. Sodium is the most important osmotic solute in blood and determines intracellular and extracellular fluid balance.⁸ In beer potomania, the sodium levels are often exceptionally low and labile, with a high risk for dangerous and rapid normalisation, making frequent monitoring imperative.⁸

The severe consequence of overcorrecting sodium too rapidly is osmotic damage of neural tissues.⁸ Osmotic demyelination and central pontine myelinolysis were first described in the literature in chronic alcoholics who, after significant bingeing behaviour, developed significantly low sodium levels and encephalopathy.⁸ These patients after treatment and rapid correction of their sodium levels had improvement of encephalopathy, but days later developed flaccid paralysis.⁸ Brain MRI on these patients will show diffuse demyelinating disease of the rostral pons.⁸ While devastating, it is a rare presentation and often requires long-standing hyponatraemia to be rapidly corrected at rates exceeding 8 mg/dL in a 24-hour period to develop.⁸ More acute hyponatraemia such as those developed over the course of hours or a day is unlikely to cause osmotic damage.⁸

The aetiology of hyponatraemia in our patient is multifactorial, with the most important causes being beer potomania and then later SIADH/SIAD. Beer potomania is a hypotonic hyponatraemia that affects predominately chronic alcoholics.^{9 10} Physiologically it is represented by increased total body fluid, reduced solute intake and suppressed ADH levels.^{9 10} Generating the reduced solute intake is the fact that beer, like many alcoholic beverages, possesses a low amount of solute in respect to its caloric and fluid content.^{10 11} Overtime, a diet predominately of beer or low solute alcohols produces a solute and fluid volume mismatch that causes a slow shedding of electrolytes by the kidney.^{9 10} Furthermore, this low ADH state allows for rapid correction of sodium with increase in solute, such as with saline infusions, leading to dangerous diuresis of free fluid.^{11 12}

SIADH or rather its more appropriate name SIAD is an important differential in our patient’s hyponatraemia. This was the second process needing to be addressed after solute replacement began to partially resolve their hyponatraemia. This disease state develops through either increased secretion of ADH or deregulated vasopressin receptor activity.¹³ ADH is a crucial hormone for water balance and exerts its effects on vasopressin receptors causing increased absorption of water in the kidney.¹³ Excessive ADH secretion and or activity of vasopressin receptors in absence of appropriate stimulating factors results in an inability to excrete adequate fluid and maintains an increased total body water.¹³ This impairs the ability of the kidney to dilute urine and consequentially decreases the serum sodium level.¹³

Our patient’s hyponatraemia is significant in that it required multiple distinct treatment phases. First, with slow and frequently monitored solute infusion, to support DKA management and replete the electrolyte deficient state. But then afterwards with furosemide and demeclocycline to correct the concomitant SIADH/SIAD supported by persistently increased total body fluid. This paradoxical vasopressin receptor activity resulted in a stabilisation of sodium at 120 mg/dL that required treatment to enhance kidney dilution and induce diuresis of free water. Only afterwards, we were able to overcome the increased vasopressin receptor activity and eventually normalise both the total body water and sodium level, preventing further decreases.

Conclusion

These conditions may seem mutually exclusive of each other as DKA often lead to hypovolaemia and beer potomania is a condition of increased total body water. This may be reconciled as they are conditions separated by their time in development. The low sodium level is due to an equilibrium established by chronic alcohol use and low solute intake over the course of weeks to months. DKA is, however, an acute process in the setting of worsening glycaemic control that was produced over days. Our patient’s bacteraemia and non-compliance with diabetes medications exacerbated his insulin deficiency. This resulting in him is developing DKA in the setting of chronic hyponatraemia.

The patient experienced resolution of both hyponatraemia and DKA through a slower modified protocol with many different phases of treatment. This shows importance of frequent monitoring and modification of care to prevent the consequences of osmotic injury. Slow improvement and complications with re-establishing a normal and appropriate ADH response further show the importance of understanding the underlying physiology behind both the neuroendocrine and renal systems in managing hyponatraemia.

Learning points.

• Treating diabetic ketoacidosis and concomitant hyponatraemia can be difficult, and protocoled systems while effective for managing either condition might not be adaptable to all cases.

• Chronic hyponatraemia is often a complicated disorder with features of impaired antidiuretic hormone activity. In our patient, beer potomania led to a total body fluid increase, which required diuresis and demeclocycline to restore normal levels.

• This case most importantly reiterates the importance that sodium correction must be done slowly to achieve normalisation without complications.

Ethics statements

Patient consent for publication

Obtained.