Search Menu. Joint British Diabetes Societies Guideline Hyperglycemid the Management of Diabetic Ketoacidosis: Diabetic Ketoacidosis Guidelines. Van Zyl DG, Rheeder P, Delport E. Umpierrez GE, Murphy MB, Kitabchi AE. Intensive Care Med. Nephrol Dial Transplant. Advanced Search.

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Diabetic Ketoacidosis (DKA) \u0026 Hyperglycemic Hyperosmolar Syndrome (HHS)

Hyperglycemic crisis and hyperkalemia -

They found no significant difference in DKA resolution at 48 hours, ICU, and hospital length of stay. However, PL group had significantly reached more DKA resolution at 24 hours in comparison to 0.

In conclusion, designing an appropriate fluid repletion therapy for DKA and HHS management will need careful planning and monitoring for choosing the appropriate fluid type, volume, and rate for the patient.

Insulin is considered to be one of the three fundamental elements of DKA and HHS management 2 , 6 , It reduces hepatic glucose synthesis, enhances peripheral glucose utilization, and inhibits lipolysis, ketogenesis, and glucagon secretion, lowering plasma glucose levels and decreasing ketone bodies production 6 , Insulin should be given immediately after the initial fluid resuscitation 2 , 6 , The aim of using insulin in DKA and HHS is to close the anion gap generated by the production of ketone bodies rather than aiming for euglycemia 6 , Intravenous administration of insulin regular mixed in NaCl 0.

Insulin can also be used as frequent subcutaneous or intramuscular injections for the treatment of DKA in mild-moderate DKA patients 6 , However, a continuous intravenous insulin regimen is preferred over subcutaneous insulin for DKA management overall due to its short half-life, fast onset, and easy titration 6 , The use of basal insulin analogs in conjunction with regular insulin infusions may speed up the resolution of DKA and minimize rebound hyperglycemia events, resulting in less ICU length of stay and less healthcare cost 6 , Insulin is currently recommended as a continuous infusion at 0.

Insulin loading dose has been linked to increasing the risk of cerebral edema and worsening shock Thus, insulin loading dose should be avoided at the beginning of therapy However, an insulin loading dose of 0.

Multiple factors must be considered when titrating intravenous insulin continuous infusion 2. The rate of blood glucose reduction, insulin sensitivity, prandial coverage, and NPO status should all be taken into consideration 2.

A rapid reduction in BG might be harmful and linked to cerebral edema 2. Moreover, the insulin infusion rate can be increased based on BG around major meals time and can be continued at a higher rate for hours following any major meal 2.

Lastly, it is necessary to monitor BG among NPO patients closely. Randomized clinical trials compared the two strategies and found no difference 27 , Intravenous LD insulin administration has been associated with an increased risk of cerebral edema 27 , An acceptable alternative for patients with mild to moderate DKA could be a bolus of 0.

Patients with end-stage renal disease ESRD and acute kidney injury AKI are considered a high-risk category that necessitates extra care 32 , To avoid rapid increases in osmolality and hypoglycemia in these patients; it is recommended that insulin infusions begin at 0.

Subcutaneous insulin should overlap with intravenous insulin for at least minutes before its discontinuation to ensure the optimal transition of care 6 , A transition to subcutaneous long-acting insulin in addition to ultra-short acting insulin such as glargine and glulisine after resolution of DKA may result in reduced hypoglycemic events compared to other basal bolus regimens such as NPH insulin and insulin regular 24 , For newly diagnosed insulin-dependent diabetes patients, subcutaneous insulin may be started at a dose of 0.

The transition process in patients who were previously using insulin or antidiabetic agents before to DKA admission is still unclear 24 , In ICU settings, clinicians tend to hold all oral antidiabetic agents and rely on insulin regimens for in-patient management given the shorter half-life of insulin and its predictability 24 , This could potentially be an area for further investigation on the transition process and its implication on patient outcomes 24 , Insulin sequestering to plastic IV tubing has been described, resulting in insulin wasting and dose inaccuracy 34 , Flushing the IV tube with a priming fluid of 20 mL is adequate to minimize the insulin losses to IV tube 34 , Patients with hyperglycemic crisiss are at a higher risk of developing hypokalemia due to multifactorial process 1 , Insulin therapy, correction of acidosis, and hydration all together lead to the development of hypokalemia 1 , Additionally, volume depletion seen with hyperglycemic crisis leads to secondary hyperaldosteronism, which exacerbates hypokalemia by enhancing urinary potassium excretion 1 , Serum potassium level should be obtained immediately upon presentation and prior to initiating insulin therapy 1 , Potassium replacement is required regardless of the baseline serum potassium level due to hydration and insulin therapy, except among renal failure patients 1 , It is suggested to administer 20 —30 mEq potassium in each liter of intravenous fluid to keep a serum potassium concentration within the normal range 1 , In addition to possible hypokalemia, patients with the hyperglycemic crisis could present with hypophosphatemia 1 , Osmotic diuresis during hyperglycemic crisis increases the urinary phosphate excretion, and insulin therapy enhances intracellular phosphate shift 1 , Phosphate replacement is not a fundamental part of hyperglycemic crisis management, given the lack of evidence of clinical benefit 1 , 29 , A special consideration with phosphate administration is the secondary hypocalcemia 1 , 29 , Acidemia associated with DKA results from the overproduction of ketoacids, generated from the haptic metabolism of free fatty acids.

This hepatic metabolism occurs as a result of insulin resistance and an increase in the counterregulatory hormones contributing to the pathophysiology of DKA 37 , Tissue acidosis could lead to impaired myocardial contractility, systemic vasodilatation, inhibition of glucose utilization by insulin, and lowering the levels of 2,3-diphosphoglycerate 2,3-DPG in erythrocytes 37 — Sodium bicarbonate decreases the hemoglobin-oxygen affinity leading to tissue hypoxia; moreover, it is associated with hypernatremia, hypocalcemia, hypokalemia, hypercapnia, prolonged QTc interval, intracellular acidosis, and metabolic alkalosis 39 , The use of adjuvant sodium bicarbonate in the setting of DKA consistently shows a lack of clinical benefit and should be prescribed on a case-by-case basis.

Although this recommendation was not supported by solid evidence; many clinicians adopt the practice to avoid the unwanted side effect of severe metabolic acidosis.

Sodium bicarbonate moves potassium intracellularly, however, clinical benefit is uncertain, and the use is controversial 41 , Prompt therapy for patients with hyperglycemic crisis is essential in reducing morbidity and mortality 6 , If not treated or treated ineffectively, the prognosis can include serious complications such as seizures, organ failures, coma, and death 6 , When treatment is delayed, the overall mortality rate of HHS is higher than that of DKA, especially in older patients.

This difference in prognoses was comparable when patients were matched for age In DKA, prolonged hypotension can lead to acute myocardial and bowel infarction 6 , The kidney plays a vital role in normalizing massive pH and electrolyte abnormalities 6 , Patients with prior kidney dysfunction or patients who developed end-stage chronic kidney disease worsen the prognosis considerably 6 , In HHS, severe dehydration may predispose the patient to complications such as myocardial infarction, stroke, pulmonary embolism, mesenteric vein thrombosis, and disseminated intravascular coagulation 6 , The VTE risk was higher than diabetic patients without hyperglycemic crisis or diabetic acidosis patients Management of hyperglycemic crisis may also be associated with significant complications include electrolyte abnormalities, hypoglycemia, and cerebral edema 7.

This is due to the use of insulin and fluid replacement therapy 4 , 5. Therefore, frequent electrolytes and blood glucose concentrations monitoring are essential while insulin infusions and fluid replacements are continued 4 , 5.

Cerebral edema is a rare but severe complication in children and adolescents and rarely affects adult patients older than 28 7. This could be due to the lack of cerebral autoregulation, presentation with more severe acidosis and dehydration among children and adolescents The exact mechanism of cerebral edema development is unknown.

Some reports suggest that the risk of cerebral edema during hyperglycemic crisis management might be induced by rapid hydration, especially in the pediatric population.

However, a recent multicenter study for children with DKA who were randomized to receive isotonic versus hypotonic sodium IV fluid with different infusions rates did not show a difference in neurological outcomes Early identification and prompt therapy with mannitol or hypertonic saline can prevent neurological deterioration from DKA management 7 , Furthermore, higher blood urea nitrogen BUN and sodium concentrations have been identified as cerebral edema risk factors Thus, careful hydration with close electrolytes and BUN is recommended Other serious complications of hyperglycemic crisis may include transient AKI, pulmonary edema in patients with congestive heart failure, myocardial infarction, a rise in pancreatic enzymes with or without acute pancreatitis, cardiomyopathy, rhabdomyolysis in patients presented with severe dehydration 7 , All authors have contributed equally in writing, organizing, and reviewing this publication.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.

Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic Crises in Adult Patients With Diabetes.

Diabetes Care 32 7 — doi: PubMed Abstract CrossRef Full Text Google Scholar. Goyal A, Mathew UE, Golla KK, Mannar V, Kubihal S, Gupta Y, et al. A Practical Guidance on the Use of Intravenous Insulin Infusion for Management of Inpatient Hyperglycemia.

Diabetes Metab Syndrome: Clin Res Rev 15 5 CrossRef Full Text Google Scholar. Saeedi P. Global and Regional Diabetes Prevalence Estimates for and Projections for and Results From the International Diabetes Federation Diabetes Atlas, 9th Edition.

Diabetes Res Clin Pract Pasquel FJ, Umpierrez GE. Hyperosmolar Hyperglycemic State: A Historic Review of the Clinical Presentation, Diagnosis, and Treatment.

Dia Care 37 11 — Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI, et al. Management of Hyperglycemic Crises in Patients With Diabetes. Diabetes Care 24 1 — Kitabchi AE, Umpierrez GE, Murphy MB, Kreisberg RA.

Hyperglycemic Crises in Adult Patients With Diabetes: A Consensus Statement From the American Diabetes Association. Diabetes Care 29 12 — Karslioglu French E, Donihi AC, Korytkowski MT. Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Syndrome: Review of Acute Decompensated Diabetes in Adult Patients.

BMJ I Fayfman M, Pasquel FJ, Umpierrez GE. Management of Hyperglycemic Crises. Med Clinics North Am 3 — Rains JL, Jain SK. Oxidative Stress, Insulin Signaling, and Diabetes. Free Radical Biol Med 50 5 — Hoffman WH, Burek CL, Waller JL, Fisher LE, Khichi M, Mellick LB.

Cytokine Response to Diabetic Ketoacidosis and Its Treatment. Clin Immunol 3 — Hayami T, Kato Y, Kamiya H, Kondo M, Naito E, Sugiura Y, et al. Case of Ketoacidosis by a Sodium-Glucose Cotransporter 2 Inhibitor in a Diabetic Patient With a Low-Carbohydrate Diet.

J Diabetes Investig , 6 5 — Umpierrez GE, Murphy MB, Kitabchi AE. Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Syndrome.

Diabetes Spectr 15 1 Kraut JA, Madias NE. Serum Anion Gap: Its Uses and Limitations in Clinical Medicine. Clin J Am Soc Nephrol 2 1 — Dhatariya K, Savage M, Claydon A, et al.

Joint British Diabetes Societies for Inpatient Care JBDS-IP Revised Guidelines. The Management of Diabetic Ketoacidosis in Adults Revised Google Scholar. Kitabchi AE, Umpierrez GE, Murphy MB. Diabetic Ketoacidosis and Hyperosmolar State. In: DeFronzo RA, Ferrannini E, Zimmet P, Alberti KGMM, editors.

International Textbook of Diabetes Mellitus. Trachtenbarg DE. Diabetic Ketoacidosis. Am Fam Phys 71 9 — Katz MA.

Hyperglycemia-Induced Hyponatremia-Calculation of Expected Serum Sodium Depression. N Engl J Med 16 —4. Rudloff E, Hopper K. Crystalloid and Colloid Compositions and Their Impact. Front Vet Sci Semler MW, Kellum JA. Balanced Crystalloid Solutions. Am J Respir Crit Care Med 8 — Van Zyl DG, Rheeder P, Delport E.

QJM 4 — Mahler SA, Conrad SA, Wang H, Arnold TC. Resuscitation With Balanced Electrolyte Solution Prevents Hyperchloremic Metabolic Acidosis in Patients With Diabetic Ketoacidosis. Am J Emerg Med 29 6 —4. Self WH, Evans CS, Jenkins CA, Brown RM, Casey JD, Collins SP, et al.

Clinical Effects of Balanced Crystalloids vs Saline in Adults With Diabetic Ketoacidosis: A Subgroup Analysis of Cluster Randomized Clinical Trials. JAMA Netw. Open 3 11 :e Ramanan M, Attokaran A, Murray L, Bhadange N, Stewart D, Rajendran G, et al.

Sodium Chloride or Plasmalyte Evaluation in Severe Diabetic Ketoacidosis Scope-Dka - a Cluster, Crossover, Randomized, Controlled Trial. Intensive Care Med 47 11 — Savage MW, Dhatariya KK, Kilvert A, Rayman G, Rees JAE, Courtney CH, et al. Joint British Diabetes Societies Guideline for the Management of Diabetic Ketoacidosis: Diabetic Ketoacidosis Guidelines.

Diabetic Med 28 5 — Umpierrez GE, Jones S, Smiley D, Mulligan P, Keyler T, Temponi A, et al. During therapy, β-OHB is converted to acetoacetic acid, which may lead the clinician to believe that ketosis has worsened. Therefore, assessments of urinary or serum ketone levels by the nitroprusside method should not be used as an indicator of response to therapy.

During therapy for DKA or HHS, blood should be drawn every 2—4 h for determination of serum electrolytes, glucose, blood urea nitrogen, creatinine, osmolality, and venous pH for DKA. Generally, repeat arterial blood gases are unnecessary; venous pH which is usually 0.

With mild DKA, regular insulin given either subcutaneously or intramuscularly every hour is as effective as intravenous administration in lowering blood glucose and ketone bodies Thereafter, 0.

Once DKA is resolved, if the patient is NPO, continue intravenous insulin and fluid replacement and supplement with subcutaneous regular insulin as needed every 4 h.

When the patient is able to eat, a multiple-dose schedule should be started that uses a combination of short- or rapid-acting and intermediate- or long-acting insulin as needed to control plasma glucose.

Continue intravenous insulin infusion for 1—2 h after the split-mixed regimen is begun to ensure adequate plasma insulin levels. An abrupt discontinuation of intravenous insulin coupled with a delayed onset of a subcutaneous insulin regimen may lead to worsened control; therefore, some overlap should occur in intravenous insulin therapy and initiation of the subcutaneous insulin regimen.

Patients with known diabetes may be given insulin at the dose they were receiving before the onset of DKA or HHS and further adjusted as needed for control. Finally, some type 2 diabetes patients may be discharged on oral antihyperglycemic agents and dietary therapy.

Despite total-body potassium depletion, mild to moderate hyperkalemia is not uncommon in patients with hyperglycemic crises. Insulin therapy, correction of acidosis, and volume expansion decrease serum potassium concentration.

To prevent hypokalemia, potassium replacement is initiated after serum levels fall below 5. Rarely, DKA patients may present with significant hypokalemia. Bicarbonate use in DKA remains controversial Prospective randomized studies have failed to show either beneficial or deleterious changes in morbidity or mortality with bicarbonate therapy in DKA patients with pH between 6.

In patients with a pH of 6. Insulin, as well as bicarbonate therapy, lowers serum potassium; therefore, potassium supplementation should be maintained in intravenous fluid as described above and carefully monitored. See Fig. Thereafter, venous pH should be assessed every 2 h until the pH rises to 7.

See Kitabchi et al. Phosphate concentration decreases with insulin therapy. Prospective randomized studies have failed to show any beneficial effect of phosphate replacement on the clinical outcome in DKA 32 , and overzealous phosphate therapy can cause severe hypocalcemia with no evidence of tetany 17 , No studies are available on the use of phosphate in the treatment of HHS.

Continuous monitoring using a flowsheet Fig. Commonly, patients recovering from DKA develop hyperchloremia caused by the use of excessive saline for fluid and electrolyte replacement and transient non-anion gap metabolic acidosis as chloride from intravenous fluids replaces ketoanions lost as sodium and potassium salts during osmotic diuresis.

These biochemical abnormalities are transient and are not clinically significant except in cases of acute renal failure or extreme oliguria. Cerebral edema is a rare but frequently fatal complication of DKA, occurring in 0. It is most common in children with newly diagnosed diabetes, but it has been reported in children with known diabetes and in young people in their twenties 25 , Fatal cases of cerebral edema have also been reported with HHS.

Clinically, cerebral edema is characterized by a deterioration in the level of consciousness, with lethargy, decrease in arousal, and headache. Neurological deterioration may be rapid, with seizures, incontinence, pupillary changes, bradycardia, and respiratory arrest.

These symptoms progress as brain stem herniation occurs. The progression may be so rapid that papilledema is not found. Although the mechanism of cerebral edema is not known, it likely results from osmotically driven movement of water into the central nervous system when plasma osmolality declines too rapidly with the treatment of DKA or HHS.

There is a lack of information on the morbidity associated with cerebral edema in adult patients; therefore, any recommendations for adult patients are clinical judgements, rather than scientific evidence. Hypoxemia and, rarely, noncardiogenic pulmonary edema may complicate the treatment of DKA.

Hypoxemia is attributed to a reduction in colloid osmotic pressure that results in increased lung water content and decreased lung compliance. Patients with DKA who have a widened alveolo-arteriolar oxygen gradient noted on initial blood gas measurement or with pulmonary rales on physical examination appear to be at higher risk for the development of pulmonary edema.

Many cases of DKA and HHS can be prevented by better access to medical care, proper education, and effective communication with a health care provider during an intercurrent illness. The observation that stopping insulin for economic reasons is a common precipitant of DKA in urban African-Americans 35 , 36 is disturbing and underscores the need for our health care delivery systems to address this problem, which is costly and clinically serious.

Sick-day management should be reviewed periodically with all patients. It should include specific information on 1 when to contact the health care provider, 2 blood glucose goals and the use of supplemental short-acting insulin during illness, 3 means to suppress fever and treat infection, and 4 initiation of an easily digestible liquid diet containing carbohydrates and salt.

Most importantly, the patient should be advised to never discontinue insulin and to seek professional advice early in the course of the illness. Adequate supervision and help from staff or family may prevent many of the admissions for HHS due to dehydration among elderly individuals who are unable to recognize or treat this evolving condition.

Better education of care givers as well as patients regarding signs and symptoms of new-onset diabetes; conditions, procedures, and medications that worsen diabetes control; and the use of glucose monitoring could potentially decrease the incidence and severity of HHS.

The annual incidence rate for DKA from population-based studies ranges from 4. Significant resources are spent on the cost of hospitalization.

Many of these hospitalizations could be avoided by devoting adequate resources to apply the measures described above. Because repeated admissions for DKA are estimated to drain approximately one of every two health care dollars spent on adult patients with type 1 diabetes, resources need to be redirected toward prevention by funding better access to care and educational programs tailored to individual needs, including ethnic and personal health care beliefs.

In addition, resources should be directed toward the education of primary care providers and school personnel so that they can identify signs and symptoms of uncontrolled diabetes and new-onset diabetes can be diagnosed at an earlier time.

This has been shown to decrease the incidence of DKA at the onset of diabetes 30 , Protocol for the management of adult patients with DKA.

Normal ranges vary by lab; check local lab normal ranges for all electrolytes. Obtain chest X-ray and cultures as needed. IM, intramuscular; IV, intravenous; SC subcutaneous.

Protocol for the management of adult patients with HHS. This protocol is for patients admitted with mental status change or severe dehydration who require admission to an intensive care unit. For less severe cases, see text for management guidelines. IV, intravenous; SC subcutaneous. From Kitabchi et al.

See text for details. Data are from Ennis et al. The highest ranking A is assigned when there is supportive evidence from well-conducted, generalizable, randomized controlled trials that are adequately powered, including evidence from a meta-analysis that incorporated quality ratings in the analysis.

An intermediate ranking B is given to supportive evidence from well-conducted cohort studies, registries, or case-control studies. A lower rank C is assigned to evidence from uncontrolled or poorly controlled studies or when there is conflicting evidence with the weight of the evidence supporting the recommendation.

Expert consensus E is indicated, as appropriate. For a more detailed description of this grading system, refer to Diabetes Care 24 Suppl. The recommendations in this paper are based on the evidence reviewed in the following publication: Management of hyperglycemic crises in patients with diabetes Technical Review.

Diabetes Care —, The initial draft of this position statement was prepared by Abbas E. Kitabchi, PhD, MD; Guillermo E. Umpierrez, MD; Mary Beth Murphy, RN, MS, CDE, MBA; Eugene J. Barrett, MD, PhD; Robert A. Kreisberg, MD; John I.

Malone, MD; and Barry M. Wall, MD. The paper was peer-reviewed, modified, and approved by the Professional Practice Committee and the Executive Committee, October Revised Sign In or Create an Account.

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Advanced Search. User Tools Dropdown. Sign In. Skip Nav Destination Close navigation menu Article navigation. Previous Article. Article Navigation. Position Statements January 01 Hyperglycemic Crises in Diabetes American Diabetes Association American Diabetes Association.

This Site. Google Scholar. Get Permissions. toolbar search Search Dropdown Menu. toolbar search search input Search input auto suggest. Figure 1—. View large Download slide. Figure 2—. Figure 3—.

Figure 4—. Table 1— Diagnostic criteria for DKA and HHS. View Large. Table 3— Summary of major recommendations. Therefore, to avoid the occurrence of cerebral edema, follow the recommendations in the position statement regarding a gradual correction of glucose and osmolality as well as the judicious use of isotonic or hypotonic saline, depending on serum sodium and the hemodynamic status of the patient.

McGarry JD, Woeltje KF, Kuwajima M, Foster DW: Regulation of ketogenesis and the renaissance of carnitine palmitoyl transferase. Diabetes Metab Rev.

DeFronzo RA, Matsuda M, Barrett E: Diabetic ketoacidosis: a combined metabolic-nephrologic approach to therapy. Diabetes Rev. Atchley DW, Loeb RF, Richards DW, Benedict EM, Driscoll ME: A detailed study of electrolyte balances following withdrawal and reestablishment of insulin therapy.

J Clin Invest. Halperin ML, Cheema-Dhadli S: Renal and hepatic aspects of ketoacidosis: a quantitative analysis based on energy turnover. Malone ML, Gennis V, Goodwin JS: Characteristics of diabetic ketoacidosis in older versus younger adults.

J Am Geriatr Soc. Matz R: Hyperosmolar nonacidotic diabetes HNAD. In Diabetes Mellitus: Theory and Practice. Morris LE, Kitabchi AE: Coma in the diabetic. In Diabetes Mellitus: Problems in Management. Kreisberg RA: Diabetic ketoacidosis: new concepts and trends in pathogenesis and treatment.

Ann Int Med. Klekamp J, Churchwell KB: Diabetic ketoacidosis in children: initial clinical assessment and treatment. Pediatric Annals. Glaser NS, Kupperman N, Yee CK, Schwartz DL, Styne DM: Variation in the management of pediatric diabetic ketoacidosis by specialty training.

Arch Pediatr Adolescent Med. Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI, Wall BM: Management of hyperglycemic crises in patients with diabetes mellitus Technical Review.

Abbas E. KitabchiGuillermo Hyperkalemla. Hyperglycemic crisis and hyperkalemiaJohn M. MilesJoseph N. Fisher; Hyperglycemic Crises in Adult Patients With Diabetes. The prevalence of hyperkalemia Hyperglycemic crisis and hyperkalemia hospitalized Hypergllycemic is between 1 and 10 percent. Hypperkalemia these patients, acute Delectable Fruit Popsicles often Hyperglycemic crisis and hyperkalemia precipitated by stressors such as illness, Hyprrglycemic, or initiation of medicines that alter potassium homeostasis Table 2 4 — Two mechanisms normally regulate potassium levels in response to variation of potassium intake. First, ingested potassium rapidly enters the portal circulation, stimulating the pancreas to release insulin. Elevated insulin levels induce rapid transport of potassium from the extracellular space into cells via cellular sodium-potassium adenosine triphosphatase.