diabetes ketoacidosis case study

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Severe diabetic ketoacidosis – a remarkable case study

Summarized from Van de Vyver C, Damen J, Haentjens C et al . An exceptional case of diabetic ketoacidosis. Case Reports in Emergency Medicine 2017.

Diabetic ketoacidosis (DKA) is a potentially life-threatening acute complication of type 1 diabetes caused by insulin deficiency. It is characterized by raised blood glucose (hyperglycemia), metabolic acidosis, and increased blood/urine ketones. Dehydration and electrolyte disturbance are common and affected patients may develop some degree of acute kidney injury (AKI) consequent on fluid loss (hypovolemia) due to osmotic diuresis associated with severe hyperglycemia. DKA evolves rapidly over a short time frame (hours rather than days) and can occur (rarely) in those with type 2 diabetes.  This DKA case study is particularly noteworthy because of the severity of the hyperglycemia and acid-base disturbance, and the fact that the patient survived such profound metabolic disturbance and associated life-threatening hemodynamic changes. The case concerns a 33-year-old woman with ”brittle” type 1 diabetes treated with continuous subcutaneous insulin infusion (insulin pump). She had, in common with many brittle diabetics, a history of gastroparesis (delayed stomach emptying).  Some 36 hours prior to emergency hospital admission she complained of abdominal pain and vomiting after attending a party. Her condition deteriorated before transfer to hospital. The ambulance team reported a rapid decline in Glasgow Coma Score (GCS) from 13 to 3 in only 10 minutes, sinus tachycardia, undetectable peripheral pulse, and hypotension (BP 99/52 mmHg). 

Clinical examination revealed severe dehydration and respiratory distress (respiration rate 40 breaths/min). Urgent intubation was necessary and systolic blood pressure dropped further to 55 mmHg. Initial (fingerstick) blood glucose was above the upper detection limit of the analyzer and blood ketones were >8.0 mmol/L. Blood gas analysis revealed severe metabolic acidosis (pH 6.74, bicarbonate 5 mmol/L, p CO 2 39.9 mmHg (5.3 kPa) and hypoxemia ( p O 2 50.2 mmHg, 6.7 kPa). Among other abnormal laboratory test results, perhaps the most remarkable was serum glucose 107 mmol/L (1924 mg/dL). (Serum glucose >33 mmol/L (600 mg/dL) is rarely seen in patients with DKA.)  White blood count (32.8x10 9 /L), C-reactive protein (789 nmol/L) and lactate (4.6 mmol/L) were also grossly elevated. Other laboratory testing revealed severe hyponatremia (sodium 113 mmol/L), severe hyperkalemia (6.7 mmol/L) and acute kidney failure (serum creatinine 332 µmol/L).  Following presumptive diagnosis of DKA, sepsis and acute renal failure, the patient was treated with aggressive IV fluids, norepinephrine, bicarbonate, and insulin, IV bolus and drip. Intensive investigation for evidence of infection proved fruitless. With treatment, the patient’s condition improved over the following days and she was extubated. Normal renal function was restored after 2 days.  In discussion of this case history, the authors briefly review the pathogenesis and treatment of DKA in general terms. They also highlight some interesting features of this case. One aspect discussed relates to the blood gas results on admission, in particular the curiously normal p CO 2 (39.9 mmHg, 5.3kPa). 

Metabolic acidosis usually provokes compensatory hyperventilation and reduced p CO 2 . The authors propose plausible theories to explain the much higher than expected p CO 2 in this case. They also propose that the remarkably high blood glucose in this case is the result of the combined effect of reduced glucose elimination consequent on renal failure and the presence of gastroparesis. 

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Case Presentation

Case study: a patient with uncontrolled type 2 diabetes and complex comorbidities whose diabetes care is managed by an advanced practice nurse.

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Geralyn Spollett; Case Study: A Patient With Uncontrolled Type 2 Diabetes and Complex Comorbidities Whose Diabetes Care Is Managed by an Advanced Practice Nurse. Diabetes Spectr 1 January 2003; 16 (1): 32–36. https://doi.org/10.2337/diaspect.16.1.32

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The specialized role of nursing in the care and education of people with diabetes has been in existence for more than 30 years. Diabetes education carried out by nurses has moved beyond the hospital bedside into a variety of health care settings. Among the disciplines involved in diabetes education, nursing has played a pivotal role in the diabetes team management concept. This was well illustrated in the Diabetes Control and Complications Trial (DCCT) by the effectiveness of nurse managers in coordinating and delivering diabetes self-management education. These nurse managers not only performed administrative tasks crucial to the outcomes of the DCCT, but also participated directly in patient care. 1  

The emergence and subsequent growth of advanced practice in nursing during the past 20 years has expanded the direct care component, incorporating aspects of both nursing and medical care while maintaining the teaching and counseling roles. Both the clinical nurse specialist (CNS) and nurse practitioner (NP) models, when applied to chronic disease management, create enhanced patient-provider relationships in which self-care education and counseling is provided within the context of disease state management. Clement 2 commented in a review of diabetes self-management education issues that unless ongoing management is part of an education program, knowledge may increase but most clinical outcomes only minimally improve. Advanced practice nurses by the very nature of their scope of practice effectively combine both education and management into their delivery of care.

Operating beyond the role of educator, advanced practice nurses holistically assess patients’ needs with the understanding of patients’ primary role in the improvement and maintenance of their own health and wellness. In conducting assessments, advanced practice nurses carefully explore patients’ medical history and perform focused physical exams. At the completion of assessments, advanced practice nurses, in conjunction with patients, identify management goals and determine appropriate plans of care. A review of patients’ self-care management skills and application/adaptation to lifestyle is incorporated in initial histories, physical exams, and plans of care.

Many advanced practice nurses (NPs, CNSs, nurse midwives, and nurse anesthetists) may prescribe and adjust medication through prescriptive authority granted to them by their state nursing regulatory body. Currently, all 50 states have some form of prescriptive authority for advanced practice nurses. 3 The ability to prescribe and adjust medication is a valuable asset in caring for individuals with diabetes. It is a crucial component in the care of people with type 1 diabetes, and it becomes increasingly important in the care of patients with type 2 diabetes who have a constellation of comorbidities, all of which must be managed for successful disease outcomes.

Many studies have documented the effectiveness of advanced practice nurses in managing common primary care issues. 4 NP care has been associated with a high level of satisfaction among health services consumers. In diabetes, the role of advanced practice nurses has significantly contributed to improved outcomes in the management of type 2 diabetes, 5 in specialized diabetes foot care programs, 6 in the management of diabetes in pregnancy, 7 and in the care of pediatric type 1 diabetic patients and their parents. 8 , 9 Furthermore, NPs have also been effective providers of diabetes care among disadvantaged urban African-American patients. 10 Primary management of these patients by NPs led to improved metabolic control regardless of whether weight loss was achieved.

The following case study illustrates the clinical role of advanced practice nurses in the management of a patient with type 2 diabetes.

A.B. is a retired 69-year-old man with a 5-year history of type 2 diabetes. Although he was diagnosed in 1997, he had symptoms indicating hyperglycemia for 2 years before diagnosis. He had fasting blood glucose records indicating values of 118–127 mg/dl, which were described to him as indicative of “borderline diabetes.” He also remembered past episodes of nocturia associated with large pasta meals and Italian pastries. At the time of initial diagnosis, he was advised to lose weight (“at least 10 lb.”), but no further action was taken.

Referred by his family physician to the diabetes specialty clinic, A.B. presents with recent weight gain, suboptimal diabetes control, and foot pain. He has been trying to lose weight and increase his exercise for the past 6 months without success. He had been started on glyburide (Diabeta), 2.5 mg every morning, but had stopped taking it because of dizziness, often accompanied by sweating and a feeling of mild agitation, in the late afternoon.

A.B. also takes atorvastatin (Lipitor), 10 mg daily, for hypercholesterolemia (elevated LDL cholesterol, low HDL cholesterol, and elevated triglycerides). He has tolerated this medication and adheres to the daily schedule. During the past 6 months, he has also taken chromium picolinate, gymnema sylvestre, and a “pancreas elixir” in an attempt to improve his diabetes control. He stopped these supplements when he did not see any positive results.

He does not test his blood glucose levels at home and expresses doubt that this procedure would help him improve his diabetes control. “What would knowing the numbers do for me?,” he asks. “The doctor already knows the sugars are high.”

A.B. states that he has “never been sick a day in my life.” He recently sold his business and has become very active in a variety of volunteer organizations. He lives with his wife of 48 years and has two married children. Although both his mother and father had type 2 diabetes, A.B. has limited knowledge regarding diabetes self-care management and states that he does not understand why he has diabetes since he never eats sugar. In the past, his wife has encouraged him to treat his diabetes with herbal remedies and weight-loss supplements, and she frequently scans the Internet for the latest diabetes remedies.

During the past year, A.B. has gained 22 lb. Since retiring, he has been more physically active, playing golf once a week and gardening, but he has been unable to lose more than 2–3 lb. He has never seen a dietitian and has not been instructed in self-monitoring of blood glucose (SMBG).

A.B.’s diet history reveals excessive carbohydrate intake in the form of bread and pasta. His normal dinners consist of 2 cups of cooked pasta with homemade sauce and three to four slices of Italian bread. During the day, he often has “a slice or two” of bread with butter or olive oil. He also eats eight to ten pieces of fresh fruit per day at meals and as snacks. He prefers chicken and fish, but it is usually served with a tomato or cream sauce accompanied by pasta. His wife has offered to make him plain grilled meats, but he finds them “tasteless.” He drinks 8 oz. of red wine with dinner each evening. He stopped smoking more than 10 years ago, he reports, “when the cost of cigarettes topped a buck-fifty.”

The medical documents that A.B. brings to this appointment indicate that his hemoglobin A 1c (A1C) has never been <8%. His blood pressure has been measured at 150/70, 148/92, and 166/88 mmHg on separate occasions during the past year at the local senior center screening clinic. Although he was told that his blood pressure was “up a little,” he was not aware of the need to keep his blood pressure ≤130/80 mmHg for both cardiovascular and renal health. 11  

A.B. has never had a foot exam as part of his primary care exams, nor has he been instructed in preventive foot care. However, his medical records also indicate that he has had no surgeries or hospitalizations, his immunizations are up to date, and, in general, he has been remarkably healthy for many years.

Physical Exam

A physical examination reveals the following:

Weight: 178 lb; height: 5′2″; body mass index (BMI): 32.6 kg/m 2

Fasting capillary glucose: 166 mg/dl

Blood pressure: lying, right arm 154/96 mmHg; sitting, right arm 140/90 mmHg

Pulse: 88 bpm; respirations 20 per minute

Eyes: corrective lenses, pupils equal and reactive to light and accommodation, Fundi-clear, no arteriolovenous nicking, no retinopathy

Thyroid: nonpalpable

Lungs: clear to auscultation

Heart: Rate and rhythm regular, no murmurs or gallops

Vascular assessment: no carotid bruits; femoral, popliteal, and dorsalis pedis pulses 2+ bilaterally

Neurological assessment: diminished vibratory sense to the forefoot, absent ankle reflexes, monofilament (5.07 Semmes-Weinstein) felt only above the ankle

Lab Results

Results of laboratory tests (drawn 5 days before the office visit) are as follows:

Glucose (fasting): 178 mg/dl (normal range: 65–109 mg/dl)

Creatinine: 1.0 mg/dl (normal range: 0.5–1.4 mg/dl)

Blood urea nitrogen: 18 mg/dl (normal range: 7–30 mg/dl)

Sodium: 141 mg/dl (normal range: 135–146 mg/dl)

Potassium: 4.3 mg/dl (normal range: 3.5–5.3 mg/dl)

Lipid panel

    • Total cholesterol: 162 mg/dl (normal: <200 mg/dl)

    • HDL cholesterol: 43 mg/dl (normal: ≥40 mg/dl)

    • LDL cholesterol (calculated): 84 mg/dl (normal: <100 mg/dl)

    • Triglycerides: 177 mg/dl (normal: <150 mg/dl)

    • Cholesterol-to-HDL ratio: 3.8 (normal: <5.0)

AST: 14 IU/l (normal: 0–40 IU/l)

ALT: 19 IU/l (normal: 5–40 IU/l)

Alkaline phosphotase: 56 IU/l (normal: 35–125 IU/l)

A1C: 8.1% (normal: 4–6%)

Urine microalbumin: 45 mg (normal: <30 mg)

Based on A.B.’s medical history, records, physical exam, and lab results, he is assessed as follows:

Uncontrolled type 2 diabetes (A1C >7%)

Obesity (BMI 32.4 kg/m 2 )

Hyperlipidemia (controlled with atorvastatin)

Peripheral neuropathy (distal and symmetrical by exam)

Hypertension (by previous chart data and exam)

Elevated urine microalbumin level

Self-care management/lifestyle deficits

    • Limited exercise

    • High carbohydrate intake

    • No SMBG program

Poor understanding of diabetes

A.B. presented with uncontrolled type 2 diabetes and a complex set of comorbidities, all of which needed treatment. The first task of the NP who provided his care was to select the most pressing health care issues and prioritize his medical care to address them. Although A.B. stated that his need to lose weight was his chief reason for seeking diabetes specialty care, his elevated glucose levels and his hypertension also needed to be addressed at the initial visit.

The patient and his wife agreed that a referral to a dietitian was their first priority. A.B. acknowledged that he had little dietary information to help him achieve weight loss and that his current weight was unhealthy and “embarrassing.” He recognized that his glucose control was affected by large portions of bread and pasta and agreed to start improving dietary control by reducing his portion size by one-third during the week before his dietary consultation. Weight loss would also be an important first step in reducing his blood pressure.

The NP contacted the registered dietitian (RD) by telephone and referred the patient for a medical nutrition therapy assessment with a focus on weight loss and improved diabetes control. A.B.’s appointment was scheduled for the following week. The RD requested that during the intervening week, the patient keep a food journal recording his food intake at meals and snacks. She asked that the patient also try to estimate portion sizes.

Although his physical activity had increased since his retirement, it was fairly sporadic and weather-dependent. After further discussion, he realized that a week or more would often pass without any significant form of exercise and that most of his exercise was seasonal. Whatever weight he had lost during the summer was regained in the winter, when he was again quite sedentary.

A.B.’s wife suggested that the two of them could walk each morning after breakfast. She also felt that a treadmill at home would be the best solution for getting sufficient exercise in inclement weather. After a short discussion about the positive effect exercise can have on glucose control, the patient and his wife agreed to walk 15–20 minutes each day between 9:00 and 10:00 a.m.

A first-line medication for this patient had to be targeted to improving glucose control without contributing to weight gain. Thiazolidinediones (i.e., rosiglitizone [Avandia] or pioglitizone [Actos]) effectively address insulin resistance but have been associated with weight gain. 12 A sulfonylurea or meglitinide (i.e., repaglinide [Prandin]) can reduce postprandial elevations caused by increased carbohydrate intake, but they are also associated with some weight gain. 12 When glyburide was previously prescribed, the patient exhibited signs and symptoms of hypoglycemia (unconfirmed by SMBG). α-Glucosidase inhibitors (i.e., acarbose [Precose]) can help with postprandial hyperglycemia rise by blunting the effect of the entry of carbohydrate-related glucose into the system. However, acarbose requires slow titration, has multiple gastrointestinal (GI) side effects, and reduces A1C by only 0.5–0.9%. 13 Acarbose may be considered as a second-line therapy for A.B. but would not fully address his elevated A1C results. Metformin (Glucophage), which reduces hepatic glucose production and improves insulin resistance, is not associated with hypoglycemia and can lower A1C results by 1%. Although GI side effects can occur, they are usually self-limiting and can be further reduced by slow titration to dose efficacy. 14  

After reviewing these options and discussing the need for improved glycemic control, the NP prescribed metformin, 500 mg twice a day. Possible GI side effects and the need to avoid alcohol were of concern to A.B., but he agreed that medication was necessary and that metformin was his best option. The NP advised him to take the medication with food to reduce GI side effects.

The NP also discussed with the patient a titration schedule that increased the dosage to 1,000 mg twice a day over a 4-week period. She wrote out this plan, including a date and time for telephone contact and medication evaluation, and gave it to the patient.

During the visit, A.B. and his wife learned to use a glucose meter that features a simple two-step procedure. The patient agreed to use the meter twice a day, at breakfast and dinner, while the metformin dose was being titrated. He understood the need for glucose readings to guide the choice of medication and to evaluate the effects of his dietary changes, but he felt that it would not be “a forever thing.”

The NP reviewed glycemic goals with the patient and his wife and assisted them in deciding on initial short-term goals for weight loss, exercise, and medication. Glucose monitoring would serve as a guide and assist the patient in modifying his lifestyle.

A.B. drew the line at starting an antihypertensive medication—the angiotensin-converting enzyme (ACE) inhibitor enalapril (Vasotec), 5 mg daily. He stated that one new medication at a time was enough and that “too many medications would make a sick man out of me.” His perception of the state of his health as being represented by the number of medications prescribed for him gave the advanced practice nurse an important insight into the patient’s health belief system. The patient’s wife also believed that a “natural solution” was better than medication for treating blood pressure.

Although the use of an ACE inhibitor was indicated both by the level of hypertension and by the presence of microalbuminuria, the decision to wait until the next office visit to further evaluate the need for antihypertensive medication afforded the patient and his wife time to consider the importance of adding this pharmacotherapy. They were quite willing to read any materials that addressed the prevention of diabetes complications. However, both the patient and his wife voiced a strong desire to focus their energies on changes in food and physical activity. The NP expressed support for their decision. Because A.B. was obese, weight loss would be beneficial for many of his health issues.

Because he has a sedentary lifestyle, is >35 years old, has hypertension and peripheral neuropathy, and is being treated for hypercholestrolemia, the NP performed an electrocardiogram in the office and referred the patient for an exercise tolerance test. 11 In doing this, the NP acknowledged and respected the mutually set goals, but also provided appropriate pre-exercise screening for the patient’s protection and safety.

In her role as diabetes educator, the NP taught A.B. and his wife the importance of foot care, demonstrating to the patient his inability to feel the light touch of the monofilament. She explained that the loss of protective sensation from peripheral neuropathy means that he will need to be more vigilant in checking his feet for any skin lesions caused by poorly fitting footwear worn during exercise.

At the conclusion of the visit, the NP assured A.B. that she would share the plan of care they had developed with his primary care physician, collaborating with him and discussing the findings of any diagnostic tests and procedures. She would also work in partnership with the RD to reinforce medical nutrition therapies and improve his glucose control. In this way, the NP would facilitate the continuity of care and keep vital pathways of communication open.

Advanced practice nurses are ideally suited to play an integral role in the education and medical management of people with diabetes. 15 The combination of clinical skills and expertise in teaching and counseling enhances the delivery of care in a manner that is both cost-reducing and effective. Inherent in the role of advanced practice nurses is the understanding of shared responsibility for health care outcomes. This partnering of nurse with patient not only improves care but strengthens the patient’s role as self-manager.

Geralyn Spollett, MSN, C-ANP, CDE, is associate director and an adult nurse practitioner at the Yale Diabetes Center, Department of Endocrinology and Metabolism, at Yale University in New Haven, Conn. She is an associate editor of Diabetes Spectrum.

Note of disclosure: Ms. Spollett has received honoraria for speaking engagements from Novo Nordisk Pharmaceuticals, Inc., and Aventis and has been a paid consultant for Aventis. Both companies produce products and devices for the treatment of diabetes.

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The psychopathology of recurrent diabetic ketoacidosis: A case-control study

Affiliations.

• 1 Diabetes and Metabolism Department, Barts Health NHS Trust, London, UK.
• 2 Diabetes, Psychiatry and Psychology Research Group, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
• 3 Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
• 4 Division of Diabetes and Nutritional Sciences, King's College London, London, UK.
• 5 Division of Psychology and Language Sciences, University College London, London, UK.
• PMID: 33368581
• DOI: 10.1111/dme.14505

Background: Despite its poor prognosis, the psychological factors associated with recurrent diabetic ketoacidosis are poorly understood. In people with type 1 diabetes, we assessed for psychopathology in those with and without recurrent diabetic ketoacidosis (DKA).

Method: The design was a case-control study. Cases were defined as people with two or more DKA episodes in a 12-month period (recurrent DKA). Cases and controls were matched for gender and age. We compared groups for scores on Beck's Anxiety Inventory (BAI), Beck's Depression Inventory II, Difficulty in Emotion Regulation Scale (DERS), Experiences in Close Relationships-Revised, Standardised Assessment of Personality-Abbreviated Scale (SAPAS), Interpersonal Problem Inventory, Eating Disorder Examination Questionnaire and Problem Areas in Diabetes (PAID) using unpaired t-tests or Mann-Whitney U tests for parametric and non-parametric data, respectively. Correction was made for multiple testing.

Results: In all, 23 cases and 23 controls were recruited with mean age 31.0 (11.4) years and 65.2% were men. Cases had higher HbA 1c levels than controls (101.1 (23.2) vs. 85.7 (21.7) mmol/mol, (p = 0.02)). Compared to controls, people with recurrent DKA had higher scores on the BAI (p = 0.004), PAID (p = 0.004), DERS (p = 0.001) and SAPAS (p < 0.001). Sixteen of 23 (69.6%) cases screened positive for a personality disorder compared to 6 of 23 (26.1%) controls.

Conclusions: People with recurrent DKA have elevated levels of anxiety and diabetes distress, greater difficulty with emotion regulation and personality dysfunction compared to matched controls.

Keywords: health care delivery; other complications; psychological aspects.

© 2020 The Authors. Diabetic Medicine published by John Wiley & Sons Ltd on behalf of Diabetes UK.

Publication types

• Research Support, Non-U.S. Gov't
• Anxiety / diagnosis
• Case-Control Studies
• Depression / diagnosis
• Diabetic Ketoacidosis / psychology*
• Emotional Regulation
• Glycated Hemoglobin / analysis
• Personality Disorders / diagnosis
• Psychological Distress
• Glycated Hemoglobin A
• hemoglobin A1c protein, human

Grants and funding

• NF-SI-0514-10157/DH_/Department of Health/United Kingdom

Diabetic Ketoacidosis (DKA)

• Pathophysiology |
• Symptoms and Signs |
• Diagnosis |
• Treatment |
• Prognosis |
• Key Points |

Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus. It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia.

(See also Diabetes Mellitus and Complications of Diabetes Mellitus .)

Diabetic ketoacidosis (DKA) occurs in patients with type 1 diabetes mellitus and is less common in those with type 2 diabetes. It develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 diabetes in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin ) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress).

Common physiologic stresses that can trigger DKA include

Acute infection (eg, pneumonia , urinary tract infection , COVID-19 )

Myocardial infarction

Pancreatitis

Missed insulin doses

Some medications implicated in causing DKA include

Corticosteroids

Thiazide diuretics

Sympathomimetics

Sodium-glucose co-transporter 2 (SGLT-2) inhibitors

DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes (also referred to as Flatbush diabetes) is a variant of type 2 diabetes, which sometimes occurs in patients with obesity, often those with African (including African American or Afro-Caribbean) ancestry. Patients with ketosis-prone diabetes can have significant impairment of beta-cell function with hyperglycemia, and are therefore more likely to develop DKA when significant hyperglycemia occurs.

SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 diabetes. In pregnant patients and in patients taking SGLT2 inhibitors, DKA may occur at lower or even normal blood glucose levels.

Euglycemic DKA can also occur with alcohol overuse or cirrhosis.

Pathophysiology of DKA

Insulin deficiency and an increase in counterregulatory hormones ( glucagon , catecholamines, cortisol ) causes the body to metabolize triglycerides and amino acids instead of glucose for energy. Serum levels of glycerol and free fatty acids rise because of unrestrained lipolysis. Alanine levels rise because of muscle catabolism. Glycerol and alanine provide substrate for hepatic gluconeogenesis, which is stimulated by the excess of glucagon that accompanies insulin deficiency.

Glucagon also stimulates mitochondrial conversion of free fatty acids into ketones. Insulin normally blocks ketogenesis by inhibiting the transport of free fatty acid derivatives into the mitochondrial matrix, but ketogenesis proceeds in the absence of insulin . The major ketoacids produced, acetoacetic acid and beta-hydroxybutyric acid, are strong organic acids that create metabolic acidosis . Acetone derived from the metabolism of acetoacetic acid accumulates in serum and is slowly disposed of by respiration.

Hyperglycemia due to insulin deficiency causes an osmotic diuresis that leads to marked urinary losses of water and electrolytes. Urinary excretion of ketones obligates additional losses of sodium and potassium. Serum sodium may fall due to natriuresis or rise due to excretion of large volumes of free water.

Potassium is also lost in large quantities. Despite a significant total body deficit of potassium, initial serum potassium is typically normal or elevated because of the extracellular migration of potassium in response to acidosis. Potassium levels generally fall further during treatment as insulin therapy drives potassium into cells. If serum potassium is not monitored and replaced as needed, life-threatening hypokalemia may develop.

Symptoms and Signs of DKA

Symptoms and signs of diabetic ketoacidosis include symptoms of hyperglycemia with the addition of nausea, vomiting, and—particularly in children—abdominal pain. Lethargy and somnolence are symptoms of more severe decompensation. Patients may be hypotensive and tachycardic due to dehydration and acidosis; they may breathe rapidly and deeply to compensate for acidemia (Kussmaul respirations). They may also have fruity breath due to exhaled acetone. Fever is not a sign of DKA itself and, if present, signifies underlying infection. In the absence of timely treatment, DKA progresses to coma and death.

Acute cerebral edema, a complication in about 1% of DKA patients, occurs primarily in children and less often in adolescents and young adults. Headache and fluctuating level of consciousness herald this complication in some patients, but respiratory arrest is the initial manifestation in others. The cause is not well understood but may be related to too-rapid reductions in serum osmolality or to brain ischemia. It is most likely to occur in children < 5 years when DKA is the initial manifestation of diabetes mellitus . Children with the highest BUN (blood urea nitrogen) levels and lowest PaCO2 at presentation appear to be at greatest risk. Delays in correction of hyponatremia and the use of bicarbonate during DKA treatment are additional risk factors.

Diagnosis of DKA

Arterial pH

Serum ketones

Calculation of anion gap

In patients suspected of having diabetic ketoacidosis, serum electrolytes, blood urea nitrogen (BUN) and creatinine, glucose, ketones, and osmolarity should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas measurement.

DKA is diagnosed by an arterial pH < 7.30 with an anion gap > 12 and serum ketones. Guidelines differ on specific levels of hyperglycemia to be included in the diagnostic criteria for DKA. A blood glucose level > 200 (11.1 mmol/L) or > 250 mg/dL (13.8 mmol/L) is most often specified; however, because DKA can occur in patients with normal or mildly elevated glucose levels, some guidelines do not include a specific level ( 1, 2 ).

A presumptive diagnosis may be made when urine glucose and ketones are positive on urinalysis. Urine test strips and some assays for serum ketones may underestimate the degree of ketosis because they detect acetoacetic acid and not beta-hydroxybutyric acid, which is usually the predominant ketoacid.

Blood beta-hydroxybutyrate can be measured, or treatment can be initiated based on clinical suspicion and the presence of anion gap acidosis if serum or urine ketones are low.

Symptoms and signs of a triggering illness should be pursued with appropriate studies (eg, cultures, imaging studies). Adults should have an ECG to screen for acute myocardial infarction and to help determine the significance of abnormalities in serum potassium.

Other laboratory abnormalities include

Hyponatremia

Elevated serum creatinine

Elevated plasma osmolality

Hyperglycemia may cause dilutional hyponatremia, so measured serum sodium is corrected by adding 1.6 mEq/L (1.6 mmol/L) for each 100 mg/dL (5.6 mmol/L) elevation of serum glucose over 100 mg/dL (5.6 mmol/L).

To illustrate, for a patient with serum sodium of 124 mEq/L (124 mmol/L) and glucose of 600 mg/dL (33.3 mmol/L), add 1.6 ([600 − 100]/100) = 8 mEq/L (8 mmol/L) to 124 for a corrected serum sodium of 132 mEq/L (132 mmol/L).

As acidosis is corrected, serum potassium drops. An initial potassium level < 4.5 mEq/L (

Serum amylase and lipase are often elevated, even in the absence of pancreatitis (which may be present in patients with alcoholic ketoacidosis and in those with coexisting hypertriglyceridemia).

Diagnosis references

1. Buse JB, Wexler DJ, Tsapas A, et al : 2019 Update to: Management of Hyperglycemia in Type 2 Diabetes, 2018. A Consensus Report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetes Care 43(2):487–493, 2020. doi: 10.2337/dci19-0066

2. Garber AJ, Handelsman Y, Grunberger G, et al : Consensus statement by the American Association of Clinical Endocrinologists and American College of Endocrinology on the comprehensive type 2 diabetes management algorithm--2020 executive summary. Endocrine Practice 26:107–139, 2020.

Treatment of DKA

IV 0.9% saline

Correction of hypokalemia

IV insulin (as long as serum potassium is ≥ 3.3 mEq/L [3.3 mmol/L])

< 7 after 1 hour of treatment)

The most urgent goals for treating diabetic ketoacidosis are rapid intravascular volume repletion, correction of hyperglycemia and acidosis, and prevention of hypokalemia ( 1, 2 ). Identification of precipitating factors is also important.

Treatment should occur in intensive care settings because clinical and laboratory assessments are initially needed every hour or every other hour with appropriate adjustments in treatment.

Volume repletion

Intravascular volume should be restored rapidly to raise blood pressure and ensure glomerular perfusion; once intravascular volume is restored, remaining total body water deficits are corrected more slowly, typically over about 24 hours. Initial volume repletion in adults is typically achieved with rapid IV infusion of 1 to 1.5 L of 0.9% saline solution in the first hour, followed by saline infusions at 250 to 500 mL/hour. Additional boluses or a faster rate of infusion may be needed to raise the blood pressure. Slower rates of infusion may be needed in patients with heart failure or in those at risk for volume overload. If the serum sodium level is normal or high, the normal saline is replaced by 0.45% saline after initial volume resuscitation. When plasma glucose falls to < 200 mg/dL ( <

For children, fluid deficits are estimated at 30 to 100 mL/kg body weight. Pediatric maintenance fluids < 300 mg/dL (16.7 mmol/L) and blood pressure is stable and urine output adequate. The remaining fluid deficit should be replaced over 24 to 48 hours, typically requiring a rate (including maintenance fluids) of about 2 to 5 mL/kg/hour, depending on the degree of dehydration.

Correction of hyperglycemia and acidosis

≥ 3.3 mEq/L ( ≥ 3.3 mmol/L) . Insulin adsorption onto IV tubing can lead to inconsistent effects, which can be minimized by preflushing the IV tubing with insulin solution. If plasma glucose does not fall by 50 to 75 mg/dL (2.8 to 4.2 mmol/L) in the first hour, insulin doses should be doubled. Children should be given a continuous IV insulin infusion of 0.1 unit/kg/hour or higher with or without a bolus.

Ketones should begin to clear within hours if insulin is given in sufficient doses. However, clearance of ketones may appear to lag because of conversion of beta-hydroxybutyrate to acetoacetate (which is the “ketone” measured in most hospital laboratories) as acidosis resolves.

Serum pH and bicarbonate levels should also quickly improve, but restoration of a normal serum bicarbonate level may take 24 hours. Bicarbonate should not be given routinely because it can lead to development of acute cerebral edema (primarily in children). If bicarbonate is used, it should be started only if the pH is < 7, and only modest pH elevation should be attempted with doses of 50 to 100 mEq (50 to 100 mmol) given over 2 hours, followed by repeat measurement of arterial pH and serum potassium.

When plasma glucose becomes < 200 mg/dL ( < insulin dose can be reduced to maintain glucose 150 to 200 mg/dL (8.3 to 11.1 mmol/L), but the continuous IV infusion of regular insulin should be maintained until the anion gap has narrowed on 2 consecutive blood tests and blood and urine are consistently negative for ketones. A longer duration of treatment with insulin

When the patient is stable and able to eat, a typical is begun. IV insulin should be continued for 2 hours after the initial dose of basal subcutaneous insulin is given. Children should continue to receive 0.05 unit/kg/hour insulin infusion until subcutaneous insulin is initiated and pH is > 7.3.

Hypokalemia prevention

Prevention of hypokalemia requires replacement of 20 to 30 mEq (20 to 30 mmol) potassium in each liter of IV fluid to keep serum potassium between 4 and 5 mEq/L (4 and 5 mmol/L). If serum potassium is < 3.3 mEq/L ( < 3.3 mmol/L), insulin should be withheld and potassium given at 40 mEq/hour until serum potassium is ≥ 3.3 mEq/L ( ≥ 3.3 mmol/L); if serum potassium is > 5 mEq/L ( > 5 mmol/L), potassium supplementation can be withheld.

Initially normal or elevated serum potassium measurements may reflect shifts from intracellular stores in response to acidemia and belie the true potassium deficits that almost all patients with DKA have. Insulin replacement rapidly shifts potassium into cells, so levels should be checked hourly or every other hour in the initial stages of treatment.

Other measures

Hypophosphatemia

Treatment references

1. Gosmanov AR, Gosmanova EO, Dillard-Cannon E : Management of adult diabetic ketoacidosis.  Diabetes Metab Syndr Obes 7:255–264, 2014. doi:10.2147/DMSO.S50516

2. French EK, Donihi AC, Korytkowski MT : Diabetic ketoacidosis and hyperosmolar hyperglycemic syndrome: review of acute decompensated diabetes in adult patients. BMJ 365:l1114, 2019. doi: 10.1136/bmj.l1114

Prognosis for DKA

Overall mortality rates for diabetic ketoacidosis are 1, 2, 3 ). Another study had lower rates of persistent neurologic sequelae and death ( 4 ).

Prognosis references

1. Edge JA, Hawkins MM, Winter DL, Dunger DB : The risk and outcome of cerebral oedema developing during diabetic ketoacidosis. Arch Dis Child 85(1):16-22, 2001. doi:10.1136/adc.85.1.16

2. Marcin JP, Glaser N, Barnett P, et al : Factors associated with adverse outcomes in children with diabetic ketoacidosis-related cerebral edema. J Pediatr 141(6):793-797, 2002. doi:10.1067/mpd.2002.128888

3. Glaser N . Cerebral edema in children with diabetic ketoacidosis.  Curr Diab Rep 2001;1(1):41-46. doi:10.1007/s11892-001-0009-7

4. Kuppermann N, Ghetti S, Schunk JE, et al . Clinical Trial of Fluid Infusion Rates for Pediatric Diabetic Ketoacidosis.  N Engl J Med 2018;378(24):2275-2287. doi:10.1056/NEJMoa1716816

Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis.

DKA can occur when acute physiologic stressors (eg, infections, myocardial infarction) trigger acidosis, moderate glucose elevation, dehydration, and severe potassium loss in patients with type 1 diabetes.

Diagnose by an arterial pH < 7.30, with an anion gap > 12 and serum ketones in the presence of hyperglycemia.

Acidosis typically corrects with IV fluid and insulin ; consider bicarbonate only if marked acidosis (pH < 7) persists after 1 hour of therapy.

Withhold insulin until serum potassium is ≥ 3.3 mEq/L ( ≥ 3.3 mmol/L).

Acute cerebral edema is a rare (about 1%) but lethal complication, primarily in children and less often in adolescents and young adults.

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When his mother got home from work, 15 year old Roberto Cruz was found very lethargic and lying in vomit at his home. His heart was racing and he was breathing abnormally. His mother called 911 when she could not get him to the car to transport him to urgent care. When the paramedics arrived at the house, Roberto was complaining that he needed to go to the bathroom and repeatedly asking for water. He was transported to the ER.

On ER admission, Roberto’s VS were BP 85/53. HR 119, RR 32, T 99.1 and O2 96% on room air. He was A&O x3 (name, place, date) but drowsy, lethargic, and slow to respond to questions. His breathing was deep and labored with “fruity breath.” He had polydipsia and polyuria, with abdominal pain rated 5/10.

Significant lab values: Blood glucose 444, ABGs: pH 7.22, Bicarb 14, paCO2 33, anion gap 13.0, paO2 90. Positive urine ketones and acetone. Potassium 5.3. He has no medical history and no health insurance.

Diagnosis: Diabetic Ketoacidosis

• Administer oxygen and provide airway support
• Establish IV access
• Administer NS fluid resuscitation
• Regular insulin via IV drip
• Monitor potassium, assess for signs of hypokalemia or hyperkalemia
• Provide electrolyte replacement as needed.
• Monitor vital signs
• Blood sugar checks Q1H
• Monitor blood pH
• Assess for changes in mental status
• Monitor intake and output
• Provide seizure and safety precautions
• Report any critical lab values or changes in patient status to physician

Patient is transferred to the ICU for correction of acidosis, slow stabilization of blood glucose levels, fluid resuscitation, potassium replacement, and monitoring.

At discharge, the diabetic educator provided the patient with diabetes education with return demonstration of correct blood glucose check and subcutaneous insulin injection. Social services met with the patient and family to assist them with financial and insurance questions, follow up appointment was scheduled with primary physician.

• As Roberto was initially triaged and treated, what were the priority assessments and treatments?
• What risk factors did Roberto have for developing DKA?
• As Roberto is discharged from the hospital, what continued health care and education needs will he and his family have? What are appropriate long term goals for Roberto and how can they be measured?

Nursing Case Studies by and for Student Nurses Copyright © by jaimehannans is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License , except where otherwise noted.

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Diabetic Ketoacidosis Upon Diagnosis

A Biochemistry Case Study

By Ali Chaari, Aisha Kafoud

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This directed case study is designed to help students integrate biochemical and physiological concepts with clinical aspects of disease. The case tells the story of a little girl who experiences diabetic ketoacidosis and is diagnosed with type 1 diabetes mellitus (T1DM). The story is based on an actual patient and the presented data are authentic. The case can be delivered as an individual assignment by using the case study handout or displayed in class with optional role play by using the PowerPoint presentation (see Supplemental Materials).  Both versions of the case cover the same basic content, but the questions are somewhat different. Upon successful completion of the case, students should understand the basics of metabolic acidosis in T1DM, differences between T1DM and T2DM, and the behavior of the blood buffer equilibrium in response to physiological change. The case was originally written for an intermediate biochemistry course, but it could also be used in a physiology or an advanced biology course.

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Date Posted

• Discuss the basics of metabolic acidosis in T1DM.
• Distinguish T1DM from T2DM.
• Predict the behavior of the blood buffer equilibrium in response to a physiological change.
• Use Winter’s formula to perform calculations with real patient data.
• Correlate real clinical data with biochemical tests.
• Explain the role of insulin and how ketoacidosis can occur due to insulin insufficiency.

Diabetes; type 1 diabetes; T1DM; ketoacidosis; blood buffer; acidosis; Winter’s formula; insulin insufficiency

Subject Headings

EDUCATIONAL LEVEL

Undergraduate lower division, Undergraduate upper division, Clinical education

TOPICAL AREAS

TYPE/METHODS

Teaching Notes & Answer Key

Teaching notes.

Case teaching notes are protected and access to them is limited to paid subscribed instructors. To become a paid subscriber, purchase a subscription here .

Teaching notes are intended to help teachers select and adopt a case. They typically include a summary of the case, teaching objectives, information about the intended audience, details about how the case may be taught, and a list of references and resources.

Download Notes

Answer Keys are protected and access to them is limited to paid subscribed instructors. To become a paid subscriber, purchase a subscription here .

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Materials & Media

Supplemental materials.

The PowerPoint presentation below offers an alternative way to deliver the case in class.

• PowerPoint Presentation (~3.9 MB)

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Impella support for refractory cardiogenic shock accompanied by diabetic ketoacidosis: a case report

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• Masaki Nakagaito 1 ,
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• Teruhiko Imamura   ORCID: orcid.org/0000-0002-7294-7637 1 ,
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Sodium–glucose cotransporter 2 (SGLT2) inhibitors are strongly recommended in patients with heart failure, regardless of the presence of diabetes mellitus. A 74 year-old woman with a reduced left ventricular ejection fraction and diabetes mellitus (the types were unknown), receiving insulin and SGLT2 inhibitor, was hospitalized for altered consciousness with systemic hypotension. Upon admission, she was diagnosed with cardiogenic shock due to diabetic ketoacidosis. Intensive fluid resuscitation under Impella CP support successively improved her metabolic acidosis, preventing worsening pulmonary congestion by mechanically unloading the heart. After hemodynamic stabilization, she was diagnosed with type 1 diabetes mellitus for the first time. She was discharged on day 54 and was followed for 6 months without any recurrences. We must remain vigilant regarding the risk of diabetic ketoacidosis in patients using SGLT2 inhibitors, particularly those on insulin therapy or with diabetes mellitus of unknown types. Impella device shows promise as a circulatory support system in alleviating the left ventricle’s workload and averting exacerbated pulmonary congestion, especially in cases where patients necessitate aggressive fluid replacement therapy, such as in the treatment of diabetic ketoacidosis concurrent with compromised cardiac function.

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Perioperative implications of sodium-glucose cotransporter-2 inhibitors: a case series of euglycemic diabetic ketoacidosis in three patients after cardiac surgery

Successful treatment of diabetic ketoacidosis secondary to fulminant type 1 diabetes mellitus using a closed-loop artificial pancreas in a pediatric patient

Empagliflozin-associated postoperative mixed metabolic acidosis. Case report and review of pathogenesis

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Second Department of Internal Medicine, University of Toyama, 2630 Sugitani Toyama, Toyama, 930-0194, Japan

Masaki Nakagaito, Makiko Nakamura, Teruhiko Imamura, Hiroshi Ueno & Koichiro Kinugawa

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Masaki Nakagaito wrote a draft. Makiko Nakamura interpreted the patient data. Makiko Nakamura, Teruhiko Imamura and Hiroshi Ueno reviewed the draft. Koichiro Kinugawa supervised this report. All authors have read and agreed to the published version of the manuscript.

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Nakagaito, M., Nakamura, M., Imamura, T. et al. Impella support for refractory cardiogenic shock accompanied by diabetic ketoacidosis: a case report. J Artif Organs (2024). https://doi.org/10.1007/s10047-024-01450-2

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A Case of Diabetic Ketoacidosis Presenting with Hypernatremia, Hyperosmolarity, and Altered Sensorium

Vinod kumar.

1 Department of Internal Medicine, St. Joseph's University Medical Center-New York Medical College, USA

Sushant M. Nanavati

Gabriel melki, mira upadhyaya, raman dhillon.

2 Department of Family Medicine, St. Joseph's University Medical Center-New York Medical College, USA

Sandra Gibiezaite

3 Department of Endocrinology, St. Joseph's University Medical Center-New York Medical College, USA

Patrick Michael

Monisha singhal.

Diabetic Ketoacidosis commonly presents with hyponatremia, but hypernatremia is a rare entity. We report a unique case of a 50-year-old woman admitted with altered sensorium with blood glucose 979 milligrams/deciliter, serum osmolarity 363 mOsm/kilograms, and serum sodium 144 milliequivalents/liter. Patient was given initial bolus of isotonic saline and continued on half isotonic saline for correction of hypernatremia along with insulin infusion therapy. Patient was successfully treated with intravenous fluids, insulin infusion, and the altered sensorium was resolved without any sequelae. This case illustrates a teaching point in the use of intravenous fluids for the treatment of Diabetic Ketoacidosis with hypernatremia.

1. Introduction

In the increasingly expanding population, Diabetes Mellitus accounts for 20-50% of new-onset diabetic patients in young adult population [ 1 ]. And Diabetic Ketoacidosis (DKA) continues to be the most severe medical emergency requiring admission to Intensive Care Unit (ICU). Here we discuss a unique case about a 44-years-old female presenting with hypernatremia in DKA secondary to severe hypotonic fluid loss and the management for this condition.

2. Case Presentation

A 50-years-old African female with medical history of hypertension, Diabetes Mellitus Type-2, and Major Depression Disorders presented with intractable vomiting and altered sensorium. About eight–ten hours prior to presentation, patient started to experience multiple episodes of nonbloody & nonbilious vomiting along with nausea leading to fatigue and altered sensorium requiring to be transported to hospital. Prior to initiation of the symptoms, she had suppressed appetite and skipped her dosage of Metformin 500 mg because of decreased oral intake and emesis. On presentation, patient was obtunded, responsive to pain, and poorly receptive to verbal stimuli. She had blood pressure of 123/81 mm Hg, respiratory rate of 25 breaths per minute, heart rate of 124 beats/minute, pulse oximetry of 97% on ambient air, and temperature of 97.6 Fahrenheit. On physical exam, she had mild distress, tachycardia, tenderness around epigastric area on deep palpation, and dehydration with poor skin turgor.

Due to state of presentation, computed tomography (CT) scan of the head showed no intracranial pathologies or cerebral edema presence. Venous blood gas showed pH 7.39, pCO 2 31 mm Hg, pO 2 52 mm Hg, HCO 3 18.8, sodium 148 mmol/L, potassium 3.5 mmol/L, glucose 750 mg/dl, and lactate 2.9 mmol/L. Initial biochemistry analysis showed serum sodium 144 meq/L, potassium 4.8 meq/L, chloride 98 meq/L, bicarbonate 14 meq/L, albumin 4.2 g/L, and serum glucose 979 mg/dl. Corrected sodium was calculated to be 158 meq/L, anion gap 32, delta gap: 2, and serum osmolality 363 mOsm/kg. Ketone bodies were strongly positive in the blood and urine. Table 1 shows additional biochemical values appropriate to the time interval.

∗ T: Time denoted in hours from admission.

Patient had received initial fluid resuscitation and, later, she was admitted to ICU requiring administration of normal saline, initiation of intravenous insulin infusion, and electrolytes repletion. Serum glucose levels were appropriately improving with goal of 50-70 mg/dl per hours, though serum sodium continued initially to peak before the values started to decrease. Patient started to be alert, awake, and responsive to commands with tolerating oral diet and improvement from admission assessment. Serum sodium levels were gradually controlled within normal range over 72 hours within admission. Patient was eventually transferred to medical floor for optimization of diabetic medication and education prior to discharge without any further events.

3. Discussion

As hyperglycemia-induced osmotic fluid and osmotic diuresis occur between compartments, electrolyte disturbances are expected resultant in patients with DKA. In addition, they may present with complex metabolic interplay: Ketoacidosis or Ketoalkalosis [ 2 ].

Patients with DKA commonly present with hyponatremia on admission to the hospital. Uncontrolled plasma glucose causes increase in plasma tonicity, creating a driving force for the movement of water from intracellular space to extracellular space, which dilutes the extracellular concentration of sodium. In addition, secretion of vasopressin limits water loss via kidney, which all leads to hyponatremia [ 1 , 3 ], while hypernatremia in DKA occurs from hypotonic renal losses, which is water excretion in excess of sodium and potassium, due to glycosuria-induced osmotic diuresis and inappropriate water replacement [ 3 ]. As per consensus statement guidelines, a correction factor of 1.6 mg per deciliter is added to the measured plasma sodium concentration for each 100 mg per deciliter of glucose above 100 mg per deciliter to account for the dilution effect of glucose. Corrected serum sodium provides a handy tool in monitoring and management during acute hyperglycemic crisis [ 1 , 3 ]. In cases of high anion-gap acidosis, delta-delta or delta gap is employed to evaluate additional underlying metabolic acid-base disorder [ 1 ]. In our case, the anion gap was 32 mmol/liter and change (delta) in the concentration of bicarbonate ions was 10 mmol/liter with a calculated delta ratio of 2, which interprets anion-gap acidosis with concurrent metabolic alkalosis. In ketoacidosis, there is 1:1 correlation between the increase in the anion gap and the decrease in the concentration of bicarbonate, but the patient had severe hypernatremia that may have contributed to the anion gap causing increased delta gap [ 1 ].

There are numerous pediatric cases reported about hypernatremia in DKA secondary to new-onset Type 1 Diabetes Mellitus, carbonated carbohydrate beverages, and herbal product ingestion [ 4 ]. Most of these cases presented with the patient exhibiting altered sensorium, attributing to hypernatremia causing severe cellular dehydration with central nervous system (CNS) [ 4 ].

Some studies suggest altered sensorium determined by the levels of serum sodium, especially in non-ketotic hyperglycemia hyperosmolar syndrome [ 5 , 6 ].

Management of hypernatremia in DKA constitutes of infusing 0.9% normal (isotonic) saline, at a rate of 15-20 milliliters per kilogram per hour or 1-1.5 liters during the first hour, to maintain effective plasma osmolality, in addition to supplementation of potassium [ 1 , 7 , 8 ]. Subsequently, fluids should be changed to 0.45% sodium chloride as the corrected sodium concentration may be in excess of 145 mmol/liter. One should take precautions to avoid risking cerebral edema, from overcorrecting acute hypernatremia, by decreasing plasma sodium concentration by 2 mol/liter/hour until plasma concentration is 145 mmol/liter [ 7 ].

In conclusion, our case provides clinicians with a refresher on the use of corrected sodium to guide the fluid therapy, altered sensorium driven by acute hypernatremia, and approach to the management of this condition.

Conflicts of Interest

The authors declare that there are no conflicts of interest regarding the publication of this paper.

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If you have gestational diabetes , you can manage your blood glucose level by following a healthy eating plan and doing a moderate-intensity physical activity, such as brisk walking for 150 minutes, each week. If consuming healthy food and beverages and getting regular physical activity aren’t enough to keep your blood glucose level in your target range, a doctor will work with you and may recommend you take insulin. Insulin is safe to take while you are pregnant.

No matter what type of diabetes you have, taking diabetes medicines every day can feel like a burden sometimes. New medications and improved delivery systems can help make it easier to manage your blood glucose levels. Talk with your doctor to find out which medications and delivery systems will work best for you and fit into your lifestyle.

Several types of insulin are available. Each type starts to work at a different speed, known as “onset,” and its effects last a different length of time, known as “duration.” Most types of insulin reach a peak, which is when they have the strongest effect. After the peak, the effects of the insulin wear off over the next few hours or so. Table 1 lists the different types of insulin, how fast they start to work, when they peak, and how long they last.

Table 1. Types of insulin and how they work 1,2

Another type of insulin, called premixed insulin, is a combination of insulins listed in Table 1. Premixed insulin starts to work in 15 to 60 minutes and can last from 10 to 16 hours. The peak time varies depending on which insulins are mixed.

Your doctor will work with you to review your medication options. Talk with your doctor about your activity level, what you eat and drink, how well you manage your blood glucose levels, your age and lifestyle, and how long your body takes to absorb insulin.

Follow your doctor’s advice on when and how to take your insulin. If you're worried about the cost, talk with your doctor. Some types of insulin cost more than others. You can also find resources to get financial help for diabetes care .

The way you take insulin may depend on your lifestyle, insurance plan, and preferences. Talk with your doctor about the options and which one is best for you. Most people with diabetes take insulin using a needle and syringe, insulin pen, or insulin pump. Inhalers and insulin jet injectors  are less common ways to take insulin. Artificial pancreas systems are now approved by the U.S. Food and Drug Administration (FDA). Talk with your doctor to see if an artificial pancreas is an option for you.

Needle and syringe

You can give yourself insulin shots using a needle and syringe . You draw up your dose of insulin from the vial—or bottle—through the needle into the syringe. Insulin works fastest when you inject it in your belly, but your doctor may recommend alternating the spot where you inject it. Injecting insulin in the same spot repeatedly could cause the tissue to harden, making it harder to take shots in that area over time. Other spots you can inject insulin include your thigh, buttocks, or upper arm, but it may take longer for the insulin to work from those areas. Some people with diabetes who take insulin need 2 to 4 shots a day to reach their blood glucose targets. Others can take a single shot. Injection aids can help you give yourself the shots.

An insulin pen looks like a writing pen but has a needle for its point. Some insulin pens come filled with insulin and are disposable. Others have room for an insulin cartridge that you insert and replace after use. Many people find insulin pens easier to use, but they cost more than needles and syringes. You may want to consider using an insulin pen if you find it hard to fill the syringe while holding the vial or cannot read the markings on the syringe. Different pen types have features that can help with your injections. Some reusable pens have a memory function, which can recall dose amounts and timing. Other types of “connected” insulin pens can be programmed to calculate insulin doses and provide downloadable data reports, which can help you and your doctor adjust your insulin doses.

An insulin pump is a small machine that gives you steady doses of insulin throughout the day. You wear one type of pump outside your body on a belt or in a pocket or pouch. The insulin pump connects to a small plastic tube and a very small needle. You insert the plastic tube with a needle under your skin, then take out the needle. The plastic tube will stay inserted for several days while attached to the insulin pump. The machine pumps insulin through the tube into your body 24 hours a day and can be programmed to give you more or less insulin based on your needs. You can also give yourself doses of insulin through the pump at mealtimes.

Another type of pump has no tubes. This pump attaches directly to your skin with a self-adhesive pad and is controlled by a hand-held device. The plastic tube and pump device are changed every several days.

Another way to take insulin is by breathing powdered insulin into your mouth from an inhaler device. The insulin goes into your lungs and moves quickly into your blood. You may want to use an insulin inhaler to avoid using needles. Inhaled insulin is only for adults with type 1 or type 2 diabetes. Taking insulin with an inhaler is less common than using a needle and syringe.

Jet injector

A jet injector is a device that sends a fine spray of insulin into the skin at high pressure instead of using a needle to deliver the insulin. It is used less commonly than a needle and syringe or a pen.

Artificial pancreas

An artificial pancreas is a system of three devices that work together to mimic how a healthy pancreas controls blood glucose in the body. A continuous glucose monitor (CGM)  tracks blood glucose levels every few minutes using a small sensor inserted under the skin that is held in place with an adhesive pad. The CGM wirelessly sends the information to a program on a smartphone or an insulin infusion pump. The program calculates how much insulin you need. The insulin infusion pump will adjust how much insulin is given from minute to minute to help keep your blood glucose level in your target range. An artificial pancreas is mainly used to help people with type 1 diabetes.

You may need to take medicines to manage your type 2 diabetes, in addition to consuming healthy foods and beverages and being physically active. You can take many diabetes medicines by mouth. These medicines are called oral medicines.

Most people with type 2 diabetes start with metformin pills. Metformin also comes as a liquid. Metformin helps your liver make less glucose and helps your body use insulin better. This drug may help you lose a small amount of weight.

Other oral medicines act in different ways to lower blood glucose levels. Combining two or three kinds of diabetes medicines can lower blood glucose levels better than taking just one medicine.

Read about different kinds of diabetes medicines (PDF, 2.8 MB) from the FDA.

If you have type 1 diabetes, your doctor may recommend you take other medicines, in addition to insulin, to help control your blood glucose. Some of these medicines work to slow how fast food and beverages move through your stomach . These medicines also slow down how quickly and how high your blood glucose levels rise after eating. Other medicines work to block certain hormones  in your digestive system  that raise blood glucose levels after meals or help the kidneys to remove more glucose from your blood.

Besides insulin, other types of injected medicines (PDF, 2.8 MB) are available that will keep your blood glucose level from rising too high after you eat or drink. These medicines, known as glucagon-like peptide-1 (GLP-1) receptor agonists, 3 may make you feel less hungry and help you lose some weight. GLP-1 medicines are not substitutes for insulin.

Side effects are problems that result from taking a medicine. Some diabetes medicines can cause hypoglycemia , also called low blood glucose, if you don’t balance your medicines with food and activity.

Ask your doctor whether your diabetes medicine can cause hypoglycemia or other side effects, such as upset stomach and weight gain. Aim to take your diabetes medicines as your doctor instructs you, to help prevent side effects and diabetes problems.

If medicines and lifestyle changes are not enough to manage your diabetes, there are other treatments that might help you. These treatments include weight-loss (bariatric) surgery  for certain people with type 1 or type 2 diabetes, or pancreatic islet transplantation  for some people with type 1 diabetes.

Weight-loss surgery

Weight-loss surgery  are operations that help you lose weight by making changes to your digestive system. Weight-loss surgery is also called bariatric or metabolic surgery.

This type of surgery may help some people who have obesity and type 2 diabetes lose a large amount of weight and bring their blood glucose levels back to a healthy range. How long the improved response lasts can vary by patient, type of weight-loss surgery, and the amount of weight the person lost. Other factors include how long a person had diabetes and whether the person used insulin. Some people with type 2 diabetes may no longer need to use diabetes medicines after weight-loss surgery . 4

Researchers are studying whether weight-loss surgery can help control blood glucose levels in people with type 1 diabetes who have obesity. 5

Pancreatic islet transplantation

Pancreatic islet transplantation is an experimental treatment for people with type 1 diabetes who have trouble controlling their blood glucose levels. Pancreatic islets  are clusters of cells in the pancreas that make the hormone insulin. In type 1 diabetes, the body’s immune system attacks these cells. A pancreatic islet transplantation replaces destroyed islets with new islets from organ donors. The new islets make and release insulin. Because researchers are still studying pancreatic islet transplantation , the procedure is only available to people enrolled in research studies.

The NIDDK conducts and supports clinical trials in many diseases and conditions, including diabetes. The trials look to find new ways to prevent, detect, or treat disease and improve quality of life.

What are clinical trials for insulin, medicines, and other diabetes treatments?

Clinical trials—and other types of clinical studies —are part of medical research and involve people like you. When you volunteer to take part in a clinical study, you help health care professionals and researchers learn more about disease and improve health care for people in the future.

Find out if clinical trials are right for you .

Researchers are studying many aspects of diabetes medicines, including

• new types of insulin
• the most effective times to take diabetes medicines
• new types of monitoring devices and delivery systems

Watch a video of NIDDK Director Dr. Griffin P. Rodgers explaining the importance of participating in clinical trials.

What clinical trials for insulin, medicines, and other diabetes treatments are looking for participants?

You can view a filtered list of clinical studies on insulin, medicines, and other diabetes treatments covered in this health topic that are federally funded, open, and recruiting at www.ClinicalTrials.gov . You can expand or narrow the list to include clinical studies from industry, universities, and individuals; however, the National Institutes of Health does not review these studies and cannot ensure they are safe. Always talk with your health care provider before you participate in a clinical study.

This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by NIDDK is carefully reviewed by NIDDK scientists and other experts.

The NIDDK would like to thank Stuart A. Weinzimer, M.D., Yale University School of Medicine