diabetes mellitus case study with answers

Diabetes Mellitus Case Study (45 min)

Watch More! Unlock the full videos with a FREE trial

Included In This Lesson

Study tools.

Access More! View the full outline and transcript with a FREE trial

What additional nursing assessments should be performed at this time?

• POC glucose
• Heart and lung sounds and respiratory effort – ensure she is protecting her airway
• Assess skin and mucous membranes
• Level of consciousness and orientation

What history questions would you like to ask of the patient and/or her parents?

• Has she been excessively thirsty or hungry lately
• Has she been urinating a lot
• Has she lost weight unintentionally?
• Is there a history of diabetes in the family?
• Has she been told previously that she has diabetes?
• Does she take any medications on a daily basis?

Upon further questioning, the parents report that their daughter has been weak a lot lately. Miss Matthews reports but she’s always hot and exhausted. She reports a 10-pound weight loss over the last 2 months despite eating all the time and agrees that she has been thirsty and peeing a lot.

What diagnostic tests should be run for Miss Matthews?

• Serum glucose level
• BMP – electrolytes, anion gap, etc.
• ABG to assess for acidosis
• Urine ketones

What is an appropriate response by the nurse?

• Your daughter has Type 1 diabetes, which means that she has an autoimmune disorder that attacks the cells in her pancreas that make insulin. Type 1 diabetes typically has nothing to do with diet and lifestyle and usually has more to do with genetics.
• Your daughter’s healthy lifestyle will continue to help her control her blood sugar levels, but unfortunately, there is no cure for type 1 diabetes at this time.

What treatments do you expect to be ordered for Miss Matthews at this time?

• Miss Matthews will need intensive insulin therapy and IV fluids to counteract the ketoacidosis and bring her blood sugars down.
• She will then need to be started on long-acting insulin like Lantus and short-acting insulin-like NovoLog for correction with meals.

Miss Matthews is treated for diabetic ketoacidosis over the next 2 days and is now feeling much better. The diabetic nurse educator comes by to teach Miss Matthews how to self-administer SubQ insulin using an insulin pen. Miss Matthews says “I  can’t stand needles, isn’t there a pill I can take instead?”

What is the most appropriate response by the nurse?

Unfortunately, at this time insulin is not available in pill form. It has to be taken via injection. Otherwise, it will not work correctly.

What options does Miss Matthews have for insulin administration?

• Insulin vial with needles
• Insulin pen
• Insulin pump

Miss Matthews is able to demonstrate proper technique for glucose monitoring and self-administration of insulin with the insulin pen. Her blood glucose levels are stable between 140 and 180 mg/dL,  and the provider has said that she could go home today.

In addition to the insulin education, she has already received, what other education topics should be included in discharge teaching for Miss Matthews?

• Miss Matthews should be taught how to count carbohydrates to determine the amount of insulin required.
• She should be given a prescribed sliding scale or insulin protocol to follow.
• Miss Matthews should also be instructed on when to take her long-acting insulin and when to take regular insulin in relation to meal times. It is important that she does not take short-acting insulins without being ready to eat.
• Miss Matthews should be educated on the possibility of morning hyperglycemia due to the Somogyi effect or Dawn phenomenon, and be given suggestions to try an evening dose of insulin or an evening snack.
• The importance of follow-up appointments with her primary care provider and/or endocrinologist should be stressed. She should have her Hgb A1c checked every 3 months to start with.
• She should also be educated on foods to avoid, such as desserts and sweets, and foods that are beneficial, such as fruits and vegetables and high-quality proteins.
• Miss Matthews should carry some candy or glucose tablets with her in case of a hypoglycemic reaction.

View the FULL Outline

When you start a FREE trial you gain access to the full outline as well as:

• SIMCLEX (NCLEX Simulator)
• 6,500+ Practice NCLEX Questions
• 2,000+ HD Videos
• 300+ Nursing Cheatsheets

“Would suggest to all nursing students . . . Guaranteed to ease the stress!”

Nursing Case Studies

This nursing case study course is designed to help nursing students build critical thinking.  Each case study was written by experienced nurses with first hand knowledge of the “real-world” disease process.  To help you increase your nursing clinical judgement (critical thinking), each unfolding nursing case study includes answers laid out by Blooms Taxonomy  to help you see that you are progressing to clinical analysis.We encourage you to read the case study and really through the “critical thinking checks” as this is where the real learning occurs.  If you get tripped up by a specific question, no worries, just dig into an associated lesson on the topic and reinforce your understanding.  In the end, that is what nursing case studies are all about – growing in your clinical judgement.

Nursing Case Studies Introduction

Cardiac nursing case studies.

• 6 Questions
• 7 Questions
• 5 Questions
• 4 Questions

GI/GU Nursing Case Studies

• 2 Questions
• 8 Questions

Obstetrics Nursing Case Studies

Respiratory nursing case studies.

• 10 Questions

Pediatrics Nursing Case Studies

• 3 Questions
• 12 Questions

Neuro Nursing Case Studies

Mental health nursing case studies.

• 9 Questions

Metabolic/Endocrine Nursing Case Studies

Other nursing case studies.

Sorry. You need a frames capable broswer to view this page.

An official website of the United States government

The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

• Publications
• Account settings

Preview improvements coming to the PMC website in October 2024. Learn More or Try it out now .

• Advanced Search
• Journal List
• J Obes Metab Syndr
• v.26(1); 2017 Mar

Two Cases of Successful Type 2 Diabetes Control with Lifestyle Modification in Children and Adolescents

Seon hwa lee.

1 Department of Pediatrics, Konkuk University Medical Center, Seoul, Korea

Myung Hyun Cho

Yong hyuk kim.

2 Department of Pediatrics, Wonju College of Medicine, Yonsei University, Wonju, Korea

Sochung Chung

Obesity and obesity-related disease are becoming serious global issues. The incidence of obesity and type 2 diabetes has increased in children and adolescents. Type 2 diabetes is a chronic disease that is difficult to treat, and the accurate assessment of obesity in type 2 diabetes is becoming increasingly important. Obesity is the excessive accumulation of fat that causes insulin resistance, and body composition analyses can help physicians evaluate fat levels. Although previous studies have shown the achievement of complete remission of type 2 diabetes after focused improvement in lifestyle habits, there are few cases of complete remission of type 2 diabetes. Here we report on obese patients with type 2 diabetes who were able to achieve considerable fat loss and partial or complete remission of diabetes through lifestyle changes. This case report emphasizes once again that focused lifestyle intervention effectively treats childhood diabetes.

INTRODUCTION

Obesity and obesity-related diseases are serious public health issues worldwide, and the increased incidence of type 2 diabetes in children and adolescents is associated with the increased incidence of obesity. 1 , 2 Excess weight gain is a risk factor for both type 2 diabetes and insulin resistance. Obesity refers to excessive fat accumulation and may affect the clinical course of diabetes in terms of insulin resistance. Therefore, the accurate assessment of obesity is important. 3 Body mass index (BMI) is used as an indicator to evaluate weight excess or obesity. 4 However, BMI is limited in that it is the sum of fat-free mass index (FFMI) and fat mass index (FMI) and does not only reflect excess fat. 5 , 6 Therefore, it may be helpful to use body composition analysis that measures fat mass (FM) without fat-free mass (FFM) as a tool to evaluate obesity. Although type 2 diabetes is considered a chronic disease that is difficult to completely cure 7 , 8 , studies have reported complete remission of type 2 diabetes in adults after intensive lifestyle modification. 9 Here we report two cases of type 2 diabetes with partial or complete response to lifestyle modification, particularly FM decrease. Our findings emphasize that lifestyle modifications including dietary treatment and exercise therapy comprise the first-line treatment in obese patients with type 2 diabetes. 10

CASE REPORT

Ms. L, 17 years and 5 months, female

Polydipsia, polyuria

Family history

Mother with hypertension, father with heart failure.

Past medical/social history

No significant history

History of present illness

This 17-year-old girl was diagnosed with diabetes at another hospital after a 1-month history of persistent polydipsia and polyuria. She presented to Konkuk University Medical Center for further diagnosis and treatment of her persistent symptoms.

Physical examination

On admission, her height was 173.1 cm (>97th percentile), weight was 107.2 kg (>97th percentile), and BMI was 35.8 kg/m 2 (>97th percentile) ( Table 1 ). She appeared obese but did not look ill and her mental status was intact. Her vital signs were normal except for a blood pressure of 137/81 mmHg (95–99th percentile). Her skin was warm and no dry mucous membranes were observed. A chest examination was unremarkable. No enlargement of the liver or spleen was appreciated on an abdominal examination. The rest of the physical exam was unremarkable.

Anthropometric data and patient body composition profiles of adolescent girls with type 2 diabetes who achieved remission after stopping medications

BMI, body mass index; FFM, fat free mass; FM, fat mass; FFMI, fat free mass index; FMI, fat mass index; FFMIZ, fat free mass index Z score; FMIZ, fat mass index Z score; PBF, percent body fat.

Lab findings

Labs on admission revealed a glycated hemoglobin (HbA1c) of 11.1%, fasting plasma glucose level of 102 mg/dL, insulin level of 23.12 μIU/mL, and C-peptide level of 4.13 ng/mL. Liver function tests revealed an elevated serum aspartate transaminase (AST) level of 115 IU/L and serum alanine transaminase (ALT) level of 141 IU/L. A lipid panel demonstrated a total cholesterol level of 133 mg/dL, triglycerides of 71 mg/dL, and high-density lipoprotein cholesterol (HDL-C) of 49 mg/dL ( Table 2 ). The total protein and albumin level was 7.0 g/dL and that of albumin was 4.5 g/dL. The free fatty acid level was elevated at 1214 μEq/L.

Biochemical profiles of adolescent girls with type 2 diabetes who achieved remission after stopping medications

HbA1c, glycated hemoglobin A1c; HDL, high lipoprotein; AST, aspartate transaminase; ALT, alanine transaminase.

Radiologic findings

There were no abnormal findings on a chest radiograph. An abdominal ultrasound showed severe fatty infiltration of the liver.

Treatment and progress

For glycemic control, the patient was started on oral medications (metformin 500 mg BID, glimepiride 1 mg QD) as well as a diet and exercise program as a lifestyle modification. Her dietary and nutritional knowledge were evaluated, and she was counseled to have regular meals with 70–75 g of proteins per day and maintain daily nutritional requirements of approximately 1,800 kcal. She was recommended to consume a low-carb, low-fat diet, limit high saturated fats, track her intake, and attend outpatient appointments every 1–2 months. She was instructed to perform aerobic and weight exercises that improve muscle strength for more than 1 hour at least 3 times per week. For 1 year, she did aerobic and anaerobic exercises for an hour or more per day. After 1 year, she incorporated a 7 km walk daily and Pilates more than 3 times per week to her exercise program. In the outpatient setting, we assessed her adherence to therapy at 1–2 month intervals, offered motivational support, and advised her to gradually increase her exercise duration rather than intensity. We measured her height and weight every year and used InBody720, a type of bioelectrical impedance analysis (BIA), to accurately evaluate her obesity. On diagnosis, the patient’s BMI was 35.8 kg/m 2 (FMI, 18.0 kg/m 2 ; FFMI, 17.8 kg/m 2 ), scoring >97th percentile, and percent body fat (PBF) was 50.4%. During the 2 years of outpatient monitoring, she had no difficulty controlling her blood sugar level using the combination of oral medication and lifestyle modification. However, the dose of metformin was increased to 1,000 mg BID due to difficulty maintaining her HbA1c <7.0% on the previous regimen; at that time, she was still considered obese with a BMI of 35.1 kg/m 2 (FMI, 17.2 kg/m 2 ; FFMI, 17.9 kg/m 2 ) and PBF of 48.9%. Her weight and body composition during treatment are shown in Fig. 1 .

Plot of changes in FFMI and FMI in two adolescent girls with T2DM who achieved remission. T2DM, type 2 diabetes; BMI, body mass index; PBF, percent body fat; FFMI, fat free mass index; FMI, fat mass index.

Three years later, the patient’s dietary therapy and exercise program resulted in an increased FFMI at 18.3 kg/m 2 and reduced FMI at 14.9 kg/m 2 , leading to discontinuation of the glimepiride and a reduction in the metformin dose to 500 mg BID.

Four years later, her HbA1c decreased to 5.4% and the metformin was discontinued due to her successful glycemic control. At that time, her fasting blood glucose level was 97 mg/dL, insulin level was 5.62 μIU/mL, and C-peptide level was 2.13 ng/mL. Her BMI was 27.1 kg/m 2 (FMI, 10.3 kg/m 2 ; FFMI, 16.8 kg/m 2 ) and PBF was 38.2%, which is still considered obese based on the World Health Organization diagnostic criteria for Asian adults; however, it was 8.7 kg/m 2 less than her BMI prior to treatment and her FMI had decreased by 7.7 kg/m 2 . Her FFMI was also reduced by 1.0 kg/m 2 , but still belonged to the 90–95th percentile; thus, her nutritional status was not a concern ( Table 1 ). Liver function tests and a lipid panel revealed AST 20 IU/L, ALT 12 IU/L, total cholesterol 114 mg/dL, triglycerides 59 mg/dL, and HDL-C 51 mg/dL ( Table 2 ). Her HbA1c has remained at <5.7% for more than a year without oral medications and will continue to be followed.

Ms. A, 12 years and 10 months, female

Hyperglycemia

Father with type 2 diabetes under treatment

12-year-old female who presented to Konkuk University Medical Center with post-prandial hyperglycemia of 330 mg/dL measured by her father one day prior to admission. Menarche occurred 1 year prior and her menstrual cycles were regular.

On admission, the patient’s height was 158.9 cm (25–50th percentile), weight was 75.5 kg (>97th percentile), and BMI was 29.9 kg/m 2 (>97th percentile) ( Table 1 ). Her vital signs were within the normal range with a blood pressure of 112/68 mmHg, pulse of 72 beats/min, respiratory rate of 20 breaths/min, and temperature of 36.6°C. She had a clear mental status, warm skin, and moist mucous membranes. A chest examination revealed no specific findings, while an abdominal examination revealed no hepatomegaly or splenomegaly. The rest of the physical examination was unremarkable.

Laboratory findings

Laboratory tests at the time of admission revealed an HbA1c level of 9.9%, fasting blood glucose level of 202 mg/dL, insulin level of 15.85 μIU/mL, and C-peptide level of 2.97 ng/mL. Liver function tests showed an elevated AST level at 47 IU/L and ALT level at 69 IU/L. A lipid panel and comprehensive metabolic panel showed a total cholesterol level of 165 mg/dL, triglyceride level of 104 mg/dL, HDL-C of 50 mg/dL, total protein of 7.6 g/dL, and albumin of 4.8 g/dL ( Table 2 ). The free fatty acid level was elevated at 671 μEq/L.

Radiologic finding

There were no significant findings on a chest radiograph. An abdominal ultrasound showed moderate fatty liver.

For glycemic control, combination therapy of oral medication (metformin 500 mg BID) and lifestyle modification through adjustments in dietary habits was prescribed. We evaluated her dietary and nutritional knowledge and then counseled her to consume regular meals with 70–90 g of protein per day, maintain daily nutritional requirements of approximately 1800 kcal, and eat a low-carb, low-fat diet. She was recommended to modify her habitual preference of salty and spicy foods, reduce her salt intake, track her meals, and attend outpatient monitoring appointments every 1–2 months.

For an exercise program, she was instructed to include aerobic and weight exercises that improve muscle strength. She was advised to walk >1 hour at least 5 days per week and visit a health training center for ≥1 hour of strength exercises at least 3 times per week. We measured her height and weight every 2 months, and used InBody720, a type of BIA for accurate assessment of obesity. On diagnosis, patient’s BMI was 29.9 kg/m 2 (FMI, 12.7 kg/m 2 ; FFMI, 17.2 kg/m 2 ) and PBF was 42.5%. Two years later after the diagnosis, an abdominal ultrasound showed improvements in her fatty liver and her HbA1c was successfully reduced to 6.0%. The oral medication was discontinued due to the successful glycemic control. At the time, her fasting blood sugar was 97 mg/dL, insulin level was 5.62 μIU/mL, and C-peptide level was 2.79 ng/mL. Her BMI (FMI+FFMI) was 23.2 kg/m 2 (7.0 kg/m 2 +16.2 kg/m 2 ), which was within the overweight range (85–90th percentile), and her PBF was 30.2%. Her BMI at that point was 6.7 kg/m 2 lower than that prior to therapy, with a 5.7 kg/m 2 reduction observed in her FMI ( Table 1 ). Liver function tests and a lipid panel revealed the following: AST, 20 IU/L; ALT, 34 IU/L; total cholesterol, 115 mg/dL; triglycerides, 70 mg/dL; and HDL-C, 30 mg/dL ( Table 2 ). The changes in the patient’s weight and body composition during treatment are shown in Fig. 1 . Since discontinuing the oral medication, the patient has maintained an HbA1c level <6.5%.

The prevalence of type 2 diabetes is increasing with changes in dietary habits and increases in the incidence of obesity among children and adolescents. Although it is already known that a reduced caloric intake and weight loss through lifestyle modifications can treat diabetes, few cases demonstrating such an effect have been reported to date. 9 As discussed previously in two cases, a notable reduction in FM resulted in an HbA1c level <6.5% and improved glycemic control as well as successful maintenance of HbA1c at goal level without medications. According to the 2009 consensus statement reported by the American Diabetes Association, a complete response is defined as blood sugar in the normal range for >1 year without any medications (fasting blood sugar <100 mg/dL, HbA1c <5.7%). Partial response is defined as a blood sugar level below the diabetes range for >1 year without any medications or medical procedures (HbA1C <6.5%; fasting blood sugar, 100–125 mg/dL). 11 In the two cases presented above, significant decreases in BMI and PBF were observed as well as subsequent improvements in HbA1c and fasting blood sugar level. In developing children, weight gain occurs with increasing age, and increases in BMI are common. However, such increases in BMI are due to increases in FFM, not FM. 6 Appropriate growth is one of the important objectives of pediatric diabetes management and treatment. Since proper nutrition and hormonal balance are essential for growth, it is more important to achieve a reduction in FM than a reduction in weight by having regular meals that are low in carbs and fat with a normal protein intake.

Weight loss through lifestyle modification generally affects FFM. In the cases discussed above, both patients had elevated FM and FFM on admission. By balancing appropriate dietary changes with aerobic and anaerobic exercises, the patient was able to maintain FFM and incur no significant effect on growth. In the present case, the patient was instructed to spend 1 hour exercising at least 3 times per week, assessed for compliance as an outpatient every 1–2 months, offered continuous motivational support, and told to gradually increase her exercise duration.

A recent study reported that oral medication was eventually needed to control hyperglycemia in patients with diabetes refractory to management with proper lifestyle modification. 12 However, lifestyle modification is important, and is a cornerstone in the treatment of diabetes, and it should be a mandatory treatment for type 2 diabetes. In females, it is common to see an increase in PBF with progression of puberty. 13 , 14 However, here we report cases of complete remission of diabetes in teenage girls with lifestyle modification and emphasize once again that intensive lifestyle improvement is an effective early treatment for diabetes. 15

Our results demonstrate that intensive lifestyle modification including regular exercise and dietary changes is very effective in the treatment of obese patients with type 2 diabetes.

CONFLICTS OF INTEREST

The authors declare that there are no conflicts of interest.

Ohio State nav bar

The Ohio State University

• BuckeyeLink
• Find People
• Search Ohio State

Pathophysiology and Correct Diagnosis

Normal physiology of the pancreas.

The pancreas is an organ that produces digestive enzymes and is located behind the stomach. 

• Inside the pancreas are cells called the islets of Langerhans. These cells secrete hormones that regulate the metabolism of carbohydrates, fats, and proteins. 
• Beta cells are one type of hormone-secreting cells in the islets of Langerhans.  The main function of beta cells is to produce insulin. 
• Insulin binds with receptors throughout the body to signal the body to send glucose into the cell. Once the glucose is inside cells, the body can excrete the glucose. 

      (McCance & Huether, 2019)

Figure 8.  Islets of Langerhans (Darling, 2016)

Al terations in Pancreatic Physiology

When specific genetic and environmental factors combine, the function of the Pancreas can be altered. These alterations can lead to insulin resistance and hyperglycemia which then leads to type 2 diabetes mellitus (DM). Genetic predisposition to type 2 DM may include inherited beta-cell dysfunction and insulin resistance (McCance & Huether, 2019).

Risk Factors for DM:

Parent or sibling have type 2 DM

American Indian or Alaskan Native

Sedentary lifestyle

Hypertension

Lack of a balanced and healthy diet

(McCance & Huether, 2019; Bellou, Belbasis, Tzoulaki, & Evangelos, 2018)

Figure 9.  Pathophysiology of Diabetes Mellitus (Skyler et al., 2017)

Obesity is the major factor that contributes to insulin resistance via different mechanisms. 

• Adipokines are hormones produced in adipose (fat) tissue. When these hormone levels are increased in the blood, production of insulin is decreased and insulin resistance increases (McCance & Huether, 2019).
• High levels of cholesterol and triglycerides interfere with insulin secretion and can cause beta-cell death (McCance & Huether, 2019). 
• Obesity causes an increase of inflammatory cytokines which cause insulin resistance by depositing fat in the liver and muscles (Skylar et al., 2017). 

When a patient develops insulin resistance, beta-cells can not produce enough insulin to support the needs of the body. Eventually, this leads to beta-cell and islet inflammation, and then eventually beta-cell death (Skylar et al., 2017). 

• When the beta-cells cannot produce enough insulin, glucose uptake into the cell is decreased resulting in hyperglycemia. 
• Dysfunction in the beta-cells leads to type 2 DM. 
• In type 2 DM, beta-cell function progressively worsens over time, resulting in even further increased insulin resistance and hyperglycemia (Skylar et al., 2017).
• Type 2 DM effects 9.3% of adults in the United States (McCance & Huether, 2019)

Diagnostic Criteria for Type 2 DM

• HbA1c: ≥ 6.5%
• Fasting (≥ 8 hours) blood glucose: ≥126 mg/dL
• 2 hour plasma glucose:  ≥ 200 mg/dL
• Random plasma glucose in a patient with classic symptoms of hyperglycemia:  ≥ 200 mg/dL

     (McCance & Huether, 2019)

Correct Diagnosis:

The correct diagnosis for J.S. is type 2 diabetes mellitus.

J.S. has a Hb A1c of 10% and a fasting blood glucose of 240 mg/dL. Both of these values fit in the diagnostic criteria for DM. The patient also has obesity, a lack of a balanced diet, and he is a smoker. These are all risk factors for DM. In J.S.’s case, obesity is probably the largest factor that led to the development of DM. J.S. also presents with other common signs and symptoms of DM such as: polydipsia, polyuria, delayed wound healing, tingling in his feet, and blurred vision.

 (McCance & Huether, 2019)

• Previous Article

Presentation

Clinical pearls, article information, case study: diabetic ketoacidosis in type 2 diabetes: “look under the sheets”.

• Split-Screen
• Article contents
• Figures & tables
• Supplementary Data
• Peer Review
• Open the PDF for in another window
• Cite Icon Cite
• Get Permissions

Brian J. Welch , Ivana Zib; Case Study: Diabetic Ketoacidosis in Type 2 Diabetes: “Look Under the Sheets”. Clin Diabetes 1 October 2004; 22 (4): 198–200. https://doi.org/10.2337/diaclin.22.4.198

Download citation file:

• Ris (Zotero)
• Reference Manager

Diabetic ketoacidosis (DKA) is a cardinal feature of type 1 diabetes. However, there is a strong, almost dogmatic, errant perception by physicians that DKA is a complication that only occurs in patients with type 1 diabetes. This is not true. DKA does occur in type 2 diabetes; however, it rarely occurs in the absence of a precipitating event.

R.T., a 25-year-old African-American man with type 2 diabetes presented with a 5-day history of nausea and vomiting. He also reported a 2-week history of polyuria and polydipsia and a 10-lb weight loss. A review of symptoms was pertinent for a 5-day history of persistent lower back pain.

The patient was diagnosed with type 2 diabetes 5 years ago when he presented to a different hospital with symptoms of polyuria, polydipsia, and weight loss. He was given a prescription for a sulfonylurea, which he says he took until his initial prescription ran out 1 month later. He had not taken any other medication since that time.

Physical examination revealed an afebrile, obese man (BMI 40 kg/m 2 ) with prominent acanthosis nigricans, no retinopathy by direct funduscopic exam, and a normal neurological exam, including motor function and sensation. The patient had no tenderness to palpation over the lumbrosacral spine or paraspinous muscles despite his complaint of lower back pain.

The laboratory data showed an anion gap, metabolic acidosis, and hyperglycemia (pH of 7.14, anion gap of 24, bicarbonate 6 mmol/l, urinary ketones 150 mg/dl, glucose 314 mg/dl) consistent with the diagnosis of DKA. His white blood count was 20,400/μl. Urinalysis demonstrated no evidence of infection. The patient's hemoglobin A 1c (A1C) was 13.5%.

The patient was admitted and treated aggressively with intravenous fluid and an insulin-glucose infusion. A non-contrast magnetic resonance imaging(MRI) of the lumbosacral spine (L-spine) was obtained because of the patient's persistent complaint of lower back pain. The L-spine MRI results were negative for pathology. However, R.T. reported increasing discomfort and now noted weakness and numbness in his bilateral lower extremities.

Neurology was consulted, and during their assessment, the patient became incontinent and was found to have 0/5 strength in the lower extremities,severely compromised sensation, and decreased rectal tone. A contrast MRI of both the thoracic and lumbar spine was ordered, and the patient was found to have a T10-T12 epidural abscess ( Figure 1 ).

Epidural abscess precipitating DKA in a type 2 diabetic patient.

The patient's antibiotic coverage was broadly expanded, high-dose intravenous steroids were initiated, and neurosurgery was urgently consulted. Emergent evacuation of the epidural abscess with laminectomies of T10-T12 was performed without complication.

R.T.'s neurogenic bladder resolved without further intervention. After intensive inpatient rehabilitation, he had 3/5 strength in bilateral lower extremities and was still unable to ambulate.

S.D., a 39-year-old white man with type 2 diabetes and mild mental retardation, presented with a 3-week history of polyuria and polydipsia, as well as dysuria, left hip pain, and a feeling of incomplete bladder emptying. Because of the severity of his left hip discomfort, the patient required a cane to ambulate.

The patient was diagnosed with type 2 diabetes 4 years ago on the basis of an elevated fasting blood glucose level during a routine medical examination. He was started on oral hypoglycemic agents, but he discontinued them after 1 month because he was unable to pay for them.

On physical exam, S.D. was afebrile but tachycardic (heart rate 131 bpm)and hypertensive (blood pressure 192/118 mmHg). General examination revealed a wasted, severely volume-depleted man. Thrush was observed on oropharyngeal exam. Cardiopulmonary and abdominal examinations were unremarkable. The patient had point tenderness on the anterior aspect of his left hip. Rectal examination revealed a non-tender prostate.

The laboratory data showed an anion gap, metabolic acidosis, and hyperglycemia (pH 7.24, bicarbonate 9 mmol/l, anion gap 24, urinary ketones 150 mg/dl, and glucose 322 mg/dl) consistent with the diagnosis of DKA. Urinalysis was remarkable for large blood, 4+ bacteria, and > 400 white blood cells. S.D.'s serum white blood count was 22,200, and his erythrocyte sedimentation rate was 109 mm/hour. His A1C result was 12.6%.

The patient was admitted and treated with intravenous fluids and an insulin-glucose infusion. Cultures were obtained. S.D. was started empirically on ticarcillin/clavulanic acid because of concern for left hip osteomyelitis and complicated urinary tract infection. An MRI of the left hip was ordered to evaluate for suspected osteomyelitis. Unexpectedly, it revealed left hip myonecrosis and a large loculated prostatic abscess( Figure 2 ).

Prostatic abscess precipitating DKA in a type 2 diabetic patient.

Urology was consulted, and the patient underwent transurethral drainage of the prostatic abscess. Methicillin-sensitive Staphylococcus aureus grew from both blood and urine cultures. S.D. was treated with intravenous antibiotics per culture sensitivities. The myonecrosis was treated conservatively.

The patient recovered well. He was started on subcutaneous insulin and discharged home to complete a 2-week course of intravenous antibiotics.

What is the mechanism of DKA?

Why does DKA occur in type 2 diabetes?

DKA is a cardinal feature of type 1 diabetes, which has led to the widespread errant perception that it is a complication unique to type 1 diabetes. However, it has been repeatedly reported that DKA does occur in patients with type 2 diabetes. 1 - 5   Moreover, as the cases presented here illustrate, it can occur even in patients who were previously insulinindependent.

A recent study evaluating 138 consecutive admissions for DKA at a large academic center observed that 21.7% had type 2 diabetes. 6   Nearly 70% of the admissions involved discontinuation of medications, and almost half had an identifiable infection when an intensive search was undertaken.

A review of the mechanism of DKA is important. Ketoacidosis occurs as a function not only of severe insulin deficiency, but also of elevated glucagon levels. Insulin is an anabolic hormone. Severe insulin deficiency results in decreased glucose utilization by muscle and an unregulated increase in lipolysis. This leads to an enhanced delivery of gluconeogenetic precursors(glycerol and alanine) to the liver. Furthermore, removal of the normal suppressive effect of insulin causes glucagon elevation. 7 , 8   Glucagon is a catabolic hormone. Glucagon promotes gluconeogenesis, decreases oxidation of free fatty acids to triglycerides, and promotes hepatic ketogenesis. 9  

Importantly, the concentration of insulin required to suppress lipolysis is only one-tenth of that required to promote glucose utilization. 10   Typically, moderate insulin deficiency (as observed in patients with type 2 diabetes) is associated with sufficient insulin to block lipolysis (and therefore ketoacid formation), but not enough to promote glucose utilization. This leads to hyperglycemia without formation of the ketoacids.

When DKA occurs in patients with type 2 diabetes, the presumed mechanism of ketoacidosis is the combination of relative insulin deficiency and increased secretion of glucagon (as well as other counteregulatory hormones such as cortisol, catecholamines, and growth hormone) in response to stress from 1 ) overwhelming infection, 2 ) infarction of tissue, or 3 ) other severe illness. The elevated catecholamines further suppress insulin secretion to perpetuate a downward spiral. The increased glucagons-to-insulin ratio causes a mismatch that promotes unregulated lipolysis and proteolysis with subsequent uninterrupted formation of ketoacids.

To summarize, DKA is not a unique feature of type 1 diabetes. Though much more common in type 1 diabetes, it does occur in patients with type 2 diabetes, as illustrated by these case reports. However, it is rare for DKA to occur in type 2 diabetes in the absence of some precipitating event. When DKA occurs in an individual with type 2 diabetes, the clinician should “look under the sheets” and initiate an intensive search for the precipitating factor. Once identified, the trigger should be treated promptly and appropriately.

DKA does occur in type 2 diabetes.

DKA in type 2 diabetes rarely occurs without a trigger.

When it does, an intensive search for the precipitating factor should be undertaken.

Brian J. Welch, MD, and Ivana Zib, MD, are fellows in the Division of Endocrinology and Metabolism at the University of Texas Southwestern Medical Center in Dallas.

The authors thank Philip Raskin, MD, for his support and guidance.

Email alerts

• Online ISSN 1945-4953
• Print ISSN 0891-8929
• Diabetes Care
• Clinical Diabetes
• Diabetes Spectrum
• Standards of Medical Care in Diabetes
• Scientific Sessions Abstracts
• BMJ Open Diabetes Research & Care
• ShopDiabetes.org
• ADA Professional Books

Clinical Compendia

• Clinical Compendia Home
• Latest News
• DiabetesPro SmartBrief
• Special Collections
• DiabetesPro®
• Diabetes Food Hub™
• Insulin Affordability
• Know Diabetes By Heart™
• About the ADA
• Journal Policies
• For Reviewers
• Advertising in ADA Journals
• Reprints and Permission for Reuse
• Copyright Notice/Public Access Policy
• ADA Professional Membership
• ADA Member Directory
• Diabetes.org
• X (Twitter)
• Cookie Policy
• Accessibility
• Terms & Conditions
• Get Adobe Acrobat Reader
• © Copyright American Diabetes Association

This Feature Is Available To Subscribers Only

Sign In or Create an Account