type 1 diabetes ati case study

Nursing Case Study for Type 1 Diabetes

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Michael is a 14-year-old male brought into a small ER by his mother. They were driving a long distance after he competed in a wrestling tournament. He had not felt well on the bus ride with the team so his mother decided he should ride with her. His mother denies a history of chronic illness but did say he had “like a cold but with a stomachache” about 3 months ago.

She also says that he has been very thirsty, and they had to stop several times for him to urinate. She is also worried because he almost missed his wrestling “weight class” parameters because he was significantly lighter this past weekend than he has been in the past. And that is even with him eating more than usual.

What symptoms are most worrisome to the triage nurse?

• He has 2 of the 3 “p’s” – polydipsia (thirst), polyuria (frequent urination), polyphagia (hunger) which are trademarks of diabetes mellitus (DM) and/or diabetic ketoacidosis (DKA). They happen in response to the body lacking insulin and its response is to try to achieve homeostasis with these mechanisms. His weight loss could be indicative of DM as well. 
• They describe a recent viral-like illness which may precipitate a diagnosis of DM (it is thought the body has an inappropriate immune response to the illness leading to DM)

In triage, the nurse obtains a point-of-care blood glucose (BG) level and the machine gives no value. Instead, an error message indicating “hi” displays on the machine.

Why did the nurse do this test? What should they do next?

• Clues point to possible DM or DKA. Getting a BG immediately can help guide care. Always follow the facility protocol/procedure on “hi” or “lo” (often spelled this way on glucometers) readings. The protocol might dictate (standing order) stat venous draw and send it to the lab. It may be advised to try again on a different machine with a new sample. Whatever the guidance, a BG level is imperative for this patient.

Michael is AAO x 4. He complains of a “stomachache” and reports he has nausea and experienced vomiting shortly before arrival. His skin is warm and dry, but his face is flushed. When asked about pain, he says he has a headache, and his vision is blurry. The nurse notices a fruity odor on his breath when obtaining vital signs. 

BP 90/54 mmHg SpO 2 98% on Room Air

HR 122 bpm and regular

RR 26 bpm at rest

The patient and his mother are placed into an exam room immediately and the triage nurse verbally reports this to the accepting nurse.

How does the nurse interpret these symptoms?

• Michael’s symptoms are consistent with hyperglycemia (link here to cheatsheet?) DKA

What orders does the accepting nurse anticipate?

• Labs, ABGs, urinalysis, IV access (bilateral upper extremities, largest possible in case patient deteriorates). One lab, in particular, can give the provider an idea of the last 2-3 month BG average, the hemoglobin A1C.

The provider orders stat labs, urinalysis and ABGs then examines the patient. 

Why stat orders?

• This patient’s condition could deteriorate rapidly, and treatment should begin ASAP. Labs are needed to guide the plan of care. The nurse should watch for changes in the level of consciousness, respiratory changes, his response to potential fluid & electrolyte imbalances. Place on continuous cardiac monitoring as well.

Lab results are as follows:

WBC 15000 cells/mcL

Glucose 420 mg/dl

BUN 21 mg/dl

Creatinine 0.77 mg/dl

Anion gap 12

Glucose positive

Ketones positive

What do these results mean?

• CBC WBC 15000 cells/mcL – an immune response, possibly to viral illness or another issue HgbA1C 9% – indicates the average BG over the past 2-3 months has been about 212mg/dLBMP Glucose 420 mg/dl – hyperglycemia K 5.8 – electrolyte imbalance, can cause cardiac changes and need to monitor closely if IV insulin is started (will need frequent checks of this and BG) BUN 21 mg/dL – fluid imbalance Creatinine 0.77 mg/dL – normal but necessary to check for kidney function Anion gap 12 – indicative of DKAABG – metabolic acidosis Ph 7.25 HCO3 15 PaCo2 35 PaO2 88Urine – indicative of DKA Glucose positive Ketones positive

What medication orders should the nurse anticipate?

• IV fluids, insulin (either IV or SQ). NOTE: only REGULAR INSULIN can be given IV, and if it is, then IV dextrose and potassium chloride should be included in the insulin IV titration protocol/order). SQ insulin may be ordered using a sliding scale. O2 via NC possibly due to potential respiratory concerns (Kussmaul respirations)

The provider tells Michael and his mother that he suspects diabetic ketoacidosis which is not uncommon for new type I diabetics. He plans to transfer Michael to a nearby city via helicopter for a higher level of care.  The patient’s mother asks why he has to be transferred.

How does the nurse explain the transfer to the mother and patient?

• DKA requires monitoring in a critical care unit. Because of his age and new-onset DM, a higher level of care is recommended in order to have access to the best resources

The flight team arrives and assesses the patient. The ER completes a report using SBAR format at the bedside. The patient and his mother are given the chance to ask questions.

What are the transport team’s priorities as they move this patient?

• Airway, breathing, and circulation (ABC) status; Mental status; Volume status.

Upon arrival to the higher level of care, Michael is admitted to the ICU overnight. By the morning he is transferred to a pediatric floor for further observation. His mother remains at his bedside. They plan to return to their home after discharge. 

How should the pediatric medical unit prepare this family for discharge? What specific teaching should be provided?

• Condition-specific education is vital including DM management with medications, exercise, nutrition, psychosocial concerns, preventative care (i.e. vaccinations), parental/family involvement. A specialized diabetic educator and/or dietician would be ideal. Assessing their education preferences and literacy level is important as well. How to give insulin injections and check BG (glucometer use) are key takeaways (have patient and parent return-demonstrate). Case management may need to get involved for prescription/supplies. An endocrinologist may be consulted so education about his specialist is also important.

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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.

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• v.9(11); 2021 Nov

A case report: First presentation of diabetes mellitus type 1 with severe hyperosmolar hyperglycemic state in a 35‐month‐old girl

1 Division of Pediatric Intensive Care, Department of Pediatrics, Shiraz University of Medical Sciences, Shiraz Iran

Homa Ilkhanipoor

2 Division of Pediatric Metabolism and Endocrinology, Department of Pediatrics, Shiraz University of Medical Sciences, Shiraz Iran

Associated Data

All data generated or analyzed during this study are included in this published article.

Hyperglycemic hyperosmolar syndrome (HHS) is a rare complication of diabetes mellitus among pediatric patients. Since its treatment differs from diabetic ketoacidosis (DKA), hence, pediatricians should be aware of its diagnosis and management.

1. BACKGROUND

Hyperglycemic hyperosmolar syndrome (HHS), which is characterized by increased serum glucose concentrations and hyperosmolality with low or absence of ketonemia or ketonuria, has been rarely reported in children. Herein, we report a 35‐month‐old girl, who was newly diagnosed with diabetes mellitus type1 (T1DM), with presentation of HHS that developed some complications.

Hyperosmolar hyperglycemic state (HHS), a rare diabetic hyperglycemic emergency, is most often observed in adult patients, but seldom seen in pediatric patients. Nevertheless, it can present in younger adults and teenagers as the first presentation of diabetes mellitus type 2 (T2DM). 1

HHS is diagnosed by the following criteria: plasma glucose more than 600 mg/dl, venous pH > 7.25, serum bicarbonate >15 mmol/L, small amount of ketonuria or its absence, effective serum osmolality >320 mOsm/kg, and obtundation, combativeness, or seizures (in approximately 50% of all cases). 1 , 2

The incidence of HHS has merely been reported in 0.8–2% of all pediatric patients, 3 , 4 but it has a higher mortality rate in children compared to DKA (~10–35%). 5

Among the precipitating factors for HHS, the main one is infection which has to be diagnosed and treated immediately.

DKA mostly develops within hours of its onset, and the main presentations are as follows: hyperventilation, vomiting, and abdominal pain which force the parents to take their children to a physician. On the contrary, HHS develops over several days and presents itself later on. In this case, patients have polyuria and polydipsia for a longer period; hence, it might not be recognizable, and ultimately present itself with severe dehydration and electrolyte disturbance. It should be noted that the degree of dehydration, electrolyte, and metabolic disturbances are more severe.

Although in HHS there is substantial loss of electrolyte, and volume, the signs of dehydration are not recognizable, due to either obesity or hypertonicity. Hence, clinical assessment of dehydration becomes more difficult. Moreover, treatment of children with HHS differs from DKA; as in patients with HHS, intravascular volume should be replaced more and faster compared to DKA in order to avoid vascular collapse.

The recommendations in the treatment of HHS in pediatric patients are based on adult experiences. The first step is fluid therapy in order to expand intra‐ and extravascular fluid to preserve renal perfusion; hence, the rate of hydration becomes much faster than DKA. 1 , 2

Nonetheless, there are some HHS’ related complications that can be life‐threatening, such as vascular complications (eg, myocardial infarction, stroke, and peripheral arterial thrombosis), central nervous system complications (eg, seizures, cerebral edema, and central pontine myelinolysis (CPM)), which are uncommon, but described as HHS complications. 1 , 2

In this case report, a 3‐year‐old girl is presented with HHS who developed some complications.

2. CASE PRESENTATION

A previously healthy 35‐month‐old girl was brought to the emergency room of the Namazi hospital, Shiraz, Iran, due to reduced level of consciousness. She was well up to five days prior to her admission, after that she presented with dysuria and loss of appetite, and then developed polyuria, polydipsia, and weight loss (14 kg → 11 kg). There was no history of DM in her family.

On arrival, her height was measured 92 cm (25th−50th) percentile), she weighed 11 kg (5th–10th) percentile), and her Body Mass Index (BMI) (BMI‐for‐age) was at the 72nd percentile. Her vital signs were as follows: temperature: 38°C, heart rate (HR): 160, blood pressure (BP): 95/50, and her Glasgow coma scale (GCS) was 11/15. During her physical examination, capillary refilling time was more than 3 s with weak pulses. When checked with a capillary blood glucose meter, her glucose level was too high, so a serum glucose test was performed. Moreover, her first VBG was as follows: pH 7.26, PCO 2 : 32, PO 2 : 39, HCO 3 : 15.8, and BE: −12.6. Due to the decreased level of consciousness, brain CT scan was performed in which brain edema was reported.

As the first line of treatment, she was hydrated with normal saline (10 cc per kg), then the laboratory report revealed; blood sugar: 1124 mg/dl, BUN: 71 mg/dl, creatinine: 1.9 mg/dl, Na: 170 mEq/L (corrected Na: 186), and K: 5.1 mEq/L (effective osmolality was 402). Additionally, urine analysis was SG: 1.010, GLU: 3+, Ketone: trace. VBG after first hydration was as follows: pH: 7.27, PCO 2 : 34.8, and HCO 3 : 15.8. Based on the laboratory report; HHS was confirmed as diagnosis; hence, she was transferred to the Pediatric Intensive Care Unit (PICU).

On arrival at PICU, she developed generalized convulsion, and her GCS declined to less than 8; so she was intubated.

She was hydrated with normal saline again; then, the intravenous fluid was administered with 15 percent deficit and maintenance of fluid in addition to urine output replacement. Due to brain edema, deficit was given over 72 h, but according to urine output and serum sodium level, the amount of deficit increased up to 18 percent, and the sodium content of IV fluid decreased.

The first sodium level reported in PICU was 185 mEq/L, but it gradually decreased as hydration continued, and the amount of fluid increased (with the target level of 10 mEq/L decrease per day); then, it became stable around 145 mEq/L over the next five days. Our primary goal in her treatment was to correct sodium level maximum 10 mEq/L per day, to decrease osmolality maximum 3–5 mosm/L/h, and to reduce blood sugar maximum 75 mg/dl per hour.

On the 3rd day, HHS was resolved, but the patient became febrile, and the amount of endotracheal tube (ETT) secretion increased. The culture of ETT secretions revealed candida non‐albicans and pseudomonas aeruginosa; hence, antibiotic was prescribed. Subsequently, the patient developed hypotension, so inotrope was initiated. On the same day, her blood creatine phosphokinase (CPK) increased to 6400 IU/L, and it reached 13,400 on the fifth day. Then, she developed hemoglobinuria; thereafter, hydration continued until the CPK level returned normal level on the 18th day (Table  1 ).

Laboratory findings

Although enoxaparin was initiated for deep venous thrombosis (DVT) prophylaxis, she presented with the left forearm and hand swelling, on the 6th day. Doppler ultrasonography revealed thrombosis of the distal part of the brachial artery, so the therapeutic dose was initiated. Consequently, her conditions improved after 2 days, and a week later, Doppler sonography was normal.

On the 9th day, she was weaned off the ventilator, and on the 21st day, the patient was discharged from hospital without any sequela.

3. DISCUSSION AND CONCLUSIONS

Hyperglycemic hyperosmolar syndrome (HHS) is a rare presentation of DM in pediatric patients, especially as the first presentation of T1DM, with a high mortality rate. HHS is not easy to diagnose according to physical examination, patient's past medical history or even with availability of laboratory data. However, physicians do not need to be too concerned of HHS in young children, especially if the patient is not obese. 5

Contrary to the frequent symptoms of DKA, such as vomiting, abdominal pain, and drowsiness that force parents to refer to a hospital, the gradual increase of HHS symptoms can cause delayed referral which can ultimately result in severe dehydration and electrolyte imbalance. As a result, proper diagnosis can lead to appropriate management.

HHS generally occurs among obese people and in T2DM, 6 but there are some rare reports on HHS in non‐obese patients and HHS in T1DM. 7 It should be noted that our patient had a normal BMI and T1DM.

Fluid deficits in HHS patients are frequently 12–15% that has to be corrected gradually and uniformly over 24–48 h, but it can be increased up to 20% or more to gradually decline serum sodium and osmolality. 1 , 2

At present time, there is no standard therapeutic guideline for HHS in children. Nonetheless, the two most important points in HHS management are fluid replacement, and gradually reduction of serum osmolality and sodium level. Fluid replacement in children with HHS should be carried out more swiftly with more amount of fluid in comparison with children with DKA. To gradually reduction of hypernatremia, we constantly measured her serum sodium level in order to adjust fluid sodium concentration. Due to the presence of brain edema, reaching the aforementioned goals became more difficult and required more attention.

The insulin infusion strategy might differ from insulin infusion rate, which is 0.1 unit/kg/h in patients with DKA, whereas it should be 0.025–0.05 unit/kg/h in patients with HHS. 1 Our patient was first diagnosed with DKA and treated as DKA in the emergency room; she was hydrated with 10 cc/kg normal saline, and deficit volume was estimated 10%; Insulin treatment was initiated, but after 3 h sodium level increased to 185 mEq/L. According to HHS protocol in PICU, insulin infusion was stopped and the patient hydrated up to 40 cc/kg with normal saline till the patient's hemodynamic became stable. Then, after the initial rehydration, insulin infusion was initiated with 0.03 units per kg per hour, and after 8 h, the sodium content of IV fluid was steadily reduced to 100 mEq/L.

Initially, the degree of dehydration was estimated 15%, but according to serum osmolality, serum sodium, and urine out, the percentage of deficit had increased to 18%.

There are some serious complications in HHS, for example, brain edema, arterial and venous thrombosis, and rhabdomyolysis. 8 In our patient, the complications were brain edema, rhabdomyolysis, and arterial thrombosis (distal part of brachial artery). The patients with HHS are at risk of venous thrombosis, especially those who are immobile more than 48 h, and for those who central venous catheter is inserted. 1 , 8 Although at the beginning of PICU admission we started enoxaparin for prophylaxis, she presented arterial thrombosis.

Altered level of consciousness is commonly seen in adult patients with osmolality more than 330 mOsm/kg, but brain edema rarely occurs in HHS. 1 , 9 At the time of admission, our patient's level of consciousness was low, which was due to high osmolality and brain edema (it was diagnosed clinically, and confirmed by brain CT scan). She also developed generalized convulsion; hence, she was intubated. Our goal was to gradually decrease serum osmolality and to administer fluids over a 72‐h period. Based on serum osmolality, urine out, and sodium level, we increased the amount of fluid. Moreover, neuroprotection was started for her (head of bed elevation 30‐degree, mannitol 20%, assuring adequate oxygenation by saturations >90%, avoiding hypercapnia by PaCO 2 between 34 and 38, and appropriate mean arterial pressure (MAP) to maintain adequate cerebral perfusion pressure in the range of 50–70, and aggressive fever control). 9

Deficit of potassium, magnesium, and phosphate in HHS is much greater than DKA. In our patient, on the 4th day of admission, serum phosphate decreased to 0.75 mg/dl.

In the previous studies, mortality rate has been reported up to 35% depending on the severity of dehydration, hyperosmolality, and patient's age. 5 However, by following the aforementioned therapeutic procedures, our patient was cured without any sequelae.

HHS is a rare complication of DM among pediatric patients, but with more complications and poorer outcome. Hence, pediatrician should be well aware of its presentations and signs for a timely diagnosis and treatment.

CONFLICT OF INTERESTS

The authors declare that they have no competing interests.

AUTHOR CONTRIBUTIONS

AS designed the study and wrote the manuscript, in addition to data collection as well as submitting the manuscript. HI was the scientific consultant. AS and HI edited the manuscript collectively. Both authors discussed the results and contributed to the final manuscript.

ETHICAL APPROVAL

This study was approved by the local ethics committee of Shiraz University of Medical sciences with approval ID: IR.sums.med.rec.1398.134. Written informed consent was obtained from patient's parents and delivered to the ethics committee.

Written informed consent was obtained from the parents of the patient for publication purposes of this case report and any accompanying images. A copy of the written consent is available for review by the Chief Editor of the Journal.

ACKNOWLEDGEMENTS

The authors are grateful to the PICU nurses who were involved in the care of this patient, and they also would like to thank Dr. H. Argasi at the RT Publication for his invaluable assistance in editing this manuscript.

Saeed A, Ilkhanipoor H. A case report: First presentation of diabetes mellitus type 1 with severe hyperosmolar hyperglycemic state in a 35‐month‐old girl . Clin Case Rep . 2021; 9 :e04984. 10.1002/ccr3.4984 [ PMC free article ] [ PubMed ] [ CrossRef ] [ Google Scholar ]

The authors have not declared a specific grant for this research from any funding agency in the public, commercial or none‐profit sectors

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Clinical pearls, case study: symptoms in a diabetes client: type 1, type 2, or type 1.5.

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Judy Friesen; Case Study: Symptoms in a Diabetes Client: Type 1, Type 2, or Type 1.5?. Clin Diabetes 1 April 2003; 21 (2): 93–94. https://doi.org/10.2337/diaclin.21.2.93

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W.G. is a 41-year-old white man who was diagnosed with diabetes 15 months ago. He is now beginning diabetes education and medical nutrition therapy (MNT) to gain weight upon referral from his primary care physician. His most recent hemoglobin A1c (A1C) was 5.0%. His current diabetes medication is metformin (Glucophage), 500 mg with breakfast, and he was started on pioglitazone (Actos) 2 weeks ago. He takes no other medications; denies smoking, alcohol, and drug use; and knows of no health problems other than diabetes.

His history revealed a blood glucose level >500 mg/dl at the time of diagnosis, with negative ketones. He checked ketones occasionally in the first year of diabetes, and all tests were negative. His mother had diabetes and was on insulin. He reports that he was on glimepiride (Amaryl) during the first year of diabetes, but that it was discontinued when he was started on metformin.

He complains of frequent urination, hunger, and thirst, which leads to drinking more than 1 gallon of water daily. He is very concerned because he is often agitated, anxious, and impatient to the point that it is affecting his family and work life. He was employed as a technician but is on leave until he feels better. His physician prescribed alprazolam (Xanax) for anxiety, but he did not fill the prescription.

Physical assessment reveals a height of 74 inches, weight of 174 lb, and body mass index of 22 kg/m 2 . He reports a 35-lb weight loss over the past 15 months of diabetes, including a recent 10-lb weight loss resulting in the referral for MNT.

W.G. reports that his doctor has prescribed a 2,500-calorie daily meal plan. He includes no fruits and no sweets in his diet and has small snacks between meals. He eats a moderate breakfast and lunch and a bigger dinner before his exercise in the evening. He reports that he is not currently able to maintain his usual 1.5 hours per day of lifting weights and playing basketball because of fatigue and lack of energy. Instead, he is exercising in short intervals as he can tolerate. He also reports symptoms of hypoglycemia but has not checked his blood glucose.

Why is this patient losing weight?

Does this patient have type 1 or type 2 diabetes, and does it make a difference in his treatment?

Are other interventions needed considering his symptoms and most recent A1C?

Nutrition assessment revealed that W.G. was eating ∼1,800 calories daily rather than 2,500 calories, as prescribed. He had a good appetite but appeared to be controlling his blood glucose by exercising and eating less than his energy requirement. An 1,800-calorie meal plan would result in weight loss of 1 lb per week for a man of his height, weight, and activity level.

W.G.’s records from self-monitoring of blood glucose (SMBG) showed an average fasting blood glucose of 118 mg/dl, which is consistent with his A1C result of 5.0%. Previous A1Cs were 5.1 and 5.6%.

His classic diabetes symptoms of polyuria, polyphagia, and polydipsia indicated that diabetes education and MNT were not adequate diabetes care for this patient. His physician readily provided a referral to an endocrinologist/diabetologist. A new treatment plan would need to address nutrition, exercise, and medications.

MNT for W.G. began with an increase to 3,000 calories daily to gain weight and to observe the effect of adequate calories on his blood glucose before his appointment with the diabetologist. He was willing to increase his calories but needed education on meal planning. He was educated about calorie points for a 3,000-calorie daily meal plan. One calorie point equals 75 calories, so his 40 daily calorie points were distributed into meals and snacks and based on healthy eating guidelines for diabetes. The meal plan was individualized based on his usual food and eating habits. 1 His SMBG results with the 3,000-calorie meal plan showed a postprandial glucose average of 150 mg/dl and a fasting glucose average of 135 mg/dl.

Medication options included increasing the dosages of his current medications, adding new oral medications, or using a combination of oral agents and insulin. W.G. was quite willing to start insulin. Because of his marked symptoms and in light of this willingness, the diabetologist at his first visit discontinued his oral medications and initiated insulin therapy. Insulin was adjusted daily during the first week, and the regimen that allowed for normal blood glucose without hypoglycemia was 10 units of glargine (Lantus) at 10:00 p.m. daily and 4 units of aspart (Novolog) with each meal.

W.G.’s education also included exercise recommendations, including safety issues such as how to recognize and treat hypoglycemia.

Laboratory tests were ordered during his first visit to the diabetologist. Because abnormal thyroid function can affect weight and anxiety, a thyroid-stimulating hormone reading TSH was ordered, with results in the normal range. A fructosamine measurement, which reflects glycemic control over the previous 3–4 weeks, was also in the normal range. Fasting C-peptide, which is a measure of insulin secretion, was 2.5 ng/ml (normal: 1.1–4.0 ng/ml) and islet cell antibodies were 10 JDF units (normal: 0–4.9 JDF units). The basic metabolic profile results were within normal range.

At a follow-up visit 4 months after insulin initiation, W.G. had gained 5 lb, felt more energetic and less anxious, was exercising, and had A1C results of 6.1%. Based on his SMBG results showing occasional hyperglycemia, his insulin was increased to 11 units of glargine at 10:00 p.m. daily and 5 units of aspart with each meal, which is 1/3 unit/kg of body weight. He was advised to continue following a 3,000-calorie daily meal plan, adjusted with exercise.

Recent research has identified a slowly progressive autoimmune diabetes in adult patients. Known as latent autoimmune diabetes of adulthood (LADA) or type 1.5 diabetes, 2 it is a slowly progressive form of type 1 diabetes. 3 After months to years, affected individuals become increasingly insulin-dependent. This type of diabetes could be the explanation for W.G.’s symptoms and progression of disease. He may have been preventing more severe hyperglycemia by exercising and restricting calories, but this also resulted in weight loss. His A1C and fructosamine results may have been surprisingly low because of his frequent hypoglycemic episodes.

Diabetes management should be based on more than A1C results if the results do not fit with the rest of the clinical picture. In this case, symptoms were the clue to the patient’s actual condition and indicated the need for treatment.

In the presence of frequent hypoglycemia, A1C levels may not accurately reflect the level of hyperglycemia present.

Nutrition, medications, and exercise must each be assessed and addressed individually in diabetes management.

Insulin initiation may be more acceptable to patients than some health professionals believe. 4  

Judy Friesen, RD, LD, FADA, CDE, is a diabetes educator at the Diabetes Treatment and Research Center of Via Christi Regional Medical Center in Wichita, Kans.

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