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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

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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.

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Diabetic Ketoacidosis (DKA) Case Study (45 min)

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Mr. Logan is a 32-year-old male with a history of DM Type I. He presented to the Emergency Department (ED) after being found by his family with decreased LOC, rapid heavy breathing, and fruity breath. His family reports flu-like symptoms for the last few days.

Before even gathering further information - what do you think is going on? Why?

Diabetic Ketoacidosis – he is a Type I Diabetic with heavy breathing (Kussmaul Respirations) and fruity breath. These are classic signs. It’s important to recognize them and immediately begin anticipating the patient’s needs.

What diagnostic or lab tests would you expect the provider to order?

• Complete metabolic panel to check serum glucose, anion gap, potassium, etc.
• Arterial Blood Gas to assess for acidosis
• Urinalysis to look for ketones

The nurse draws a Complete Metabolic Panel and notifies the Respiratory Therapist to obtain an Arterial Blood Gas. Upon further assessment, the patient is oriented x 2 and drowsy. He is breathing heavily. Lungs are clear to auscultation, S1/S2 present, bowel sounds active, pulses present and palpable x 4 extremities. A POC glucose reads >450 (meter max).

Vital signs are as follows: HR 87 RR 32 BP 123/77 SpO 2 96%

Mr. Logan’s labs result and show the following: Glucose 804 mg/dL K 6.1 mEq/L BUN 39 mg/dL pH 7.12 Cr 1.9  mg/dL pCO 2 30 Anion Gap 29 mEq/L HCO 3 – 17 Urine = Positive for Ketones

Using these lab results, explain what is going on physiologically with Mr. Logan.

• His glucose is extremely high and he is positive for ketones, which says that his body is having to break down fatty acids to make energy
• His anion gap is high, meaning there are other “ions” in the system besides the electrolytes – in this case, the extra acids are creating this ‘gap’
• He is in metabolic acidosis because of the ketoacids – this is what’s causing the Kussmaul respirations – his body is trying to breathe off CO2 to bring his pH up
• His potassium is high because the body will kick potassium out of the cells to compensate for an acidotic state. This way instead of having H+ (acids) in the blood stream, we have K+ – this protects many tissues, but puts our heart at risk
• His BUN/Cr are elevated because of the dehydration caused by osmotic diuresis (caused by hyperglycemia and hyperosmolarity)

What is the #1 priority for Mr. Logan at this time?

• The #1 priority for DKA is to get the blood sugar down and get insulin into the system. Getting insulin into the system allows the gluconeogenesis to STOP (so that the body will STOP making ketoacids and start using the glucose it has).
• The #2 priority is fluid replacement due to severe dehydration from osmotic diuresis

The provider writes an order for an Insulin Lispro infusion IV, titrating to decrease blood glucose per protocol, 1L NS bolus NOW, and a continuous infusion of Normal Saline IV at 250 mL/hr, and to change the fluids to D5 ½ NS at 125 mL/hr once the blood glucose level falls below 250 mg/dL.

What is the first action you should take after receiving these orders?

Remind the provider that the only insulin that can be given IV is Regular Insulin and request that he change the order. Call the Pharmacist if you have to

• **Note – most facilities have a computerized ordering that prevents something like this from happening, but it’s important that you know this!!

The provider adjusts the order to Regular Insulin IV infusion.  Orders are also written for hourly POC glucose checks and a q2h BMP.

Why is it important to check a BMP frequently? What are we monitoring for?

• Frequent BMP’s are important to confirm the blood glucose when the POC meter is just reading MAX.  
• It’s also important to monitor the Anion Gap to see when it “closes” – indicating resolution of the acidosis
• We are also monitoring potassium levels. They will start elevated, but insulin drives potassium into the cells – causing it to decrease rapidly.

After 4 hours and another 1L bolus of NS, Mr. Logan’s blood glucose level has dropped to 174 mg/dL, but his anion gap is still 19. The nurse changes his fluids to D5 ½ NS per the order and continues the insulin infusion. The most recent BMP showed a K of 3.7, down from 6.1, so the provider orders to give 40 mEq of KCl PO.

Why is the insulin continued even after the blood glucose decreases?

• The goal is to stop gluconeogenesis and reverse the acidosis. The glucose may fall rapidly while there are still ketoacids being made.
• By giving D5 ½ NS infusion with the insulin, we can continue to bring down the acidosis process while maintaining safe blood sugars.

After another 4 hours, Mr. Logan’s anion gap is now 12, a repeat ABG shows a pH of 7.36 with normal CO 2 and HCO 3 – levels.  The nurse begins to transition Mr. Logan off of the IV infusion to SubQ insulin per protocol.  He is feeling much better and says he’s embarrassed that he had to be brought to the hospital.  

What education can you provide Mr. Logan to help him understand why this happened and how to prevent it from recurring in the future?

• When you are ill, you should check your blood sugar more often as sometimes the body’s healing processes and stress response can make your sugar go higher than normal
• Notify your provider if you’re ill, they may recommend increasing your long-acting insulin
• Notify your provider or go to the ED at the FIRST indication of DKA – fruity breath, heavy breathing, feeling dry and hot, excessive urination, blurry vision, or a blood glucose over 400 mg/dL or over your meter MAX.  
• If you have an insulin pump, make sure it is working appropriately – if not, notify your provider or turn the pump OFF and switch to SubQ insulin until the pump can be fixed
• **Note – if a patient comes in with an insulin pump, it should always be turned OFF – we will manage their sugars with SubQ insulin and don’t want them to receive a double dose.

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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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Diabetic ketoacidosis

On this page, when to see a doctor, risk factors, complications.

Diabetic ketoacidosis is a serious complication of diabetes.

The condition develops when the body can't produce enough insulin. Insulin plays a key role in helping sugar — a major source of energy for muscles and other tissues — enter cells in the body.

Without enough insulin, the body begins to break down fat as fuel. This causes a buildup of acids in the bloodstream called ketones. If it's left untreated, the buildup can lead to diabetic ketoacidosis.

If you have diabetes or you're at risk of diabetes, learn the warning signs of diabetic ketoacidosis and when to seek emergency care.

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Diabetic ketoacidosis symptoms often come on quickly, sometimes within 24 hours. For some, these symptoms may be the first sign of having diabetes. Symptoms might include:

• Being very thirsty
• Urinating often
• Feeling a need to throw up and throwing up
• Having stomach pain
• Being weak or tired
• Being short of breath
• Having fruity-scented breath
• Being confused

More-certain signs of diabetic ketoacidosis — which can show up in home blood and urine test kits — include:

• High blood sugar level
• High ketone levels in urine

If you feel ill or stressed or you've had a recent illness or injury, check your blood sugar level often. You might also try a urine ketone test kit you can get at a drugstore.

Contact your health care provider right away if:

• You're throwing up and can't keep down food or liquid
• Your blood sugar level is higher than your target range and doesn't respond to home treatment
• Your urine ketone level is moderate or high

Seek emergency care if:

• Your blood sugar level is higher than 300 milligrams per deciliter (mg/dL), or 16.7 millimoles per liter (mmol/L) for more than one test.
• You have ketones in your urine and can't reach your health care provider for advice.
• You have many symptoms of diabetic ketoacidosis. These include excessive thirst, frequent urination, nausea and vomiting, stomach pain, weakness or fatigue, shortness of breath, fruity-scented breath, and confusion.

Remember, untreated diabetic ketoacidosis can lead to death.

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Sugar is a main source of energy for the cells that make up muscles and other tissues. Insulin helps sugar enter the cells in the body.

Without enough insulin, the body can't use sugar to make the energy it needs. This causes the release of hormones that break down fat for the body to use as fuel. This also produces acids known as ketones. Ketones build up in the blood and eventually spill over into the urine.

Diabetic ketoacidosis usually happens after:

• An illness. An infection or other illness can cause the body to make higher levels of certain hormones, such as adrenaline or cortisol. These hormones work against the effects of insulin and sometimes cause diabetic ketoacidosis. Pneumonia and urinary tract infections are common illnesses that can lead to diabetic ketoacidosis.
• A problem with insulin therapy. Missed insulin treatments can leave too little insulin in the body. Not enough insulin therapy or an insulin pump that doesn't work right also can leave too little insulin in the body. Any of these problems can lead to diabetic ketoacidosis.

Other things that can lead to diabetic ketoacidosis include:

• Physical or emotional trauma
• Heart attack or stroke
• Pancreatitis
• Alcohol or drug misuse, particularly cocaine
• Certain medicines, such as corticosteroids and some diuretics

The risk of diabetic ketoacidosis is highest if you:

• Have type 1 diabetes
• Often miss insulin doses

Sometimes, diabetic ketoacidosis can occur with type 2 diabetes. In some cases, diabetic ketoacidosis may be the first sign of having diabetes.

Diabetic ketoacidosis is treated with fluids, electrolytes — such as sodium, potassium and chloride — and insulin. Perhaps surprisingly, the most common complications of diabetic ketoacidosis are related to this lifesaving treatment.

Possible complications of the treatments

Treatment complications include:

• Low blood sugar, also known as hypoglycemia. Insulin allows sugar to enter cells. This causes the blood sugar level to drop. If the blood sugar level drops too quickly, the drop can lead to low blood sugar.
• Low potassium, also known as hypokalemia. The fluids and insulin used to treat diabetic ketoacidosis can cause the potassium level to drop too low. A low potassium level can affect the heart, muscles and nerves. To avoid this, potassium and other minerals are usually given with fluid replacement as part of the treatment of diabetic ketoacidosis.
• Swelling in the brain, also known as cerebral edema. Adjusting the blood sugar level too quickly can cause the brain to swell. This appears to be more common in children, especially those with newly diagnosed diabetes.

Untreated, diabetic ketoacidosis can lead to loss of consciousness and, eventually, death.

There are many ways to prevent diabetic ketoacidosis and other diabetes complications.

• Manage your diabetes. Make healthy eating and physical activity part of your daily routine. Take diabetes medicines or insulin as directed.
• Monitor your blood sugar level. You might need to check and record your blood sugar level at least 3 to 4 times a day, or more often if you're ill or stressed. Careful monitoring is the only way to make sure that your blood sugar level stays within your target range.
• Adjust your insulin dosage as needed. Talk to your health care provider or diabetes educator about how to make your insulin dosage work for you. Consider factors such as your blood sugar level, what you eat, how active you are, and whether you're ill. If your blood sugar level begins to rise, follow your diabetes treatment plan to return your blood sugar level to your target range.
• Check your ketone level. When you're ill or stressed, test your urine for excess ketones with a urine ketones test kit. You can buy test kits at a drugstore. If your ketone level is moderate or high, contact your health care provider right away or seek emergency care. If you have low levels of ketones, you may need to take more insulin.
• Be prepared to act quickly. If you think you have diabetic ketoacidosis because your blood sugar is high and you have too many ketones in your urine, seek emergency care.

Diabetes complications are scary. But don't let fear keep you from taking good care of yourself. Follow your diabetes treatment plan carefully. Ask your diabetes treatment team for help when you need it.

Oct 06, 2022

• DKA (ketoacidosis) and ketones. American Diabetes Association. https://diabetes.org/diabetes/dka-ketoacidosis-ketones. Accessed Sept. 17, 2022.
• Diabetic ketoacidosis (DKA). Merck Manual Professional Version. https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/diabetes-mellitus-and-disorders-of-carbohydrate-metabolism/diabetic-ketoacidosis-dka?query=Diabetic ketoacidosis (DKA). Accessed Sept. 17, 2022.
• Hirsch IB, et al. Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis. https://www.uptodate.com/contents/search. Accessed Sept. 17, 2022.
• Hirsch IB, et al. Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment. https://www.uptodate.com/contents/search. Accessed Sept. 17, 2022.
• Ferri FF. Diabetic ketoacidosis. In: Ferri's Clinical Advisor 2023. Elsevier; 2023. https://www.clinicalkey.com. Accessed Sept. 17, 2022.
• Evans K. Diabetic ketoacidosis: Update on management. Clinical Medicine. 2019; doi:10.7861/clinmed.2019-0284.
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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. 

May contain information that is not supported by performance and intended use claims of Radiometer's products. See also Legal info .

has a master's degree in medical biochemistry and he has twenty years experience of work in clinical laboratories.

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• v.9(5); 2017 May

Diabetic Ketoacidosis: An Emergency Medicine Simulation Scenario

Reuben addison.

1 Human Kinetics and Recreation, Memorial University of Newfoundland

Tate Skinner

2 Biochemistry Nutrition, Memorial University of Newfoundland

3 Medical Education, Memorial University of Newfoundland

Michael Parsons

4 Emergency Medicine, Memorial University of Newfoundland

Simulation provides a safe environment where learning is enhanced through the deliberate practice of skills and controlled management of a variety of clinical encounters. This is particularly important for core cases and low-frequency, high-stakes procedures and encounters. Competency-based medical education has seen widespread adoption in the field along with ongoing work in the areas of undergraduate and postgraduate training. Similarly, effective professional development activities stand to benefit greatly from a more stringent integration of simulation and competency-based approaches. This particularly makes sense when considering the goals of patient safety and achievement of optimal clinical outcomes. The current report describes a simulation training session designed to acquaint emergency medicine residents with the presentation and management of diabetic ketoacidosis (DKA) through the use of simulation.

Introduction

Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus, most commonly occurring in patients with type I diabetes. As individuals with uncontrolled type I diabetes develop an insulin deficiency, the cells in their body are unable to utilize glucose properly to meet their energy demands. In response, the body begins to metabolize other nutrients (fat, proteins, glycogen) to prevent starvation. As a result of these metabolic pathways, acidic ketones are produced leading to metabolic acidosis that is characteristic of DKA. Some typical presenting symptoms include dehydration and altered mental status [ 1 - 3 ].

Roughly 30% of children with type 1 diabetes present with DKA at the time of their diagnosis [ 4 ]. DKA is the most common cause of hospitalization and mortality in children with type I diabetes, occurring in 1% to 10% of patients per year [ 5 - 6 ]. Initial presentation at a later age is less common and presenting symptoms can be confused with a variety of other conditions. Given the frequency with which diabetic patients present with DKA and the severe consequences if left untreated, it is vital that emergency department (ED) physicians are familiar with the presentation and management of this condition. The reader should keep in mind that the management of DKA in the pediatric population requires particular caution due to the risk of cerebral edema. This technical report describes a simulation teaching session on DKA that is designed for a cohort of post-graduate emergency medicine trainees. The objective of this case is to provide learners with the following knowledge/skills:

Objective 1: Assess the patient with an undifferentiated altered level of consciousness (LOC) - relevant to the CanMEDS Medical Expert role.

Objective 2: Diagnose and treat DKA - relevant to the CanMEDS Medical Expert role.

Objective 3: Demonstrate effective communication skills for team interactions and conflict management - relevant to the CanMEDS communicator, collaborator, and professional roles.

Simulation has developed as an important tool to complement traditional teaching methods. The traditional “see one, do one, teach one” approach has fallen out of favor. A transition to a more rigorous competency-based education and assessment system is well under way, with an increased focus on patient safety and quality assurance as they are important drivers of this change. Grant, et al. [ 7 ] provide a succinct review of the evolution and advancement of simulation to its current role and highlight its importance in medical education. They cite evidence to support the use of the safe and controlled environment of simulation. They also highlight its benefits in learning different skills from procedural tasks to more team-based and interpersonal skills. Simulation integrated with traditional teaching methods serves to supplement and enhance learning. In our program, we broadly work from the Kolb’s learning cycle framework [ 8 ]. We strive to create a “safe” learning environment where learners are active participants [ 9 ]. We do our best to optimize fidelity of the cases and enhance the emotional engagement of learners – aiming for a balance of “activation” and a “pleasant” experience as depicted in the circumplex model of affect [ 10 - 11 ]. 

Technical report

A 19-year-old male presented to the ED with decreased LOC. The patient was found in his dorm room in the morning. An ambulance was called and the patient was transported to the hospital. Few historical details are available as the patient is from another province. Aside from that, he may have consumed some alcohol the previous night. The patient did attest he has no known past medical history. His family is not present with him and the emergency medical services (EMS) crew has departed. The patient is drowsy, but responsive (depending on the level of case difficulty chosen) and has some dried vomit on his clothing. The patient has just arrived in the ED and no interventions have yet been performed. There is a single nurse confederate to help with the case.

The Context, Input, Process, Product (CIPP) model is applied below to give a clear overview of the current case design and to demonstrate how to modify the case to meet the needs of various learners [ 12 ].

The case details can be adjusted to accommodate the available physical space, learners, modality, and the use of confederates. The case can be performed in a variety of settings including in-situ in the ED, clinic, or hospital ward. It can also be conducted in a simulation lab setting. The "difficulty" level can be easily modified to meet the needs of a variety of learners by adjusting case inputs, as outlined below in Table ​ Table1 1 .

The advantages of a high-fidelity simulator can also be leveraged by utilizing standardized patients (SP) to fill the role of patients, nurses, and confederates to improve realism. A hybrid setup is sometimes applied during the scenario to include the challenge of performing procedures such as central line placement.

See Table ​ Table2 2 below.

A pre-briefing session is conducted prior to the start of the simulation scenario. The main goal is to establish a safe learning environment for the learner [ 9 , 13 ]. The “fiction contract” is reviewed, addressing the limitations and ‘believability’ of the simulation scenario. The “basic assumption” – that everyone is present for the purpose of learning and are viewed as intelligent, capable individuals who will try their best  – is reviewed. The evaluative nature of the session, if any, is made clear from the beginning. Learners are provided with an introductory simulation lecture and an opportunity to become familiar with the simulation lab and equipment prior to the session, usually at the beginning of the academic year.

This case was designed by the ED faculty and follows a standard format provided by a simulation lab. Most cases are based on true ED patient encounters and scenarios are written along a spectrum ranging from common cases to low-frequency, high-stakes encounters.

Following the pre-briefing, residents are directed to the simulation room and provided with the “pre-scenario” information as seen in Table ​ Table3. 3 . The nurse may add the following (passed along from the paramedic): “The patient was found on the bed, fully clothed, and very drowsy. Little is known about the patient and nothing about his medical history. His family doesn’t live in the province”.

AMPLE: Allergies, Medications, Past medical history, Last eaten, Events leading; BHB: beta-hydroxybutyrate; BP: blood pressure; CBC: complete blood count; DDx: differential diagnosis; EMS: emergency medical services; FHx: family history; GAEB: good air entry bilaterally; HEENT: head, eyes, ears, nose, throat; ICU: intensive care unit; IV NS: intravenous normal saline; HR: heart rate; LBC: lytes, BUN, creatinine; LFT: liver function tests; LOC: level of consciousness; MM: mucous membrane; NKDA: no known drug allergies; PMHx: past medical history; RR: respiratory rate; T: temperature; VBG: venous blood gas

Once in the room, the students are expected to assign roles and function as a team to diagnose and treat the patient appropriately. Using available resources including the attending SP nurse, ED triage sheet, EMS record, and interaction with the patient and their family, the student will gather key information. The team lead can utilize the skills of other learners to help complete tasks. Additional help, such as specialist backup, may be requested but is often not available. Monitors and intravenous (IV) are usually not established at the beginning of the case and learners will have to request these. A full set of vitals may not be provided up front and the student must recognize this. Early interventions and investigations should be initiated (as appropriate to the case) including fluid bolus, request for electrocardiogram (ECG), blood work, and x-ray (Figures ​ (Figures1 1 - ​ -2) 2 ) (Table ​ (Table4 4 ).

BHB: beta-hydroxybutyrate; CBC: complete blood count; eGFR: estimated glomerular filtration rate; Hct: hematocrit; Hgb: hemoglobin; LBC: lytes, BUN, creatinine; MCV: mean corpuscular volume; OSM: osmolality; VBG: venous blood gas

With an initial assessment and complete set of vitals, the learner should go through a general approach to the patient with an altered LOC and develop/verbalize an appropriate differential and treatment plan, thus meeting the requirement for Objective 1. A standard approach to primary assessment is expected. The Airway, Breathing, Circulation (ABC)-IV-O2-Monitor is generally a good start. Abnormal vitals should be addressed at this stage. The initial ECG showed tachycardia, peaked T-waves and QRS widening (Figure ​ (Figure1). 1 ). The learner should consider the differential of this finding and verbalize concern of hyperkalemia.

As labs and investigations are available, the student should consolidate the information and proceed with a more directed treatment of DKA and its associated complications to meet Objective 2. Fluid deficits should be corrected and specific treatments to address metabolic abnormalities should be initiated. Insulin infusion should be initiated and particular attention should be paid to electrolyte abnormalities, particularly potassium and the acid-base status of the patient. Triggers for the onset of DKA should be explored and addressed. Complications including dysrhythmias should be treated appropriately. Depending on the level of case difficulty chosen for the scenario, more advanced procedures such as intubation or central line placement may be integrated through the use of hybrid setups or the high-fidelity mannequin.

Integration of SP confederates helps to satisfy Objective 3 which focuses on the CanMEDS roles of communicator, collaborator, and professional. The SP nurse may be scripted to add challenges to the case to help highlight these roles. Alternatively, an SP family member can play roles ranging from a quiet/concerned parent to a loud and disruptive individual, challenging the student to direct attention and resources to deal with both the patient and the extenuating circumstances.

Table ​ Table1 1 provides suggestions for a number of input modifiers that can be used for any scenario involving high fidelity or SP (including the current case) to adjust the case difficulty by dialing up or down the “signal-to-noise” ratio, depending on the needs of the learner. Table 3 outlines the general flow of the current case.

Two faculty members are generally involved in running the scenario. One directs the changes in vitals, provides prompts and acts as the “voice” of the patient when the high-fidelity mannequin is used. This individual also communicates with the SP nurse, providing direction in the case. The second faculty member is responsible for following the temporal flow of the case and taking notes of key events for the review during the debriefing session. Particular attention is given to the pre-determined objectives.

Debriefing is centered around the key objectives of the case and uses the advocacy-inquiry approach, focusing on the three phases as described by Rudolph, et al. [ 9 , 14 ]. This portion of the session is generally longer in duration than the simulation itself and provides the opportunity for review and discussion in a small group setting. Faculty and residents who were involved in the session are present and simulated patients are also invited to give their feedback. Depending on case outcomes and progression, additional points may be selected for clarification and discussion. Particular points of interest that instructors may wish to discuss include rapid primary assessment and early intervention in the sick, undifferentiated patient. Failure to obtain a full set of vitals occasionally leads to delayed diagnosis and is more likely to happen with a junior learner. The importance of addressing abnormal vitals before a definitive diagnosis is discussed. Inability to obtain much history from the patient should prompt a further search in common areas such as online medical records, medical bracelets, and subtle contact information available from the patient’s wallet. Once the diagnosis of DKA is made, directed treatment should be established along with a definitive plan. Specific interventions and plans for disposition should be clear. Clear communication with team members, the patient, and their family is essential for the smooth progress of the case.

Post-Scenario Didactics

Post-scenario didactics are integrated into the debriefing session and focus on the key objectives of the session. The general goal is to discuss the approach and early management of the altered LOC patient. As mentioned above, the emphasis is placed on abnormal vitals and “what the patient needs at this point”, as opposed to making a final diagnosis before initiating treatment. ABC IV-O2-Monitor can help during the first encounter with the patient and a number of mnemonics have been used to help generate a differential diagnosis list. Learners are encouraged to take a practical approach by collecting full vitals and pertinent facts to help guide further actions. Overall, the treatment of DKA is reviewed in some detail. Additional focus is placed on the sicker patient with an altered LOC, acidosis, and profound electrolyte abnormalities, often with key ECG findings. The treatment of patients of different age groups is compared and reviewed with particular attention to insulin and fluid administration.

The non-medical expert CanMEDS roles are discussed, emphasizing them as a key part of effective team function. In general, this discussion reviews clear, concise, closed-loop communication and integrates references to difficulties or challenges that may have arisen during the case. As a general rule, a more experienced learner will demonstrate greater proficiency in these areas; however, it is important to include these challenges as it will help identify areas of improvement that may be hard to pick up during day-to-day clinical rotations and encounters.

Key summary information is provided to learners after the session is completed. This may include relevant articles, checklists, online resources, or important sections in key textbooks [ 2 - 3 , 15 ]. Without timely follow-up on the learning objectives and outcomes of the session, learners may lose out on the opportunity to consolidate and retain what they have learned.

Recognizing that important issues may arise during the case, there is flexibility in our approach and we adjust the plan to accommodate discussion around these topics. 

Expected outcomes focus on the CanMEDS roles and integrate both medical expert and non-medical expert roles [ 16 ]. Points on crisis resource management (CRM) are often integrated as a learning objective. Faculty, staff, or SP confederates can add additional challenges to the scenario, tying in the communicator, collaborator, and professional roles which the students should be familiar with.

Medical Expert: Approach to the patient with an undifferentiated altered LOC.

Medical Expert: Approach to diagnosis and treatment of DKA.

Communicator: Emphasis is placed on the appropriate use of closed-loop communication to ensure smooth team functioning in the case.

Collaborator: The student should use available resources to diagnose and treat the patient while dealing with any challenges that may arise during the case.

Professional: Respectful and effective communication is essential for efficient team performance and for addressing interpersonal difficulties introduced through the inclusion of confederates.

With the current focus on competency-based performance and linked milestones versus the traditional time-based approach to completion of training, simulation enables instructors to challenge learners with relevant cases and content in a timely manner, to ensure they gain proficiency. Waiting for hands-on exposure to core cases/topics in the clinical ED setting can prove inefficient and often falls short of what is needed. Patient safety and improved outcomes are the driving forces for this change [ 17 ].

This simulation scenario was developed to help learners appropriately recognize and treat a patient with DKA. A number of case modifiers are included, allowing the case difficulty to be altered depending upon the level of learners. In this case, the initially non-specific presentation of the patient with an altered level of consciousness requires the learner to step back and cast a wide diagnostic net. Once a definitive diagnosis is established, more directed treatment is necessary. Core emergency medicine references are highlighted for reviewing key information on these topics [ 2 - 3 ]. Learners must be aware of potential biases that can be encountered which can lead them off course from reaching an accurate diagnosis. In this case, the patient’s recent alcohol consumption was a confounding variable and was not directly responsible for the altered LOC but did lead to nausea, vomiting, and dehydration. The integration of scripted SP is an effective way to add challenges to a case and to evaluate non-medical expert CanMEDS roles which are essential for competent performance as a medical professional [ 16 ].

In more advanced versions of the scenario, procedural skills are also integrated. Endotracheal intubation and central line placement are important skills for emergency medicine physicians, and the simulation provides a safe, low-risk environment for learners to practice these skills. The inclusion of these skills usually requires a hybrid case set-up using task trainers; the didactic review will address the relevant background information and the discussion of hands-on performance [ 15 ]. Adaptation of the case to a low-fidelity setup may help to address the issues of cost and time effectiveness of a high-fidelity simulation-based training that are often prohibitive.

Conclusions

This technical report describes the design and implementation of a simulation scenario on DKA for emergency medicine trainees. A number of key modifiers are described that allow for the adjustment of case difficulty and enable assessment of a number of CanMEDS roles. Relevant points about CRM and effective communication are also covered. Simulation provides a safe, controlled environment where learners can implement/practice their knowledge and skills to effectively train on low-frequency, high-stakes encounters and procedures as well as core topics.

The content published in Cureus is the result of clinical experience and/or research by independent individuals or organizations. Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein. All content published within Cureus is intended only for educational, research and reference purposes. Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional. Do not disregard or avoid professional medical advice due to content published within Cureus.

The authors have declared that no competing interests exist.

Human Ethics

Consent was obtained by all participants in this study

Animal Ethics

Animal subjects: This study did not involve animal subjects or tissue.