Diabetic ketoacidosis (DKA) is a life-threatening diabetic emergency involving homeostatic imbalance and damaging compensatory processes. In order to achieve optimal patient outcomes, acute care NPs require a standardized protocol that implements best evidence and prioritizes care.1,2 Recent evidence has associated the use of standardized tools in medical institutions with improvements in patient outcomes and decreases in preventable medical errors.3,4
In clinical settings, structured mnemonics have been established as optimal tools to improve communication and recall.5 Due to the time-sensitive nature of DKA, it is imperative that care is prioritized and standardized among clinicians. With the goal of reducing inconsistencies in care while better recalling current clinical guidelines, the authors propose a structured mnemonic tool of “using your HEAD backward” in the management of DKA. In this mnemonic, “HEAD” is used in reverse order to help prioritize patient care according to the condition's most pertinent and dire complications. By “using your HEAD backward,” the NP can manage DKA and its related complications: Dehydration, Anion gap, Electrolyte imbalance, and Hyperglycemia (see Use your HEAD backward).
DKA manifests as the result of absolute or relative insulin deficiency in unmanaged diabetes mellitus (see Pathophysiology of DKA).6 Paired with the systemic depletion of insulin, a surge in counterregulatory hormones (including glucagon, cortisol, catecholamines, and growth hormones) stimulates glycogenolysis. As a result, triglycerides within adipose tissue are hydrolysed, creating a surge in free fatty acid delivery to the liver. Using free fatty acids as ketogenic precursors, the liver produces and releases ketones, including beta-hydroxybutyrate, acetoacetate, and acetone into circulation. Ketones from the liver are acidic, and as their concentrations increase in the circulation, an acidotic environment is created in the body, characterized by a decrease in serum pH and a widening anion gap.6
A series of signs and symptoms have been associated with the clinical presentation of DKA.7 Due to hyperglycemia, the NP may notice polyuria, polydipsia, and weakness. In a state of acidosis, the patient will likely experience nausea and abdominal pain as well as air hunger in the form of Kussmaul respirations. The NP should be mindful for the presence of acetone-odor breath, indicating the intrinsic ketogenesis process.
The NP plays an essential role in decreasing the occurrence of DKA through patient education and increasing blood glucose self-monitoring. NPs should offer education and care planning related to “sick day” management, which involves special precautions in the occurrence of illness due to fluctuations in blood glucose levels. Recent guidelines published by Diabetes Canada recommend that blood glucose self-monitoring should occur every 2 to 4 hours, and maintaining hydration with sugar-free fluids and water is essential when the patient is sick.7 A blood ketone test is recommended in type 1 diabetes mellitus (T1DM) if preprandial blood glucose levels exceed 14 mmol/L (252 mg/dL) and/or symptoms of DKA are present.
Health teaching should also include insulin adjustment in the event of a sick day as well as medications to avoid during this period of time. Diabetes Canada recommends that when ill, the patient should temporarily stop sulfonylureas, ACE inhibitors, diuretics, direct renin inhibitors, metformin, angiotensin receptor blockers, nonsteroidal anti-inflammatories, and sodium-glucose cotransporter-2 (SGLT2) inhibitors.7
A clinical diagnosis of DKA lacks definitive criteria; however, certain diagnostic markers will guide the NP toward a DKA diagnosis.7 The presence of hyperglycemia (greater than 11.0 mmol/L or approximately 200 mg/dL) or a history of diabetes, an elevated serum ketone concentration (greater than 3.0 mmol/L or 3 mEg/L) or ketonuria (greater than 2+), a low serum pH (less than 7.3), and/or low bicarbonate levels (less than 15.0 mmol/L or 15 mEg/L) as well as an increased anion gap (greater than 12 mmol/L or 12 mEg/L) indicate a DKA diagnosis and should be treated as a life-threatening emergency.8,9
The NP should have consideration for the occurrence of euglycemic diabetic ketoacidosis (eu-DKA), which may develop in patients with unmanaged T1DM or type 2 diabetes mellitus.8 Patients experiencing eu-DKA will often present with less extreme hyperglycemia (less than 11.0 mmol/L or approximately 200 mg/dL). While the etiology of eu-DKA is not widely understood, its precipitating factors may include decreased hepatic production of glucose in fasting state or excessive urinary excretion of glucose due to surges in counterregulatory hormones.
A recent case study published in the International Journal of Emergency Medicine has indicated that the use of SGLT2 inhibitors is associated with a higher incidence of eu-DKA. While SGLT2 inhibitors cause glycosuria by lowering renal glucose threshold, thus leading to lower blood glucose levels, SGLT2 inhibitors also stimulate pancreatic glucagon release, increasing lipolysis and subsequent ketone body formation.10 Patients experiencing eu-DKA will present with evidence of ketosis and dehydration as seen in DKA; however, patients will experience a milder hyperglycemia due to a less severe insulin resistance. It is recommended that rapid fluid balance be prioritized in eu-DKA treatment followed by the normalization of electrolytes and acidosis through an insulin drip. A higher dextrose concentration (10% or 20%) is required in managing eu-DKA to prevent rebound hypoglycemia.8
DKA management involves progressive treatment implementation in order of clinical priority. Once the DKA diagnosis is confirmed, the NP should begin treatment using the mnemonic “HEAD” in reverse order, specifically prioritizing the management of Dehydration, Anion gap, Electrolytes, and Hyperglycemia.
Dehydration. Managing the fluid deficit DKA patients is a critical initial step to restore extracellular fluid volume and increase urinary glucose excretion.7 Additionally, hyperosmolality due to dehydration poses a risk to the DKA patient. According to guidelines from Diabetes Canada, adult patients experiencing a mild-to-moderate fluid deficit should be administered 0.9% NaCl I.V. 500 mL/h for 4 hours followed by 250 mL/h for 4 hours. In the severely deficient adult patient, the NP should first administer 1 to 2 L/h 0.9% NaCl solution to correct hypotension or shock and once stable, administer 500 mL/h for 4 hours followed by 250 mL/h for 4 hours.7
DKA management in pediatric patients requires careful consideration, as excessive fluid replacement can negatively impact patient outcomes.9 Current guidelines recommend crystalloid fluid volumes ranging between 10 mL/kg and 20 mL/kg. In order to determine an optimal I.V. fluid volume for pediatric patients experiencing DKA, Bakes and colleagues conducted a randomized control trial conducted in the US (n = 50), comparing the efficacy of higher versus lower I.V. fluid volumes in reaching metabolic normalization.11 The higher volume patient group (n = 25) received 20 mL/kg of 0.9% NaCl I.V. bolus over the first hour, followed by 0.675% saline and potassium replacement at 1.5 times maintenance. Alternately, the low volume group (n = 25) received 10 mL/kg of 0.9% NaCl I.V. bolus over the first hour, followed by 0.675% saline and potassium replacement at 1.25 times maintenance.
Over a 3-year study period, it was determined that pediatric DKA patients treated with a higher volume of I.V. fluid experienced the shortest time to metabolic normalization, specifically (P = 0.04). To increase perfusion and normalize metabolic processes in the pediatric patient presenting with DKA, the NP should administer 20 mL/kg normal saline over the first hour, followed by 0.675% saline and potassium replacement at 1.5 times maintenance.11
While current guidelines recommend initiating fluid repletion with the standard one-bag method of normal saline and supplemental electrolytes, recent studies conducted in the US have evaluated the efficacy and feasibility of a two-bag titration approach, one bag containing saline and supplemental electrolytes and another bag containing identical solution composition with additional 10% dextrose.12,13 The two-bag method allows for the titration of dextrose delivery by varying the relative infusion rate in order to better control blood glucose levels among adult patients. In both studies, it was determined that the use of a two-bag approach was associated with an earlier correction of the anionic gap, earlier discontinuation of insulin infusion, and fewer associated episodes of hypoglycemia during insulin infusion.
Anion gap. As the ketones produced in DKA are acidic in nature, their production and presence in the body inevitably leads to anion gap elevation and a systemic state of acidosis.14 The balanced equation below represents the electrical gap that exists between the most commonly measured positive and negative ions:15
(Na+ + K+) – (Cl– + HCO3–)
In a state of ketoacidosis, the production of liver ketones yields increase in positive ion concentration, thereby creating a disequilibrium in the above equation. The anion gap “widens,” which clinically refers to an increased difference in the number of circulating cations comparatively to anions within the body.15
Administering fluids aids in clearing ketone bodies, while insulin halts the processes of lipolysis and ketogenesis to resolve DKA. Additionally, administering insulin promotes potassium reuptake by cells, therefore reducing its presence in the extracellular space and circulating plasma. Insulin administration should be timed accordingly to prevent negative patient outcomes, including cerebral edema.9
The Diabetes Canada Clinical Practice Guidelines Expert Committee has developed an algorithm to help NPs in managing acidosis in DKA.7 If the serum potassium concentration is greater than or equal to 3.3 mmol/L, it is recommended that the NP proceed with a continuous infusion of regular insulin at a measurement of 0.1 units/kg/h.7,14 However, the NP should correct hypokalemia prior to insulin administration if the patient's serum potassium concentration level is below 3.3 mmol/L. The patient should be continuously monitored for treatment efficacy, specifically in resolving ketosis via anion gap normalization.7
Ketoacidosis is resolved when blood glucose is less than 11 mmol/L (200 mg/dL), paired with two of the following: serum bicarbonate greater than or equal to 15 mmol/L (15 mEg/L), venous pH greater than 7.3, and an anion gap below 12 mmol/L (12 mEg/L).14 When serum glucose falls below 11 mmol/L (200 mg/dL), the I.V. insulin dose should be reduced to 0.02 to 0.05 units/kg/h. It is recommended that the NP transition to a multidose subcutaneous insulin regimen beginning at a dose of 0.5 to 0.8 units/kg/day when DKA resolves and the patient is able to eat.15 However, the American Diabetes Association recommends that a subcutaneous basal insulin injection should be administered for 2 to 4 hours prior to discontinuing I.V. insulin.16
Electrolytes. DKA management requires careful monitoring and consideration for electrolyte imbalance, as treatment with I.V. fluid replacement and insulin administration can cause fluctuations that may influence patient outcomes. Specifically, serum potassium levels pose a substantial risk, as the DKA patient is at risk for developing hyperkalemia and/or hypokalemia. In addition to measuring serum potassium levels every 2 hours, NPs should proceed with continuous cardiac monitoring, as this method has been established as the ideal approach for assessing cardiac risk among patients with severe hyperkalemia.9,14,17
Hyperkalemia manifests in the initial stages of DKA as insulin depletion prevents potassium's reentry into the cell via the sodium-potassium ATPase pump, therefore causing its increase in concentration in the extracellular space. Additionally, hyperkalemia manifests due to intrinsic compensatory mechanisms to restore acid-base balance in the presence of acidosis, wherein cells secrete potassium into the bloodstream to restore electrical neutrality. In the instance of hyperkalemia in DKA—specifically serum potassium levels greater than 5.5 mmol/L—the NP should continue with insulin treatment to counteract acidosis, as insulin will effectively move potassium ions from the blood back into the cell.6
Due to the abrupt egression of potassium from the blood into the cell via insulin administration, hypokalemia development (less than 3.5 mmol/L or 3.5 mEg/L) poses a risk to the DKA patient.6 If the DKA patient initially presents with normokalemia or hypokalemia, the NP should proceed with I.V. potassium replacement immediately, with a recommended dose between 10 mmol/L (10 mEg/L) and 40 mmol/L (720 mEg/L) depending on severity of potassium deficit, at a rate not surpassing 40 mmol/h.7 Alternately, if hypokalemia develops throughout DKA treatment, potassium replacement may be indicated when plasma potassium concentrations are less than 5.0 to 5.5 mmol/L (5 to 5.5 mEg/L); however, administering potassium replacement is contingent on whether diuresis is present.7
In addition to potassium balance, NPs should have consideration for serum sodium concentration due to alterations in blood osmolality during the initial fluid resuscitation phase of treatment. Diabetes Canada recommends that if serum sodium concentration is normal or high, and effective plasma osmolality decreases at a rate of less than 3 mmol/kg/h, the NP should switch to a 0.45% NaCl solution.7 However, if the corrected plasma sodium concentration is low, or plasma osmolality is decreasing at a rate greater than or equal to 3 mmol/kg/h, the NP should continue with the administration of 0.9% NaCl.
It is imperative that magnesium concentration be monitored and managed when restoring electrolyte balance. Due to the rapid administration of fluids to restore fluid balance and flush excess glucose, magnesium may be lost in the urine, placing the patient at risk for magnesium deficiency. It is imperative that NPs consider that normokalemia cannot be achieved without managing magnesium deficiency due to the interplay between these ions within the renal tubules. In the distal tubular and cortical collecting duct cells, potassium ions are secreted into the luminal fluid via potassium-channels, specifically the maxi-K channels and the renal outer medullary potassium (ROMK) channels.18 The ROMK channels, specifically, are directly influenced by magnesium concentration. Under normal conditions, magnesium ions block the ROMK channel, therefore reducing potassium efflux. In a state of magnesium deficiency (as commonly seen in the patient being treated for DKA), potassium is freely secreted. Potassium replacement without magnesium replacement will not successfully treat hypokalemia.18
Hyperglycemia. The final stage in the DKA management, and the NP's last clinical priority, is treating hyperglycemia. The hasty correction of hyperglycemia increases the risk cerebral edema, due to water and glucose reuptake into cells with insulin administration, particularly among children.9 When blood glucose levels reach 14 mmol/L, the NP should administer D5W or D10W to prevent rebound hypoglycemia and allow time for acidosis to be reversed within the body. For optimal outcomes, the patient's blood glucose levels should be maintained between 12.0 and 14.0 mmol/L (216 to 252 mg/dL).7 The NP should monitor neurologic status hourly. In the event of altered level of consciousness, headache, and bradycardia indicating the development of cerebral edema, the NP should administer 0.5 to 1.0 g/kg of mannitol while adjusting I.V. fluids to maintain ideal BP.9
By using the mnemonic learning tool “use your HEAD backward,” acute care NPs will be able to prioritize care and apply best evidence in clinical settings to improve patient outcomes. Poor prognoses in DKA are associated with deviations from standardized protocols and inconsistencies in care. By addressing complications in a systematic order, first by Dehydration, Anion gap, Electrolytes and lastly, Hyperglycemia, NPs can ensure that mortality from an associated comorbidity is avoided.14
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