to 30 mEq of potassium per liter to restore the intracellular potassium debt, provided kidney function is normal (see Figure 24-3).24 In patients without normally functioning kidneys and in those with cardiopulmonary disease, careful attention must be paid to the volume of fluid replacement to avoid fluid overload.
After the serum glucose level decreases to 200 mg/dL, the infusing solution is changed to a 50/50 mix of hypotonic saline and 5% dextrose. Dextrose is added to replenish depleted cellular glucose as the circulating serum glucose decreases to 200 mg/dL.24 Dextrose infusion also prevents unexpected hypoglycemia when the insulin infusion is con-tinued but the patient cannot take in sufficient carbohydrate from an oral diet.
Replacing Insulin
In moderate to severe DKA, an initial IV bolus of regular insulin at 0.1 unit for each kilogram of body weight may be administered. Subsequently, a continuous infusion of regular insulin at 0.1 unit/kg/hr is infused simultaneously with IV fluid replacement (see Figure 24-3).24 In a 70-kg adult, the infusion would be 7 units of insulin per hour. If the plasma glucose concentration does not fall by 50 to 70 mg/dL during the first hour of treatment, the glucose measurement should be rechecked. When the plasma glucose level is decreasing as expected, the insulin infusion will be increased each hour until a steady glucose decline of between 50 and 70 mg/dL per hour is achieved.24
Frequent assessment of the patient’s blood glucose concen-tration is mandatory in moderate to severe DKA. Initially, blood glucose tests are performed hourly. The frequency then decreases to every 2 to 4 hours as the patient’s blood glucose level stabilizes and approaches normal. After the level has decreased to 200 mg/dL, the acidosis has been corrected, and rehydration has been achieved, the insulin infusion rate may be decreased to 0.05 to 0.1 unit/kg/hr. This usually represents 3 to 6 units per hour in an adult receiving a continuous IV insulin infusion. It is important to verify that the serum potassium concentration is not lower than 3.3 mEq/L and to replace potassium if necessary, before administering the initial insulin bolus.24
Reversing Ketoacidosis
Replacement of fluid volume and insulin interrupts the ketotic cycle and reverses the metabolic acidosis. In the pres-ence of insulin, glucose enters the cells, and the body ceases to convert fats into glucose.
Adequate hydration and insulin replacement usually correct the acidosis, and this treatment is sufficient for many patients with DKA. As shown in Figure 24-3, replacement of bicarbonate is no longer routine except for the severely aci-dotic patient with a serum pH value lower than 7.0.24 An indwelling arterial line provides access for hourly sampling of arterial blood gases (ABGs) to evaluate pH, bicarbonate, and other laboratory values in the patient with severe DKA.
Hyperglycemia usually resolves before the ketoacidemia does.24 Type 1 diabetes patients with DKA can require 6 L of IV fluid replacement even for mild DKA.25 In one clinical report, patients with previously diagnosed type 1 diabetes in DKA took an average of 21 hours after being started on an IV insulin protocol to clear ketones from the urine. The insulin infusion was continued for 36 hours until the patients
FIG 24-3 Protocol for the management of diabetic ketoacidosis (DKA) and hyperglycemic hyper-osmolar state (HHS). (From Kitabchi AE, et al. Hyperglycemic crises in adult patients with diabetes:
a consensus statement from the American Diabetes Association. Diabetes Care. 2009;32[7]:1335.) Complete initial evaluation. Check capillary glucose and serum/urine ketones to confirm hyperglycemia and
ketonemia/ketonuria. Obtain blood for metabolic profile. Start IV fluids: 1.0 L of 0.9% NaCl per hour.
IV Fluids
Determine hydration status.
Severe hypovolemia
Administer 0.9%
NaCl (1.0 L/hr).
Hemodynamic monitoring/
pressors Cardiogenic
shock Mild
dehydration K 3.3 mEq/L
Hold insulin and give 20-30 mEq/hr until K 3.3 mEq/L.
Do not give K , but check serum K
every 2 hours.
K 5.2 mEq/L
K 3.3-5.2 mEq/L
Give 20-30 mEq K in each liter of IV fluid to keep serum K between 4-5 mEq/L.
Evaluate corrected serum Na .
Serum Na high
Serum Na normal
Bicarbonate
pH 6.9
No HCO3
100 mmol in 400 mL H2O
20 mEq KCL, infuse
for 2 hours
Repeat every 2 hours until pH 7.
Monitor serum K
every 2 hours.
pH 6.9
Insulin: Regular
IV route (DKA and HHS)
0.1 U/kg/Bwt as IV bolus
0.1 U/kg/hr IV continuous insulin infusion
0.14 U/kg/Bwt/hr as IV continuous insulin infusion
If serum glucose does not fall by at, least 10% in first hour, give 0.14
U/kg as IV bolus, then continue previous Rx.
When serum glucose reaches 200 mg/dL, reduce
regular insulin infusion to 0.02-0.05 U/kg/hr IV, or give
rapid-acting insulin at 0.1 U/kg SC every 2 hrs. Keep serum glucose between 150 and 200 mg/dL until resolution
of DKA.
When serum glucose reaches 300 mg/dL, reduce
regular insulin infusion to 0.02-0.05 U/kg/hr IV. Keep serum glucose between 200 and 300 mg/dL until patient is
mentally alert.
Check electrolytes, BUN, venous pH, creatinine, and glucose every 2-4 hours until stable.
After resolution of DKA or HHS and when patient is able to eat, initiate SC multidose insulin regimen. To transfer from IV to SC, continue IV insulin infusion for 1-2 hours
after SC insulin begun to ensure adequate plasma insulin levels. In insulin-naive patients, start at 0.5 U/kg to 0.8 U/kg body weight per day and adjust insulin as needed.
Look for precipitating cause(s).
IV route (DKA and HHS)
Potassium
Establish adequate renal function (urine output — 50 mL/hr).
Serum Na low
0.9% NaCl (250-500 mL/hr)
depending on hydration state
When serum glucose reaches 200 mg/dL (DKA) or 300 mg/dL
(HHS), change to 5% dextrose with 0.45% NaCl at 150-250 mL/hr.
0.45% NaCl (250-500 mL/hr)
depending on
hydration state DKA HHS
could tolerate an oral diet; during this time, the patients received a total of 9.5 L of normal saline for rehydration.26 Patients who are newly diagnosed with type 1 diabetes take longer to clear urine ketones and require more insulin to achieve normal glycemic control, compared with long-term diabetics.26
Replenishing Electrolytes
Low serum potassium (hypokalemia) occurs as insulin pro-motes the return of potassium into the cell and metabolic acidosis is reversed. Replacement of potassium by adminis-tration of potassium chloride (KCl) begins as soon as the serum potassium falls below normal. Frequent verification of
Vital signs, especially heart rate (HR), hemodynamic values, and blood pressure (BP), are continuously monitored to assess response to the fluid replacement. Evidence that fluid replacement is effective includes normal central venous pres-sure (CVP), decreased HR, and normal BP. Box 24-6 lists the standard features to be included in an assessment of hydra-tion status. More invasive hemodynamic monitoring, such as a pulmonary artery catheter, is rarely needed. Further evi-dence of hydration improvement includes a change from a previously weak, thready pulse to a pulse that is strong and full and a change from hypotension to a gradual elevation of systolic BP. Respirations are assessed frequently for changes in rate, depth, and presence of the fruity acetone odor.
Blood glucose is measured each hour in the initial period.
Sometimes potassium is measured just as frequently. The serum osmolality and serum sodium concentration are evalu-ated, and blood urea nitrogen (BUN) and creatinine levels are assessed for possible kidney impairment related to decreased renal perfusion. The purpose of these frequent assessments is to determine that the patient’s clinical status is improving.
After the patient has stable laboratory indicators and is awake and alert, the transition to subcutaneous insulin and an oral diet can be made. Hypoglycemia is a risk during the transi-tion period. For example, in anticipation of discontinuing the insulin and IV dextrose infusion, a patient receives a subcu-taneous dose of insulin and is expected to eat a meal. However, if the patient is then unable to eat an adequate amount, hypo-glycemia results from the administration of subcutaneous insulin without adequate glucose.
Surveillance for Complications
The patient in DKA can experience a variety of complica- tions, including fluid volume overload, hypoglycemia, hypo-kalemia or hyperkalemia, hyponatremia, cerebral edema, and infection.
Fluid volume overload. Fluid overload from rapid volume infusion is a serious complication that can occur in the patient with a compromised cardiopulmonary system or kidneys.
Neck vein engorgement, dyspnea without exertion, and pul-monary crackles on auscultation signal circulatory overload.
Reduction in the rate and volume of infusion, elevation of the head of the bed, and provision of oxygen may be required to manage the increased intravascular volume. Hourly urine measurement is mandatory to assess kidney function and adequacy of fluid replacement.
the serum potassium concentration is required for the DKA patient receiving fluid resuscitation and insulin therapy.
The serum phosphate level is sometimes low (hypophos-phatemia) in DKA. Insulin treatment may make this more obvious as phosphate is returned to the interior of the cell. If the serum phosphate level is less than 1 mg/dL, phosphate replacement is recommended.24
Nursing Management
Nursing management of the patient with DKA incorporates a variety of nursing diagnoses (Box 24-5). The goals of nursing management are to administer prescribed fluids, insulin, and electrolytes; monitor response to therapy; maintain surveil-lance for complications, and provide patient education.
Administering Fluids, Insulin, and Electrolytes
Rapid IV fluid replacement requires the use of a volumetric pump. Insulin is administered intravenously to patients who are severely dehydrated or have poor peripheral perfusion to ensure effective absorption. Patients with DKA are kept on NPO status (nothing by mouth) until the hyperglycemia is under control. The critical care nurse is responsible for moni-toring the rate of plasma glucose decline in response to insulin. The goal is to achieve a fall in glucose levels of approximately 50 to 70 mg/dL each hour.24 The coordination involved in monitoring blood glucose, potassium, and often blood gases on an hourly basis is considerable.
When the blood glucose level falls to 200 mg/dL, a 5%
dextrose solution (D5W) with 0.45% NaCl solution is infused to prevent hypoglycemia.24 At this time, it is likely that the insulin dose per hour will also be decreased. The regular insulin drip is not discontinued until the ketoacidosis sub-sides, as identified by absence of ketones and a normal pH by arterial blood gas analysis.24
Insulin is given subcutaneously after glucose levels, dehy-dration, hypotension, and acid–base balance are normalized;
the patient is in stable condition and taking an oral diet.
Monitoring Response to Therapy
Accurate intake and output (I&O) measurements must be maintained to monitor reversal of dehydration. Hourly urine output is an indicator of kidney function and provides infor-mation to prevent overhydration or insufficient hydration.
• Hourly intake
• Blood pressure changes
• Orthostatic hypotension
• Pulse pressure
• Pulse rate, character, rhythm
• Neck vein filling
• Skin turgor
• Skin moisture
• Body weight
• Central venous pressure
• Hourly urine output
• Complaints of thirst
BOX 24-6 Hydration Assessment BOX 24-5 NURSING DIAGNOSES:
DIABETIC KETOACIDOSIS
• Decreased Cardiac Output related to alterations in preload, p. 579
• Deficient Fluid Volume related to absolute loss, p. 584
• Anxiety related to threat to biologic, psychologic, and social integrity, p. 576
• Disturbed Body Image related to functional dependence on life-sustaining technology, p. 587
• Ineffective Coping related to situational crisis and personal vulnerability, p. 599
• Powerlessness related to lack of control over current situ-ation or disease progression, p. 600
• Deficient Knowledge related to lack of previous exposure to information, p. 585 (see Box 24-8, Patient Education for Diabetic Ketoacidosis)
manifestations of hyponatremia include abdominal cramp-ing, postural hypotension, and unexpected behavioral changes. Sodium chloride is infused as the initial IV solution.
Maintenance of the saline infusion depends on clinical mani-festations of sodium imbalance and serum laboratory values.
Risk for cerebral edema. Changes in the patient’s neuro-logic status may be insidious. Alterations in level of con-sciousness, pupil reaction, and motor function may be the result of fluctuating glucose levels and cerebral fluid shifts. Confusion and sudden complaints of headache are ominous signs that may signal cerebral edema. These obser-vations require immediate action to prevent neurologic damage. Neurologic assessments are performed every hour or as needed during the acute phase of hyperglycemia and rehydration. Assessment of level of consciousness serves as the index of the patient’s cerebral response to the rehydra-tion therapy.
Risk for infection. Skin care takes on new dimensions for the patient with DKA. Dehydration, hypovolemia, and hypo-phosphatemia interfere with oxygen delivery at the cell site and contribute to inadequate perfusion and tissue break-down. Patients must be repositioned frequently to relieve capillary pressure and promote adequate perfusion to body tissues. The typical patient with type 1 diabetes is of normal weight or underweight. Bony prominences must be assessed for tissue breakdown, and the patient’s body weight must be repositioned every 1 to 2 hours. Irritation of skin from adhe-sive tape, shearing force, and detergents should be avoided.
Maintenance of skin integrity prevents unwanted portals of entry for microorganisms.
Oral care, including tooth brushing and use of lip balm, helps keep lips supple and prevents cracking. Prepared sponge sticks or moist gauze pads can be used to moisten oral mem-branes of the unconscious patient. Swabbing the mouth moistens the tissue and displaces the bacteria that collect when saliva, which has a bacteriostatic action, is curtailed by dehydration. The conscious patient must be provided the means to self-remove oral bacteria by tooth brushing and frequent oral rinsing.
Strict sterile technique is used to maintain all IV systems.
All venipuncture sites are checked every 4 hours for signs of inflammation, phlebitis, or infiltration. Strict surgical asepsis is used for all invasive procedures. Sterile technique is used if urinary catheterization is necessary to obtain urine samples for testing. Urinary catheter care is provided every 8 hours.
Patient Education
It is important to be aware of the knowledge level and adher-ence history of patients with previously diagnosed diabetes to formulate an appropriate teaching plan. Learning objec-tives include a discussion of target glucose levels, definition of hyperglycemia and its causes, harmful effects, symptoms, and how to manage insulin and diet when one is unwell and unable to eat. Additional objectives include a definition of DKA and its causes, symptoms, and harmful consequences.
The patient and family are also expected to learn the princi-ples of diabetes management. Universal precautions must be emphasized for all family caregivers. The patient and family must also learn the warning signs of DKA to report to the attention of a health care practitioner. Education of the patient, family, or other support persons to achieve Hypoglycemia. Hypoglycemia is defined as a serum
glucose level lower than 70 mg/dL.24 Most acute care hospi- tals have specific procedures for management of the hypogly-cemic patient. For example, if hypoglycemia is detected by finger-stick point-of-care testing at the bedside, a blood sample is sent to the laboratory for verification, the physician is notified immediately, and replacement glucose is given intravenously or orally, depending on the patient’s clinical condition, diagnosis, and level of consciousness.
Unexpected behavior change or decreased level of con-sciousness, diaphoresis, and tremors are physical warning signs that the patient has become hypoglycemic. These symptoms are especially important to recognize if the frequency of glucose testing has lengthened to 2- to 4-hour intervals. A comparison between the physical symptoms expected with hypoglycemia and those of hyperglycemia is provided in Box 24-7.
Hypokalemia and hyperkalemia. Hypokalemia can occur within the first hours of rehydration and insulin treatment. Con-tinuous cardiac monitoring is required because low serum potassium (hypokalemia) can cause ventricular dysrhythmias.
Hyperkalemia occurs with acidosis or with overaggressive administration of potassium replacement in patients with renal insufficiency. Severe hyperkalemia is demonstrated on the cardiac monitor by a large, peaked T wave; flattened P wave, and widened QRS complex. See Figure 11-46 in Chapter 11. Ventricular fibrillation can follow.
Hyponatremia. Sodium elimination from the body results from the osmotic diuresis and is compounded by the vomit-ing and diarrhea that can occur durfrom the osmotic diuresis and is compounded by the vomit-ing DKA. Clinical
HYPOGLYCEMIA HYPERGLYCEMIA
• Restlessness
• Apprehension
• Irritability
• Trembling
• Weakness
• Diaphoresis
• Pallor
• Paresthesia
• Pallor
• Headache
• Hunger
• Difficulty thinking
• Loss of coordination
• Difficulty walking
• Difficulty talking
• Visual disturbances
• Blurred vision
• Double vision
• Tachycardia
• Shallow respirations
• Hypertension
• Changes in level of consciousness
• Seizures
• Coma
• Excessive thirst
• Excessive urination
• Hunger
• Weakness
• Listlessness
• Mental fatigue
• Flushed, dry skin
• Itching
• Headache
• Nausea
• Vomiting
• Abdominal cramps
• Dehydration
• Weak, rapid pulse
• Postural hypotension
• Hypotension
• Acetone breath odor
• Kussmaul respirations
• Rapid breathing
• Changes in level of consciousness
• Stupor
• Coma
BOX 24-7 Clinical Manifestations of Hypoglycemia and
Hyperglycemia
elevation in serum hyperosmolality causing osmotic diuresis.
Ketosis is absent or mild. Inability to replace fluids lost through diuresis leads to profound dehydration and changes in level of consciousness. The overall mortality rate from HHS ranges from 5% to 20%.24 Because patients with HHS have type 2 diabetes as an underlying disorder, they are gen-erally older adults with cardiovascular comorbidities.
The diagnostic criteria for HHS are as follows and as shown in Table 24-4:24
• Blood glucose greater than 600 mg/dL
• Arterial pH greater than 7.3
• Serum bicarbonate greater than 18 mEq/L
• Serum osmolality greater than 320 mOsm/kg H2O (320 mmol/kg)
• Absent or mild ketonuria
Most patients with this level of metabolic disruption expe-rience visual changes, mental status changes, and potentially hypovolemic shock.
HHS occurs when the pancreas produces a relatively insuf-ficient amount of insulin for the high levels of glucose that flood the bloodstream. HHS primarily affects older, obese persons with underlying cardiovascular conditions. Infection is the primary reason that type 2 diabetics develop HHS; the most common infections are pneumonia and urinary tract infections. The patient may have type 2 diabetes treated with diet and oral hypoglycemic agents that is destabilized by an infection. Other precipitating causes of HHS include stroke, myocardial infarction, trauma, major surgery, and the stress of critical illness.
Differences between Hyperglycemic Hyperosmolar State and Diabetic Ketoacidosis
Clinically, HHS is distinguished from DKA by the presence of extremely elevated serum glucose, more profound dehy-dration, and minimal or absent ketosis (Table 24-5). Another major difference is that protein and fats are not used to create new supplies of glucose in HHS as they are in DKA; as a result, the ketotic cycle is never started or does not occur until the glucose level is extremely elevated.
Pathophysiology
HHS represents a deficit of insulin and an excess of glucagon (Figure 24-4). Reduced insulin levels prevent the movement of glucose into the cells, allowing glucose to accumulate in the plasma. The decreased insulin triggers glucagon release from the liver, and hepatic glucose is poured into the circula-tion. As the number of glucose particles increases in the blood, serum hyperosmolality increases. In an effort to decrease the serum osmolality, fluid is drawn from the intra-cellular compartment (inside the cells) into the vascular bed.
Profound intracellular volume depletion occurs if the patient’s thirst sensation is absent or decreased. HHS may evolve over days or even weeks.24
Hemoconcentration persists despite removal of large amounts of glucose in the urine (glycosuria). The glomerular filtration and elimination of glucose by the kidney tubules is ineffective in reducing the serum glucose level sufficiently to maintain normal glucose levels. The hyperosmolality and reduced blood volume stimulate release of ADH to increase the tubular resorption of water. ADH, however, is powerless to overcome the osmotic pull exerted by the glucose load.
Excessive fluid volume is lost at the kidney tubule, with knowledge-based, independent self-management of blood
glucose level and avoidance of diabetes-related complications are the ultimate goals of the teaching process (Box 24-8).
Collaborative Management
In all aspects of patient care management, health care profes-sionals work as a team with the major collaborative goal of providing the best possible outcome for each patient. Current guidelines related to Collaborative Management of patients with hyperglycemia crisis are listed in Box 24-9.