Assessment and treatment of hypoglycemia in elders: cautions and recommendations.
Critical care practitioners define severe hypoglycemia as BG less than 50 mg/dL for men, 45 mg/dL for women, and 40 mg/dL for infants and children (Smeeks, 2008). Similarly, Moses (2007) distinguishes four categories of hypoglycemia:
* Mild hypoglycemia = BG 60-70 mg/dl
* Moderate hypoglycemia = BG 45-59 mg/dl
* Severe hypoglycemia = BG <45 mg/dl with affected individual alert and awake
* Unconscious with severe hypoglycemia = BG<45 and individual unresponsive
Most primary care practitioners treating older adults use serum glucose of 70 mg/dL to define hypoglycemia. Rapid response to older adult patients with BG below 70 mg/dL is necessary to prevent injuries and additional morbidity, as they may be less aware of or unable to respond to symptoms of hypoglycemia (Frier & Fisher, 2007).
Pathophysiology of hypoglycemia
Hormonal regulation. Hypoglycemic symptoms are mediated through both the central and peripheral nervous systems. Once plasma glucose concentrations fall below 70 mg/dL, a sequence of events begins with release of neuroendocrine hormones (counter-regulatory or anti-insulin hormones), stimulation of the autonomic nervous system, and finally, production of neurogenic and neuroglycopenic symptoms. Peripheral autonomic symptoms (adrenergic), including sweating, irritability, tremulousness, anxiety, tachycardia, and hunger, serve as an early warning system and precede the central neuroglycopenic symptoms due to cerebral glucose deprivation (e.g., confusion, paralysis, seizures, and coma) (Zammitt & Frier, 2005).
The normal response to hypoglycemia includes suppression of insulin release with secretion of glucagon and pancreatic polypeptide from the pancreas, epinephrine from the adrenal medulla, norepinephrine from sympathetic postganglionic nerve terminals and the adrenal medulla, cortisol from the adrenal cortex, and growth hormone from the anterior pituitary gland. Glucagon and epinephrine are the initial fast-acting substances released in acute hypoglycemia, activating the sympathetic nervous system and causing increased lipolysis in adipocytes, with increased release of free fatty acids as an additional energy source and glucose-sparing maneuver (Frier & Fisher, 2007). A deficiency in any one of these systems may contribute to prolonged hypoglycemia.
Evaluation. Recurrent or acute hypoglycemia indicates the need for further diagnostic testing to rule out infection, renal disease, medication interaction, or dietary or oncologic causes (Cryer et al., 2009). A comprehensive metabolic profile, complete blood count, liver function tests, pre-albumin/albumin, serum insulin, serum cortisol, C-peptide, and thyroid panels should be obtained (Raghavan et a]., 2007). Occult infections account for approximately 20% of new onset, acute hypoglycemic episodes among older adults (diabetic and non-diabetic). Consequently, the patient with acute, unexplained hypoglycemia should have a complete physical examination with consideration of anterior and posterior chest x-ray and urine culture and sensitivity. Blood cultures also may be pursued if other tests are non-diagnostic (Frier & Fisher, 2007; Smeeks, 2008).
Disease-Related Hypoglycemia in Older Adults
Type 2 diabetes. Among adults age 65 and older in the United States, the prevalence of diabetes is 15.3% (5.4 million persons). The prevalence of undiagnosed diabetes is estimated at 6.9%, or 2.4 million persons (Selvin, Coresh, & Brancati, 2006). Risk factors for type 2 diabetes include age greater than 45; Hispanic, Native American, African American, Asian American, or Pacific Islander descent; family history of type 2 diabetes in a first-degree relative; history of previous impaired glucose tolerance; impaired fasting glucose; hypertension (>140/90 mmHg); and dyslipidemia (high-density lipoprotein cholesterol <40 mg/dL or triglyceride >150 mg/dL) (Zammitt & Frier, 2005). The United Kingdom Prospective Diabetes Study found 2.4% of those using metformin (Glucophage[R]), 3.3% of those using a sulfonylurea, and 11.2% of those using insulin had major hypoglycemic episodes; more than 30% of them were over age 65 (Cryer, Davis, & Shamoon, 2003).
Persons with type 2 diabetes, many of whom are older adults, average 16 hypoglycemic events each year. Predictors of hypoglycemia in patients with type 2 diabetes include treatment with insulin, a history of previous hypoglycemia, and duration of insulin treatment (Briscoe & Davis, 2006). Primary risk factors for hypoglycemia in decreasing importance have been reported as age over 64, current insulin treatment, sulfonylurea treatment, polypharmacy, renal impairment, and previous hypoglycemic episodes (Miller et al., 2001). One recent study found hypoglycemic episodes no more frequent among nursing home residents with type 2 diabetes with dementia versus nondiabetic patients with dementia matched for age, reinforcing the need to monitor all nursing home residents for hypoglycemia (Arinson, Fidelman, Berner, & Adunsky, 2007). Strict glycemic control is associated frequently with increased hypoglycemic episodes in older adults (Guettier, 2006). Maintaining consistent carbohydrate intake with nighttime snacks is important. It remains to be seen whether morbidity, mortality, or quality of life improve with strict glycemic control in older adults with diabetes (Goldman & Ausiello, 2004; Guettier, 2006; Holmes, Hayley, Alexander, & Sachs, 2006).
Renal disease. Kidney disease is a frequent cause of adverse medication reactions and therefore causing hypoglycemia in older adults (Pham & Dickman, 2007; Pistrosch, Bussemaker, & Gross, 2006). Over 300,000 patients in the United States had end-stage renal disease (ESRD) in 1997, with the number expected to double by 2010 (Swedko, Clark, Paramsothy, & Akbari, 2003). Because older patients often have milder renal disease, with impaired medication elimination prolonging medication effects, it is important to determine their glomerular filtration rate (GFR) and creatinine clearance (C1Cr) in order to assess drug dosing that may contribute to hypoglycemia as well as other symptoms (Pham & Dickman, 2007; Swedko et al., 2003).
In the past, serum creatinine (Cr) has been used to evaluate renal function (Levey et al., 2007). In older adults and women with lower muscle mass, however, Cr can be within normal ranges even with severe renal disease (Levey et al., 2007). The 24-hour creatinine clearance test is the most accurate assessment of GFR, but time consuming and costly (Swedko et al., 2003). Two alternative methods for computing age/weight-adjusted GFR and creatinine clearance ([Cl.sub.Cr]) are the Cockcroff-Gault formula and the Modification of Diet in Renal Disease ([MDRD.sub.version 4]) (Fadem, 2007a). Nurses can determine [Cl.sub.Cr] and GFR quickly with a patient's current Cr value, age, weight, gender, and race using free online [Cl.sub.Cr] and GFR calculators (Fadem, 2007b). It is important to obtain the corrected GFR in any patient prescribed oral diabetic and blood pressure medications; significant reductions in GFR require dosing adjustments in these patients.
Adrenal insufficiency. Adrenal crisis is relatively rare, but may cause prolonged hypoglycemia secondary to decreased secretion or depleted stores of epinephrine and norepinephrine from the adrenal medulla (Klaner, 2008).
Infections. Hypoglycemia often occurs during or following acute infections in older adults (Raghavan et al., 2007). Infection-related hypoglycemia (IRH) increases the risk of death and morbidity among persons over age 70 (Arinson et al., 2007). Increased comorbidities (e.g., congestive heart failure, coronary artery disease, ESRD); decreased functional status; and increased Cr, albumin and C-reactive protein are associated with IRH (Cryer et al., 2009). Sepsis also has been the leading cause of hypoglycemia among patients initially admitted to geriatric and internal medicine services, with severity of hypoglycemia correlated with risk of death while in the hospital (Kagansky et al., 2003).
Hypoglycemic unawareness. Secretion of glucagon, epinephrine, and growth hormone during hypoglycemia diminishes significantly after age 65, reducing autonomic warning symptoms in older adults (Chau, Shumaker, & Plodkowski, 2003; Frier & Fisher, 2007; Meneilly, 2000). In addition, repeated episodes of hypoglycemia produce accommodation or autonomic desensitization, making low blood glucose difficult to appreciate and creating increased risk for subsequent hypoglycemia, fails, and injuries (Briscoe & Davis, 2006; Miller et al., 2001; Veneman & Erkelens, 1997; Zammitt & Frier, 2005). Many older adult patients with chronic hypoglycemia have few if any symptoms with BG values as low as 45 mg/dL (Chau & Edelman, 2001; Frier & Fisher, 2007; Selvin et al., 2006). Some theorize older patients are more likely to be desensitized to the release of catecholamines associated with low serum glucose or may have depleted catecholamine stores (Frier & Fisher, 2007). Selective serotonin reuptake inhibitors (SSRIs) also have been associated with decreased perception of hypoglycemia. The exact mechanism by which SSRIs cause hypoglycemia unawareness is unknown, although one hypothesis posits an atypical serotonin syndrome resulting in autonomic dysfunction (White, 2007). Beta adrenergic blockers (B-blockers) also reduce awareness and may mask the presence of hypoglycemia by dampening usual adrenergic responses (Zammitt & Frier, 2005). This unawareness phenomenon also has been identified as hypoglycemia-associated autonomic failure (HAAF), resulting in recurrent neurogenic symptoms and recurrent severe hypoglycemia in older adults (Cryer, 2004; Cryer et al., 2003).
Oncologic factors. Insulin-producing tumors of the pancreas can cause severe hypoglycemia; among these are islet cell adenoma and carcinoma (insulinoma), which are rare and easily treated in adults (Raghavan et al., 2007). These tumors are most common in women (60%), with median age of diagnosis 50 years (Le Roith, 1999); 10% of patients with insulinoma are age 70 or older. Hypoglycemia also can result from large non-insulin-secreting tumors, most commonly retroperitoneal or mediastinal malignant mesenchymal tumors. These tumors secrete abnormal insulin-like growth factor (Raghavan et al., 2007).
Hepatic disease. Glycogen stores rapidly disappear as liver disease (including cirrhosis due to alcoholism) progresses, causing recurrent hypoglycemia (Cryer, 2004). Dextrose infusions (10%) or IV bolus treatments of 25% or 50% dextrose are required because glucagon will be ineffective due to depleted glycogen stores. Hemodynamic instability, respiratory failure, and metabolic acidosis also are common in these cases (Cryer et al., 2003).
Reactive hypoglycemia. In some cases, hypoglycemia occurs immediately following meals, with no known causes (idiopathic reactive hypoglycemia [RH]). Alimentary hypoglycemia, another form of RH related to prior upper GI surgery (Guettier, 2006), results from rapid glucose absorption into the intestine and increased insulin secretion after every meal. RH is treated easily by eliminating simple sugars from the diet and increasing the frequency of meals, with smaller total carbohydrate intake at each meal (Raghavan et al., 2007).
Medication-Related Causes of Hypoglycemia
Secretagogues. Sulfonylureas, the most common oral medication in the treatment of type 2 diabetes in older adults, are associated with hypoglycemic events by enhancing insulin secretion from pancreatic islet cells. Sulfonylureas are named for their core configuration, consisting of one sulfonylurea group attached to a benzene ring. First-generation sulfonylureas, including chlorpropamide (Diabinese[R]), tolbutamide (Orinase[R]), tolazamide (Tolinase[R]), and acetohexamide (Dymelor[R]), have substituents that are small, polar, and hydrophilic, making them more water-soluble and less potent, in the second and third-generation sulfonylureas, (glyburide [Micronase[R]], glipizide [Glucotrol[R]], gliclazide [Diamicron[R], Dianorm-In[R]], and glimepiride [Amaryl[R], DIAPRIDE[R]]), substituents are large, nonpolar, lipophilic groups that more readily penetrate cell membranes and therefore are more potent in increasing insulin release (Spiller & Sawyer, 2006). A comparison of these medications is presented in Table 1.
Risk factors for sulfonylurea induced hypoglycemia include age over 65, inadequate caloric intake, polypharmacy interactions (e.g., [beta]-blockers, sulfonamides, insulin), and recent initiation of sulfonylurea therapy with limited prior exposure (Doyle & Egan, 2003; Lewis, 2004; Spiller & Sawyer, 2006). Renal disease can delay hypoglycemia onset 1-3 days through accumulation of medication and metabolites. In the United States, glyburide has been associated with the highest number of serious hypoglycemic episodes. Mefformin in combination with glyburide (Glucovance[R]) also has caused severe hypoglycemic incidents (Ben-Ami, Nagachandran, Mendelson, & Edoute, 1999; Briscoe & Davis, 2006; Guettier, 2006; Raghavan et al., 2007).
Psychotropic medications. The link between haloperidol (Haldol[R]) and episodes of severe, life-threatening hypoglycemia has been noted in the literature since 1969 (Kojak, Barry, & Gastineau, 1969; Walter, Hoofnagle, Lanum, & Collins, 2006). Although haloperidol is not listed specifically in the Revised Beers List of Potentially Inappropriate Medications for the Elderly (Fick et al., 2003), it should be avoided in older adults with a history of hypoglycemia, or sulfonylurea or insulin use, due to the risk of severe hypoglycemic interactions. Tricyclic antidepressants, chlorpromazine, MAO inhibitors, and lithium also have been reported to cause severe hypoglycemia (Burks & Gopalan, 2005; Doyle & Egan, 2003).
Quinolines. Quinine (Qualaquin[R]) is used as an anti-malarial and anti-arrhythmic agent, and in the treatment of leg cramps. Other drugs in the same class are quinidine (Biguin Durules[R]), chloroquine (Aralen[R]), mefloquine (Lariam[R]), and halofantrine (Halfan[R]). All drugs in this class have strong hypoglycemic properties, increasing insulin secretion as the sulfonylureas do (Doyle & Egan, 2003).
Antibiotics. Pentamidine (Nebu Pent[R], Pentam[R]), used in treating opportunistic infections associated with immunosuppression (e.g. Pneumocystis pneumonia) and protozoan parasites, causes severe hypoglycemia by increasing insulin secretion (Lehne, 2004; Raghavan et al., 2007). Isoniazid (Niazid[R]) has been reported to potentiate the effects of glyburide and also cause hypoglycemia through cytotoxic hepatic damage (Burks & Gopalan, 2005; Doyle & Egan, 2003; Service, 1995).
Since they were used to treat typhoid fever in 1942, sulfonamides such as trimethoprim/sulfamethoxazole (TMP/SMX[R]; Bactrim DS[R]; Septra DS[R]) have been known to cause significant, life-threatening hypoglycemia by increasing insulin secretion (Arem, Garber & Field, 1983; Burks & Gopalan, 2005). Fluorquinolones generally have low rates of hypoglycemia tmless prescribed with a sulfonylurea, increasing risk for hypoglycemic events by a factor of 1.5-2 (Mohr et al., 2005). Gatifloxacin (Tequin[R], Zymar[R]) has the highest rate of hypoglycemia among this drug class in older adults (Lodise et al., 2007). In contrast, moxifloxacin (Avelox[R]), ciprofloxacin (Ciloxan[R]), and the cephalosporins have lower observed hypoglycemic effects in older patients (Park-Wyllie, Juurlink, & Kopp, 2006).
Alcohol. Ethanol is a potent hypoglycemic agent causing decreased endogenous glucose production and glycogenolysis. Volume of alcohol intake is correlated with the degree of resulting hypoglycemia and can be life-threatening in elders (Al-Sanouri, Dikin, & Soubani, 2005; Raghavan et al., 2007; Smeeks, 2008).
Cardiac medications, [beta]-blockers with marked antidysrhythmic (quinidine-like) effects (e.g., propranolol [Inderal[R]], sotalol [Betapace[R]], oxprenolol [Trasicor[R]]) inhibit glycogenolysis and are most likely to be associated with hypoglycemia in older adults (Burks & Gopalan, 2005; Sharma, Tefera, & Aminzay, 2009). Isolated reports indicate angiotensin-converting enzyme inhibitors can cause hypoglycemia by increasing insulin sensitivity (Herings, de Boer, Stricker, Leufkens, & Porsius, 1995). Disopyramide phosphate (Norpace[R]) is an antiarrhythmic (procainamide family) that also has caused increased insulin secretion and hypoglycemia (Burks & Gopalan, 2005).
Salicylates. Over 100 years ago, salicylates were considered a first-line treatment for diabetes mellitus due to their observed hypoglycemic activity (Williamson, 1901). It has been determined more recently that salicylates such as aspirin decrease serum glucose by reversing or inhibiting the process of insulin resistance related to generalized inflammatory responses (Shoelson & Goldfine, 2006).
Treatment of Hypoglycemia
The ADA (2009) indicates 15-20 grams of glucose is the preferred treatment for hypoglycemia. However, any form of carbohydrate can be administered with close follow up every 15 minutes until blood glucose reaches 70 mg/dL. For patients at risk for severe hypoglycemia, glucagon kits should be prescribed and family members instructed in their use. Treatment of hypoglycemia (plasma glucose <70 mg/dl) "requires ingestion of glucose- or carbohydrate-containing foods," although "pure glucose is preferred" (ADA, 2009). In severe cases of hypoglycemia with unresponsiveness, emergency glucagon kits should be used to reverse the low blood sugar levels (see Table 2).
Glucose. In adults, intravenous glucose is the preferable first-line treatment for severe hypoglycemia (Guettier, 2006; Moses, 2007). Dextrose is a simple, inexpensive, and effective solution for all cases of hypoglycemia. For patients with severe hypoglycemia and altered mental status, IV infusion of 10% dextrose solution is effective as well as IV bolus doses of 25% or 50% dextrose adjusted to maintain a blood glucose concentration greater than 70 mg/dL (Moore & Woollard, 2005). In mild, moderate, or severe hypoglycemia without altered mental status, supplementation with glucose tablets, gels, liquids, or other sources of carbohydrates such as juices should be attempted before IV dextrose (Cryer et al., 2003; Moses, 2007). Pre-measured, commercially available oral glucose products (tablets, gels, and liquids) are designed for rapid absorption and availability (15 minutes or less), unlike complex carbohydrates in foods and juices (Moses, 2007).
Glucagon. Glucagon is a linear peptide of 29 amino acids related to the secretin family of peptide hormones and produced in alpha cells of the pancreatic islets. glucagon's primary action is to increase blood concentration of glucose by stimulating hepatocytes and breakdown of glycogen in the liver, and by activating hepatic gluconeogenesis, which allows amino acids to be converted to glucose. It also increases lipolysis of triglycerides in adipose tissue (Spiller & Sawyer, 2006). The only FDA-approved uses for glucagon include emergency treatment of severe hypoglycemic reactions in unconscious patients or those unable to swallow (if IV glucose is unavailable), psychiatric patients receiving insulin shock therapy, diagnosis of insulinoma, and relaxation of smooth muscle in the GI tract for radiologic studies (ADA, 2009; Lehne, 2004; Wilson, Shannon, Shields, & Stang, 2008).
Eli Lilly and Company (2005) packages glucagon emergency kits in bright orange, hard plastic cases that contain one Hyporet [R] syringe, a 1 gm vial of lyophilized glucagon (powder form), and one vial of 1 ml vial of sterile water as the diluent solution. The glucagon should be reconstituted at the time it is needed and should not be saved for future use. The recommended dose for severe hypoglycemia is 1 mg/ml subcutaneously (SC), intramuscularly (IM), or IV for adults or children weighing 44 pounds or more. Onset of action for IM administration is 15 minutes, with a 30-minute duration of effect. Severe hypoglycemia should be treated first with IV glucose prior to use of glucagon. Nurses should be careful to ensure physician orders for glucagon use are consistent with FDA guidelines and recommended use instructions, including unconscious or non-responsive patients and blood glucose consistent with severe hypoglycemia (usually below 60 mg/dL).
As of March 2009, only two reports had been published regarding either adverse or non-therapeutic reactions to IM, IV, or SC glucagon injections (Marri, Cozzolino, & Palumbo, 1968; Thoma, Glauser, & Genuth, 1996). In addition, according to staff at Eli Lilly and Company, no known published studies within the past 5 years documented the presence of adverse reactions to glucagon in patients over age 65 (personal communication, December 12, 2007). Nurses should be aware that clinical studies of glucagon lacked sufficient numbers of subjects age 65 and older to determine if they have a different response than younger subjects. Prescribers should start at the low-end dosing range (0.5 mg/ml) for geriatric patients due to greater risks of co-morbid hepatic, renal, or cardiac disease (Eli Lilly and Company, 2005).
More importantly, the most extensive and well reviewed geriatric pharmaceutical guide (endorsed by the American Geriatrics Society) does not list glucagon within its accepted formulary for older adults (Omnicare, 2004). Acute injections of glucagon can cause nausea and constipation, or complicate treatment of postoperative patients and those with acute or chronic gastrointestinal disease (Eli Lilly and Company, 2005; Wilson et al., 2008). Many older adults with hypoglycemia have comorbid diagnoses of congestive heart failure, coronary artery disease, and renal failure, and may be prescribed [beta]-blockers, calcium channel blockers, angiotensin receptor blockers, or a combination of the three. Tang (2003) noted glucagon exerts positive inotropic and chronotropic effects on the heart, and administration can cause acute hypertensive crises. Yet, Eli Lilly and Company (2005) denies any reports of such events in older adults.
Octreotide (Sandostatin LAR[R]). Emergency services and hospital emergency departments have used this drug for patients with difficult-to-manage hypoglycemia (Lheureux, Zahir, Penaloza & Gris, 2005). Octreotide also has been used for sulfonylurea overdose, although this is an off-label use in the United States (U.S. Food and Drug Administration [FDA] 2007; Kleinschmidt, 2005; Novartis, 2007; Omnicare, 2004). When used to treat episodes of hypoglycemia, dextrose itself can induce insulin secretion, contributing to rebound episodes of hypoglycemia. Octreotide is thought to block the elevated insulin levels that result from both sulfonylurea and dextrose use (McLaughlin, Crandall, & McKinney, 2000). The demonstrated safety and efficacy of octreotide for the treatment of sulfonylurea-induced hypoglycemia (Lheureux et al., 2005) has led the FDA to sponsor at least one new clinical trial investigating the use of the drug for this purpose (Fasano, 2008).
Treatment Algorithm for Hypoglycemia in Older Adults
The algorithm presented in Table 3 represents a safe, rational approach for treating hypoglycemia in older adults. Treatment emphasizes use of glucose tablets, liquids, or gels starting at 15 mg glucose/dose to be administered to elders who are awake and responsive, with 15-minute monitoring to document return of BG greater than 70 mg/dL (Moses, 2007). This approach emphasizes frequent monitoring and avoidance of severe hypoglycemia. However, dextrose infusions or ampules for IV administration related to persistent, severe hypoglycemia also should be available for patients who do not respond to oral glucose (Briscoe & Davis, 2006; Frier & Fisher, 2007).
Glucagon is indicated for persistent severe hypoglycemia unresponsive to oral glucose or glucose infusions (Eli Lilly and Company, 2005; Moses, 2007). Orders for glucagon should be reviewed in advance, and its use specified only if the patient is unresponsive and unable to receive oral glucose or if IV glucose infusions have been ineffective or are unavailable; nursing documentation also should reflect this (ADA, 2009; Eli Lilly and Company, 2005; Wilson et al., 2008).
Polypharmacy, type 2 diabetes, occult infections, and renal disease continue to increase in frequency, often resulting in recurrent hypoglycemic episodes among older adults. The medical-surgical nurse should pursue these and other clinical clues to determine causes of recurrent hypoglycemia, keeping in mind insulin or insulin secretagogue treatment of diabetes is still the most common cause of hypoglycemia. Other frequent causes of iatrogenic hypoglycemia include unexpected nutritional interruption/discordance, low body mass index, congestive heart failure, chronic kidney disease, and use of [beta]-blockers (Maynard, Huynh, & Renvall, 2008).
Hypoglycemia risk-reduction efforts by nursing staff should include addressing the issues highlighted here through knowledge of current renal function and medication interactions. Inexpensive and effective commercial products for hypoglycemic treatment are available readily for nurse use. They should be present in emergency departments, medical-surgical care areas, geropsychiatry units, and long-term care settings. Hypoglycemic treatment protocols similar to those presented here should be present in unit policy and procedure manuals detailing each level of intervention based on both patient clinical status and blood glucose measures. Regular inservices or reviews of these protocols should occur on all nursing units (Cryer et al., 2009). When hypoglycemic events occur with unconsciousness or inability to swallow, clearly written orders for glucagon administration should be in place. Intravenous glucose/ dextrose administration always should be attempted prior to glucagon use. Nurses employed in nursing home (NH) settings particularly should be aware of these guidelines. A number of authors in the United States and the United Kingdom reported on the inconsistency in clinical policy documentation, follow-through, and knowledge of appropriate treatment for acute hypoglycemia among NH staff (Munshi & Lipsitz, 2007). For example, Ouslander, Osterweil, and Morley (1997) provide the following suggestions for care of the hypoglycemic NH patient:
Where possible, nursing staff should be allowed to administer 50 ml of 50 percent dextrose when starting an intravenous line on a diabetic resident suspected of being hypoglycemic. In addition, diabetic NH residents should have a standing order for 1 mg of glucagon intramuscularly in case of hypoglycemia associated with confusion and/or lethargy ... give glucagon if BS<30 or if acute confusion or delerium occurs (pp. 293-294).
In the United States, Medicare regulations permit "short-term intravenous lines or tubing" (Cress, 2007, p. 214). Consequently, most patients in nursing homes will not have available IV access should IV dextrose solutions be required for an acute hypoglycemic episode. In addition, most NHs employ a higher percentage of LPN versus RN staff who may be the first to respond to or be aware of hypoglycemia in a resident (Seago, Spetz, Chapman, Dyer, & Grumbach, 2004). In many states, LPNs may not be certified or permitted to initiate IV access or provide IV medications, requiring the intervention of an RN during an acute hypoglycemic episode (National Association of Practical Nurse Educators, 2009). Although there have been no published studies at this time on the frequency or circumstances of use of glucagon in NHs, it is possible that confusing or poorly written orders or policies could lead to use of glucagon as a first-line treatment in an acute hypoglycemic episode when the patient currently is prescribed [beta]- blockers and/or calcium channel blockers. Given these realities, a best-practice approach to the treatment of acute, severe hypoglycemia in the NH would require intervention by a RN or nursing supervisor.
The nurse should be aware of co-morbidities in patients prescribed glucagon, especially those receiving B-blockers and calcium channel blockers. Intravenous administration of glucagon can have marked positive inotropic and chronotropic effects on the heart, leading many experts to support its use as an antidote for overdoses of any medications which reduce heart rate and/or blood pressure including: [beta]-blockers, calcium channel blockers, and dilitiazem (Cardizem [R]) (Bailey, 2003; Mahr, Valdes, & Lamas, 1997; Shepherd, 2006; White, 1999). A transient increase in both blood pressure and pulse rate usually occurs following the administration of glucagon. Patients taking [beta]-blockers or calcium channel blockers might be expected to have a greater increase in both pulse and blood pressure, which usually will be transient (15-30 minutes) because of glucagon's short half-life. However, increased blood pressure and pulse rate in patients with coronary or renal disease may require additional interventions due to slowed elimination of the drug (Abernethy & Schwartz, 1999; White, 1999). Hence, close monitoring of patients taking these cardiac medications is suggested following glucagon administration.
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Note: The author and all MEDSURG Nursing Editorial Board members reported no actual or potential conflict of interest in relation to this continuing nursing education article.
Perry C. Goldstein, BSN, RN, CMSRN, is a Staff Member and Charge Nurse, Medical Surgical Unit, Box Butte General Hospital, Alliance, NE.
Table 1. Sulfonylureas Medication Characteristics 1st Generation Sulfonylureas Low potency Chlorpropamide (Diabinese[R]) Small polar molecules Tolazamide (Tolinase[R]) Hydrophilic, water soluble Tolbutamide (Orinase[R]) Large daily doses Acetohexamide (Dymelor[R]) 2nd Generation Sulfonylureas High potency Glyburide (Diabeta Micronase[R]) Large, nonpolar molecules Glyburide-micronized (Glynase Lipophilic, membrane permeable Prestabs[R]) Small daily doses Glipizide (Glucatrol[R]), High risk for hypoglycemia (Glucatrol XL[R]) Gliclazide (Diamicron[R]) Gliquidone (Glurenorm[R]) 3rd Generation Sulfonylureas High potency Glimepiride (Amaryl[R]) Large, nonpolar molecule Lipophilic, membrane permeable Small daily dose High risk for hypoglycemia * Not available in the United States Source: Lewis, 2004; Spiller & Sawyer, 2006 Table 2. Available Rapid-Acting Glucose Supplements/Hypoglycemic Treatments Brand Name Glucose/ Retail Cost ($USD) Tab BD[R] 5 grams 1.99/6 tabs (http://www.bd.com) (multi flavors) Dex-4[R] 4 grams 16.95/100 tabs (http://www.dex4.comn (multi flavors) CVS 4 grams 5.49/50 tabs (http://www.cvs.com) (multi flavors) Walgreens 4 grams 5.49/50 tabs (http://www.walgreens.comn (multi flavors) Walmart 4 grams 4.78/50 tabs (http://www.walmart.com) (multi flavors) ReliOnTablets[R] 4 grams 4.78/50 tabs (http://www.relion.com) (multi flavors) ReliOn Gel[R] 15 grams/ 9.98/3, 15 gram (http://www.relion.com) tube tubes Glutol Liquid[R] (180 ml) 100 gram/180 6.40-9.40/180 ml (http://www.paddocklabs.com/ ml (0.55 diabetes.html) gm/ml) Glutose Gel[R] 15 grams/ 14.00/3, 15 gram (http://www.drugstore.com) tube tubes Glutose Gel[R] 45 grams/ 14.00/1, 45 gram (http://www.drugstore.com) tube tubes GlucoBurst Geh 15 grams/ 42.00/18 foil (http://www.glucoburst.com) tube packages GlucoBurst Tabs[R] 5 grams 9.00/3, 24 et (http://www.glucoburst.com) bottles Insta Glucose Geh 24 grams/tube 13.00/3, 24 gram (http://www.walgreens.com) tubes D25/D50 Amputes 25 grams/50ml 10.00-12.00/ampute (http://www.hospital- pharmacy.com) Glucagon[R] Emergency Kit 1 mg/ml 110.00-124.00/kit (http://www.lilly- reconstituted from U.S. pharmacies diabetes.com) Speed Brand Name Dose of Action BD[R] 3 tabs 15 min (http://www.bd.com) Dex-4[R] 4 tabs 15 min (http://www.dex4.comn CVS 4 tabs 15 min (http://www.cvs.com) Walgreens 4 tabs 15 min (http://www.walgreens.comn Walmart 4 tabs 15 min (http://www.walmart.com) ReliOnTablets[R] 4 tabs 15 min (http://www.relion.com) ReliOn Gel[R] 1 tube 15 min (http://www.relion.com) Glutol Liquid[R] (180 ml) 30 ml 15 min (http://www.paddocklabs.com/ diabetes.html) Glutose Gel[R] 1 tube 15 min (http://www.drugstore.com) Glutose Gel[R] 1/3 tube 15 min (http://www.drugstore.com) GlucoBurst Geh 1 tube 15 min (http://www.glucoburst.com) GlucoBurst Tabs[R] 3 tabs 15 min (http://www.glucoburst.com) Insta Glucose Geh 1 tube 15 min (http://www.walgreens.com) D25/D50 Amputes 1 ampute 15 min (http://www.hospital- pharmacy.com) Glucagon[R] Emergency Kit 1 vial 15-30 min (http://www.lilly- diabetes.com) Table 3. Algorithm for Treatment of Hypoglycemia at Different Severity Levels Mild Hypoglycemia Moderate BG 60-70 mg/dl Hypoglycemia Give 15 grams carts BG 45-59 mg/dl give 20 grams carbs 1. Glucose oral gei 40% 1. Glucose oral gel 40% 15 grams orally, or grams orally, or 2. Glucose 3 tablets 2. Glucose 4 tablets orally @ orally @ 5 gms or 5 gms, or 5 tablets @ 4 4 tablets @ 4 gms, or gms, or 3. Juice 4 ounces (120 ml) 3. Juice 6 ounces (180 ml), or 4. Monitor BG q15 min 4. Dextrose 50% 25 ml IV bolus 5. Monitor BG q15 min Severe Unconscious Hypolycemia with Severe Awake, BG <45 Hypolycemia Give 30 grams carbs bg<45 1. Glucose oral gel 40% 30 1. Dextrose 50% 25 ml IV grams orally, or bolus, or 2. Glucose 6 tablets orally @ 2. Glucagon 1 mg SC or IM * 5 gms or 8 tablets @ 4 Vomiting and aspiration gms, or risk: Roll patient on side after 3. Juice 8 ounces (240 ml) 3. Monitor BG, HR, and or respirations q15 min 4. Dextrose 50% 25 ml IV bolus 5. Monitor BG q15 min Source: Chau & Edelman, 2001; Moses, 2007; Raghavan et al., 2007; Zammitt & Frier, 2005. (BG = blood glucose, Garbs = carbohydrates, IV = intravenous, IM = intramuscular, SC = subcutaneous, HR = heart rate) * Octreotide acetate (Sandostatin LAR[R]) 50-100 pg (IM and SC) has been used as an off-label treatment in emergent hypoglycemic situations with unconsciousness in the U.S. and U.K. At this time, the FDA has not approved octreotide for primary or off-label use in severe hypoglycemia.
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|Author:||Goldstein, Perry C.|
|Date:||Jul 1, 2009|
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