About

Flap Surgery: The Basics

Introduction

Flap surgeries can be a critical treatment for various wounds to provide bulk tissue. It is a tad more detailed than skin grafts, as it involves a circulatory supply from a donor site to a recipient site. It is important to recognize what flap surgery entails, the indications, and types of flap surgeries. Nurses should be knowledgeable on care plans and assessment for flap surgery, positioning techniques, patient education topics, and how to identify possible complications such as infection or flap dehiscence. Are you ready to dive into the interesting course topic of flap surgery?

Flap Surgery: What is it?

Flap surgery involves removing healthy, live tissue from one location of the body and transporting it to another area that needs it for healing purposes. Flap surgeries are commonly used to transfer this healthy tissue to areas of lost skin, fat, muscle movement, and/or skeletal support (9). A tissue flap has its own system for vascularization and does not depend on the recipient’s wound bed to perfuse the donor tissue, which differs from non-vascularized skin grafts (8). Essentially, a flap is tissue with a substantiated blood supply that is transferred from a donor site to a recipient site. If the flap surgery was a party, the damaged host site would send out an invite saying “BYOB- Bring Your Own Blood-Supply!”

The flap continues to be fed by the same blood supply from where it was taken, until new blood vessels grow from the recipient site and the wound heals completely. The recipient site is called the primary defect and the wound that is created by cutting, lifting, or sliding the flap to fill the primary defect is called the secondary defect (8). The base, or pedicle, of the flap is the tissue that remains attached to the skin adjacent to the defect, it contains the vascular supply required for initial flap survival (8).

Surgeons have used skin flaps to repair wounds and tissue damage for centuries. The term “flap” was derived from the Dutch word “flappe” during the 16th century (8). Around 700 B.C., the Sushruta Samhita (an ancient text on surgery and medicine) first documented a technique of reconstructing a large nasal tip defect with a flap of cheek tissue (8). New techniques are constantly being developed to meet various needs. Flap surgeries are used for a variety of wounds from pressure ulcers to breast reconstruction following mastectomy.

Types of Flap Surgeries 

Flap surgeries are classified in the following ways: (9) 

• Blood supply  

• Type/composition of tissue  

• Distance of the healthy site from the recipient tissue  

• Locations of donor and recipient tissue 

• Movement 

Figure 1: Classification of Flaps 

Classification by Blood Supply 

Flaps can be named based on the supply of blood. The understanding of the circulation of blood to the donor tissue is critical when describing the type of flap. The terms random and axial are used to categorize the blood supply. 

• Random Flaps 

• Not based on a specific vessel 

• Uses subdermal plexuss (network of blood vessels between the deep reticular portion of the dermis and subcutaneous fat tissue beneath it) (7) 

• Axial Flaps 

• Single, direct cutaneous artery in the axis of the flap 

• Named according to the pathway 

Classification by Tissue Type 

Flaps can be named according to their composition. The tissue composition may be skin, fascia, muscle, bone, nerve, cartilage, or a combination. Fascia is the thin lining of connective tissue that surrounds and holds each blood vessel, bone, nerve fiber, and muscle in place (7). Cutaneous refers to the layers of skin. Pedicle flaps are those that are still attached to the original site and the other end is moved to cover the recipient area; a free flap is an area of tissue completely removed from one part of the body and surgically placed in another area (8). 

Common flaps: (5) 

• Skin Flap: Skin and superficial fascia 

• Fascio-cutaneous Flap: Skin and deeper layer of deep fascia 

• Fascial Flap: Deep fascia only 

• Muscle Flap: Muscle only 

• Myo-cutaneous Flap: Muscle and skin 

• Osteomyocutaneous Flap: Muscle, bone, and skin 

• Bone Flaps: Bone (vascularized) 

• Innervated Flaps: Flaps that contain a motor or sensory nerve and function 

Fascio-cutaneous Flap  

This flap includes the skin, subcutaneous tissue, and the underlying deep fascia (5). The musculocutaneous perforators or direct septocutaneous branches of major arteries act as vascular supply (5). Perforator flaps are named based on their location, arterial supply, or the muscle of origin. The indications for fasciocutaneous flaps are based on its advantages of being more simple, reliable, thin, and easily mobilized (8). These flaps can come from many potential donor sites (8). 

Muscle Flap 

Muscle tissue can be used as donor tissue in flap surgery. Surgeons may utilize the benefits of flap surgery in wound closure following major surgeries. For example, median sternotomy (vertical inline incision through the sternum of the chest) is the most commonly used approach for cardiac surgery (6). Cardiac surgeons face the risk of deep sternal wound infections following surgery, which is associated with significant morbidity and mortality rates. The use of soft tissue flaps for sternal closure is helpful for patients with extensive tissue deficits after debridement (6). It can be used for immediate or delayed closure. Options for donor tissue for sternal flap closure include the pectoralis major, rectus abdominis, and latissimus dorsi muscles, or an omental flap (6).  

Remember, flaps are transplanted with blood supply intact, so it’s important to know the supply. For instance, if tissue from the pectoralis major muscle is used, the nurse must recognize that this muscle’s primary and secondary blood supply is the thoracoacromial artery and perforators from the internal mammary artery (6). 

Musculocutaneous Flap 

This type of flap, which includes muscle and skin layers, is often used when the area to be covered needs more bulk and an increased blood supply. Musculocutaneous flap surgery is frequently used to rebuild a breast after a mastectomy (5). 

Bone Flap 

A bone flap is comprised of bone with a vascular supply. An example of this flap surgery is for a surgical site infection (SSI) following a craniotomy; in this procedure, operative debridement occurs, and the bone flap is removed, cleaned, and replaced (4). An alternate therapy for this is titanium cranioplasty (implant instead of native bone flap), which has similar outcomes. 

Classification by Location and Movement 

• Local flap: Donor tissue is located next to the area receiving the tissue; the skin remains attached at one end to allow the blood supply to be left intact (5). 

• Regional flap: Donor tissue is a section that is attached by a specific blood vessel.  

• Distant flap: Donor and recipient tissues are distally located from each other. This flap surgery involves detaching and reattaching skin and blood vessels from one site of the body to another site; microsurgery is used to connect the blood vessels (5).  

Figure 2: Example of Flap Type 

The movement of the flap is also used to describe flap surgery. You may hear terms such as advancement, sliding, rotation, and pivotal. Sliding flaps is when the tissue is moved or "slid" directly into the adjacent defect without "jumping" over other tissue (5).  Advancement flaps are considered simple movements for local flaps and fall within the group of sliding flaps. Pivotal (geometric) flaps include rotation, transposition, and interpolation (5). Local, random pattern flaps are common for the reconstruction of cutaneous defects. 

Image 1: Image of a local flap surgical procedure to cover nasal tip defect/wound (9) 

Indications for Surgery 

There is an incredible breadth of possibilities for flap reconstructive surgery, from small, skin-only defects to large, multi-tissue defects. There is a wide range of etiologies, such as traumatic, oncological, and congenital (9). The transferred tissue flap can contain multiple types of tissue, including skin, muscle, nerve, fascia, and bone (9). The larger the volume of tissue transferred, the greater the need for perfusion. A common indication is the need for a large bulk of tissue. Flaps are helpful when wounds are large, complex, or need large amounts of tissue for closure.  

General Indications: 

• Protection of the greater vessels 

• Correction of congenital defect 

• Abdominal wall reconstruction 

• Deep, gaping wounds 

• Reconstruction after tumor excision 

• Trauma 

• Debridement procedure to remove infected or necrotic tissue 

• Venous ulcers (non-healing) 

• Pressure ulcers (non-healing) 

• Breast reconstruction 

• Rhinoplasty 

• Scar Revision 

• Skin Cancer 

• Burns 

Each type of wound has unique indications. Commonly, skin flap surgery is required when a wound is too big for the edges to be brought together directly, so the flap covers the area and depth of the wound (10).

Risks versus Benefits 

Flap survival depends on factors of blood flow, angiogenesis (formation of new blood cells), vascularization, edema, wound closure tension, postoperative complications (hematoma/seromas) and infection (8). Before the initial incision, the flap is fully vascularized and viable, but once the flap is raised, it is immediately ischemic. The tissue can survive up to 12 to 13 hours of avascularity at 37°F and many research studies have proven it is viable even longer (8). This time is invaluable to preserve the tissue. Sufficient blood flow through attachment of the base of the flap is essential in the initial 24 to 48 hours after surgery (8). There is a risk for loss of tissue with no meaningful contribution to the needed area, along with a new wound. This risk reminds me of a neighbor who once removed carpet from a closet to patch carpet in a bedroom, only to find the cutting was too small and they were left with two gaping carpet holes.  

There is also risk for bleeding, infection, or necrosis at both sites. A recent study found that more than 27% of patients will experience a minor complication (wound dehiscence, infection, fistula, and donor-site problems) after surgery, and 6% of patients will suffer a major complication (flap failure, pneumonia, and cerebrovascular accidents) following surgery (11). Chronic flap complications can also be aesthetic in nature; include scarring, contracture, color/texture mismatch, and lack of hair growth. Patients may experience pain or numbness at the sites on a chronic basis as well (9). 

Most flap surgeries are considered safe with a low complication rate, and surgeons report that flap surgery is not avoidable in certain circumstances. However, the surgery preparation itself and anesthesia presents considerations for elderly patients or those with heart disease, uncontrolled diabetes, smokers, or bleeding disorders (2). Nutrition is a key factor in these surgical procedures. Poor nutritional status has been linked with a greater incident of negative outcomes (11). The healthier the patient is before surgery increases, the chances of reduced complications, so glucose control and weight management are examples of risk reduction strategies. 

Preparing for Surgery 

Patients undergoing flap surgery need an abundance of education on what to expect throughout this procedure. There are many opportunities to optimize patient outcomes before going to the operating room. Preoperative education, for example, has been suggested to have an important, positive effect on clinical outcomes (11). Many patients are also experiencing other issues, such as cancer diagnoses, poor circulation, comorbidities, bed sores, among others. Taking time to holistically prepare each patient is essential.  

Addressing Comorbidities and Other Conditions 

Multiple studies have found an increased surgical complication rate in patients with diabetes mellitus, older age, female gender, malnutrition, anemia, and nicotine intake (11). Prior to surgery, the goal is to improve and optimize the modifiable conditions as much as possible, for instance, reduction in nicotine or improvement in glucose control and anemia. Further, patients with advanced cancer can have hypothyroidism affecting postoperative healing if left uncorrected (11). Non-modifiable factors such as a history of radiotherapy, age, advanced cancer stage, or chronic kidney disease, cannot be altered prior to surgery, but can guide care planning and education following the surgery. 

Adequate nutrition before and after flap surgery has been demonstrated in numerous studies to improve outcomes. An estimated 35% of patients with head and neck cancers present in a state of malnutrition, and the Enhanced Recovery After Surgery (ERAS) Society recommends that all patients undergo a comprehensive preoperative nutritional assessment and consult with nutritionist (11). Improved nutrition status can hopefully yield enhanced wound healing problems and reduction in risk of infection. 

Lab assessment is key to preparation before flap surgery. An example is assessment for anemia prior to surgery. Patients who are anemic at the time of free flap surgery have been found to have poor outcomes (11). Remember, hemoglobin transporting the oxygen to the sites of flap insertion and removal is vital to the survival of the flap. Preoperative hemoglobin values below 10 g/dL have historically been a significant predictor of flap failure and thrombosis (11). A hematocrit level of 30 to 40% with normovolemic hemodilution is ideal to optimize patient outcomes.  

Blood transfusions during or following surgery impacts flap success as well.  Transfusion can increase blood viscosity and immunosuppression, thus leading to decreased blood flow and flap compromise from poor perfusion (11). Studies also show a link between blood transfusions and increased wound infections (11). Steps and treatments should be taken prior to surgery to improve anemia or blood component abnormalities to give these patients a greater chance for successful flap surgery. 

Preoperative considerations should include: (9) 

• Patient age  

• Diabetes status 

• Smoking history 

• Atherosclerosis 

• Peripheral vascular disease 

• Steroid use 

• Previous surgeries 

• The extent and location of the defect 

Providing Preoperative Instructions 

A lack of education, difficulty in understanding complex medical information, fear and anxiety about the surgery, and language barriers are some of the challenges a patient for surgery may have. Patients may also have limited access to reliable health resources or be unable to recall important information due to stress or preoperative medications. As a result, they may not be fully informed about the surgical process, potential risks, and postoperative care.  

Preoperative education list: 

• Assess the patient’s level of understanding. 

• Each facility should have a preoperative teaching program with specific content on surgery, but you must assess if the patient understands this information. 

• Review specific pathology and anticipated surgical procedure.  

• Verify that consent has been obtained / signed. 

• Informed surgical choices and consent for the procedure is required, not only a signature. 

• Use resource teaching materials, and audiovisuals as available on flap surgery and implement an individualized preoperative teaching plan.  

• Preoperative or postoperative procedures and expectations, output (urinary and bowel) changes to expect following surgery, dietary considerations, anticipated intravenous (IV) lines and tubes (nasogastric [NG] tubes, drains, and catheters). 

• Preoperative instructions: NPO guidance prior to surgery, shower or skin preparation, medications to take and hold, prophylactic antibiotics or anticoagulants, anesthesia premedication. 

• Discuss postoperative pain management plan and options.   

• Some patients may expect to be pain-free or are hesitant to take narcotic agents. 

• Provide education and encourage practice of coughing and deep breathing. 

• Confirm and recheck the surgery schedule, patient identification band, chart, and signed operative consent for the surgical procedure. 

• Offer pastoral spiritual care or counseling. 

Post-Operative Considerations 

This section will cover assessment, drains, positioning, and negative pressure wound therapy during the post-operative period. 

Assessment 

Frequent monitoring of free flaps in the acute postoperative period is important. It is strongly recommended that flap assessments are performed at least hourly for the first 24 hours postoperatively, then continued at a reduced increment for the duration of the patient's hospitalization (11). Each facility should have standing orders for flap assessment based on the directive of the surgeon or regulatory body.  

In addition to conventional assessments of flaps (physical exam of flap warmth, turgor, capillary refill, color, and Doppler assessment of the vascular pedicle), many adjuncts have been developed including implantable Dopplers to assess blood flow (11). Assessments should include a head-to-toe physical assessment and a focused wound assessment. A focused cardiovascular (circulation and perfusion) and integumentary assessment is appropriate. Review of lab work indicative of healing status, hemodynamics, and infection should be a priority. Standard post-operative assessments following anesthesia, such as respiratory and orientation, should be performed according to facility protocol. 

Assess circulation of the flap: 

• Color of the flap (dusky, blue, pink, pale) 

• Warmth 

• Dry/Intact? Leaking Fluids? 

• Changes in size 

• Edema 

• Indications of hematoma (sutures over the flap pulling apart, or palpable crepitus beneath the skin) 

Assess amount and type of exudate (drainage): (3) 

• Amount (scant, small/minimal, moderate, or large/copious)  

• Color and thickness: (7) 

• Sanguineous: fresh bleeding  

• Serous: clear, thin, watery plasma 

• Serosanguinous: serous drainage with small amounts of blood noted 

• Purulent: thick and opaque; color can be tan, yellow, green, or brown (this is an abnormal finding and should be reported to physician or wound care provider) 

Use of Doppler to assess deeper circulation of flap: (11) 

• Color duplex ultrasound 

• Near-infrared spectroscopy 

• LASER Doppler flowmetry 

• Implantable Doppler (useful for buried flaps) 

Assess circulation distal to the flap: 

• Capillary refill 

• Color  

• Temperature 

• Pulses  

• Edema 

Drains 

Drains may be used for removal of fluid around both the donor and recipient surgical areas to enhance healing (7). 

Patients may have the following drains after flap surgery: 

• Jackson Pratt (JP) drains 

• JP drains are closed-suction devices that remove fluids from the surgical sites. 

• JP drains contain a flexible bulb that has a plug that can be opened to remove collected fluid.  

• Each time fluid is removed from the JP drain, the nurse should squeeze the air out of the bulb and replace the plug before releasing the bulb.  

• This suction creates a vacuum that pulls fluid into the drainage tubing and bulb. 

• Penrose drains: 

• A Penrose drain is a soft, flexible tube inserted into the surgical site that drains fluid away from the wound bed (7).  

• Nurses should assess the drain and express fluid when appropriate to prevent accumulation. 

Positioning 

The goal of positioning following flap surgery is to promote and improve tissue perfusion. Positioning and elevation of the flap recipient will promote venous return and reduce fluid accumulation to improve tissue perfusion. Activity, exercise, and repositioning improve tissue perfusion. Massage of the erythematous area is avoided because damage to the capillaries and deep tissue may occur (10). Patients should never lay on the wound and extremities should never “dangle” (if the donor or recipient site is on the extremities). Positioning may require creativity when there are multiple drains, NG tube, wound therapy devices, IV tubes, and multiple dressings. Positioning should be free of restrictive clothing and flap sites should be visible for assessment of dressings. It is imperative for the surrounding skin to be sanitary and free of debris.  

Negative Pressure Wound Therapy 

Negative pressure wound therapy (NPWT) is typically used for soft-tissue salvage after the development of complications after flap surgery. For example, NPWT may be applied if an infection occurs in the donor or recipient flap. Immediate postoperative application of NPWT over the flap coverage is not as common (2). However, nurses should be aware of this treatment, the application, and its mechanisms of action. 

NPWT is also known as a wound vac. NPWT uses sub-atmospheric pressure to help reduce inflammatory exudate and promote granulation tissue in an effort to enhance wound healing (4). The idea of applying negative pressure therapy is that once the pressure is lower around the wound, the gentle vacuum suction can lift fluid and debris away and give the wound a fighting chance to heal naturally. NPWT systems consist of a sterile foam sponge applied to the wound bed, a semi-occlusive adhesive cover, a fluid collection system or cannister, and the suction pump (1). The foam sponge is applied to the wound and covered. A fenestrated tube is embedded in the foam, the wound is sealed with adhesive tape to make it airtight, and the machine delivers continuous or intermittent suction, ranging from 50 to 125 mmHg (1). 

Figure 3. Negative Pressure Wound Therapy Visual 

Home Care and Patient Education 

Educating clients and caregivers about wound care and skin integrity empowers them to actively care for their flap sites. With proper wound cleaning, dressing changes, and preventive measures, individuals can confidently perform their own self-care and enhance the healing process. The use of pamphlets, printouts, websites, and referrals to specialists will give the patients a stronger foundation of knowledge. 

• Wound Assessment  

• Teach the patient and caregiver about skin and wound assessment, ways to monitor for signs and symptoms of infection, complications, and proper healing. 

• Signs of Infection 

• Signs of a localized wound infection include redness, warmth, tenderness, and abnormal purulent drainage around the wound. 

• Importance of proper nutrition, hydration, and methods to maintain tissue integrity 

• Adequate caloric intake and balance of protein and essential vitamins has been shown to improve the healing of flaps (3). 

• Dressing changes, wound cleansing, and hand hygiene 

• Methods to prevent skin breakdown 

• The flap surgery is often for the treatment of a deep pressure wound, so education is needed on impaired skin integrity due to friction. 

• Common areas: Sacrum, heels, elbows. 

• Avoidance of raising the head of bed often, causing weight to be applied to sacrum. 

• Importance of turning, mobility, and ambulation 

• Pain management 

• Medications 

• Heat/cold therapy applications and precautions 

• Negative Pressure Wound Therapy devices (wound vac) 

• Home healthcare is applicable for these devices and should be changed by a certified individual, but patients should be aware of basic care and troubleshooting. 

• Drain maintenance 

• Showering restrictions 

• Reduction of stress and tension at wound site 

• Avoid constipation, strenuous movements, and lifting 

• Restrictions vary for location of flaps and per surgeon instructions 

• Follow-up appointments 

Flap Dehiscence or Loss 

Flap dehiscence is a complication in which the incision made to either the donor or recipient site reopens. A flap loss refers to the flap not re-establishing blood flow and surviving, leading to necrosis of the tissue. As we mentioned earlier, the survival of the flap is impacted by blood flow, new vascularization and tissue formation, edema, wound closure tension, postoperative complications (hematoma/seromas), and infection (8).   

Prevention Strategies 

Nurses should apply their basic knowledge on causes of wound dehiscence. Factors that influence dehiscence risk include the ability to synthesize collagen, strength of suture material, closure technique, and stress on the incision, such as coughing, strenuous movement, or obesity (7). Consider areas that have greater stress and tension, such as the abdomen. Dehiscence is most common following abdominal flap surgeries (7). NPWT has been shown to be a great preventative measure for wound dehiscence as studies found a roughly 50% reduction in stress and tension at the incision site with its use (7). This reduction in stress is attributed to the reduction in subcutaneous fluid accumulation and enhanced healing time.  

The location of the flap surgical sites will impact prevention. For example, immobilization and stabilization devices are unique to sites such as the abdomen, chest, extremities, and sacral region. Infection prevention measures for wounds are essential for nursing care. Incisions from flap procedures also have a higher chance of opening if the wound becomes infected (7). Prevention of hematomas is also meaningful, including the use of blood thinners. However, the safety precautions for blood thinners is different for each client. 

Management and Treatment 

It is estimated that 80% of free flaps can be salvaged if dehiscence or compromise is recognized early enough (11). As we mentioned, it is more common for flaps that are removed from (or applied to) the abdomen to open. The following terms describe the depth: 

• Superficial dehiscence: the skin wound alone opens, but the rectus sheath remains intact. 

• Full thickness dehiscence: the rectus sheath fails to heal and “bursts,” with protrusion of abdominal content. 

• This commonly occurs secondarily to intra-abdominal pressure (example: ileus) or poor surgical technique. 

The treatments for flap compromise will be determined by the provider once a cause is identified. Treatment may be a return to the operating room for additional surgical intervention or a simple evacuation of hematoma through suctioning.  

Recovery 

The focus of recovery is the healing and thriving of the flap site and surgical wounds. The time of flap healing varies, and some may heal much quicker than others. There are four phases of wound healing to recognize: hemostasis, inflammatory, proliferative, and maturation (7). 

• Hemostasis. This phase begins immediately after surgery when platelets release growth factors that alert various cells to start the repair process.  

• Inflammatory. This process involves vasodilation so that white blood cells in the bloodstream can move into the wound to begin cleaning the wound bed. Signs include edema and erythema.  

• Proliferative. This phase generally begins a few days after the injury and includes capillary repair and growth, granulation tissue formation, collagen formation, and wound contraction (7). 

• Maturation. During this phase, collagen continues to be created to strengthen the wound and fill in the wound gaps. 

The healing process can be enhanced in many ways, including nutrition therapy, topical agents, compression therapy, and hyperbaric oxygen therapy (HBOT). The recovery process for flap surgery will include management of pain and discomfort, disturbance of body image, impaired skin integrity, swelling, bruising, and gastrointestinal upset.  

Outcomes for recovery should be measurable and achievable. Each patient will have unique recovery goals, integrating comorbidities and psychosocial aspects.  

Examples of Patient Outcomes following flap surgery: (3) 

• Patient safety: Patient will be able to attain safety by maintaining intra- and extra-cellular environment. 

• Healing of wounds: Wounds should heal properly, complications will be prevented or maintained 

• Management of pain 

• Prevention of further damage or skin breakdown 

Conclusion

As discussed throughout this course on flap surgery, nurses are a key team member in the care and survival of flaps. Hopefully you now understand what flap surgery is, the indications, and types of flap surgeries. Critical knowledge includes pertinent assessment, drain or NPWT management, patient teaching, and prevention and management of possible complications.

Diabetic Ketoacidosis Management

Introduction   

Diabetic ketoacidosis is considered one of the most life-threatening complications of diabetes mellitus. More importantly, it is also one of the most preventable complications of diabetes. Through proper education and empowerment of persons with diabetes to self-manage this chronic medication condition, the overall mortality rates associated with this complication have steadily declined in the United States. An interdisciplinary team approach (including medical providers, social workers, case managers, and community resources) has been proven to reduce recurrences of DKA in vulnerable populations. (2)

Definition

DKA, or diabetic ketoacidosis, is defined as the potentially life-threatening medical condition that occurs in people with diabetes. While it usually occurs in persons with type 1 diabetes mellitus, who are dependent on daily insulin injections, it may also occur in individuals with type 2 diabetes for a variety of reasons (underlying physiologic stress, such as an acute infection or trauma, or uncontrolled blood glucose levels and missed routine diabetic medications).

In an acute case of diabetic ketoacidosis, the body is not producing enough insulin to move glucose into the cell for energy, and the liver then begins to break down fat for fuel instead, producing ketones. This buildup of ketones in the body results in ketoacidosis. Left untreated, diabetic ketoacidosis can lead to a diabetic coma and eventual death. (3)

Epidemiology

Epidemiology is the study of how often a disease process occurs in different populations. By studying the rates of occurrence, epidemiologists are able to evaluate treatment options and develop long term strategies to lower the risk of ongoing or recurrent disease related episodes.

Diabetic ketoacidosis is currently a leading cause of both morbidity and mortality in children with Type 1 diabetes. It usually occurs at the time of the initial diagnosis in as much as 30-40 percent of the children in the United States alone. In children living with a confirmed Type 1 diabetes condition (previously diagnosed), these percentages decrease to average rates of 6-8 percent annually.

The drastic reduction of such occurrences is believed to be directly related to ongoing patient and family education and medication adherence. Diabetic ketoacidosis is potentially life-threatening, but it is for the most part, also preventable. Throughout this educational offering, key components of patient education in diabetic self-management, including reducing the risk of diabetic ketoacidosis, will be discussed (4) (5).

By comparison, other countries, challenged by annual income, healthcare access, cost management, and food insecurity, do not fare so well. Various studies were funded by the Leona M. and Harry B. Helmsley Charitable Trust, and the Juvenile Diabetes Research Foundation Ltd. Several countries included in these studies were deemed “LLMIC” (low and low middle-income countries). Countries, including Haiti, Ethiopia, Senegal, Nepal, and Tanzania, to name a few were found to have inadequate supplies, medications, and equipment to both initially diagnose, and successfully manage diabetes mellitus long term. Critical items necessary for the treatment and stabilization of acute diabetic ketoacidosis were in even shorter supply. These barriers to treatment resulted in delayed or missed diagnosis, increased overall complication rates and premature deaths.

“Evidence from single-center studies suggest that DKA in new-onset T1D is more common in LLMICs compared to upper and upper-middle income countries, with rates ranging from 62.2 to 77.1% in Nigeria, 69.8% in South Africa, and 92.1% in Sudan. In comparison, in upper and upper-middle income countries in North America and Europe the rates range from 14.7% (Denmark) to 42.0% (France”). (6)

Ongoing education of healthcare professionals and patients/families alike, coupled with availability of and easy access to self-management medications, and monitoring equipment, positively affect DKA related health outcomes and quality of health and well-being.

The development of insulin delivery systems (insulin pumps) has further positively impacted the rate of DKA occurrence. Patient comfort, ongoing education, streamlined medication delivery and enhanced monitoring systems have afforded patients with diabetes a better understanding of their condition and empowered them to successfully self-manage their health conditions. While reported rates of DKA in previously diagnosed persons with T1DM were 6.3% in one study, that number decreased to 2.2% at 3 years out.

Ongoing improvements in closed insulin delivery systems medication continues to improve (lower) DKA occurrence rates, when compared to those previously using multiple daily injection therapy. The development of continuous glucose monitoring (CGM) devices, in addition to insulin delivery systems, provides for early detection and treatment of both hypoglycemia and hyperglycemia. The addition of remote app devices further allows constant monitoring and two-way communication between patients, family members, and even healthcare providers.

Sadly, the population identified as being at highest risk for DKA is that of children who are uninsured/underinsured, lacking the insurance coverage for many closed delivery medication systems as well as specialty care (pediatric endocrinology) provider access.

The acute complications associated with DKA account for a high percentage of premature deaths in T1DM patients under the age of 30 years old. (7) Given these statistics of prevalence and incident rates, DKA is an ever-increasing global concern which is best addressed and managed through ongoing, patient specific disease management education.

The prognosis for DKA worsens in the presence of coma, hypotension and in the presence of severe (chronic and acute) comorbidities. Yet, with early identification, ongoing education, and improved glucose monitoring/treatment options, DKA, often life threatening, is also highly preventable. The goal, therefore, is to ensure all patients with diabetes mellitus are given equal opportunity to access both the education and materials necessary to successfully monitor their health condition. (8)

Pathophysiology

Diabetic ketoacidosis occurs when the body is under stress and responds with an increase in catecholamines, cortisol and growth hormones. The release of such hormones decreases the ability of insulin, further increasing insulin resistance and resulting in serum hyperglycemia. Without cellular glucose for energy the body then begins to break down fat and protein for energy, resulting in increased levels of serum ketones. The combination of hyperglycemia and ketosis, as well as dehydration and various electrolyte imbalances, form the basis of diabetic ketoacidosis. (9)

While it is believed that the omission of insulin (nonadherence/ noncompliance, or mechanical failure of insulin delivery systems) accounts for the largest percentage of DKA admissions, other factors may be responsible for the development of this condition. Any disease process that increases insulin resistance, impairs insulin secretion, or interferes with carbohydrate metabolism may contribute to the onset of acute diabetic ketoacidosis in a vulnerable, health compromised patient.

Clinical Signs and Symptoms

Diabetic ketoacidosis is caused by the underlying presence of hyperglycemia, ketoacidosis and ketonuria. Early signs and symptoms may include any of the following:

• Generalized weakness and fatigue.
• Nausea and vomiting
• Diffuse abdominal pain.
• Decreased appetite and anorexia.
• Decreased/ altered levels of consciousness, such as mild disorientation and confusion.
• Dry skin and mucus membranes and decreased perspiration
• Tachycardia (increased heart rate) and tachypnea (increased respiratory rate)
• Acetone/ketone smell on breath
• Significant weight loss (usually a rapid onset in the newly diagnosed Type 1 diabetes mellitus patients)
• A patient history of noncompliance with prescribed insulin therapy (due to coexisting medical issues in which patient may have intentionally stopped insulin due to decreased food/fluid intake), costs factors (unable to afford prescribed therapy) and missed insulin doses (mechanical failure of the patient’s current insulin delivery system).

Additional signs and symptoms may be present, related to the patient’s age. While an adult patient would be able to verbalize symptoms, a child may not be able to do so, especially in cases where the diagnosis of T1DM is done during their initial presentation to an emergency department for suspected DKA.

In all cases, there may be other factors (illness, injury, medication side effects) that cause DKA to occur; thus, thorough examination and diagnostic testing must be done in all cases prior to initiation of treatment. Likewise, discharge planning and ongoing follow-up care must be patient specific to address behaviors and treatments required for optimal health maintenance.

Teens/Young Adults

In the teenager/ young adult population, the following symptoms may occur: (11)

• Increases in urination, thirst, and appetite.
• Unintentional/ unexplained weight loss despite increases in food and fluid intake.
• Changes in energy level (increased fatigue)
• Vision changes

Please note that normal growth and development stages/patterns in a teenager/young adult will influence glucose metabolism (related to hormone levels).

Young Children

In the young children’s population, symptoms usually strike suddenly and, unlike the adult population, are usually not related to a specific lifestyle or dietary practice. Most children present with the following symptoms:

• Increased urination
• Increased thirst
• Fatigue
• Vision problems (blurred vision)
• Acetone/ketone “fruity smell” on breath
• Unexplained weight loss, often despite appearing to eat (and drink) more.
• Changes in mood and behavior

Infants/Toddlers

In the infant/toddler population, symptoms may present as follows:

• Increased food and fluid intake (always appearing thirsty despite normal fluid intake)
• Frequent urination (in the potty-trained child, this may present as a new onset of bed wetting behaviors)
• Increasing fatigue and changes in normal activity levels
• Unexplained weight loss despite increased food and fluid intake
• Increased occurrences in diaper rashes (suspected increase in yeast infection)
• Fruity/acetone smell to breath
• Unusual behavior (child specific)

Etiology

Etiology: Causes of Diabetic Ketoacidosis

Hyperglycemia and low insulin levels lead to diabetic ketoacidosis. Common causes include the following:

• Acute illness, altering a person’s intake of food or drink, makes glucose management more difficult. This is a two-fold situation. The person with diabetes, recognizing the change in their normal food/fluid intake may also choose to intentionally decrease/skip their routine diabetic medications to avoid episodes of hypoglycemia.
• Insufficient levels of insulin due to the demands of normal growth and development patterns in children and young adults.
• Missed insulin doses (intentional decision to take inadequate doses, inadvertently held doses, inaccurate dose amounts, clogged insulin pump tubing).

Other causes of DKA, unrelated to insulin dose administration, are thought to be related to increased stress levels (inflammation/ infection) and normal hormone disruption, physiologic stressors. Persons with Type 2 diabetes may experience DKA due to prolonged, untreated hyperglycemia. (12), (13)

• Myocardial infarction
• Neurological stroke
• Motor vehicle accident with physical injuries (inflammatory response to blunt force/penetrating trauma)
• Abuse of alcohol and illegal drugs
• Medication side effects (diuretic and corticosteroid *use) see below
• Severe or prolonged illness (such as pneumonia and urinary tract infection/ urosepsis/wound infections)

Etiology: Precipitating Factors

Common precipitating factors for diabetic ketoacidosis include the following (14):

• Poor compliance with prescribed insulin therapy (intentional, nonintentional)
• Infections (especially T2DM in the elderly/ adult population)
• Newly diagnosed diabetes (especially T1DM in the pediatric/juvenile population)
• Physiologic based stressors, including coronary syndrome, cerebral vascular accidents, ischemic injuries, shock like states, chronic alcoholism, illicit drug use and certain antipsychotic medications.

Etiology: Diabetic Ketoacidosis and Corticosteroid Use

Diabetic ketoacidosis is related to long term corticosteroid usage. yperglycemia has been reported in a large percentage of patients who are using corticosteroids long term, often as high as “64-71%”. The elevated glucose levels combined with the ongoing physiologic stressors warranting use of these medications, increases the risk of DKA. The benefit/risk of using these medications long term must be assessed, especially in patients with pre-existing metabolic risk factors. Ongoing patient monitoring is essential to lower the risk of long-term complications. (15) (16).

Risk factors that “may” increase the likelihood of developing type 2 diabetes after long term steroid usage include the following:

• Overweight (BMI 25.0 -29.9 percent) / obesity (BMI 30 percent or above)
• History of gestational diabetes
• History of polycystic ovarian syndrome
• History of family members with type 2 diabetes

Treatment

Emergency Treatment

The initial or emergency treatment of diabetic ketoacidosis may require complex, frequent monitoring, often necessitating an intensive care admission. The following generic guidelines refer to intensive care nursing management. Please refer to your specific organization for nursing protocols related to DKA management. Many facilities have strict admission guidelines to ensure the appropriate use of intensive care resources. With respect to patients with DKA, suitable ICU admissions may include the following:

• A newly diagnosed diabetic during an episode of DKA
• Any infectious disease condition that triggers an episode of DKA
• An episode of DKA occurring concurrently with a physiologic stressor event (acute myocardial infarction, cerebrovascular accident/stroke)

The goals of emergency treatment of diabetic ketoacidosis are multifactorial and listed below. Interventions will include, but not be limited to, insulin intravenous infusions, hourly vital sign monitoring (or more frequent), and hourly glucose checks.

• Treatment/correction of dehydration with IV fluids
• Treatment of hyperglycemia with insulin therapy
• Treatment of electrolyte imbalances
• Treatment/correction of acid-base imbalance

Initial/Emergency treatment of DKA includes (20):

• Initial assessment and stabilization ABC airway, breathing and circulation.
• Aggressive fluid therapy to restore circulating volume.
• Isotonic saline IV infusion
• IV with dextrose component once glucose level 200-250mg/dl

Laboratory Findings

The following laboratory ranges provide a generic overview of normal ranges and abnormal findings associated with DKA (17) (18) (19). The confirmation of acute diabetic ketoacidosis is dependent on both laboratory findings as well as patient assessment. Please refer to your specific medical organization (unit specific) for further guidance and treatment parameters.

• Serum potassium levels: Normal range (3.5 to 5.0 mEq/L) hyperkalemia range approximately 5.0 to 5.5mEq/L. 
• Serum sodium levels: Normal range (137 to 142 mEq/L) severe hyponatremia range approximately 125mEq/L or lower; severe hypernatremia range above 145mE/L 
• Serum Amylase level: Normal range (40 to 140 units per liter) (U/L); may be elevated in cases of pancreatitis/ pancreatic inflammation, which may coexist with DKA 
• Serum Lipase level: Normal range (0-160 units per liter) (U/L); may be elevated in cases of pancreatitis/ pancreatic inflammation, which may coexist with DKA 
• Serum Osmolality level: Normal range 275-295 mOsm/kg: may be elevated to between 300-320 mOsm/kg in DKA       
• Arterial blood gas analysis: Arterial ph below 7.3 (normal range 7.35-7.45)   
• Anion Gap: Normal 4-12 mEq/L ; levels above  > 10 may indicate existing acidosis in DKA 
• Serum glucose level (normal fasting below 100mg/dl). Hyperglycemia range above 250mg/dl 
• Serum ketone level (normal negative); serum ketones detected in blood; usually greater than 5mEq/L       
• Serum bicarbonate level (normal 22-29 mEq/l); usually less than 18mEq/L  
• Anion gap level (normal 4-12mmol/L); usually greater than 12 mmol/L)

To rule out physiologic stressors associated with the development of DKA (systemic infections, acute myocardial infarction, pneumonia, urosepsis), refer to your medical organization (unit specific) guidelines regarding these additional diagnostics:

• Serial blood and wound cultures
• Serial EKG and Troponin levels
• Sputum cultures and sensitivity
• Urinalysis and culture with sensitivity
• Chest Xray

Fluid Resuscitation Guidelines

The American Diabetes Association (ADA) recommends the following initial fluid resuscitation in the adult population; additional boluses may be required after each hourly reassessment: (21). Please refer to your unit specific guidelines regarding fluid boluses, and fluid resuscitation. Caution in use with patients with preexisting heart failure, kidney failure or other medically indicated “fluid restrictions”.

0.9% SC (Sodium Chloride Solution) initially as a 15–20 mL/Kg bolus for hemodynamic resuscitation

• then 250–500 mL/h of fluid until glucose is normalized (usually faster than DKA resolution) 
• then 150–250 mL/h until DKA resolution  
• For the replenishment, 0.45% SC (Sodium Chloride Solution) unless hyperglycemia-corrected hyponatremia is present.

In the pediatric population, fluid resuscitation boluses are indicated in children who present with the following symptoms: (22)

• Dry mucus membranes 
•  Poor skin turgor 
•  Lethargy; altered level of consciousness. 
• Nausea and vomiting 
• Tachycardia and tachypnea 
• Kussmaul type respirations (deep and labored respiratory breathing patterns)

Fluid recommendation: 10–20 mL/kg bolus of isotonic saline given over 30–60 mins.

Insulin Therapy and Acute Diabetic Ketoacidosis

Intravenous use of insulin is preferred in patients with acute diabetic ketoacidosis, as subcutaneous absorption of insulin would most likely be ineffective in light of dehydration.

Intravenous continuous infusion of insulin at a rate of at 0.14 U/kg/hour or

Insulin bolus of 0.1U/kg, followed by insulin continuous infusion at a rate of 0.1U/kg/hour.

Hourly (or more frequent glucose checks) with a decrease in insulin delivery dose when glucose level is 250mg/dl or less. At this time, insulin dose is further decreased to 0.05 or 0.1U/kg hourly until DKA is resolved. 

• Patients, once stabilized and deemed able to eat, can be transitioned to subcutaneous insulin administration and routine glucose monitoring (point of care/ POC glucometers)

Laboratory Tests Guidelines Therapy Goals

• Serum glucose levels below 200mg/dl 
• Serum bicarbonate level greater than 15mEq/L 
• Serum potassium level 4.0 -5.0 mEq/L 
• Venous pH greater than 7.30  
• Anion gap equal to/less than 12eEq/l. (23)

Electrolyte Imbalance (Hyperkalemia-> Hypokalemia)

Serum potassium levels are usually high/elevated due to the cellular changes occurring as the result of acidosis and decreased insulin. Electrolyte replacement should be monitored very closely in diabetic ketoacidosis. During the rehydration/ volume restoration phase and insulin administration, extracellular potassium shifts back into the intracellular space (causing hypokalemia). In addition, insufficient insulin levels may deplete various serum electrolytes; thus, frequent serum electrolyte levels with appropriate intravenous replacement ensure proper cellular activity.

Treatment-Related Complications

• Hypoglycemia (blood glucose levels below 70mg/dl); treat; accordingly, patient should be transitioned to subcutaneous insulin injections when serum glucose level 200-250mg/dl, and patient is able to tolerate oral intake.
• Hypokalemia (blood potassium levels below 3-3.4 mmol/L); intravenous therapy to include potassium supplements; oral supplements as tolerated once patient transitions to diabetic diet.
• Cerebral edema

Cerebral Edema

Cerebral edema, or brain swelling, occurs for a variety of conditions (brain tumors, blunt trauma, inflammatory conditions, and even infections). Diabetic ketoacidosis and hyponatremia can cause cerebral edema. (24) Cerebral edema is the leading cause of mortality in children. A normal ICP (intracranial pressure) reading is 7-15mmHG; an increased reading in excess of 20-25mmHG, coupled with the following symptoms, may be indicative of cerebral edema.

Initial symptoms of cerebral edema may include the following:

• Headache 
• Visual changes (double vision (diplopia) or blurred vision) 
• Changes in speech/ ability to talk/ personality. 
• Nausea and vomiting 
• Changes in level of consciousness (lethargy-> unresponsiveness) 
• Changes in respirations/ difficulty breathing

Symptoms that may indicate worsening of cerebral edema. 

• decorticate and decerebrate posturing. 
• cranial nerve palsies  
• fluctuating level of consciousness 
• sustained heart rate deceleration, 
• increased vomiting, headache, and lethargy 

Confirmation Testing: 

• CT (Computerized Tomography) scan 
• MRI Magnetic Resonance Imaging

Treatment for DKA Related Cerebral Edema

When cerebral edema is confirmed by radiologic testing, the administration of Mannitol (or hypertonic sodium) is recommended as follows (25) (26):

• 0.5-1 g/kg intravenous mannitol may be given over the course of 20 minutes and repeated if no response is seen in 30-120 minutes.  
• If no response to mannitol occurs, hypertonic saline (3%) may be given at 5-10 mg/kg over the course of 30 minutes. 
• Additional treatments may be warranted, including diuretics, corticosteroids, and possible surgical intervention (to prevent herniation syndrome).

Nursing Care and Management

Nursing Care: Patient Placement

Initial/hourly (or more frequent) assessment to include the following:

Due to the frequency of monitoring and medication administration during the acute phase of DKA, patients are usually placed in the Intensive Care Unit. ICU treatment often includes hourly physical assessments (intake, output, neurological assessment, vital signs; frequent laboratory testing (glucose testing); and rapid identification of complications (cerebral edema, hypoglycemia, hypokalemia).

Transfer to a step-down unit usually occurs when the patient is fully awake, tolerating oral intake (both solid food and liquids), vital signs are stable, and fluid and electrolyte replacements are complete. The average timeline may be 1-2 clinical days. The focus of care now shifts to discharge planning, patient education, and ongoing management.

Nursing Care: Acute Phase

• Monitoring of vital signs, level of consciousness/ neurological status, urine output
• Administration of IV fluids as ordered.
• Frequent blood glucose assessment and insulin administration

Nursing Care: Patient Education, Discharge Planning, and Follow-up Care

• Compliance with medications, healthy diet, glucose monitoring, sick day management
• Signs and symptoms of infection
• Importance of follow-up care with primary medical provider/endocrinologist
• Lifestyle behavior changes (smoking cessation, physical activity, healthy diet)
• Medical Alert ID bracelet or wallet insert regarding chronic medical conditions and medication.
• Coordination of follow-up care to ensure ongoing medical support, educational services and financial assistance when appropriate (medical provider, endocrinologist, pharmacist, social worker/ case management services, DSMES classes) (27)

Patient Education

Diabetes Self-Management Education and Support (DSMES)

The Centers for Disease Control and Prevention offer a Diabetes Self-Management Education and Support Toolkit on their website available to the public, designed for various health organizations/ community organizations and others interested in educating persons with diabetes to live a healthier lifestyle. Studies have shown that people who receive such education have better overall health and wellbeing. Despite these studies, a very low percentage of those qualified to receive such services access them. Check out the link below for more information.

• DSMES Program Review: https://www.cdc.gov/diabetes/dsmes/index.html
• DSMES Tooliit: https://www.cdc.gov/diabetes/dsmes-toolkit/index.html

Additional Resources

The following websites are being provided to assist the healthcare professional in accessing appropriate diabetes related information, including insulin coverage, food insecurities, food bank locations, and DSMES information. https://diabetes.org/

The American Diabetes Association provides information on prediabetes, Type 1, and Type 2 diabetes, as well as gestational diabetes. Included on their website are sections on medications, support groups, diet and activity, advocacy efforts, and prevention efforts. https://www.jdrf.org/

The Juvenile Diabetes Research Foundation is a global organization for Type 1 diabetes mellitus. The site offers information on all things T1DM, including sections for those newly diagnosed, those interested in fundraising, research and clinical trials, daily diabetes management, volunteer opportunities, and access to local chapters worldwide. From the healthcare provider perspective, this website offers continuing education programs and pdf downloads for patient specific education. https://getinsulin.org/

The Get Insulin website provides information for persons with diabetes to access affordable insulin coverage. The site also offers information and guidance on health insurance plans, an insulin related newsletter, and external links to food sources (for patients with food insecurity issues) https://www.feedingamerica.org/find-your-local-foodbank

The Feeding America website enables persons with food insecurities to access food banks in their area, according to state location and zip code.

Patient Education and Follow-up Care (DSMES)

DSMES, or Diabetes Self-Management Education and Support, is the gold standard when it comes to patient education on this chronic medical condition. The goal of this education is to educate and empower the patient to successfully manage their medical condition, in efforts to lower the risk of long term, lifetime complications. DSMES is considered an ongoing process, and is recognized as an integral part of patient education at various critical points in their lifetime:

• At time of initial diagnosis
• During all patient medical appointments and routine follow-up care
• At time of onset for newly diagnosed complications
• Anytime a patient expresses concern over current diabetic management challenges.

Medicare and Medicaid

Medicare (Medicare Part B) and Medicaid plans currently offer the following coverage for diabetes related education (28):

• 10 hours of education (combined individual and group training) for an initial diagnosis of diabetes
• 2 hours of follow-up training annually after initial training completion

Qualifying Labs for DSMES

In general, a patient must be diagnosed with type 1, type 2, or gestational diabetes to qualify for DSMES, such as:

• Fasting Blood glucose of 126 mg/dL on 2 separate occasions
• 2-hour Post-Glucose Challenge of ≥200 mg/dL on 2 separate occasions
• Random Glucose Test of >200 mg/dL with symptoms of unmanaged diabetes

DSME Contents Overview

• Diabetes disease process pathophysiology and treatment to increase risk reduction for long term complications.
• Healthy eating includes meal planning, food label reading, carbohydrate counting, and strategies for eating out.
• Physical activity includes the benefits of activity as they related to better weight control, sleep habits and stress reduction.
• Medication usage overview to include medication administration, side effects, storage and cost issues.
• Blood glucose monitoring and management to include proper use of monitoring devices and associated equipment cleaning/repair.
• Prevention of complications (early detection, treatment, acute and chronic complications such as kidney disease and nerve damage; proper foot care)
• Healthy coping strategies to include stress reduction, effective self-management behaviors, and symptom recognition (hypoglycemia/hyperglycemia)
• Sick day management includes intake/output monitoring, over the counter medication usage, carbohydrate counting, ketone assessment, fever control and when to seek emergency services.
• Problem solving to include diabetes management during emergencies (power outages, flooding, tornados, hurricanes)

For more DSMES information visit: https://www.cdc.gov/diabetes/dsmes/dsmes-living-with-diabetes.html

Safety Considerations (Sick Day Management)

Successful management (prevention) of diabetic ketoacidosis requires patient education and empowerment in managing situations where glucose levels may be elevated and/or insulin levels (doses) are substandard (29).

There are many situations that can put a patient at risk for the development of DKA, including the following (29):

• Illness (acute and chronic), affecting normal food and fluid intake which negatively affects glucose management.
• Missed medication (insulin therapy) due to a clogged insulin pump tubing, a malfunctioning insulin pump, partial doses/skipped doses of insulin (whether related to costs, cognition, or mental health issues {diabetes distress}),
• Medication side effects
• Concurrent use of alcohol or drugs
• Physiologic stress (heart attack, stroke, physical injury)

Patient Education: Sick Day Management

Home treatment/ self-care (30)

The importance of preplanning cannot be understated. All persons with diabetes should have adequate supplies at home, to address an acute illness, including medications to treat basic symptoms before they escalate. These medications may include over the counter medications to treat pain, nausea, vomiting, diarrhea, as well as adequate supplies to manage their diabetes (alcohol prep pads, syringes, prescription medications).

In addition, it is important to stock up on diabetic friendly foods and drinks to maintain nutrition and hydration levels during an acute illness. Such items might include sports drinks, soft drinks, instant cooked cereals, puddings, soups. In the event that a patient cannot eat their regular meals, the goal is to eat or drink 50 grams of carbohydrate every 4 hours to maintain glucose levels.

Sick Day Management Guidelines

• Monitor glucose levels every 4 hours.
• Stay hydrated – 4 to 6 ounces of fluid every ½ hour to prevent dehydration.
• Daily weight
• Temperature checks (rule out underlying infection)
• Current medication compliance- do not stop taking insulin or diabetic oral agents ** notify provider immediately if you choose to stop medications.

Seek emergency care for the following signs/ symptoms:

• Persistent vomiting/diarrhea to the point that you cannot tolerate any food or fluid intake for several hours
• Ongoing glucose levels above 240mg/dl
• The presence of moderate/high levels of ketones in urine
• Unexplained weight loss during an illness
• Any difficulty breathing
• Fruity/acetone smell on breath
• Changes in gait/balance/ vision

Research Findings

Research: Diabetes Distress and Burnout

Diabetes is a 24/7/365 chronic medical condition. Unlike many conditions that are simply managed with lifestyle changes or a single, once a day medication regimen, diabetes mellitus requires lifelong, around the clock commitment. Whether diet, activity, or medication management, a person with diabetes may easily feel overwhelmed by even the basic requirements for self-management. (31)

Ongoing health challenges, comorbid medical conditions, medication and diet cost issues and family dynamics can all affect a person’s ability to successfully manage any health condition. When emotions (sadness, anger, hostility, frustration, and even fear) become overwhelming, diabetic distress (a feeling of defeat) can often occur. Without prompt, patient specific interventions (mental health services, financial assistance, self-management education), these feeling will progress to diabetic burnout, and increase the risk of unhealthy habits (poor medication adherence and overall glycemic control). (32)

Diabetes distress can easily progress to diabetes burnout without appropriate ongoing medical treatment and mental health interventions. When a person with diabetes reaches the point of burnout, they often appear to disconnect from their routine healthcare, exhibiting indifference towards their overall health and well-being. They may become both mentally and physically exhausted from the daily requirements of this chronic medical condition. At this point, it is not uncommon to observe a person’s total disregard for their ongoing medical treatments, daily medications, routine self-care, and more. Missed medications, missed medical appointments, poor dietary intake, and a visible lack of basic hygienic practices are cause for concern.

A multidisciplinary approach to treating suspected diabetic distress and burnout is highly encouraged. From ongoing education, physical and mental health assessments, and enrollment in therapies (individual therapy sessions, and support groups), the person with diabetes needs a supportive environment in which to become empowered in the self-management of their disease progress. In doing so, it is believed that health outcomes are optimal, and the risk of long-term complications is lowered. (33)

Reserach: Diabulimia

Bulimia nervosa is a potentially life-threatening eating disorder characterized by episodic binge eating of large amounts of food, followed by forced vomiting and possibly laxative use to then “purge” the food. These alternating behaviors are the result of a person fearful of weight gain and willingness to lose weight in unhealthy ways. (34) (35)

Diabulimia is a serious, life threatening eating disorder affecting persons with Type 1 diabetes. Through intentional restricted/ limited use of prescribed insulin, weight loss occurs. This eating disorder is more common in young female adolescents and young adults. (34) (35)

Signs and symptoms may include the following (34) (35):

• Unexplained weight loss
• Hemoglobin A1C > 9
• Multiple episodes of DKA
• Unfilled insulin prescriptions, missed diabetes related medical appointments,
• Expressed fear of insulin related weight gain
• Anxiety related to body image
• Obsessive interest in calories and dieting

Research: Insulin Affordability

For many persons with diabetes, the perceived noncompliance with therapy (on behalf of the healthcare professional) is actually that of a cost related issue. Many persons cannot afford ongoing therapies related to management of this chronic medical condition. In attempts to “cut costs”, patients have admitted to skipping certain medications, cutting medications in half, reducing prescribed doses of insulin, and purchasing poorer quality, less expensive foods (that are often lacking in nutritional value). Poorly controlled / uncontrolled diabetes heightens the risk of both acute and chronic complications.

In an attempt to ensure accessibility and affordability of insulin therapy to persons with diabetes, the Inflation Reduction Act of 2022 in part ensures that persons with diabetes on Medicare pay no more than $35 for a month’s supply of insulin product under their prescription drug coverage. Similar drug coverage benefits were also extended to many state-based insurance plans. (36)

In addition, most Medicaid insurance plans, as well as private insurance companies have now enacted reduced insulin costs/ cost sharing programs. Finally, for patients with no insulin costs benefits, many national insurance providers offer free/ reduced cost insulin through their patient assistance program. For a comprehensive list of these resources, please see the following website link (American Diabetes Association): https://diabetes.org/tools-resources/affordable-insulin

Research: Insulin Delivery Systems

With the creation of advanced insulin delivery /monitoring devices (insulin pumps, and continuous glucose monitoring devices), the person with diabetes is afforded a more streamlined process to control their chronic medical condition. Most patients using such devices report better glucose control {“time in range”}, meaning the time their blood glucose levels remained in an acceptable range, ease of portability (of supplies), increased comfort (no more finger sticks), and decreased rates of anxiety, depression and distress.

The following website links represent various insulin delivery devices. Consider making a resource book containing various delivery devices for your specific unit (or hospital organization). Many have 24/7 customer service representatives available if you need to trouble shoot a device suspected of malfunctioning or require additional staff/patient educational resources.

This list contains a variety of websites but is not all inclusive. If you are caring for a patient with an insulin delivery device in place, please contact that specific company for more directions on its usage, removal, replacement parts and more.

Examples of insulin delivery devices:

• Makers of the MiniMed 780G System and the MiniMed 630G system: https://www.medtronic.com/us-en/healthcare-professionals/products/diabetes/insulin-pump-systems.html
• Makers of the Omnipod 5 and the Omnipod DASH Insulin Management System: https://www.omnipod.com/
• Quick overview of various insulin pumps currently on the market: https://consumerguide.diabetes.org/collections/pumps

Case Studies

Case Study #1

A 3-year-old female child is sent, by ambulance, from her local pediatrician’s office with reports of increased lethargy, increased thirst and appetite, and new onset of bedwetting (child had stopped wearing diapers at age 2.5 years). Parents report that the child’s appetite appears increased lately, but pediatrician noted several pounds weight loss since last visit.

• Based on these signs and symptoms alone, what is your initial diagnosis for this child?
• What are your priority nursing interventions for this child?
• How would you assess hydration status on a 3-year-old child?

The child is diagnosed with new onset Type 1 Diabetes and stabilized in the Emergency Department. The parents of this child are visibly distraught over the diagnosis, stating “no one in our family is diabetic; this can’t be happening”.

• What are some of the initial nursing patient/family education areas you could address at this time?
• What are some in hospital consultations that should be considered for this patient and her family?
• What are some community resources you have in your area that you could offer this family?

Case Study #2

A 78-year-old female, with a previous history of CVA, is transferred to your facility from a local nursing home for evaluation of fever and hyperglycemia. The nursing home staff reported the patients’ blood glucose level was 400mg/dl earlier today and her WBC count was 14,500. Upon arrival, the patient is unresponsive, with a temperature 102F , her glucose is 350mg/dl, with +ketones (moderate) and a urinalysis (indwelling catheter) confirms a UTI.

Patient past medical history includes old CVA, T2DM.

• Based on these signs and symptoms alone, what is your initial diagnosis for this patient?
• What diagnostic studies would be warranted in light of hyperglycemia, fever, urinary tract infection, and altered level of consciousness?
• What questions would you ask the nursing home staff, in light of this patient’s initial presentation?
• When this patient is stabilized for transfer back to the nursing home, what information should be included in the discharge instructions/ transfer of care?

Case Study #3

A 60-year-old male present to the Emergency Department with an Acute Myocardial Infarction.

Patient past medical history includes borderline hypertension, and prediabetic HgbA1C 5.8.

The patient was found to have severe coronary artery disease and received Coronary Artery Bypass Graft x 3. During the immediate post operative recovery phase, he receives insulin therapy to control glucose levels >300mg/dl. He is eventually sent home on insulin therapy, pending follow-up with his cardiologist as well as a new consultation for an endocrinologist.

At the time of discharge, the patient is adamant that he was “prediabetic and could easily control my glucose levels with diet alone”; he doesn’t understand how he is now “an insulin diabetic”.

• What are key points in nursing education for this patient, regarding his new “diabetic status”
• How would you explain to the patient the connection between his myocardial infarction, bypass surgery, and currently elevated glucose levels?
• What nursing interventions can you provide PRIOR to discharge to assess his comfort level with insulin injections and glucose monitoring?
• What community resources are available to your patient for a new diagnosis of diabetes?
• The patient wants to know when he can stop the insulin injections. What is your response?

Successful management of acute diabetic ketoacidosis requires resuscitation with intravenous fluids and insulin therapy, replacement of electrolytes and early identification of any events (medical, surgical, and psychological) that contributed to this medical emergency. With the continued increase in diagnosis of diabetes, and ongoing challenges in healthcare costs and coverage, chronic medical conditions will continue to burden the already overwhelmed healthcare arena. By educating and empowering patients to self-manage their disease process, we can lower the risk of long-term complications and improve health outcomes worldwide.

Conclusion

The International Diabetes Federation reports that, in 2021, approximately 10.5 % of the global adult population (ages 20-79 years old) has diabetes, and that nearly 50% of this population are unaware that they are living with this chronic condition. Left untreated, the rates of long-term, nonreversible complications are quite alarming. (37) By the year 2045, it is projected that 1 in every 8 persons (approximately 12.5 %) will be living with diabetes. This will equate to an increase of 46 percent, with nearly 783 million people being affected. This single health condition will represent staggering health expenditures and increased mortality and morbidity associated rates worldwide.

Diabetes ketoacidosis continues to be a potentially life-threatening complication for persons with diabetes. DKA is also, in most cases, a highly preventable condition, with early identification and treatment. The importance of ongoing, patient specific education to address all aspects of diabetes self-management is a key factor in lowering the occurrence of DKA. Dr William Polonsky, a licensed clinical psychologist and certified diabetes educator, is the President of the Behavioral Diabetes Institute in San Diego, California. With regards to the importance of patient education and empowerment, he said the following:

“Well-controlled diabetes is the leading cause of nothing!” Dr William Polonsky. (38)

As healthcare professionals, we have the responsibility to ensure that our patients with diabetes are afforded the education and ongoing support necessary for them to successfully manage their specific disease process. In doing so, we positively impact patient satisfaction, improve medication adherence rates, and lower the risk of long-term complications.

Heart Disease Prevention & Management

Introduction   

Heart disease is an umbrella term encompassing a range of cardiovascular conditions, and stands as the leading cause of death worldwide, claiming millions of lives. Both heart disease and stroke are types of cardiovascular disease. The impact of heart disease transcends individual health, posing a significant economic burden through reduced labor and workforce participation. In 2018, the mean labor income losses were $13,463 for heart disease and $18,716 for stroke. Total labor income losses were estimated at $203.3 billion for heart disease and $63.6 billion for stroke [1].  

Heart disease manifests in various forms, each with its unique characteristics and implications. Coronary artery disease, the most common type, arises from the buildup of plaque in the coronary arteries [2]. This narrowing can restrict blood flow to the heart, causing symptoms such as chest pain or shortness of breath [2]. Other prevalent forms include heart failure, rhythm abnormalities, heart valve defects, and congenital heart defects [4]. These conditions can lead to a spectrum of complications, including heart attacks, strokes, and heart failure, significantly impairing quality of life and survival [3]. By understanding the underlying mechanisms, risk factors, and clinical presentations of heart disease, participants will gain a deeper understanding of the disease's impact on the cardiovascular system and overall health.  

Prevention, the cornerstone of combating heart disease, will be a central focus. Participants will explore lifestyle modifications that play a pivotal role in reducing the risk of heart disease, including diet, physical activity, weight management, smoking cessation, and stress reduction. Identification and management of risk factors, such as high blood pressure, high cholesterol, and diabetes, is prioritized. 

Types of Heart Disease  

Heart disease encompasses a spectrum of conditions, each with unique underlying mechanisms and dietary management strategies [5]. Coronary artery disease (CAD), heart failure (HF), hypertensive heart disease (HTN), and arrhythmias constitute a significant portion of these prevalent ailments. Coronary artery disease (CAD) is the most common type of heart disease [6]. The four main types of cardiovascular disease (CVD) include coronary heart disease, stroke, peripheral arterial disease, and aortic disease [7].  Cerebrovascular disease is the second most common type of heart disease [7]. Other forms of heart disease include congenital heart disease, heart valve disease, cardiomyopathy, pericardial disease, arrhythmia, and aortic dissection.  

Congenital heart disease (CHD) 

Congenital heart disease (CHD) is the most common type of birth defect, affecting about one in 100 babies born in the United States [8]. CHDs can range from mild to severe and can affect the heart's structure, function, or both [8].  

Heart Valve Disease 

Heart valve disease is a condition in which one or more of the heart valves are damaged or diseased which causes blood to flow backward through the valves, damaging the heart and other organs [9]. Heart valve disease affects 2.5% of the U.S population and can be caused by several factors, including infection, injury, and aging [9].  

Heart Failure 

Heart failure is a condition in which the heart's weakened pump fails to meet the body's demands for blood and oxygen, leading to a range of debilitating symptoms including fatigue, shortness of breath, swelling, chest pain, palpitations, weight gain, swelling in the ankles, legs, and abdomen, bloated or hard stomach, dry hacking cough, and nausea [10][11]. More than six million adults in the U.S. have heart failure [10].  

Cardiomyopathy 

Cardiomyopathy represents a collection of diverse conditions of the heart which makes it weaker and less able to pump blood. Cardiomyopathy can be caused by several factors, including infection, toxins, and genetic disorders [12]. Due to the potential for underdiagnosis, estimates of cardiomyopathy prevalence can vary. It is estimated that up to one in 500 adults may be affected by this condition [13].  

Pericardial Disease 

Pericardial disease is a condition that affects the pericardium, the sac that surrounds the heart [14]. This can cause inflammation, infection, or scarring of the pericardium, which can interfere with the heart's ability to function. Pericardial disease can manifest as acute pericarditis, pericardial effusion, cardiac tamponade, or constrictive pericarditis [14].  

Arrhythmia 

Arrhythmia is a cardiac disorder characterized by an abnormal heart rhythm, manifesting as tachycardia (excessively rapid heartbeat), bradycardia (abnormally slow heartbeat), or irregular heartbeat patterns [15]. These irregularities can induce symptoms such as palpitations, dizziness, and syncope (fainting episodes) and can arise from various etiologies, including underlying heart conditions, electrolyte imbalances, and adverse effects of certain medications [15].  

One in 18 people, or five percent of the U.S. population has an arrhythmia with afib (atrial fibrillation) being the most common [16].  

Aortic Dissection 

Aortic dissection is a rare, life-threatening condition in which the inner layer of the body’s main artery (aorta), tears [17]. This can cause blood to leak between the layers of the aorta, which can weaken the artery and cause it to rupture. Aortic dissection can be caused by several factors including high blood pressure, atherosclerosis, and connective tissue disorders [17]. Aortic dissection affects about 30 in one million people each year and more than 13,000 die each year [18]. Aortic dissection is most common in individuals over the age of 60 and if not treated, the tear can worsen, ripping the outer layer of the aorta, allowing blood to escape the artery [17] [18]. As many as 40 percent of individuals who suffer from an aortic dissection die, and the risk of death increases by 3-4 percent every hour the condition is left untreated [18]. 

Epidemiology/Statistical Evidence  

Heart disease is a global health crisis, with an estimated 17.9 million deaths attributed to cardiovascular diseases in 2019, representing 32% of all global deaths [19]. This significant number reflects the pervasive nature of heart disease, affecting individuals of all ages, socioeconomic backgrounds, and ethnicities. The distribution and determinants of heart disease plays a pivotal role in understanding the prevalence. Heart disease varies across regions, with higher rates observed in high-income countries compared to low-income countries [20]. However, the burden of heart disease is shifting, with a growing trend in low-income countries due to rapid urbanization, lifestyle changes, and increasing exposure to risk factors [20].  

Epidemiology: Modifiable and Non-Modifiable Risk Factors 

Epidemiological studies with data from 61 cohort studies, encompassing 12.7 million person-years of follow-up and 56,000 fatalities from coronary heart disease (CHD) and stroke revealed a consistent and graded increase in CVD risk. The risk was associated with higher baseline systolic blood pressure (SBP) and diastolic blood pressure (DBP) levels beyond the usual thresholds of 115 and 75 mmHg. A 20-mmHg elevation in SBP and a 10 mmHg increase in DBP was associated with a two-fold higher risk of CVD [21].  

Cardiovascular disease (CVD) is a leading cause of morbidity and mortality in individuals with type 2 diabetes mellitus (T2DM). This increased risk stems from a complex interplay of traditional and non-traditional risk factors that contribute to the initiation and progression of atherosclerosis, a pathological process characterized by the buildup of plaque within artery walls [22].  

The epidemiology of heart disease involves recognizing the associated risk factors. These can be categorized into modifiable and non-modifiable factors. Modifiable risk factors include hypertension, high cholesterol, smoking, obesity, diabetes, physical inactivity, and poor diet [23]. Non-modifiable risk factors include age, gender, and family history [23]. According to the American Heart Association (AHA), the likelihood of developing CVD in U.S. men and women is 40% between the ages of 40 and 59, 75% between 60 and 79, and 86% for those over the age of 80 [24].  

Statistics on Ethnic/Racial Minorities 

Patients from minority groups with acute coronary syndrome (ACS) are at an increased risk of heart attack (MI), readmission to the hospital, and death from ACS [25]. Black/African Americans are at 30% increased risk of heart disease and death from heart disease and double the risk of stroke with a higher risk of developing heart failure [25]. Among Asian Americans /Pacific Islanders, coronary artery disease (CAD) manifests earlier in life and affects a larger proportion of the population compared to other ethnic groups [25]. Overall CVD rates are lower among non-White Hispanic individuals. Among Hispanic subgroups, Puerto Rican Americans exhibit the highest HTN-related death rates [25]. Heart failure incidence among Hispanics falls between that of African Americans and non-Hispanic whites [25].  

Epidemiology: Genetic and Environmental Factors 

The development of heart disease is influenced by a complex interplay of genetic and environmental factors [26]. Major risk factors include sustained high blood pressure placing excessive strain on the heart, increasing the risk of heart failure, stroke, and other complications [27]. Elevated levels of low-density lipoprotein (LDL) cholesterol can accumulate in arteries, narrowing and reducing blood flow to the heart [28].  

Diabetes mellitus, characterized by high blood sugar levels that damage blood vessels and nerves throughout the body, increases the risk of heart disease and stroke [29]. Tobacco contributes to atherosclerosis – the buildup of plaque in arteries – through a cascade of mechanisms that lead to atherosclerosis, including thrombosis, insulin resistance, dyslipidemia, vascular inflammation, abnormal vascular growth, angiogenesis, and impaired endothelial repair and regeneration [30] [50].  

Obesity and excess abdominal fat can increase the risk of heart disease by elevating blood pressure, cholesterol levels, and blood sugar levels [27]. A lack of regular physical activity contributes to obesity, high blood pressure, and other risk factors for heart disease [31]. A family history of heart disease increases an individual's risk, indicating a genetic predisposition to the condition [32].  

Prevention Strategies 

Prevention for heart disease begins with addressing modifiable risk factors with an emphasis on diet, exercise, smoking cessation, and stress management. Prevention also involves regular health screenings.  

Key prevention strategies include: 

• Adopting a Heart-Healthy Diet consisting of fruits, vegetables, and whole grains, and limiting saturated and trans fats, sodium, and added sugars [33].  

• Maintaining a healthy weight through a balanced diet and regular exercise [23].  

• Engaging in regular physical activity for at least 150 minutes of moderate-intensity aerobic exercise or 75 minutes of vigorous-intensity aerobic exercise per week [34].  

• Participating in smoking cessation, managing high blood pressure, and working with healthcare providers to manage cholesterol levels through lifestyle changes or medication [23].  

Patient Education for Self-Management  

Patient education for self-management plays a vital role in preventing and managing heart disease. Healthcare professionals should begin by conducting a thorough assessment of each patient, considering their unique risk factors, medical history, and lifestyle choices related to heart disease and develop a personalized self-management plan that align with the patient's specific needs and objectives [35].  

Provide clear and concise information about heart disease, its risk factors, and prevention strategies, and address individual needs and concerns, with consideration of cultural background, lifestyle, and any underlying health conditions. Effective communication is paramount in this process. Health care professionals should employ strong communication skills to establish a meaningful connection and foster open and honest dialogue, active listening, and demonstration of empathy to gain insight into their preferences [36].  

To cater to diverse learning styles, it is essential to offer educational materials in various formats [37]. Tailor the educational approach to each patient's learning style, using plain language, visual aids, and active participation strategies. Involve the patient in setting realistic and achievable self-management goals [38]. These resources may encompass brochures, videos, or online materials. It is imperative that these materials are designed to be comprehensible and sensitive to cultural differences.  

Patients must be educated about modifiable risk factors that pertain to heart disease prevention [23]. This includes discussions on dietary choices, physical activity, smoking cessation, and responsible alcohol consumption [23]. Furthermore, healthcare professionals should articulate the significance of adhering to prescribed medications to manage cardiovascular conditions.   

Medical Management and Treatment  

In addition to lifestyle modifications, healthcare providers can prescribe medications to treat heart disease [23]. The common medications used to treat heart disease include antihypertensive medications to lower blood pressure, antihyperlipidemic medications to lower cholesterol levels, and antiplatelet medications to prevent blood clots [40]. Beta-blockers are used to slow the heart rate and lower blood pressure and angiotensin-converting enzyme (ACE) inhibitors are used to lower blood pressure and relax blood vessels. Angiotensin II receptor blockers (ARBs) are prescribed to lower blood pressure and relax blood vessels [41]. 

In some cases, invasive medical procedures may be required to treat heart disease. The common types of medical procedures used to treat heart disease include coronary angioplasty to open blocked or narrowed coronary arteries, and coronary artery bypass grafting (CABG) to create a new pathway for blood to flow around blocked or narrowed coronary arteries [39][42]. Other common procedures are heart valve surgery to repair or replace damaged heart valves, implantable cardioverter-defibrillators (ICD) to monitor the heart rhythm and deliver electrical shocks to correct abnormal heart rhythms, and implantable pacemakers to help control the heart rhythm [43]. 

Heart Health Resources 

Resources for heart disease prevention and management are essential for both healthcare professionals and patients. These resources encompass a wide range of tools, information, and support systems that play a crucial role in reducing the risk and managing heart disease. 

Educational Materials/Content 

Information is key to prevention and management. Patients and healthcare providers can access pamphlets, brochures, websites, and educational videos that explain the causes, risk factors, symptoms, and treatment options for heart disease [44]. These resources empower individuals to make informed decisions about their heart health. [44].  

Patients can benefit from resources that offer guidance on Heart-Healthy diets, including low-sodium meal plans, tips for reducing saturated fats, and strategies for incorporating more fruits and vegetables into their meals. 

Published Guidelines 

Medical organizations and government health agencies publish guidelines for heart disease prevention. These guidelines provide evidence-based recommendations for diet, exercise, smoking cessation, and medication management, with proper nutrition being a cornerstone of heart disease prevention and management [33].  

Support Groups 

Support groups provide a platform for individuals with heart disease to connect, share experiences, and receive emotional support [45]. These groups can be in-person or online and offer a sense of community for patients and their families [45].  

Technological Advancements 

Telehealth has become important in managing chronic conditions such as heart disease [46]. Patients can access virtual consultations with healthcare providers, receive remote monitoring, and access educational materials online. Smartphone apps and wearable devices can help individuals track their health metrics, such as blood pressure, heart rate, and physical activity [47]. Many of these tools provide real-time feedback and reminders to support heart-healthy habits.  

Nonprofit Organizations 

Nonprofit organizations dedicated to heart health advocacy, such as the American Heart Association, offer a wealth of resources. The American Heart Association (AHA) is a leading organization for heart disease research and education [48]. The National Heart, Lung, and Blood Institute (NHLBI) is a part of the National Institutes of Health (NIH) and offers information on heart disease prevention and management, as well as clinical trials and research studies [49]. 

Conclusion

Heart disease encompasses a spectrum of conditions with diverse underlying mechanisms and management strategies. Modifiable risk factors, including diet, exercise, smoking cessation, and stress management, play a crucial role in both prevention and management [23]. Resources for heart disease prevention and management empower individuals to take control of their heart health. These resources span from educational materials and support groups to telehealth platforms and smartphone apps, providing comprehensive guidance and support for both patients and healthcare professionals [44][45]. 

Nutrition for a Healthy Heart

Introduction   

Research indicates that a heart-healthy diet is a powerful tool for the prevention and control of cardiovascular disease [1]. A heart-healthy dietary approach to wellness emphasizes the intake of the appropriate proportions of macronutrients, essential vitamins, minerals, and fiber while minimizing the consumption of saturated fats, trans fats, cholesterol, salt (sodium), and the reduction of processed foods, trans-fats, and added sugars [2] [3]. The cornerstone of the diet includes an abundance of fresh fruits and vegetables, whole grains, lean proteins, and healthy fats [2].  

For healthcare providers and patients, the goal of adopting a heart-healthy diet is multifaceted. The diet aims for a reduction in overall cardiometabolic risk, improving blood pressure, lowering cholesterol levels, reducing the risk of developing heart disease and stroke, and preserving the overall health of the circulatory system [3].  

Nurses play a pivotal role in patient education and promoting heart-healthy lifestyles by empowering patients with knowledge and skills related to nutrition and dietary choices. This course aims to equip nurses with comprehensive knowledge of heart-healthy eating principles, enabling them to guide and educate their patients.  

The adoption of healthy lifestyle choices, with nutrition being the most important behavioral factor, is estimated to reduce the risk of myocardial infarction (MI) by 81–94% [5][6][7]. In comparison, treatment with pharmacotherapies alone results in a 20–30% reduction [8]. 

Heart Disease: A Brief Overview 

Heart disease remains one of the leading causes of morbidity and mortality worldwide, with diet and nutrition playing a crucial role in both its development and prevention [4]. Cardiovascular diseases, also known as CVDs, are the primary cause of death worldwide, claiming an estimated 17.9 million lives per year [4].  

Cardiovascular disorders affect the heart and blood vessels, manifesting in coronary heart disease, cerebrovascular disease, rheumatic heart disease, and others. More than four out of five CVD fatalities stem from heart attacks and strokes, with one-third of these deaths occurring in individuals under the age of 70 [4].  

The term "heart disease" encompasses various conditions affecting the heart's structure and function, many of which are influenced by dietary habits [9]. Cardiovascular risk factors, including malnutrition, tobacco and alcohol use, stress, obesity, sedentary lifestyle, hypertension, diabetes, hyperlipidemia, and genetic predisposition, can increase an individual's likelihood of developing cardiovascular diseases [10] [12].  

The modifiable risk factors include sedentary lifestyle, smoking, high blood pressure, diabetes, hypercholesterolemia [12]. Almost three quarters of patients (73%) had at least three risk factors compared to 31% of healthy subjects. 

Family history of cardiovascular disease (CVD) is a significant independent risk factor for premature coronary heart disease (CHD). The risk of premature CHD increases in a linear fashion as the number of affected family members grows. [11]. Cardiovascular risk factors, including malnutrition, tobacco and alcohol use, stress, obesity, sedentary lifestyle, hypertension, diabetes, hyperlipidemia, and genetic predisposition, can increase an individual's likelihood of developing cardiovascular diseases [10].  

The five modifiable risk factors include sedentary lifestyle, smoking, high blood pressure, diabetes, and hypercholesterolemia [10]. A higher proportion of cardiovascular patients (73%) had at least three risk factors compared to healthy individuals, where less than one-third had three or more risk factors [10]. 

Types of Heart Disease / Statistics 

There are multiple types of heart disease, each with distinct mechanisms and implications for dietary management [13]. Coronary artery disease (CAD), heart failure, hypertensive heart disease, and arrhythmias represent a fraction of these conditions. The four main types of CVD include coronary heart disease, stroke, peripheral arterial disease, and aortic disease [15].  

Coronary artery disease (CAD) is the most common type of heart disease [14]. Cerebrovascular disease is the second leading cause of heart disease. Other forms of heart disease include congenital heart disease, heart valve disease, cardiomyopathy, pericardial disease, arrhythmia, and aortic dissection.  

Congenital heart disease (CHD) is the most common type of birth defect, affecting about 1 in 100 babies born in the United States [16]. CHDs can range from mild to severe and can affect the heart's structure, function, or both [16].  

Heart valve disease is a condition in which one or more of the heart valves are damaged or diseased, which causes blood to flow backward through the valves, damaging the heart and other organs [17]. Heart valve disease affects 2.5% of the U.S population and can be caused by several factors, including infection, injury, and aging [17].  

Heart failure is the heart's inability to pump blood, leading to symptoms such as fatigue, shortness of breath, swelling, chest pain, palpitations, weight gain, swelling in the ankles, legs, and abdomen, bloated or hard stomach, dry and hacking cough, and nausea [18] [19]. More than 6 million adults in the United States have heart failure [18].  

Cardiomyopathy represents a collection of diverse conditions of the heart which makes it weaker and less able to pump blood. Cardiomyopathy can be caused by several factors, including infection, toxins, and genetic disorders [20]. Due to the potential for underdiagnosis, estimates of cardiomyopathy prevalence can vary. It is estimated that up to 1 in 500 adults may be affected by this condition [21].  

Pericardial disease is a condition that affects the pericardium, the sac that surrounds the heart [22]. This can cause inflammation, infection, or scarring of the pericardium, which can interfere with the heart's ability to function. Pericardial disease can manifest as acute pericarditis, pericardial effusion, cardiac tamponade, or constrictive pericarditis [22].  

Arrhythmia is a cardiac disorder characterized by an abnormal heart rhythm, manifesting as tachycardia (excessively rapid heartbeat), bradycardia (abnormally slow heartbeat), or irregular heartbeat patterns [23]. These irregularities can induce symptoms such as palpitations, dizziness, and syncope (fainting episodes) and can arise from various etiologies, including underlying heart conditions, electrolyte imbalances, and adverse effects of certain medications [23]. One in 18 people, or 5 percent of the U.S. population has an arrhythmia with a-fib (atrial fibrillation) being the most common [24].  

Aortic dissection is a rare, life-threatening condition in which the inner layer of the body’s main artery (aorta), tears [25]. This can cause blood to leak between the layers of the aorta, which can weaken the artery and cause it to rupture. Aortic dissection can be caused by several factors, including high blood pressure, atherosclerosis, and connective tissue disorders [25].  

Aortic dissection affects about 30 in 1 million people each year and more than 13,000 die each year [26]. Aortic dissection is most common in those individuals over the age of 60 and if not treated, the tear can worsen, ripping the outer layer of the aorta and allowing blood to escape the artery [25] [26]. As many as 40 percent of individuals who suffer from an aortic dissection die, and the risk of death increases by 3-4 percent every hour the condition is left untreated [26]. 

Evidence on Diet and Heart Health / Diet Options 

When considering the diet options for heart health, the Mediterranean diet, DASH diet, and plant-based diets are among the most researched and recommended. These diets share common elements such as an emphasis on whole foods, minimal intake of red meat, and a high volume of fruits and vegetables. Extensive research has demonstrated that the DASH dietary pattern lowers the risk of cardiovascular disease [37]. Numerous prospective studies have demonstrated the consistent benefits of the Mediterranean diet on cardiovascular health [30]. 

There is substantial evidence that most vascular events may be prevented by avoiding smoking, participating in regular physical activity, maintaining normal body mass index, and eating a healthy diet [27].  

Observational studies have demonstrated that dietary patterns rich in fruits and vegetables, excluding white potatoes, are linked to a lower risk of CVD [28] [29]. Regular consumption of whole grain foods has been linked to a reduced risk of cardiovascular disease (CVD), coronary heart disease (CHD), stroke, metabolic syndrome, and various cardiometabolic risk factors, as evidenced by robust observational studies and clinical trials [28]. Numerous randomized controlled intervention studies have demonstrated that replacing refined grains with whole grains leads to significant improvements in cardiovascular risk factors [28] [31].  

Except for a small trial that demonstrated a reduction in arrhythmia recurrences among regular drinkers with atrial fibrillation upon alcohol abstinence, no other studies have reported favorable outcomes associated with alcohol consumption for cardiovascular health [32].  

Dietary fiber, abundant in plant-based foods like fruits, vegetables, whole grains, nuts, seeds, beans, and legumes, have shown an inverse association with a lower risk of metabolic syndrome and cardiometabolic risk factors [33].  

A systematic review and meta-analysis provided evidence that substituting saturated fat with unsaturated fat can improve cardiovascular outcomes and reduce the risk of CVD [34]. Plant-based diets rich in foods like whole grains, fruits, vegetables, and nuts, have been linked to a reduced risk of cardiovascular events and intermediate risk factors [36].  

Current evidence does not support the widespread use of high-dose vitamin and mineral supplements for the prevention of cardiovascular disease (CVD) [28]. 

Role of Sodium and Fats 

Sodium and fats hold significant impact over heart health. High sodium intake is associated with hypertension, a risk factor for heart disease, while certain types of saturated and trans fats, are linked to an increase in LDL cholesterol and the development of atherosclerosis [28]. A systematic review and meta-analysis revealed the detrimental effects of saturated fat on cardiovascular disease (CVD) outcomes and risk factors compared to unsaturated fat. [36] 

A strong body of evidence has documented the adverse effects of trans fatty acids on cardiometabolic risk factors [37]. Adhering to current recommendations to replace saturated fat from meat and dairy with nontropical plant oils also lowers dietary trans fatty acids [38]. 

Healthy Eating Tips and Strategies 

Incorporating a heart-healthy diet into a patient’s lifestyle requires practical tips and strategies. First, make gradual changes instead of overhauling the entire diet. Meal planning can help with healthier choices.  

Setting realistic goals and collaborating with the patients to set achievable dietary goals. Controlling portion size, using smaller plates and bowls, prioritizing low-calorie, nutrient-rich foods like fruits and vegetables and limit high-calorie, high-sodium foods like refined, processed, or fast foods [39].  

Paying attention to the amount of saturated and trans fats, cholesterol, and sodium. Suggest lean protein sources such as fish, poultry, beans, and lentils and limit the intake of unhealthy fats and instead opt for healthy fats like those found in olive oil, avocados, and nuts [39].  

Consume at least five servings of fruit and vegetables daily [41]. Choose whole grains over refined grains and limit the intake of added sugars [28]. To have more control over the ingredients, cook and consume meals at home and make gradual changes to diet habits and build on those habits over time. 

Patient Education 

Nurses are well positioned to provide patient education and counseling on heart-healthy eating. The core of patient education lies in translating knowledge into practice. Nurses must communicate with consideration of cultural, linguistic, and individual patient dietary preferences. Education should be patient-centered, with actionable steps that patients can integrate into their daily lives [40].  

Effective patient education strategies can include establishing a rapport, assessing the patient's knowledge, and understanding, tailoring the educational approach, using plain language, incorporating visual aids, encouraging active participation, providing written materials and ongoing support and follow-up, and addressing any barriers and concerns [42]. 

Resources 

A wealth of resources is available to support nurses in their role as patient educators, from professional organizations like the American Heart Association to local community programs and online platforms [43]. These resources offer educational materials, dietary guidelines, and support tools that nurses can utilize to enhance their teaching.  

A heart-healthy diet is one that is low in saturated and trans fats, cholesterol, and sodium. It is also high in fiber, fruits, vegetables, and whole grains [2][3]. Eating a heart-healthy diet can help to lower your blood pressure, cholesterol levels, and risk of heart disease [2]. 

The National Heart, Lung, and Blood Institute (NHLBI) has a website with information on heart-healthy eating, including recipes, meal plans, and tips for eating out. The American Heart Association (AHA) has a website with information on heart-healthy eating, including recipes, meal plans, and tips for shopping for heart-healthy foods.  

The Dietary Approaches to Stop Hypertension (DASH) diet is a heart-healthy eating plan that has been shown to lower blood pressure [45].  

The Mediterranean diet is a heart-healthy eating plan that has been shown to have several health benefits, including reducing the risk of heart disease, stroke, and type 2 diabetes [44]. You can find information about the Mediterranean diet on the Mayo Clinic website.  

In addition to these websites, there are many cookbooks and other resources available on heart-healthy eating. Patients can also talk to their doctor or a registered dietitian for personalized advice on how to eat a heart-healthy diet. 

Conclusion

In conclusion, adopting a heart-healthy diet is a crucial step towards maintaining cardiovascular well-being and overall health [30]. The nurse's role as a patient educator in promoting a heart-healthy diet is pivotal. By leveraging a position of trust and frequency of contact with patients, nurses can champion dietary choices that can reduce the risk and impact of heart disease.  

Research underscores the importance of a balanced intake of nutrients to support the cardiovascular system's health, emphasizing whole foods, lean proteins, healthy fats, and a reduction in sodium, saturated fats, and sugars [3]. 

Patients adopting a heart healthy diet require a multifaceted approach, combining knowledge with actionable steps that are practical and sustainable. The role of healthcare professional is instrumental in this dietary transition.  

A heart-healthy diet offers a multitude of benefits beyond reducing heart disease risk. It can improve blood pressure control, lower cholesterol levels, promote healthy weight management, and enhance overall energy levels [2][3]. A heart-healthy diet can contribute to a stronger immune system, reduced inflammation, and improved mental clarity [46]. 

Adverse Childhood Experiences

Introduction   

All children should grow and thrive in a caring, nurturing environment that meets their physical, emotional, and social needs. However, many are not so fortunate. Nearly every two in three Americans (64%) have experienced adverse childhood events (ACEs) (1, 2, 4, 5).  

ACEs are highly associated with future chronic health conditions, mental illness, premature death, and more (1). In fact, the more ACEs an individual has had, the higher their risk for having poor health outcomes as adults (13).  

Fortunately, there are preventive and protective measures that can be taken with the appropriate resources (1). With better awareness of ACEs and the right support in place, healthcare professionals can help improve the quality of life for a myriad of children and the adults they grow up to be. 

Definition 

Adverse childhood events, or ACEs, can occur from birth until age 18, and are great determinants of future health (1). These are any potentially traumatic events that happened to a child. ACEs are strongly linked to mental and physical disease in adults, contributing to at least half of the leading causes of death in the United States (1).  

The ACE score is a 10-item survey to identify any negative occurrences a person had before their 18th birthday (3). The higher a person’s ACE score, the more risk they have for an unhealthy adulthood (1,2). 

ACE was a term coined in a large-scale study published in 1998, describing them as childhood abuse and household dysfunction in seven specific areas (1, 2). In subsequent years, three more areas were added (3, 13). Altogether, the ten ACEs are comprised of the following examples of three broad categories:  

• Childhood abuse 

• • Psychological 

• • Physical 

• • Sexual 

• Household dysfunction 

• • Substance abuse 

• • Mental illness 

• • Parent treated violently. 

• • Family member incarcerated. 

• Neglect 

• • Emotional  

• • Physical  

Statistics and Demographics 

The initial adverse childhood experience (ACE) study, conducted in the late 1990s, included over 17,000 adult participants and revealed the following key demographic data (1, 2, 5):  

• Nearly 66% of women and 62% of men reported at least one ACE in their lives. 

• More than 1 in 6 people (17.3%) said they had experienced four or more types of ACEs.  

• Respondents’ races who reported ACEs were: 74.8% white, 11.2% Hispanic, 7.2% Asian/Pacific Islander, 4.5% black, and 2.3% other. 

• About 49% of those with college degrees experienced at least one ACE, compared to 44% without a high school diploma.  

• The age group who reported the highest incidence of ACEs was those from 35-49, where almost 70% had experienced at least one ACE. The lowest incidence was reported by those aged 65 and older, at 40%.  

• Of all women reporting ACEs, 25% said they endured sexual abuse, 30% witnessed substance abuse in the home, and 25% of the respondents’ parents got divorced.  

• Of all men reporting ACEs, 30% went through physical abuse, 24% saw substance abuse at home, and 22% of their parents were divorced.  

More recent data shows that at least 50% of the top causes of death in the US are associated with ACEs (6). As there is also a high association between ACES and depression, preventing these experiences could reduce adult depression by 44% (6).  

Causes and Risk Factors 

The causes of adverse childhood events are varied and multifaceted. They can stem from familial or communal challenges, often referred to as social determinants of health. Many of these determinants can cause ACEs, and may include (8):  

• Lack of access to healthcare or other resources 

• Financial difficulties 

• Homelessness or frequent moving 

• Discrimination 

• Any type of disrupted living situation  

As noted earlier, most of the American population has had some sort of adverse childhood experience. However, there are some factors that make it more likely for these to occur. Societal, communal, and familial cultures all play a role in adverse experiences.  

The following situations or conditions increase the likelihood of ACEs (7):   

Community Risk Factors: 

• High rates of poverty, crime, and violence 

• Limited educational, economic, and employment opportunities  

• Lack of community activities for youth 

• Unstable housing and frequent moves by community residents   

• Readily accessible alcohol and drugs 

• Frequent experiences of food insecurity  

Family and Individual Risk Factors:  

• Social or developmental disabilities or delays  

• Mental or chronic physical illnesses 

• A history of abuse experienced by caregivers themselves. 

• Youth dating or engaging in sexual activity early. 

• Single-parent families, particularly those with young caregivers 

• Low income and/or high economic stress 

• Low education levels 

• Children with few or no friends, or friends who partake in delinquent or aggressive behaviors 

• Caregivers with limited understanding of child development  

• Use of spanking or other corporal punishment as a form of discipline  

• Inconsistent discipline and/or little parental supervision 

• Families isolated from extended family, friends, and/or neighbors 

Cultural Considerations  

Though many people experience ACEs, some populations are affected disproportionately. This includes women and those in racial or ethnic minorities, who are at greater risk for experiencing 4 or more ACEs (6, 8). Specifically, African Americans, American Indians, and Alaska Natives (AI/AN) are far more likely to have multiple ACEs than any other race or ethnicity (9,10).  

The AI/AN community is a relatively young one, with poverty rates up to four times higher than the national average (10). Furthermore, the AI/AN group is often lumped together as “other” as a race category on surveys, making data harder to come by for this population (10).  

AI/AN children, when compared to the total US population, are more likely to have:  

• Parents who are divorced (33% versus 21%) 

• Lived with someone who abused a substance (24% versus 12%) 

• Witnessed domestic violence (15% versus 6%) 

• Lived with a parent who ultimately died (4% versus 2%) 

Lifespan Impact on the Individual 

While adverse childhood experiences affect most Americans, having been through four or more puts a person at significantly higher risk of health problems as an adult (1, 2, 9). In general, the more ACEs an individual has experienced, the more likely they will have poor outcomes later in life, with a specifically high correlation to diabetes, heart disease, obesity, depression, substance abuse, smoking, poor academic achievement, and early death (4).  

In fact, ACEs can reduce an individual’s life expectancy by as many as 20 years, compared to someone who has had zero ACEs (8).  

The original ACEs study was conducted to determine the link between childhood abuse and adult health risk factors (1). The conclusion was overwhelmingly that in the United States, the main causes of morbidity and mortality are related to many of the health behaviors exhibited by those who have experienced ACEs (1). More recent studies find that ACEs contribute significantly to substance abuse, violence, and self-harming behavior (11).  

At least 5 of the top 10 leading causes of death in the United States that are strongly related to ACEs include (9,11, 12):  

• Heart disease (#1 cause of death) 

• Stroke (#5) 

• Chronic lower respiratory diseases (#6)  

• Diabetes (#8) 

• Chronic liver disease and cirrhosis (#9) 

As far as mental health goes, the link with ACEs is clear: The higher one’s ACE score, the more likely they are to be depressed, experience impaired work performance, and have suicidal tendencies (13). Harmful behaviors associated with high ACE scores include smoking, drinking, and drug abuse, as these methods are often used to cope with past traumatic experiences (13).  

Societal Implications 

Adverse childhood events are preventable and have been shown to contribute to at least half of the leading causes of death in the United States (1, 9, 11). Thus, the impact of ACEs on public health is vast. Since the CDC considers ACEs a public health concern, it is of utmost importance to decrease their incidence (1). Through the reduction and prevention of ACEs, general public health would improve markedly, drastically cutting down on healthcare costs and resources (1, 5, 6, 9).  

The societal implications for reducing ACEs are manifold:  

• Dramatic reduction of preventable causes of death 

• Longer lifespans for the general population  

• Better mental health  

• More cost-effective physical and mental healthcare 

• Lower rates of disease and depression in the general population 

Ways to Mitigate ACEs 

Though ACEs are widely pervasive in American society, they need not be so. With proper resources and support systems, many -if not all- ACEs may be eradicated. The best way to mitigate ACEs would be to prevent them in the first place (4). This requires creating safe, stable, nurturing environments for children and their families (9). Furthermore, as ACEs can occur for a wide array of reasons, they need to be addressed at both the family and communal levels. 

With individuals, a first step would be prevention of ACEs in the home. This could involve a vast array of mental health, education, and social work services such as: home visits, parenting classes, therapy sessions, and more (8, 9). Different emotion management techniques and child development concepts could be taught to at-risk families, promoting bonding and trust between children and their caregivers.  

High-quality childcare and after-school programs with trusted adults can help mitigate ACEs as well (9). Screening for ACEs at regular intervals would also be helpful. This could include annual check-ups at the doctor’s office, visits with the school nurse or counselor, or a consultation with a home health provider. Medical management of physical and mental health conditions would be made available, including routine health screenings and necessary medications (4, 8, 9).  

At the community level, prevention could take the form of free education for family members, food and housing assistance, adequate access to healthcare services, and fostering safe neighborhoods (4, 9). Economic support for families could include family-friendly work policies, earned income tax credits, and so forth. Children could partake in community events like after-school clubs and sports, helping them build bonds with trusted and supportive adults.  

Three principles are the most helpful preventing long-term effects of ACEs, (4):  

• Reducing stress by ensuring basic needs are met, as well as tending to abusive situations, community crime, substance abuse, discrimination, and poverty. 

• Strengthening life skills can strengthen the resilience of children and their family members by practicing planning, focus, and self-control. 

• Building responsive relationships by having adults listen to their children and respond adequately to their needs, thereby fostering a safe, trusting relationship. 

Reporting ACEs 

Considering there are various types of ACEs, they can be difficult to identify and thus report. However, some are clear-cut. In situations where child abuse or neglect is occurring or suspected, a mandated reporter (e.g., nurse, teacher, counselor) would need to report it as soon as possible. If the child is in imminent danger, take them to a safe place and make a report.  

To report child abuse in the United States, call or text 1-800-4-A-CHILD (1-800-422-4453). The website is https://www.childhelphotline.org/.  

If there is suspicion that a child is being sexually exploited, the phone number to call is 1-800-THE-LOST (1-800-843-5678), and the website is https://report.cybertip.org/.  

To report human trafficking, call 1-888-373-7888, use TTY at 711, text BEFREE (233733), or visit the website at https://humantraffickinghotline.org/.  

For anyone experiencing feelings of self-harm or suicide, 988 is the national Suicide and Crisis Lifeline that can be called or texted. The website is https://988lifeline.org/.  

Support and Additional Resources 

While there is no single way to prevent ACEs from occurring, there is a plethora of resources available to help mitigate the effects and to educate others. Visting a healthcare provider can connect a patient to mental health professionals, support groups, or specialty services like social work and support groups (8).  

The Substance Abuse and Mental Health Services Administration (SAMHSA) has an abundance of resources on topics like trauma-informed care, early childhood mental health programs, Native Connections for the AI/AN population, school, and campus health, and much more. More information can be found at https://www.samhsa.gov/programs.  

Healthy Outcomes from Positive Experiences (HOPE) is a national resource center offering research, training, and technical assistance in order to better the lives of children and their families. Their website is https://positiveexperience.org/.  

The Centers for Disease Control and Prevention (CDC) offers ACE-specific information at this website: https://www.cdc.gov/violenceprevention/aces/resources.html.  

Conclusion

Adverse childhood events, or ACES, affect the majority of the American population. Strongly correlated with many leading causes of death, ACEs are preventable and warrant attention from healthcare providers and the general public alike. Fortunately, many resources exist at the individual, community, and national levels to provide care and prevention for these experiences.  

Though ACEs tend to lead to negative health outcomes, they need not condemn a person to lifelong problems. Through screening tools, community food and housing programs, mental health assistance, education, and adequate medical care, ACEs can be mitigated, well managed, and prevented.  

Despite the misfortune in a child’s life, there is still much hope available when they reach adulthood.  

Conclusion

Adverse childhood events, or ACES, affect the majority of the American population. Strongly correlated with many leading causes of death, ACEs are preventable and warrant attention from healthcare providers and the general public alike. Fortunately, many resources exist at the individual, community, and national levels to provide care and prevention for these experiences.  

Though ACEs tend to lead to negative health outcomes, they need not condemn a person to lifelong problems. Through screening tools, community food and housing programs, mental health assistance, education, and adequate medical care, ACEs can be mitigated, well managed, and prevented.  

Despite the misfortune in a child’s life, there is still much hope available when they reach adulthood.  

Trauma Informed Care in Nursing

Introduction

As nurses, we have been trained to perform ongoing assessments on patients with every encounter. Many patients have gone through traumatic events that often go undiscovered by the healthcare team.

A trauma informed care approach will help healthcare providers uncover past trauma. This will allow them to tailor a plan of care that helps alleviate patient suffering by decreasing overall stress and anxiety. When the healthcare team is aware of past trauma, they can avoid conversations and situations that could potentially re-traumatize the patient.

Trauma Informed Care 

Trauma is a human experience that can affect people from all different backgrounds and walks of life. There is no race, gender, sexual orientation, or social class that is immune to the far-reaching clutches of trauma. A traumatic event is an event that is marked by sexual violence, severe injury and/or death. These events can be first-hand accounts where the people themselves were the victims of the event.  

They can also be indirectly experienced by witnessing the event take place on another person. The event can also produce vicarious trauma when it happens to a close friend or loved one. No matter how traumatic an event was experienced, it can have severe and long-lasting effects (1). 

Despite the rising accounts of traumatic events, trauma informed care is an underused skill in the healthcare field. Those who support and use trauma informed care understand that there is a large population of people seeking healthcare services who have had past traumatic experiences. They are also aware that just by seeking out care, they have the potential of being re-traumatized.  

Empowering the patient to have control over their care through collaboration will help decrease the chances of re-traumatization.  

There are six principles of trauma informed care: 

1. Safety 
2. Trustworthiness and transparency 
3. Peer support 
4. Collaboration and mutual support 
5. Cultural and historical sensitivity  
6. Empowerment of voice and choice 

Trauma informed care runs parallel to ethics in the healthcare setting. It endeavors to ease the patient’s suffering by preventing re-traumatization and empowering the patient. (3)

Principles of Trauma Informed Care 

It is meaningful to explore each of the six principles of trauma informed care 

Safety 

In trauma informed care, safety pertains to both the psychological and physical safety of the patient and their family throughout their encounter with the healthcare organization. The goal is to prevent any form of re-traumatization. This is accomplished by creating safe spaces, access to services, and engagement between the patient and the healthcare team.  

One of the greatest aspects of safety in trauma informed care is environmental. This demands that the healthcare teams create an environment that is both welcoming and accommodating to all patients regardless of their diverse backgrounds. We must understand that patients who have undergone traumatic events can be hypersensitive to their environmental safety.  

The trauma informed care plan must be individually tailored and include communication initiatives that promote the patient’s self-identity and how they would like to be addressed (1).

Trustworthiness and Transparency 

Nursing has long been recognized as the nation’s most trusted profession. This has been accomplished through the intentional focus of patient advocacy. Nation-wide policies and safety goals have promoted diversity, equity, and inclusion. Initiatives to make sure that the patient understands and agrees with their plan of care, such as using their preferred language in plain and clear terms, is an example of how nurses build that trust.  

Using the concept of patient-centered care helps demonstrate transparency, which is a way nurses further build trust. True transparency can be accomplished through encouraging patients to be involved in their care. Asking patients if it is acceptable that we document their experiences and even share our notes or computer screens to demonstrate our desire to be transparent.  

Educating patients using the teach-back method also indicates our transparency as our knowledge becomes theirs (1).

Peer Support 

Contrary to popular beliefs, the goal of peer support in trauma informed care is not fixing the individual. Rather, the goal is to assist the individual to empower themselves by connecting them with supportive groups of peers that have similar experiences, culture, beliefs, and religion. Empowerment of the patient should be the goal of peer support. Traumatic stress is often accompanied by a re-traumatization cycle that can be interrupted and ultimately stopped through individual empowerment of the patient.  

These peer support groups often contain members who themselves have survived traumatic events. To have the best probability of success, the patient should leave behind former friends who enable the re-traumatization cycle and gravitate to the peer support group members. This can leave the patient with further feelings of loss and grief. This has to be considered when developing the plan of care for the patient (1). 

Identifying Past Trauma 

Trauma informed care does not mean that the care is tailored to a patient’s specific trauma. Nor does it mean that the team endeavors to heal or even address past trauma. Rather, in simple terms, trauma informed care recognizes that the patient has been through a traumatic ordeal and that the plan of care must take that trauma into account in order to properly care for the patient.  

The patient’s reaction and compliance may be affected by their past trauma. Past trauma needs to be identified and acknowledged. Past trauma can affect all aspects of a patient’s life. Identifying and acknowledging the trauma and how the patients then needed coping mechanisms may now have become detrimental to their health is important for the overall well-being of the patient.  

Through the identification of past trauma, the team can take the opportunity to ensure that the patient does not feel responsible for the life-altering trauma and understands that the trauma was not their fault. Identifying the trauma can lead to the revelation that there is a connection between past trauma and the patient’s current coping and functioning; this can change their overall perspective, thus changing their lives (4). 

Collaboration and Mutual Support 

Collaboration and mutual support demand that the entire healthcare team see the patient as both an equal partner and the expert in their own personal experiences. The patient should be allowed to both identify and prioritize their goals, then the healthcare team can work with the patient to for the plan of care with these goals at the forefront.  

Collaboration takes more time than the traditional healthcare “do as I say” method. It helps in the trust-building process and when done properly, it helps the patient to succeed as the goals have come from them. This is something that can also interrupt the re-traumatization cycle. It also increases the probability that the patient will be compliant with the plan of care and any after-care appointments and follow-ups (1,4). 

Cultural and Historical Sensitivity 

The entirety of the patient’s identity is surrounded in cultural and historical sensitivity. Not only does this encompass aspects such as race, gender, age, etc. but it also includes life experiences and relationships right down to the base familial associations.  

It also includes beliefs, core values and experiences in open spaces. When seeking healthcare, no matter the reason, all of these aspects of the patient’s identity are brought to the facility and laid in front of the healthcare team (1).  

Empowerment of Voice and Choice 

As discussed earlier in the peer support principle, empowerment is paramount in trauma informed care. Empowerment of voice and choice is perhaps the chief cornerstone and is present in all the other principles of trauma informed care. Trauma informed care empowers patients by making them feel heard and that their voice is important for their overall well-being.  

Though the healthcare team may not always agree, trauma informed care also enforces the concept that the patient’s choices are to be respected. Through the trauma informed care journey, the patient develops their ability to navigate the healthcare setting and becomes familiar with the language of the medical community.  

This further empowers the patient as they can understand the plan of care and become an active participant in that plan, as they were involved in both the planning and implementation. Further, trauma informed care creates a safe and supportive environment where the patient is allowed to grow and mature in their knowledge and understanding of themselves and their health (1).

Effects of Traumatic Stress 

Traumatic stress has shown to increase chronic illness, mental health issues and early death. When left alone, traumatic stress can morph into enduring stress. Some forms of enduring stress include: 

• Chronic stress – this happens when trauma is continuous over a long period of time. 

• Toxic stress – this is found in children who experience long-standing and/or frequent trauma such as emotional and physical abuse, neglect, and exposure to violence.  

Traumatic stress can have altering effects on multiple brain processes. This includes the neurologic, immunologic, endocrinologic, metabolic, inflammatory, and autonomic processes. Depending on which phase of brain development the patient is in when the trauma occurs, it determines the long-lasting effects.  

Repeated trauma can cause a hormonal cascade which can result in the allostatic load phenomenon. This phenomenon distorts the normal stress mediating processes.  

Traumatic stress often leads to self-destructive behavior. Drug and alcohol use/addiction, violence and risky behavior often follows those who have had traumatic stress events. There is a fear among traumatic stress victims that they may be judged for their choices and lifestyle (1). 

Adverse Childhood Experiences 

Nearly 40% of people have been exposed to adverse childhood experiences. Of course, adverse childhood experiences harm the overall health and well-being of the child; they also have a potential great impact on the physical and mental health of the person as they transition into adulthood.  

Adverse childhood experiences and childhood trauma have shown to leave the patient with an increased risk for developing leading causes of death and disability. These conditions include heart disease, stroke, cancer, and depression with suicidal ideation. Also, childhood trauma can lead to symptoms of chronic headache and pain as an adult (2). 

As most childhood trauma is perpetrated by someone known and close to the child such as a parent, relative or close family friend, the child is often left with an altered expectation of interpersonal relationships. This may lead to severe insecurity and distrust where negative personal perception especially in relation to others may develop.  

People who develop physical symptoms of past childhood trauma are often unable to adjust and move on post-trauma. On the other hand, those who are able to form positive relationships tend to have fewer physical symptoms and are more liable to have adjusted to childhood trauma. Childhood trauma can have long-reaching effects on the ability of the adult to form positive relationships and have normal responses to stressful situations (2). 

Trauma Informed Approach 

The trauma informed approach was born out of the research on adverse childhood experiences. The research showed that the more adverse childhood experiences that took place in the patient’s life, the more it affected their mental and physical health; even leading to early death.  

Trauma informed approach begins at the organizational level, where the culture must adapt to prevent re-traumatization. There are a few aspects that need to be incorporated into the organization’s training to accomplish the changes needed.  

The organization must put on trauma glasses and view the healthcare team through the trauma lens. There is a direct correlation between trauma and mental health; this needs to be acknowledged, accepted, and viewed as part of the care plan. 

In order for the trauma informed approach to be effective, the organization must realize that trauma expands beyond Post Traumatic Stress Disorder (PTSD). Rather, trauma incorporates a multitude of differing issues that can include mental, emotional, physical, and other multiple trauma sources.  

The healthcare professional who is assessing the patient should be trained in recognizing the signs of trauma and, if disclosed, be able to respond appropriately in the moment. Training needs to be done with all front-line staff who the patient may confide in. 

The healthcare team should be aware of resources that are available in the community and be able to refer the patient to those organizations. Being as trauma specific as possible so that the patient can connect in a meaningful way with this new support system. The organization should partner with these support groups to ensure easy transitioning from the institution to the community. 

The team should also prioritize the principles of trauma informed care. For instance, to promote trustworthiness and transparency, the team could limit the number of healthcare providers who will ask the patient to repeat the story of their traumatic experience. Turning to more collaborative communication and relationships between the team and the patient; allowing the patient to be actively involved in their plan of care also promotes the trauma informed care principles. 

Promoting safety within the organization for both the patient and the healthcare team also helps to change the culture to one of a trauma informed approach. Trauma survivors could be approached and asked to help design, implement, and evaluate the trauma informed approach to be used. What better way to get to know your community resources than to actively partner with them to help meet the needs of the organization’s patients. 

It needs to be recognized that not all patients who show similar symptoms to those of past trauma have gone through a traumatic event. There is no cookie-cutter plan of care, and all patients must be properly assessed to determine what their plan of care will be (6).

Impact of Trauma Informed Care 

The impact of trauma-informed care on the patient and on the healthcare system as a whole cannot be overstated. By understanding that a great deal of the patients who seek out healthcare services have undergone a traumatic event and tailoring the assessment with that in mind, an organization can minimize the occurrence of re-traumatization.  

When we understand how trauma has affected our patients’ lives, how they perceive the healthcare system and what their previous experiences within that system have been like, steps can be taken to ensure better outcomes within this population (1).

Nursing Implications 

In order for trauma informed care to be properly accepted and put into use in the healthcare setting, the culture must be transformed to be a trauma-informed culture. Nursing is with the patient around the clock and nurses have the ability to touch patient’s lives in the most impactful way.  

Here are a few considerations that pertain to the healthcare team but when used by nurses have the ability to transform the patient’s environment into a true trauma informed care setting. 

Introductions 

Even if the nurse believes that the patient knows who they are, it is important for the nurse to reintroduce themselves with every interaction. The patient generally has many different members of the healthcare team entering their space throughout their stay. Team members tend to meld into one anonymous face to the patient; the nurse by introducing and reintroducing themselves and their role to the patient will not only foster an understanding of who does what, but they will empower the patient to be engaged and involved in their plan of care. 

Body Language 

Body language is important when caring for any patient. When caring for a patient who has experienced trauma, this becomes even more impactful. Open body language sets the stage for trust.  

Trauma survivors may often feel a sense of being trapped or confined which may lead to an overall sense of powerlessness. Unintentional threatening body language magnifies these feelings and could bring on a re-traumatization episode. By contrast, non-threatening body language decreases the trauma center and leaves the patient calm and non-triggered.  

Trauma informed care body language includes being at the patient’s level; commit to sit or raising the bed so that both patient and nurse are at the same level. Knowing the environment and deescalating trauma by the nurse positioning themselves properly in relation to the patient and the door; allowing for both to access so that the patient does not feel confined. 

Anticipatory Guidance 

Past trauma may have been unpredictable or an outright surprise. Verbally telling a patient what will be expected during their stay will reassure them even if the coming procedure or test may cause pain. Sharing who will be part of their care during their stay will also set them at ease. Knowing and understanding the expectation further empowers the patient to be involved in their plan of care.  

The expectation, when known, decreases those feelings of surprise which could bring them back to that time of trauma.

Permission 

Touch can have an incredible impact on the patient who has experienced past trauma. Unwanted or inappropriate touch quite likely may have been a part of their traumatic experience. It can activate those traumatic memories and activate the re-traumatization cycle. Touch is also inevitable when it comes to the nurse/patient relationship.  

What the nurse can control is when the touch occurs. Touch should always be preceded by the nurse explaining what they are going to do and asking for the patient’s permission to touch them. Asking permission puts the ball in the patient’s court and empowers them as they are now given a choice and are in control of their body and space.  

Permission to touch the patient should never be assumed; permission should be asked every time the nurse needs to touch the patient. 

Protect 

In many cases, patients who have experienced trauma experienced it at the hand of someone that they know. Many times, the patient will not be alone in their room; family and friends are often present. Patient advocacy has always been the primary role of the nurse.  

As part of being an advocate for the patient, the nurse should protect the privacy and safety of the patient. Asking those present in the room to leave prior to discussing the patient’s plan of care is a way to protect both privacy and safety. The patient may not feel safe asking visitors to leave their room especially if they may have been involved in the prior traumatic episode.  

By asking visitors to leave, the nurse gives control back to the patient. In private, the nurse can ask who the patient is comfortable with remaining in the room. Once again, the patient is empowered. 

Clear and Consistent 

Realistic expectations are understood when given in clear and consistent language. This will also foster trust especially if the entire healthcare team is on the same page and vocalizing the same message, consistency. Using language that the patient understands is also paramount. Avoiding medical terminology and acronyms also builds trust as the patient knows that the nurse has made it their priority that the patient understands their plan of care. 

Universal Precaution 

Finally, trauma informed care needs to be a universal precaution regardless of if the patient’s past trauma history is known or not. By treating all patients as if they had experienced past trauma, those who have will be more apt to share the experience.  

Also, nurses will be less likely to start the re-traumatization cycle by inadvertently triggering an episode. It will help treat the patient without relying on the patient to disclose something that they may not yet feel comfortable sharing. (3)

Resources 

It is not easy to become a center where trauma informed care is practiced, it does not happen overnight. Trauma informed care is an intentional shift in culture at the facility and/or system level. Trauma informed training should be implemented, and the staff need to understand the “why” behind the training in order to buy-in.  

Trauma informed care not only helps the patient to be empowered and prevent re-traumatization, but staff that have undergone past traumatic experiences can also be helped once a facility adopts this culture. This culture should be at the forefront of both staff and leadership minds. Staff meetings, unit huddles and any other opportunity where leadership actively communicates with staff should incorporate the messaging of trauma informed care.  

Facilities should actively be hiring a trauma informed workforce. People from wide varieties of racial and cultural backgrounds should be on the interview panel. Questions pertaining to trauma informed care can and should be asked to pick up on skills and traits that will promote this culture. 

A few environmental factors to create the trauma informed culture include keeping doors and common areas well-lit, keeping noise levels low and having warm, cozy colors as decoration in common areas.

Below are some websites that can be visited in order to help kickstart the culture of trauma informed care: 

• https://TraumaInformedCare.chcs.org 

• https://www.creatingpresence.net/ 

• https://www.chcs.org/resource/key-ingredients-for-successful-trauma-informed-care-implementation/ 

• https://store.samhsa.gov/product/SAMHSA-s-Concept-of-Trauma-and-Guidance-for-a-Trauma-Informed-Approach/SMA14-4884 

(5) 

Conclusion

Though not a new concept, trauma informed care is essential to help patients who have had traumatic experiences navigate through the healthcare system. Trauma informed care empowers patients to take control of their care in collaboration with the healthcare team. Ultimately, the goal of trauma informed care is to prevent re-traumatization of the patient at the hands of the healthcare team.

The trauma background of any given patient is unknown when they arrive at the facility. It is the responsibility of the nurse to use trauma informed care to both assess the patient and create trust so that they will disclose the trauma. Once known, the team will be able to work together with the patient to prevent further trauma and have positive outcomes.

Conclusion

Though not a new concept, trauma informed care is essential to help patients who have had traumatic experiences navigate through the healthcare system. Trauma informed care empowers patients to take control of their care in collaboration with the healthcare team. Ultimately, the goal of trauma informed care is to prevent re-traumatization of the patient at the hands of the healthcare team.

The trauma background of any given patient is unknown when they arrive at the facility. It is the responsibility of the nurse to use trauma informed care to both assess the patient and create trust so that they will disclose the trauma. Once known, the team will be able to work together with the patient to prevent further trauma and have positive outcomes.

Nursing Care in Lewy Body Dementia 

Introduction   

Lewy body dementia is one of the more common causes of dementia. Currently it is the second most common dementia disorder following Alzheimer’s disease [2]. This condition is shown to affect more than 1.4 million people in the United States [1] [2]. Of dementia cases in older adults, Lewy body dementia is said to make up 5% of people with dementia [2]. Lewy body dementia is a disorder that progresses over time [1]. The progression of the disease differs between individuals and the severity of the symptoms [1].  

On average an individual lives between five to eight years after diagnosis [1]. Currently there is not a cure for this disease [1]. This course will examine the causes of this disease, signs and symptoms patients might experience, diagnostic tests, types of management, and educational resources for family members. This course is designed to inform nurses about this common disease and to use this information in their daily practice to care for their patients.  

Definition

Lewy body is an umbrella term that includes two separate diagnoses: Dementia with Lewy bodies and Parkinson’s disease dementia [5]. As these diseases progress, they develop together and are seen as one entity, not two separate conditions [4]. Lewy body dementia is a condition that involves neurocognitive disorders that include hallucinations, memory loss, behavior changes, and parkinsonism features [2]. This disease can also affect intellectual abilities and cause individuals to act out dreams during REM (rapid eye movement) sleep [2]. REM sleep behavior disorder sometimes may be experienced before any other symptoms are exhibited [2].   

Lewy body dementia is known for a buildup of deposits of alpha- synuclein proteins called Lewy bodies [1]. Diagnosing this condition can be difficult because many neurological disorders have similar symptoms. Lewy body dementia and Parkinson disease dementia are very similar. For a diagnosis of Lewy body dementia, there must be a cognitive impairment with motor symptoms occuring in less than 12 months [3].  Parkinson’s disease dementia affects an individual’s movements; cognitive symptoms appear later (greater than one year) [5].  

Lewy body dementia is known to affect older adults generally between the ages of 50 and 85 [2]. This disease is said to be underdiagnosed due to a large number of diagnoses occuring post-death during autopsies [4]. Several medications used to treat neurocognitive and behavioral symptoms in other conditions can worsen the symptoms of Lewy body dementia [4]. Therefore, an accurate diagnosis can impact an individual’s quality of life.  

Epidemiology 

Lewy body dementia affects a significant number of individuals in the United States. This condition is found more often in men than women [4]. Age is thought to be the greatest risk factor for an individual developing this disease [4]. An individual who has a family history of Lewy body dementia and Parkinson’s disease is at a higher risk for developing this condition [3].

Lewy Body dementia is more widespread in European, Asian, and African ethnic groups [3].  In individuals with Parkinson’s disease, the incidence of Parkinson’s disease dementia is said to be around 25-30% [4]. The incidence of individuals with Parkinson disease developing this type of dementia after having Parkinson’s for more than 20 years increases to around 83% [4].  

Pathophysiology 

There is a buildup of alpha- synuclein proteins that causes neurons to die in Lewy body dementia [2] [5].  As mentioned above in this course, this buildup of proteins is called Lewy bodies. The death of neurons that produce dopamine result in problems with movement, cognitive impairment, a decline in cognition, and sleep disturbances [4].  In Lewy body dementia there is a deficiency of acetylcholine [3]. There is also a decrease in acetylcholine with Alzheimer’s disease, but the deficiency is greater with Lewy body dementia [3]. The decrease in neurons that produce acetylcholine causes memory loss and learning impairment [4].  

The mutation of synuclein alpha and synuclein beta genes can cause dementia with Lewy bodies [2]. Mutations in apolipoprotein E and GBA genes are potential risk factors for developing the disease [2]. There have been cases where a buildup of alpha-synuclein was found during an autopsy, but the individual did not show any clinical signs of Lewy Body dementia when alive [4]. The function of these proteins in this condition is still undetermined [5]. 

Etiology 

The exact cause of Lewy body dementia is still unknown. While research is ongoing and new developments are occuring, the specific cause has not been determined. The accumulation of Lewy bodies cause cell death which causes symptoms, however, the reason for the buildup of Lewy bodies is still under research [5]. As mentioned earlier, there are specific gene mutations that have been shown to increase the likelihood of producing altered alpha- synuclein proteins, in turn causing them to clump together (forming the Lewy bodies) [2].  

The mutation of the GBA gene interferes with the function of lysosomes, which can affect the breakdown of the alpha- synuclein proteins, causing the proteins to accumulate [2]. The e4 allele type of the APOE gene has been shown to increase the risk of developing Lewy body dementia [2]. These clumps of Lewy bodies form inside and outside of neurons in different areas of the brain, where they can alter the function of the cell and can cause the cell to die [2].

The neurons that develop the neurotransmitter dopamine are especially impacted by these clumps of Lewy bodies, which was addressed earlier in this course [2]. Further research is required to find out why these Lewy bodies develop in certain individuals. Currently, age, genetics, and environmental factors are some of the greatest risk factors [3]. 

 ​

Clinical Signs and Symptoms 

Lewy body dementia is a progressive disorder - the signs and symptoms worsen over time. The symptoms that are more common are sleep changes, impaired behavior, movement, and cognition [5]. Research shows that the location of Lewy body accumulation impacts the clinical signs and symptoms the individual experiences [3]. If Lewy bodies develop in the brainstem and cerebral cortex first, the condition is called dementia with Lewy bodies, and the onset of the dementia is early [3]. If Lewy bodies accumulate in the brain stem and then develop into the cerebral cortex as time passes, the onset of dementia appears later, and this condition is called Parkinson’s disease dementia [3].  

Rapid Eye Movement Sleep Behavior Disorder 

Rapid eye movement (REM) sleep behavior disorder is sometimes the first clinical sign of dementia with Lewy bodies [2]. Individuals with this disorder move and talk while dreaming in their sleep [2]. The movements can be violent and cause the individual to fall out of bed [5]. Individuals may kick, punch, and scream in REM sleep (the second half of their sleep) [4]. REM sleep behavior disorder is seen in 76% of patients with dementia with Lewy bodies [4].   

This disorder can cause fractures and contusions in some individuals resulting from falling out of bed [4]. This can not only affect the individual, but also the sleep partner of the patient [4]. In some cases, separate sleeping arrangements are needed for the safety of the individual and their sleeping partner. A questionnaire by the patient and sleep partner is part of the diagnosis of REM sleep behavior disorder [14]. If the individual does sleep next to someone, this questionnaire can be helpful as most of the time the patient cannot recall the events while asleep [14]. Video polysomnography is required for a complete diagnosis of this disorder [14]. These events while asleep must be repeated to meet the diagnostic criteria [14]. 

Other Sleep Disorders 

Other disorders of sleep include sleepiness in the daytime, restless leg syndrome, confusion when awakened, and obstructive sleep apnea [4]. 

Visual Hallucinations 

Visual hallucinations are present in about 80% of individuals with Lewy body dementia [1]. Visual hallucinations are a core clinical symptom of dementia with Lewy bodies [4]. They are more common in women than in men [4]. Individuals are aware of these hallucinations and can tell others what they experienced [4]. Visual hallucinations are vivid to individuals and have been said to range from people walking around the house to seeing people that have died sitting next to them [6]. During the beginning stages of the disease, the hallucinations do not seem to affect the patient as much as when the disease progresses [6]. Patients are said to be afraid of these hallucinations in the later stages of the disease [6]. Nonvisual hallucinations are less common, however can occur in some patients [1]. These hallucinations include smelling or hearing something that is not in their surroundings [1]. 

Fluctuation in Cognition 

Fluctuation in cognition is also a clinical sign that is associated with dementia with Lewy bodies [4]. This symptom includes changes in attention, concentration, and alertness [5]. These changes are random and can differ day-to-day [1]. Symptoms can include delirium, and mimic symptoms that are caused by metabolic diseases, which can further the difficulty with identifying the correct diagnosis [4]. To diagnose dementia with Lewy bodies, one of the episodes must be confirmed [4]. These fluctuations can be present in other forms of dementia in their later stages but when present in earlier stages, they point to dementia with Lewy bodies [4].  

Memory loss that impacts activities of daily living can be found in later stages of Lewy body dementia [1]. Memory loss early on is more often a characteristic sign of Alzheimer’s dementia [1]. Confusion about the individual’s whereabouts, and inability to multitask can also occur in dementia with Lewy bodies [4]. 

Problems with Movement 

Problems with movement are signs of Lewy body dementia. Bradykinesia (slow movements) and rigidity occur in about 85% of individuals with dementia with Lewy bodies [4]. Tremor at rest is less common in individuals with this condition [4]. Loss of coordination and difficultly swallowing can occur [1]. Problems with movement greatly increase the risk of falls for these individuals [4]. This can place strain on the individual’s caregivers [4]. 

Autonomic Dysfunction 

Autonomic dysfunction can be present in dementia with Lewy bodies and Parkinson’s disease dementia. This symptom is seen in about 90% of patients with Lewy body dementia [4]. The symptoms that result from autonomic dysfunction can be constipation, urinary incontinence, orthostatic hypotension, erectile dysfunction, and dizziness [1] [4]. Orthostatic hypotension appears as early as five years prior to the diagnosis of Lewy body dementia [4]. Syncope and falls are usually the result of orthostatic hypotension [4]. Constipation can also occur earlier in the disease process [4]. 

Diagnostic Tests and Evaluations  

Throughout this course, it has been mentioned that Lewy body dementia is significantly underdiagnosed. Individuals are usually diagnosed as the disease progresses due to the symptoms that overlap with other forms of dementia and other neurological and psychiatric disorders [3]. An autopsy of the brain after death is one of the only ways to have a conclusive diagnosis of Lewy body dementia [16]. There are certain diagnostic criteria and diagnostic tests that are used to diagnose an individual with Lewy body dementia. 

Diagnosis by Symptoms 

Lewy body dementia is probable when an individual experiences dementia and two main features of the disease. Lewy body dementia is a potential diagnosis if the individual experiences progressive dementia and one main feature of the disease [3]. As discussed in the clinical signs and symptoms section of this course, key features of Lewy body dementia are cognitive fluctuations, dementia that progresses, problems with movement (signs of parkinsonism), REM sleep behavior disorder, and visual hallucinations [3] [16].  

Timing of symptoms is relevant for distinguishing between the two forms of Lewy body dementia [3]. Currently healthcare providers use the time span of one year to distinguish the two forms [3]. If dementia occurs within one year of the appearance of movement problems, then a diagnosis of dementia with Lewy bodies is used [3]. If an individual is diagnosed with Parkinson’s disease and starts experiencing symptoms of dementia more than one year after their Parkinson’s diagnosis, then Parkinson’s disease dementia is used [3]. Some indicative biomarkers in addition to clinical symptoms are used in diagnosis [4]. Some of these biomarkers can be found in cerebral spinal fluid (CSF) and are still under research [4].  

Cognitive Tests 

Cognitive testing can be used to show the cognitive impairment of patients with Lewy body dementia [3]. The Mini-Mental State Examination can be used as an initial screening test [4]. This exam tests cognitive function by focusing on concentration, orientation, and memory [15]. This test can be limited since symptoms of these patients can fluctuate day to day [3]. Another cognitive function test is the Montreal Cognitive Assessment (MoCA) [15]. Providers do not usually diagnose based on a single test; instead, they use the results to look for other signs and symptoms of Lewy body dementia [4]. 

Imaging Tests 

There are certain imaging tests that can help with diagnosis and distinguishing between other dementia disorders. A single-photon emission computerized tomography (SPECT) scan can help support a diagnosis [16]. This is a nuclear scan that can sense radioactivity [16]. If the SPECT scan shows a reduced dopamine transporter uptake in the basal ganglia, this can be a sign of Lewy body dementia [16]. This will separate the diagnosis between Lewy body dementia and Alzheimer’s disease [4]. Performing this scan alone will not lead to a possible diagnosis of Lewy body dementia; however, in combination with other diagnostic tests, the scan can lead to a more certain diagnosis [4]. Results from these scans can appear normal initially, and the scan may need to be repeated [4].  

An iodine- MIBG myocardial scintigraphy can be performed to support Lewy body dementia [16]. This would show decreased communication of cardiac nerves [16]. The results may be skewed by heart disease or certain drugs [4]. A CT or MRI may be used but these imaging tests can present mixed results [4]. With Alzheimer’s disease, significant atrophy is seen in the medial temporal lobes [4]. There is normally minimal atrophy in Lewy body dementia [4].  

As mentioned earlier in the course, video polysomnography is needed for the diagnosis of REM sleep behavior disorder [14]. This sleep study without the loss of muscle tone can also point towards a diagnosis of Lewy body dementia as REM sleep behavior disorder has now moved to a key feature of this disease [14]. 

Case Studies 

Case Study #1 

A 74-year-old male presents to his primary care provider after his wife reports abnormal behavior over the past several months. His wife reports the patient kicks and screams during sleep. The patient reports seeing little people walking around the living room during the day. The wife states the patient some days will fall asleep throughout the day while completing activities.  The patient states difficulty walking and muscle stiffness.  

The wife states last week the patient was supposed to go to the local grocery store to buy milk. After two hours passed, the wife called her husband as she was worried about him. He states he got lost finding the grocery store and did not know where he was. The wife said she had to drive to find her husband and bring him home. The patient also reports dizziness when standing. After the nurse obtained an orthostatic blood pressure, the patient was positive for orthostatic hypotension. 

• Which form of dementia is the patient most likely experiencing? 
• What type of symptoms is the patient experiencing that would point to that diagnosis? 
• What diagnostic tests or evaluations should the patient undergo? 
• What types of supportive treatment should the healthcare provider include in the treatment plan for this patient? 

Case Study #2 

A 70-year-old female presents to the emergency department via EMS after falling at home. The patient’s daughter called 911 after finding her on the floor when going to visit her. Upon arrival at the emergency department the patient is oriented to self. The patient does not know where she is or what happened to precipitate the fall. The patient has a past medical history of hypertension, diabetes type II, and Parkinson’s disease.  

The patient was diagnosed with Parkinson’s disease two years prior. The daughter states the patient has been forgetful lately and not acting like herself. The daughter reports that her mom’s behavior is different from day-to-day. An MRI and the National Institutes of Health Stroke Scale (NIHSS) are used to rule out a cerebrovascular accident. A complete blood count (CBC), a complete metabolic count (CMP), and urinalysis are obtained. The patient suffered a contusion to her right cheek and a right radius fracture. The patient states that she sees figures dancing in the room and smells popcorn. The patient appears to be frightened by the hallucinations. The patient’s daughter states for the last six months the patient has had difficulty swallowing and a reduced appetite.  

• Which form of dementia is the patient most likely experiencing? 
• What would the MRI of the patient most likely show? 
• What clinical signs of dementia is the patient exhibiting? 

Management 

Currently there is not a cure for Lewy body dementia, only supportive treatment. The management of this disease involves a multifaceted approach, including therapies, pharmacological treatments, and family support. 

Therapies 

Specific therapies can help with symptom management and help improve the individual’s quality of life. Occupational therapy can help improve a patient’s ability to complete activities of daily living. Speech therapy can help with swallowing coordination and improve the clarity and volume of speech [5]. Physical therapy can aid patients with problems with movement [5]. Mental health counseling can help individuals and their families with managing behaviors and their emotions [5]. 

Medications 

Pharmacotherapy can help with supportive treatment but can also worsen symptoms if certain medications are taken. Below are some examples of medications that are used by patients with Lewy body dementia. 

• Cholinesterase Inhibitors are used to help cholinergic activity to improve cognitive function [6].  

• Rivastigmine was one of the first of these drugs to be tested [6]. Patients were noted to have improved on their cognitive exams [6]. It is also shown to reduce hallucinations and lessen anxiety [6]. This class of drugs has been said to improve the quality of life for some patients [4].   

• Donepezil and Galantamine are also used to reduce dementia symptoms of hallucinations [6]. These drugs were initially targeted for patients with Alzheimer dementia, however, they are effective for individuals with Lewy body dementia as well [3]. A study was done stating even if there is not a sign of cognitive improvement, this should not be the criteria to stop the medication as this medication has been proven to protect the individual from further impairment of cognition [4]. 

• Atypical Antipsychotics are prescribed to patients that are not seeing a reduction of symptoms while on cholinesterase inhibitors [3]. These types of drugs are seen as controversial due to the many adverse effects that have been seen in patients [4]. Drugs such as haloperidol and olanzapine should be avoided in patients with Lewy body dementia as they can cause neuroleptic malignant syndrome (a life-threatening condition) [5]. Quetiapine, clozapine, pimavanserin, and aripiprazole are atypical antipsychotic drugs that can be used to improve agitation and help prevent cognitive fluctuations [5]. 

• Carbidopa-Levodopa can be used in patients to manage problems with movement [3]. This medication can cause side effects and can result in hallucinations, delusions, and increase confusion [3]. Providers should begin with low doses of this medication [3]. 

• Clonazepam is a benzodiazepine that can lessen the REM sleep behavior disorder that patients with dementia with Lewy bodies can experience [5]. Between 33-65% of patients with REM sleep behavior disorder can experience an injury while sleeping [5]. This medication has been proven to decrease injuries that occur during sleep [5]. Clonazepam can adversely affect individuals with gait disorders or sleep apnea [5]. 

• Melatonin is a hormone that can be used for patients that are affected by REM sleep behavior disorder (5). Studies have shown that the use of melatonin lessened the frequency and the severity of symptoms associated with REM sleep behavior disorder [5]. Melatonin can have side effects such as headaches in the morning, sleepiness during the day, and hallucinations [5]. 

• Memantine is used to treat dementia symptoms [5]. This medication is an NMDA receptor antagonist that stops effects of glutamate in the brain [5]. Memantine has been shown to improve symptoms of patients early in the disease [5]. 

Nursing Care 

As mentioned before, there is not a cure for Lewy body dementia. Caring for patients with Lewy body dementia includes supportive treatment. Nurses can play a significant role in caring for these patients and providing the family with support. Home health nurses can help with frequent assessment of the patient and their environment [3]. Environmental changes may be needed to protect the patient from falls and other accidents. Home health nurses can assess the type of assistance the patient would benefit from.  

Nurses can aid the family by providing education to assist in how to care for the patient. Family members and caregivers must be aware of the changes in behavior, fluctuations in cognition, and hallucinations that the individual might experience [3]. Nurses must also provide education to the caregiver of the patient on the side effects of certain medications, as they can affect an individual with this disease [7]. 

 ​

Family Support 

Lewy body dementia is growing in recognition; however, many people might not be aware of this condition and the disease process. Family members need support from health care professionals to better care for their loved ones. Support can come in the form of education and preparing the family for the symptoms the individual may experience. The cognitive function of patients with this disease can be very limited [3]. Family members must be educated on monitoring the individual closely to promote safety [3]. These individuals are at a high risk for falling and developing aspiration pneumonia (due to swallowing difficulties) [3]. Family members should be educated in preparing for an emergency.  

Individuals with Lewy body dementia may need care and the family needs to know how to inform health care providers of their specific needs. It is important to educate family members that their roles in their past relationship with the patient will likely change due to the disease process. To prevent caregiver burnout, family members must be aware of their limitations and know when they need help [7]. Modifying the patient’s home may be needed for patient safety [3]. Each patient may have specific needs and family members should know what modifications may be necessary [3].  

Prognosis 

The prognosis of Lewy body dementia can be viewed as poor. As mentioned briefly earlier in this course, this disease is progressive and after diagnosis, the life expectancy is five to eight years [3]. The range of expectancy has also been attributed to delay in diagnosis, which can further delay supportive treatment to improve quality of life for the individual [3]. Patients can die from complications from the disease. Complications can include cardiac complications, falls, adverse effects from medications, pneumonia, and suicide [3].  

Compared to Alzheimer’s dementia, the risk of hospitalization or death due to respiratory infections is higher in patients with Lewy body dementia [8]. The median age at death is said to be similar between patients with Alzheimer’s dementia and Lewy body dementia [8]. The life expectancy from diagnosis to death is shorter in patients with Lewy body dementia [8]. The patient’s environment has been shown to play a role in the increased risk of mortality [8]. Patients in nursing homes have been shown to have a higher risk of mortality [8]. Caregivers can decrease the risk of complications by educating themselves on this disease and keeping their loved ones safe. 

Resources for Family Support  

Lewy body dementia is a diagnosis that can affect all aspects of an individual’s life and their family members lives. As nurses we must provide support for family members so they can better care for their loved ones and improve their quality of life. As recognition of this condition grows, family support resources are increasing. The Lewy Body Dementia Association is a nonprofit organization that raises awareness and provides support for families with individuals that suffer from Lewy body dementia [10]. Support groups can be found on their website to help families across the country in their local area [10].  

The Lewy Body Dementia Association was started by caregivers of individuals with this condition. They also focus on education and research into the disease. This association is a resource for family members [10]. 

Another resource for family members is The Lewy Body Dementia Resource Center. This is a nonprofit charitable organization that gives assistance and support to those who care for someone with Lewy body dementia [9]. This organization was founded by caregivers of individuals with Lewy body dementia. They have a support phone line that is available seven days a week to answer questions [9]. They also promote research and early diagnosis of this disease [9]. 

Research Programs 

Lewy body dementia is the second most common form of dementia in the United States [4]. This illness is thought to be underdiagnosed and commonly mistaken for other neurological disorders [3]. Research on Lewy body dementia can decrease the time it takes to diagnose a patient, and can help with management of the condition.  

The National Institute of Neurological Disorders and Stroke provides support for a variety of research endeavors for Lewy body dementia [11]. In 2021 The National Institute of Health spent $93 million dollars on Lewy Body dementia research [11]. One program is the Biomarkers for Lew body dementias program. This program aims to increase clinical data collection from patients with this condition, find biomarkers to expand further research, and allow access to the science community to help with further studies [11]. Another program is the Parkinson’s Disease Biomarkers Program. This program’s purpose is to collectively research with healthcare professionals, patients and family members, and technology professionals to increase biomarker research [11]. 

Biomarker research has been increasing in Lewy body dementia. A biomarker is a feature that can specifically indicate a certain disease [12]. For quite some time there were not any identified biomarkers for Lewy body dementia. There are certain biomarkers that aid in distinguishing Alzheimer’s disease from Lewy Body dementia [13]. These biomarkers can be assessed through imaging or in cerebral spinal fluid [13]. Currently these biomarkers are only helpful if another disease is doubtful [13].  

New biomarkers are needed to separate Alzheimer’s dementia from Lewy Body dementia and other neurological disorders [13]. Biomarkers that can help with early diagnosis would be beneficial for early treatment [13]. 

Conclusion  

Lewy Body dementia affects 1.4 million Americans [2]. The disease is underdiagnosed and often diagnosed incorrectly. Incorrect diagnoses can lead to worsening of symptoms and the administration of drugs that can lead to adverse effects.  

Educating healthcare providers and the community about Lewy body dementia can improve quality of life for individuals with the disease. As nurses, we must be informed about this disease to better educate our patients and their caregivers, and to know how to advocate for our patients.  

Understanding Lupus Nephritis

Introduction   

A lupus diagnosis and the complications that arise can be devastating for patients. Nurses are often looked to for support and answers, so it is important to educate ourselves on these serious conditions. Lupus nephritis (LN) is considered one of the most severe organ manifestations of the autoimmune disease systemic lupus erythematosus (SLE). Essential knowledge on lupus nephritis includes the defining features, epidemiology, pathophysiology of normal kidney function and lupus nephritis, clinical presentation, and treatments.

Lupus Nephritis 

Lupus nephritis (LN) is an organ manifestation of the autoimmune disease systemic lupus erythematosus (SLE). The cause of lupus erythematosus is not known. Researchers suggest a genetic predisposition, but a genetic link has not been identified (2). This is a difficult reality, as patients and healthcare providers usually hope for a why. We will discuss the definition, prevalence, pathophysiology, manifestations, clinical diagnosis guidelines, and treatment regimens for LN.  

Definition 

Lupus nephritis (LN) is considered a condition and a manifestation. LN is one of the most severe organ manifestations of the autoimmune disease systemic lupus erythematosus (SLE). LN is a form of glomerulonephritis, which is inflammation of the glomeruli (the tiny filters within the kidneys). This inflammation causes significant imbalances within the body due to impaired kidney function.

Overview of Systemic Lupus Erythematosus (SLE) 

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by a loss of immune tolerance of endogenous nuclear material, which leads to systemic autoimmunity that may cause damage to various tissues and organs (1). Essentially, the damage to DNA structures causes the body’s immune system to be incidentally programmed to attack its own tissue. There are two types of lupus: systemic lupus erythematosus and “discoid” lupus erythematosus. SLE is systemic, meaning it can affect almost any organ system or tissue and presents in different manifestations impacting the skin, joints, kidneys, and brain (2). “Discoid” lupus erythematosus only affects the skin tissue. Our focus will be on systemic lupus erythematosus (SLE) as we gain a deeper understanding of lupus nephritis.  

The causes of SLE are unknown but many attribute it to genetic, environmental, and hormonal factors. SLE is hard to diagnose because the symptoms are often mistaken for those of other conditions. There is no cure for SLE, but symptoms can be managed. SLE presentation and prognosis are highly variable, with symptoms ranging from minimal to life-threatening. Patients with lupus may experience periods of exacerbation of symptoms, sometimes called 'flares', as well as periods of remission. SLE is associated with substantial morbidity and mortality, particularly caused by renal and cardiovascular disease and infections. LN is considered one of the most severe manifestations of SLE.  

SLE can be compared to a guard dog intended to protect your home. The guard dog (immune system) protects you from unwanted intruders (infection), but also bites friends, family, and the mailman (your own organ tissue)!

Epidemiology and Statistical Evidence of Lupus Nephritis 

Systemic lupus erythematosus has an estimated prevalence of about 10–150 per 100,000 persons (2). However, a large number of people could be undiagnosed due to being asymptomatic or the symptoms mistaken for other diseases. An average of 40% of SLE patients develop lupus nephritis (LN). Those diagnosed with SLE at a younger age are at a higher risk of developing LN and other complications (1). 

SLE in general is more prevalent in women, especially women of reproductive age, than in men; the ratio is 9:1 (1). Therefore, 90% of SLE cases are women. However, men who have been diagnosed with SLE more commonly develop LN than women with SLE. Numerous studies have also found that the prevalence of LN in patients with SLE is higher in African American, Hispanic, and Asian populations (1). The impact of SLE disproportionately affects children and adults living in poorer geographic areas (8).  

Within 10 years of the initial SLE diagnosis, 5–20% of patients with LN develop end-stage kidney disease and the multiple comorbidities associated with immunosuppressive treatment (1). Mortality in LN is quite variable ranging in between 15% and 25% (6). It is important to remember that the treatments are also very risky because it is difficult to balance the risks and benefits of suppressing the immune system. LN is a topic of significant research, so nurses can have a meaningful impact in raising awareness and encouraging hope for more advanced treatment development.

Normal Kidney Function 

The kidneys have several life-sustaining functions. The kidney serves to maintain fluid and chemical homeostasis and to contribute to hemodynamic stability (3). The renal tubules of the kidneys have unique and vital roles. Daily urine output is about 1–2 L, and over 98% of the glomerular filtrate is reabsorbed by the renal tubules (3).  

There is a delicate balance and interdependency between the kidneys and other organs. For example, the kidneys produce hormones that help regulate blood pressure and control calcium metabolism, the kidneys also release a hormone that stimulates red blood cell production. A simple and fun mnemonic formula to help you remember the vital functions: A WET BED. 

A WET BED: Functions of the Kidneys 

A - controlling ACID-base balance 

W - controlling WATER balance 

E - maintaining ELECTROLYTE balance 

T - removing TOXINS and waste products from the body 

B - controlling BLOOD PRESSURE 

E - producing the hormone ERYTHROPOIETIN 

D - activating vitamin D 

Controlling acid-base balance 

• Our bodies always have a state of delicate equilibrium among the acids and bases, which has a parameter known as pH.  

• The kidneys excrete or retain acids and bases when there is an excess or lack of them.  

• The normal pH of the blood is 7.35 to 7.45. 

Controlling water balance 

The kidneys regulate the volume of urine produced and adapt to one’s hydration level to maintain water balance.  

Maintaining electrolyte balance 

The kidneys filter specific electrolytes from the blood, return them back into circulation, and excrete excess electrolytes into the urine. Kidneys maintain electrolyte balances like sodium and phosphate. 

Removing toxins and waste products from the body 

The kidneys remove water-soluble waste products and toxins and excrete them in urine.  

Controlling blood pressure 

The kidneys produce an enzyme called renin, which converts the angiotensinogen produced in the liver into angiotensin I, that is later converted in the lungs into angiotensin II. Angiotensin II constricts the blood vessels and increases blood pressure. Another way the kidneys help reduce elevated blood pressure is they produce more urine to reduce the volume of liquid circulating in the body to compensate. 

Producing the hormone erythropoietin 

The kidneys produce a hormone called erythropoietin, which aids in the creation of more red blood cells (erythrocytes), which are vital for the transport of oxygen throughout all the tissues and organs. 

Activating vitamin D 

The kidneys transform calcifediol into calcitriol, the active form of vitamin D.

Anatomy and Physiology of the Kidneys 

It is important to review the anatomy and physiology of the kidneys. The urinary system as a whole is composed of two kidneys, a pair of ureters, a bladder, and a urethra. The kidneys are located at the back of the abdominal wall and at the beginning of the urinary system. The size of each kidney is dependent on age, sex, and height, but the average length is approximately 10–12 cm, and the right kidney may be slightly smaller than the left kidney (3). The kidneys are made up of nephrons, which are microscopic structures composed of a renal corpuscle and a renal tubule.  

The average human kidney is composed of approximately one million individual functioning nephrons, each containing a single glomerulus or filtering unit (3). The function of filtration is accomplished by three major components of nephron activity: (1) glomerular filtration, (2) tubular reabsorption, and (3) tubular secretion. These components respond to factors including renal blood flow, neuroendocrine effects, and the fluid and nutrient supply to the body. 

Vascular Structure of the Kidneys

The kidneys are perfused with 1.2 liters of blood per minute, which represents about 25% of the cardiac output (3). From the abdominal aorta, the main renal artery carries blood into the kidney and then branches to segmental arteries, then to interlobar arteries, then branches to arcuate arteries, followed by branching to interlobular arteries, and finally onto afferent arterioles (3). Vascular resistance in the kidney is low when compared to other vascular beds within the body.

Figure 2. Vascular Structure of the Kidneys (3)

Pathophysiology of Lupus Nephritis 

Have you ever played dominos? If aligned properly, the domino effect will rapidly cause a consecutive reaction. The immune response can be compared to this domino effect. One cellular action will cause the response and activation of many other cells. A perceived foreign body activates certain immune responses. In most cases, this maintains life. In some cases, it is harmful to vital tissue.  

An autoimmune response to the renal system involves the T- and B-cell interactions stimulating interstitial plasma cell generation in the kidney; interstitial tissue leads to restricted autoantibody-producing plasma cells (6). This cascade of inflammatory response is facilitated by the production of interferon-α (IFN-α), which augments autoreactive B-cell activation and its reciprocal interaction in T-cell activation. This prolonged local injury and inflammation attracts neutrophils that try to help alleviate this inflammation, but the sustained local injury leads to neutrophil apoptosis (cell death), which further causes local injury. This injury further augments the inflammatory response by enhancing the intrarenal autoimmunity and inflammation, leading to kidney tissue injury (6). 

Lupus nephritis is considered a type-3 hypersensitivity reaction. A hypersensitivity reaction is an inappropriate or overreactive immune response to an antigen. Symptoms typically appear when an individual has had a previous exposure to the antigen. Hypersensitivity reactions can be classified into four types (9). 

• Type I - IgE mediated immediate reaction 

• Type II - Antibody-mediated cytotoxic reaction (IgG or IgM antibodies) 

• Type III - Immune complex-mediated reaction 

• Type IV - Cell-mediated, delayed hypersensitivity reaction 

In type III hypersensitivity reactions, antigen-antibody aggregates called "immune complexes” are formed. When someone has lupus, a number of DNA are damaged and have cell death, which exposes parts of the nucleus in the cell, and parts of the nucleus are recognized by the immune system as “nuclear antigens.” Remember, the immune system attacks antigens. The antigen-antibody complexes are transported by the blood and are deposited in various tissues, such as the kidneys.  

When the complexes are deposited, it initiates the recruitment of inflammatory cells (monocytes and neutrophils) that release lysosomal enzymes and free radicals at the site of immune complexes, causing damage to that tissue (9). Examples of tissues that it may deposit in include skin, joints, blood vessels, or glomeruli. In the case of LN, the site of damage is the glomeruli of the kidneys, and it can have a disastrous impact.

Clinical Presentation 

The clinical manifestations of LN can be unpredictable and very different among patients. Patients may present with no symptoms at all, while other patients may have significant proteinuria progressing to acute renal failure. Understanding the disease and its progress is vital for nurses to provide optimal care and education to the patient. Remember, these patients may have signs and symptoms from their lupus already, so isolating renal impairment is essential. 

Signs and Symptoms 

Signs and symptoms of systemic lupus erythematosus depend on the body systems that are affected by the disease. Systemic symptoms include fatigue, malaise, weight loss, anorexia, and fever. The patient may report musculoskeletal symptoms, including joint and muscle pain, joint swelling and tenderness, hand deformities, and skin lesions such as the characteristic “butterfly rash” or maculopapular rash (small, colored area with raised red pimples). Other symptoms stem from the central nervous system (visual problems, memory loss, mild confusion, headache, depression).  

It is important for the nurse to establish a history of symptoms related to the hematological system (venous or arterial clotting, bleeding tendencies), cardiopulmonary system (chest pain, shortness of breath, lung congestion), or gastrointestinal system (vomiting, difficulty swallowing, diarrhea, and bloody stools). To differential LN, it is important to focus on specific function impairment and manifestations arising from the kidneys (1).  

Nephritic symptoms related to hypertension and poor kidney function: 

• Peripheral edema 

• Headache and dizziness 

• Nausea and vomiting 

Nephrotic symptoms related to proteinuria:  

• Peripheral or periorbital edema 

• Coagulopathy 

Patients may report the following: 

• Foamy urine 

• Blood in the urine 

• Dark urine 

• Changes in the frequency of urination 

• Weight gain and swelling, including the legs and hands 

Classifications of Lupus Nephritis 

There are six classifications of lupus nephritis:  

• Class I: Minimal mesangial  
  • Prevalence 10-25% of people with lupus (SLE) 
  • 5% of lupus nephritis cases 
  • Clinical findings: Kidney biopsy shows build-up of antigen-antibody complex deposits; urinalysis is normal 
• Class II: Mesangial proliferative  
  • Prevalence: 20% of lupus nephritis cases 
  • Clinical findings: Mesangial hypercellularity of any degree with mesangial immune deposits 
• Class III: Focal LN 
  • Prevalence: 25% of lupus nephritis cases 
  • Clinical Findings: Active lesions exist in less than half of the glomeruli; hematuria and proteinuria 
• Class IV: Diffuse proliferative  
  • Prevalence: 40% of lupus nephritis cases 
  • Very severe subtype 
  • Clinical findings: More than 50% of the glomeruli are affected with active lesions 
  • Immune complex deposits exist under the endothelial when viewed with an electron microscope 
  • Hematuria and proteinuria 
  • Hypertension, elevated serum creatinine, and raises anti-dsDNA (an antibody tested to diagnose lupus) 
  • Kidney failure is common 
• Class V: Membranous  
  • Prevalence: 10% of lupus nephritis cases 
  • Clinical findings:  
  • Hematuria and proteinuria 
  • Significant systemic edema 
  • The glomerular capillary wall is thicker in segments 
  • High risk for renal vein thromboses, pulmonary embolism, or other thrombotic complications; active lesions are present 
• Class VI: Advanced sclerotic LN 
  • Global sclerosis – typically more than 90% of the glomeruli are damaged and have active lesions 
  • Clinical findings: Progressively worsening kidney function

Diagnosis 

LN is often the presenting manifestation resulting in the diagnosis of SLE (1). SLE is diagnosed clinically and serologically with the presence of certain autoantibodies. Evaluating kidney function in patients diagnosed with SLE is important as timely detection and management of renal impairment has been shown to greatly improve renal outcomes. The clinical presentation and laboratory findings for LN may differ, ranging from normal urinalysis and normal renal function test results to severe proteinuria, nephrotic syndrome, or acute nephritic syndrome, which can result in acute kidney failure (1). Monitoring for the development of lupus nephritis is done by a urinalysis, creatinine, urine albumin-to-creatine ratio, glomerular filtration rate (GFR), and a kidney biopsy.  

Laboratory tests for SLE disease activity include the following: 

• Antibodies to double-stranded DNA (dsDNA) 

• Complement (C3, C4, and CH50) 

• Erythrocyte sedimentation rate (ESR) 

• C-reactive protein (CRP) 

Laboratory tests to evaluate kidney function in SLE patients: 

• Urinalysis  

• Check for protein, red blood cells (RBCs), and cellular casts 

• Serum creatinine assessment 

• Blood urea nitrogen (BUN) testing 

• Spot urine test for creatinine and protein concentration 

• 24-hour urine test for creatinine clearance and protein excretion 

Urinalysis 

A high level of protein or red blood cells in the urine signifies kidney damage. The Systemic Lupus International Collaborating Clinics (SLICC) define renal involvement in lupus as a 24-hour urinary protein excretion of 0.5 g daily or the presence of red blood cell casts in urinary sediment (1). Urinary protein excretion in a 12-hour or 24-hour urine collection provides the best estimate of proteinuria. The most common abnormalities in urinary sediment in patients with LN are leukocyturia, hematuria, and granular casts (1).  

Blood Tests 

Creatinine is a waste product from the normal breakdown of muscles in your body. Kidneys remove creatinine from the blood. An elevated creatinine reveals damage to the kidneys because it is not functioning as it should. Glomerular filtration rate (GFR) also is an important test to determine how well the kidneys are functioning. 

Kidney Biopsy 

The next step in diagnosing LN would be a kidney biopsy. Kidney biopsy is currently the gold standard for confirming a diagnosis of LN and characterizing the LN subtype on the basis of histological patterns (1). A kidney biopsy is usually performed as a percutaneous needle biopsy with minimization of risk factors for bleeding complications. The piece of tissue removed is examined under a microscope by a pathologist. 

A kidney biopsy can (1): 

• Confirm a diagnosis of lupus nephritis 

• Help in determining how far the disease has progressed 

• Guide treatment

Treatment 

Treatment of LN is highly individualized. There is not a specific FDA-approved drug specifically given for the treatment of LN. Treatment cannot be a “one-size fits all” approach, but a plan to target renal impairment and avoid causing further damage. The goal of immunosuppressive therapy is the resolution of inflammatory and immunologic activity. Unfortunately, aggressive treatments can result in additional harm to patients. As the therapy of LN consists of potentially toxic drugs, it may be harmful to begin treatment without a definitive diagnosis (4). 

Treatment of LN usually involves immunosuppressive therapy and glucocorticoids. The goals of LN treatment are to achieve rapid remission of active disease, prevent renal flares, prevent progression of chronic kidney disease (CKD), minimize treatment-associated toxicity, and preserve fertility (1). Immunosuppressive therapy is used to treat active focal (class III) or diffuse (class IV) LN or lupus membranous nephropathy (class V); but not usually used to treat minimal mesangial (class I), mesangial proliferative (class II), or advanced sclerosing (class VI) LN.  

The treatment of focal or diffuse LN has two main components: initial therapy with anti-inflammatory and immunosuppressive agents to slow kidney injury, followed by long-term subsequent immunosuppressive therapy to control the chronic autoimmune processes of SLE and encourage the repair of damaged nephrons (1). 

Treatment Goals 

• Reduce inflammation in the kidneys 
• Decrease immune system activity by blocking immune cells from attacking the kidneys directly and making antibodies that attack the kidneys 
• Treatment of systems (hypertension, fluid retention)  
• Support kidney function 

Medications 

Medications for the treatment of LN include (2): 

• Corticosteroid  
  • Prednisone 
• Immunosuppressant 
  • Cyclophosphamide  
  • Mycophenolate mofetil 
  • Hydroxychloroquine (Quinoline drug used to treat or prevent malaria; used for autoimmune response) 

Blood pressure control: 

• Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) 
• Diuretics 
• Beta blockers 
• Calcium channel blockers 

Treatment Guidelines 

Key points of American College of Rheumatology guidelines for managing lupus nephritis (1): 

1. Patients with clinical evidence of active and previously untreated lupus nephritis should have a kidney biopsy to classify the disease according to the International Society of Nephrology/Renal Pathology Society (ISN/RPS) criteria. 
2. Patients with lupus nephritis should receive background therapy with hydroxychloroquine, unless contraindicated. 
3. Glucocorticoids plus either cyclophosphamide intravenously or mycophenolate mofetil orally should be administered to patients with class III or IV LN.  
4. Patients with class I/II nephritis do not require immunosuppressive therapy. 
5. Angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers should be administered if proteinuria reaches or exceeds 0.5 g/day (1). 
6. Blood pressure should be monitored and maintained at or below 130/80 mm Hg. 
7. Patients with class V lupus nephritis are generally treated with prednisone for one to three months, followed by tapering for one to two years if a response occurs.  

For those who progress to kidney failure, treatment options include dialysis and kidney transplant.

Complications 

Complications of LN can be categorized into comorbidities from the actual condition and treatment-associated adverse outcomes. As mentioned, immunosuppressive therapy and glucocorticoids have harmful risks of their own. Comorbidities can include complications of the renal system and cardiovascular system. Treatment-associated complications can include infections, osteoporosis, cardiovascular disease, and reproductive impairment (1).  

SLE and treatments, including glucocorticoids and calcineurin inhibitors, can cause hypertension, hyperlipidemia, and nephrotic syndrome (1). Many patients with LN have progressive CKD with associated comorbidities, such as anemia, osteoporosis, and other bone and mineral diseases. These factors contribute to vascular risks of progressive CKD and can lead to cardiovascular disease.  

The prevalence of osteopenia and osteoporosis is high in patients with LN taking immunosuppressive therapy. In patients with severe nephrotic syndrome, a loss of plasma proteins, including clotting inhibitors, transferrin, immunoglobulins, and hormone-carrying proteins (such as vitamin D-binding protein), can lead to protein malnutrition, anemia, hormonal and vitamin deficiencies, hyperlipidemia, and increased risk for venous or arterial thrombosis (1). High-dose cyclophosphamide therapy correlates with premature gonadal failure in some cases, which is a complication of male and female reproductive organs (1).  

Immunosuppressive agents increase the risk of infection, which can be further increased by disease activity, leukopenia, and CKD-related factors, such as nephrotic syndrome. Patients receiving immunosuppressive treatment can be at risk for poor outcomes with pneumocystis jirovecii pneumonia, herpes, hepatitis B, tuberculosis, influenza, and pneumococcal infection (1).  

End-stage renal disease (ESRD) is a major complication of LN. Some 5–20% of patients with LN develop ESRD (1). By definition, all patients with LN have chronic kidney disease (CKD), but not all patients with CKD progress to ESRD. Essentially, ESRD occurs when the kidneys are no longer able to function to maintain life and either dialysis or a kidney transplant is needed.

Figure 4. Complications of Lupus Nephritis

Screening and Prevention of Lupus Nephritis 

Screening for LN onset and relapses is important for prompt treatment to improve outcomes. There are many new biomarkers under exploration for predicting and assessing LN (1). Patients with SLE should be screened periodically, even during periods of remission, every six to 12 months, or more frequently when clinically indicated (1). During regular check-ups, screening for LN onset or flares in patients with SLE should include evaluation of volume status, blood pressure measurement, urinalysis, and measurement of serum parameters. Elevation of serum creatinine level, the appearance of dysmorphic erythrocytes, cellular casts and new-onset proteinuria may indicate onset of LN (1). Nurses should encourage patients to regularly attend their appointments.  

Patient Education 

Patient education must be individualized to each unique patient. Lupus or LN may be a new diagnosis, or the patient may have been diagnosed previously. Teaching topics should include education on the disease process, the purpose of treatment regimens, and the importance of compliance.  

Education on medication regimens is essential. Include the purpose, dosage, and possible side effects of all medications. Teach the patient when to seek medical attention. Provide tips such as wearing a medical alert bracelet or lanyard noting the condition and medications so appropriate action can be taken in an emergency. Provide resources on smoking cessation for patients who use tobacco. Teach the female patient the importance of planning pregnancies with medical supervision because pregnancy is likely to cause an exacerbation of the disease and the disease may cause negative pregnancy outcomes.  

Discuss all precipitating factors that need to be minimized or avoided, including fatigue, vaccination, infections, stress, surgery, certain drugs, and exposure to ultraviolet light. Teach the patient to avoid strenuous exercise, but instead set goals of steady pace and balance. Describe pain management strategies and the importance of adequate nutrition. The patients may have concerns about skin care products and cosmetics. Teach the patient that these products should be hypoallergenic and approved by a provider prior to use. Encourage the patient to contact appropriate support groups available in the area. 

Diet 

Education on diet and nutrition for patients with LN can be very helpful in managing this condition. A diet regimen can be challenging because many people with this condition may also experience weight loss or gain, inflammation, osteoporosis, high blood pressure, and atherosclerosis. Recognizing specific nutritional concerns for each condition is important. A registered dietitian would be a meaningful resource for those with LN. 

A kidney-healthy diet consists of low salt, low fat, and low cholesterol, with an emphasis on fruits and vegetables. Eating the right foods can help patients manage kidney impairment, maintain a healthy weight, and lower their blood pressure. Steroid medications can cause significant fluctuation in weight and energy.  

The provider may advise restrictions on dietary protein intake. According to nephrology research, consuming more than 1.5 g of protein per kilogram per day can overwork the kidney filters, causing hyperfiltration (5). Many proteins are composed of amino acids that are converted to acids that are harmful to the kidney in large amounts; a diet high in animal proteins also contains sulfuric and phosphate acids that promote kidney damage (5). Potassium intake is also an important aspect of diet for those with LN. Potassium is secreted by the kidneys and may rise when kidney function declines; abnormal potassium levels can impact muscle function and increase the risk of hypertension, coronary artery disease, or stroke (5). A balanced diet with special considerations is a key teaching factor. It may be helpful to seek out resources from registered dieticians when needed. 

Overview of Teaching Topics 

Topics for education: 

• Disease process 
• Treatment plan 
• Diagnostic studies and lab results 
• Medications 
  • Purpose 
  • Dosage 
  • Side effects 
  • Contraindications 
• Infection control 
• Diet 
• Tobacco cessation resources 
• Reproductive complications 
• Techniques to minimize ultraviolet exposure 

Resources 

The American College of Rheumatology (ACR) and Lupus Foundation of America (LFA) are excellent resources for patient with lupus that provide education and resources to improve overall well-being. The Lupus Foundation of America has a team of physicians, scientists, health educators, and individuals with lupus who work together to create resources, support groups, awareness initiatives, and programs. Patients can go to the “Ask our Health Educator” portal and get answers to questions they may have.

Conclusion 

Nurses need to have a good understanding of lupus nephritis to provide patients with appropriate support and advice about how to maintain wellbeing and lead meaningful active lives. Knowledge on disease pathophysiology, manifestations, treatments, and complications is valuable for this serious condition. Patients often rely on nurses to support and empower them on this pathway.

Alcohol Use Disorder: Long Term Effects and Complications

Introduction

Alcohol use disorder (AUD) is one of the most widespread psychiatric disorders and is estimated to affect approximately 29 million individuals aged 12 and older in the United States (9). According to the 2021 National Survey on Drug Use and Health, 28.6 million adults ages 18 and older have AUD and roughly 900,000 adolescents ages 12 to 17 have AUD (7).

Alcohol is the most prevalent misused substance in America with alcohol-related issues causing more than 85,000 deaths annually in the United States and three million deaths a year globally (9, 12). Globally, about 240 million people are affected by AUD, especially in Europe and America (9).

AUD is linked to motor vehicle accidents, dementia, depression, homicide, and suicide (9). The condition can also lead to social complications, such as legal problems, relationship issues, and economic stressors (due to the cost of alcohol, required medical care, missed time at work, and job loss). Individuals with AUD can end up isolating themselves from the individuals who are trying to help them most, including family members and friends.

Moderate alcohol use for most adults—no more than two drinks a day for men and one for women—is relatively harmless. An alcoholic drink includes 12 fluid ounces of regular beer, 10 fluid ounces of malt liquor, five fluid ounces of wine, or 1.5 fluid ounces of 80-proof distilled spirits (3, 4). Heavy alcohol drinking is defined as having four or more drinks per day or eight or more drinks per week for women and five or more drinks per day or 15 or more drinks per week for men (4).

Small amounts of alcohol, in particular red wine, can have beneficial cardiovascular effects, but heavy drinking can lead to serious health issues, such as cancer, cardiovascular disease, liver disease, osteoporosis, and infections (3, 4). Men are more likely than women to develop AUD, but women’s health suffers more than men’s, even at lower levels of consumption (3). Individuals with lower levels of education and of lower income experience AUD more than their counterparts (9).

Drinking can become problematic for those people who have psychological traits of impulsiveness, low self-esteem, and the constant need for attention and approval. Individuals who lack personal insight about drinking can develop AUD. For example, those who use alcohol to emotionally self-medicate (i.e., unwind from a stressful day) can develop alcohol-related issues (3).

Unfortunately, many individuals with AUD deny having a problem with alcohol and therefore do not seek treatment until faced with medical issues or legal complications. Regardless of how severe a patient’s drinking problem may seem, evidence-based treatment that includes medications, behavioral therapies, and support groups can help individuals achieve and maintain recovery.

Pathophysiology

Alcohol ethanol or ethyl alcohol is a chemical substance found in alcoholic beverages, such as beer, hard cider, malt liquor, wines, and distilled spirits (liquor). Alcohol is the byproduct of yeast fermentation of sugars and starches. Alcohol is also found in some medicines, mouthwashes, and household products, including vanilla extract and other flavorings (4).

Alcohol use disorder is defined by the National Institute on Alcohol Abuse and Alcoholism as a medical condition characterized by an impaired ability to stop or control alcohol use despite adverse social, occupational, or health consequences (7). The term alcohol use disorder includes the terms alcohol abuse, alcohol dependence, alcohol addiction, and alcoholism. The condition affects brain function and is classified as mild, moderate, or severe (7).

Several evidence-based theories explain the development of AUD in individuals. These theories are (9):

• Positive-effect regulation: This occurs when people consume alcohol to seek positive rewards like pleasure or euphoria. Alcohol may be consumed to enhance social experiences and positive emotions.
• Negative-effect regulation: Individuals may drink alcohol in response to negative or distressing situations as a means to self-medicate and alleviate feelings of anxiety, depression, or low self-worth.
• Pharmacological vulnerability: This theory explains the differences in how individuals respond to the acute and chronic effects of alcohol. Some individuals are more prone to the rewarding effects of alcohol, or they have a reduced ability to metabolize alcohol, thus increasing their chances of developing AUD.
• Deviance proneness: Individuals with a history of deviant behavior or impaired socialization during childhood are more prone to AUD because these individuals use alcohol to self-medicate to alleviate symptoms of anxiety, depression, or low self-worth.

Cytosolic alcohol dehydrogenase (ADH) is the enzyme that metabolizes alcohol in the liver, and this metabolism process produces acetaldehyde as a byproduct. Acetate is then formed by the metabolism of acetaldehyde by the enzyme aldehyde dehydrogenase (ALDH).

Acetate then enters the body’s various metabolic pathways. Additionally, ADH is present in the gastrointestinal tract as well as the liver, which leads to the initial metabolism of alcohol during its ingestion. This is referred to as first-pass metabolism. The enzyme CYP2E1 of the cytochrome P450 system is upregulated in chronic alcohol users, which leads to an increased rate of alcohol metabolism (9).

Several factors affect the metabolism of alcohol (9):

• Women have a higher initial blood alcohol concentration following consumption because they have a slower first-pass metabolism due to lower levels of ADH; however, women eliminate alcohol consumption faster than males.
• Alcohol elimination declines with age, which is why older adults may experience a lower tolerance to alcohol than when younger, or why they may experience more severe hangover symptoms.
• In pregnancy, the fetal liver has an incomplete expression of enzymes CYP2E1 and ADH, leading to slower alcohol metabolism. This means that the fetus is exposed to the mother’s consumption of alcohol for a prolonged period, increasing the risk of fetal alcohol spectrum disorders.
• Native Americans have been found to metabolize alcohol faster due to the expression of beta-3 Class 1 ADH isoforms than individuals who express only the beta-1 Class 1 ADH isoform.
• When an individual fasts, alcohol metabolism is slowed due to decreased levels of ADH during a fasting state. Alternatively, food intake increases blood flow to the liver and allows fructose and other sugars to speed the metabolism of alcohol.
• The highest rates of alcohol elimination occur in the late evening versus during the daytime hours.
• Medications that have ADH inhibition or H2 receptor-blocking properties decrease the rate of alcohol elimination. This reduces first-pass metabolism in the stomach and increases blood alcohol levels.
• Heavy drinking increases the expression of the CYP2E1 enzyme, which increases alcohol elimination; however, this is eventually slowed in individuals with advanced liver disease.

Alcohol use can permeate every organ and tissue in the body, resulting in systemic dysfunction. The Complications and Long-Term Effects section explores how alcohol use impacts the body.

Risk Factors

Several factors are believed to contribute to the development of alcohol use disorder, including the home environment, peer interactions, genetic disposition, cognitive functioning, and other mental health disorders, such as schizophrenia, depression, and personality disorders (9).

Risk factors for AUD include (3, 7, 9):

• Genetics and family history. Hereditary factors can influence AUD by as much as 60%. Parents’ drinking habits are directly correlated to the child’s development of AUD. Certain genes have been found to increase an individual’s susceptibility to AUD, including:
• GABRG2 and GABRA2, COMT Val 158Met, DRD2 Taq1A, and KIAA0040.
• Drinking at an early age. Those individuals, especially females, who begin consuming alcohol before age 15 are three times more likely to have AUD. Research indicates that younger people who wait to start consuming alcohol until age 21 are less likely to have AUD.
• Mental health disorders. Psychiatric conditions, such as depression, post-traumatic stress disorder (PTSD), and attention deficit hyperactivity disorder (ADHD) are linked to an increased risk of AUD. Childhood trauma is also strongly correlated with AUD. The presence of both AUDs and psychiatric disorders leads to a worsened prognosis for both disorders.
• Social issues. Poverty and lack of education are significant risk factors for AUD.

Additionally, the risk for developing AUD can depend on how much, how often, and how quickly the individual consumes alcohol. Binge drinking and heavy drinking over time can lead to AUD (7).

Signs and Symptoms

Nurses need to perform a thorough assessment of those individuals suspected of having AUD. The Cut Down, Annoyed, Guilty, and Eye-opener (CAGE) questionnaire is the widely accepted gold-standard assessment tool and is comprised of these questions (2):

1. Have you ever felt that you need to cut down on your drinking?

2. Have people annoyed you by criticizing your drinking?

3. Have you ever felt bad or guilty about your drinking?

4. Have you ever had a drink first thing in the morning to steady your nerves or to get rid of a hangover (eye-opener)?

The scoring for the CAGE includes 0 for “no” answers and 1 for “yes” answers with a total score of two or greater being clinically significant for AUD. However, healthcare providers are encouraged to regard a total score of one or greater as the potential for substance abuse disorder that requires further patient exploration (2).

The Alcohol Use Disorders Identification Test (AUDIT) is a 10-item screening tool created by the World Health Organization (WHO) to assess alcohol-related conditions. There is a patient test that individuals may administer to themselves, and a test designed for healthcare providers to administer to patients. Both tests ask the same questions and use a similar scoring method. The provided answers are 0 for “never”, 1 for “monthly or less”, 2 for “2-4 times a month”, 3 for “2-3 times a week”, and 4 for “4 or more times a week”. A score of 8 or more indicates harmful alcohol use (8, 12).

The AUDIT questions are (8, 12):

1. How often do you have a drink containing alcohol?
2. How many drinks containing alcohol do you have on a typical day when you are drinking? (The answer options for this question are 0 for “1 or 2”, 1 for “3 or 4”, 2 for “5 or 6”, 3 for “7 to 9”, and 4 for “10 or more”.)
3. How often do you have six or more drinks on one occasion?
4. How often during the last year have you found that you were not able to stop drinking once you had started?
5. How often during the last year have you failed to do what was normally expected to you because of drinking?
6. How often during the last year have you needed a first drink in the morning to get yourself going after a heavy drinking session?
7. How often during the last year have you had a feeling of guilt or remorse after drinking?
8. How often during the last year have you been unable to remember what happened the night before because of your drinking?
9. Have you or someone else been injured because of your drinking? (The answer options for this question are “no”, “yes, but not in the last year”, and “yes, during the last year”.)
10. Has a relative, friend, doctor, or other healthcare worker been concerned about your drinking or suggested that you cut down? (The answer options for this question are “no”, “yes, but not in the last year”, and “yes, during the last year”.)

Nurses and other healthcare professionals can ask patients the additional questions below about their alcohol use to determine the risk and presence of AUD.

In the past year, have you (7):

• Ended up drinking more or longer than you intended?
• Tried to cut back on drinking, but have been unable to do so?
• Experienced symptoms of illness (hangover) related to your drinking?
• Craved a drink so much that it distracted you from your current activity?
• Found that your drinking has interfered with maintaining your responsibilities and obligations regarding home, family, work, or education?
• Continued to drink despite knowing that it caused problems with family and friends?
• Foregone pleasurable activities (hobbies, etc.) that you enjoy to drink?
• Increased your risk for injury (driving, swimming, using machinery, walking in a dangerous area, engaging in unsafe sexual behavior) due to drinking?
• Continued to drink despite the social, health, or economic problems it causes?
• Experienced feelings of anxiety, depression, or memory blackout due to your drinking?
• Needed to drink more alcohol than in the past to get the same effects?
• Experienced alcohol withdrawal symptoms, such as tremors, restlessness, irritability, nausea and vomiting, sweating, malaise, racing heartbeat, hallucinations, or seizures?

The patient’s positive response to two to three of these criteria indicates mild symptoms, four to five indicates moderate symptoms, and six or more indicates severe symptoms (7).

Patients with AUD often report frequent falls, blackout spells, motor instability and tremors, visual disturbances, hangover symptoms (headache, nausea and vomiting, dry mouth, photophobia), hypertension, heart palpitations, seizures, confusion, mood swings, and sleep disturbances. Social symptoms include school or job instability or loss, relationship separation or divorce, estrangement from family and friends, and homelessness (9). Nurses should also assess patients suspected of AUD for post-traumatic stress disorder, bipolar disorder, panic disorder, anxiety disorder, dysthymic disorder, major depressive disorder, and insomnia (9).

During the assessment of a patient with AUD, nurses may note ataxia, fine motor skill disturbances, mental status changes, mood changes, slurred speech, tachycardia, hypotension, nystagmus, asterixis, ruddy palms, jaundiced coloring, and ascites. Signs of liver disease include hepatomegaly, splenomegaly, cirrhosis, spider angiomata, and liver atrophy (9).

Prevention

The stage in life when a person is exposed to alcohol is an important predictor for alcohol misuse. Adolescence is a time when many people begin experimenting with drinking, and research indicates that drinking before the brain is fully formed (age 26) can negatively impact brain development and compromise cognitive function. The main goal of preventing AUD is to impede, or at least delay, the onset of drinking in the youth population (6).

Adolescents and young adults seek independence and favor transitioning to adult roles. Most of this population drives automobiles and spends more time with friends than family members, thus making them easily influenced by their peer group. This also means that this population is at high risk for alcohol-related injuries, with 5,000 18- to 24-year-olds dying each year due to alcohol-related incidents (6). This group engages in binge drinking, which can lead to blackouts, alcohol poisoning, sexual assault, sexually transmitted infections, and poor academic performance.

Other factors that influence drinking behaviors that should be considered in prevention interventions are genetics, health status, cultural background, educational background, socioeconomic status, community attitudes toward alcohol use, and exposure to social media. Preventative measures should also be geared toward pregnant women and older adults since these populations have special considerations, such as the risk for fetal alcohol spectrum disorders in pregnant women and the inability to effectively metabolize alcohol in older adults that can lead to injuries (6).

Regular screenings for alcohol misuse are a key prevention strategy, and research shows that most patients do not object to being screened for alcohol use and thus are open to receiving advice about alcohol use (6). Evidence also shows that alcohol-related incidents can be prevented by both individual and environmental interventions. For example, college students who are taught to monitor their drinking and how to effectively refuse alcohol when offered can prevent AUD. College communities that restrict happy hours, enforce the minimum drinking age, and prevent alcohol price promotions can decrease the risk of AUD (6).

Diagnostics and Treatment

The preliminary source used to diagnose alcohol use disorder is the Diagnostic and Statistical Manual of Mental Disorders (DSM).

According to the DSM, the criteria for alcohol use disorder include (11):

A maladaptive pattern of substance use leading to clinically significant impairment or distress, as manifested by two or more of the following, occurring at any time in the same 12-month period:

• Alcohol is often taken in larger amounts or over a longer period than was intended.
• There is a persistent desire or unsuccessful efforts to cut down or control alcohol use.
• A great deal of time is spent in activities necessary to obtain alcohol, use alcohol, or recover from its effects.
• Craving, or a strong desire or urge to use alcohol.
• Recurrent alcohol use failing to fulfill major role obligations at work, school, or home.
• Continued alcohol use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of alcohol.
• Important social, occupational, or recreational activities are given up or reduced because of alcohol use.
• Recurrent alcohol use in situations in which it is physically hazardous.
• Alcohol use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by alcohol.
• Tolerance, as defined by either of the following:
  • A need for markedly increased amounts of alcohol to achieve intoxication or desired effect.
  • A markedly diminished effect with continued use of the same amount of alcohol.
• Withdrawal, as manifested by either of the following:
  • The characteristic withdrawal syndrome of alcohol
  • Alcohol (or a closely related substance, such as a benzodiazepine) is taken to relieve or avoid withdrawal symptoms.

Laboratory testing in patients with AUD can indicate blood disorders; vitamin, mineral, and electrolyte imbalances; cancers; cardiovascular disease; liver disease; and pancreatitis. Alcohol-related organ damage can be determined by biomarkers, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transpeptidase (GGT), phosphatidylethanol (PEth), fatty acid ethyl ester (FAEE), total serum sialic acid (TSA), mean corpuscular volume (MCV), cholesteryl ester transfer protein (CETP), carbohydrate-deficient transferrin (CDT), N-Acetyl-β-Hexosaminidase (Beta-Hex), macrophage migration inhibitory factor (MIF), and D-dopachrome tautomerase (DDT). Biomarkers like alcohol and ethyl glucuronide levels can determine recent alcohol consumption. CDT and PEth levels can help monitor abstinence (1, 9).

Treatment approaches for AUD involve pharmacological and nonpharmacological interventions.

The Federal Drug Administration (FDA) has approved three pharmacological treatments for AUD (9, 10):

• Naltrexone (Vivitrol) is a mu-opioid antagonist that blocks the effects of opioids and is widely used in treating addiction to narcotics. In alcoholism, the medication blocks the effects of naturally occurring opioids, such as endorphins. Therefore, the drinker does not experience any psychological benefits or “high” from the alcohol. Naltrexone also reduces the craving for alcohol leading to improved abstention rates, reduced number of drinking days, and reduced risk of relapse. The potential side effects—nausea, headaches, and fatigue—also work as an alcohol deterrent.
• Acamprosate is a glutamate agonist that promotes a balance of inhibitory and excitatory neurotransmitters in the brain that are disrupted by alcohol abuse. The discontinued brand name is Campral, but the generic equivalent is still available. The medication can cause weight gain and severe depression.
• Disulfiram (Antabuse) is an alcohol antagonist drug that inhibits ALDH, resulting in the accumulation of acetaldehyde in the body. The purpose of disulfiram is to promote fear in the drinker because drinking alcohol in conjunction with taking the medication can result in serious adverse reactions, including flushing, headache, dyspnea, diaphoresis, dizziness, shock, and even death.
• Gabapentin (Neurontin) and topiramate (Topamax) are not yet FDA-approved for AUD, but they are currently being used to treat the disease. Gabapentin, an anticonvulsant used to treat neuropathic pain, corrects dysregulation caused by alcohol use and cessation; it also decreases alcohol cravings. Topiramate, also an anticonvulsant, decreases alcohol cravings.

The most effective non-pharmacological approach to AUD is psychological therapy, including (9):

• Motivational interviewing. This technique is most effective in those patients who are ambivalent about changing their behaviors and quitting alcohol. The approach is client-centered and helps patients recognize and address their issues. It helps them become motivated to make long-lasting, healthy changes.
• Motivational enhancement therapy (MET). MET is a manual-based intervention that includes motivational interviewing and focuses on strengthening the motivation of the patient to change their alcohol use behaviors.
• Cognitive behavioral therapy (CBT). CBT helps individuals explore the connections among their thoughts, emotions, and behaviors. This therapy can increase motivation to stop drinking, identify triggers that prompt alcohol use, and teach effective coping mechanisms to deal with alcohol cravings and alcohol-seeking behaviors. In one study, 58% of patients receiving cognitive-behavioral treatment fared better than those who did not receive this therapy (3).

Other programs that support patients with AUD are residential facilities (in-patient rehabilitation), community programs like Alcoholics Anonymous (AA) or other 12-step programs, and faith-based programs that align with the principles of certain religions.

Complications and Long-Term Effects

AUD impacts each body system and can cause complications that have long-term negative effects. For example, alcohol impairs the brain’s ability to regulate balance, memory, speech, and judgment, which can lead to injuries. With long-term, heavy drinking the neurons reduce in size, the brain’s mass shrinks, and the brain’s inner cavity grows larger.

Alcohol interferes with glutamate action, which inhibits the creation of new memories and leads to blackouts. Alcohol also influences the neurotransmitters dopamine and serotonin, which can cause mood dysregulation, impaired concentration, and decreased motivation. Even though alcohol can cause euphoria at first, it is a depressant that can lead to suicidal ideation, behaviors, and death.

Additionally, excessive alcohol consumption can weaken the immune system, which can lead to increased rates of infection, such as pneumonia (4).

Additional complications of AUD by the organ system are (4, 5, 7):

• Cardiac/Circulatory: Cardiomyopathy, arrythmias, stroke, hypertension, ischemic heart disease, heart failure
• Endocrine: Acute and chronic pancreatitis, pancreatic cancer, diabetes
• Gastrointestinal: Esophageal cancer, oral cavity cancer, larynx cancer, pharynx cancer, gut leakiness, gastritis, ulcers, microbial dysbiosis, colorectal cancer, inflammatory bowel disease (IBD)
• Hepatic: Steatosis, steatohepatitis, fibrosis, cirrhosis, alcohol-associated hepatitis, liver cancer
• Immune/Lymphatic: Infections, such as tuberculosis
• Integumentary: Melanoma
• Neurologic: Ischemic stroke, amyotrophic lateral sclerosis (ALS), Alzheimer’s disease, multiple sclerosis (MS)
• Reproductive: Breast cancer, sexually transmitted infections
• Respiratory: Acute respiratory distress syndrome, alcohol-associated lung disease, pneumonia
• Skeletal: Muscle myopathy, muscle wasting, impaired bone fracture repair, reduced bone density (osteopenia, osteoporosis)
• Urinary: Kidney disease, prostate cancer

Alcohol is a toxic substance that contains carcinogens, such as nitrosamines, asbestos fibers, phenols, and hydrocarbons, which are the cause of 3.5% of cancer deaths in the United States (4).

Some cancers associated with alcohol consumption are (4):

• Head and neck cancer. Drinkers are at increased risk for oral cavity, pharynx, and larynx cancers. The risk increases among those individuals who both drink and use tobacco.
• Esophageal cancer. Esophageal squamous cell carcinoma risk is high in moderate to heavy drinkers.
• Liver cancer. The risk for hepatocellular carcinoma and intrahepatic cholangiocarcinoma doubles in individuals who are heavy drinkers.
• Breast cancer. Light drinkers have a slightly increased risk of breast cancer, whereas moderate to heavy drinkers increase their risk substantially. Tobacco use in conjunction with alcohol use increases the risk of breast cancer.

There are multiple ways in which alcohol can increase the risk of cancer, such as (4):

• Metabolism of ethanol to acetaldehyde, which is a toxic carcinogen, acetaldehyde damages DNA and proteins.
• Oxidation can damage DNA, proteins, and lipids.
• Inability to digest and assimilate vital nutrients that can protect against cancers, such as vitamin A, vitamin B complex, vitamin C, vitamin D, vitamin E, and carotenoids.
• Increasing levels of estrogen can lead to breast cancer.

The prognosis for patients with AUD is very challenging with less than 20% to 30% achieving long-term abstinence and with most acquiring serious to permanent health conditions that are irreversible (9).

Patient Education

Nurses play a critical role in educating patients with AUD, and they should do so in a non-judgmental and non-confrontational manner.

Educational topics nurses should address with patients include (9, 10):

• Healthy diet. Most patients with AUD suffer from malnourishment, particularly regarding folate. Foods rich in folate include legumes, eggs, leafy greens, citrus fruits, nuts and seeds, and fortified grains. Patients should be taught the importance of maintaining a healthy diet that is rich in protein, complex carbohydrates, fresh fruits and vegetables, healthy fats, and vitamins and minerals.
• Reducing risky behaviors. Individuals with AUD should be taught that alcohol consumption lowers inhibitions, which can lead to risk-taking behaviors, such as driving, swimming, operating heavy machinery, and engaging in unprotected sexual practices.
• Importance of support groups. Patients with AUD are more likely to make progress and stay motivated if they are supported by family, friends, and community resources like Alcoholics Anonymous (AA). Family members should also be encouraged to attend support groups like Al-Anon.
• Maintaining a temptation-free environment. Patients should be encouraged to remove all alcohol from their homes and offices. When traveling, they can request that hotels remove alcohol from the guest room minibar.
• Importance of maintaining health screenings. AUD can lead to other serious health conditions, such as cardiovascular disease, osteoporosis, and various cancers. Patients should be taught the importance of receiving regular medical check-ups and health screenings to maintain optimal health.

Nurses should also ensure that patients can access educational and support resources in their native language, as well as be provided with information about resources available to low-income individuals, if applicable.

Resources

There are many resources available to assist patients with AUD.

• Alcoholics Anonymous: AA is a global fellowship community that helps individuals resolve their issues with alcohol. https://www.aa.org/
• Al-Anon Family Groups: Like AA, Al-Anon is a fellowship community that helps friends and family members of alcoholics gain the support they need. https://al-anon.org/
• Alateen: Alateen is a component of Al-Anon, a fellowship group for adolescents who have been affected by someone else’s drinking. https://al-anon.org/newcomers/teen-corner-alateen/
• Centers for Disease Control and Prevention: The CDC provides resources, such as publications, online tools, and healthcare information related to individual states. https://www.cdc.gov/alcohol/resource-center/index.html
• FindTreatment.gov: This is a national website for locating treatment facilities for mental and substance use disorders. https://findtreatment.gov/locator
• National Association for Children of Addiction (NACoA): This organization provides programs, such as The Clergy Education and Training Project, Celebrating Families, and Children’s Program Kit to support the children of addicted parents. https://nacoa.org/
• Rethinking Drinking: The National Institute on Alcohol Abuse and Alcoholism (NIAAA) website provides evidence-based information for patients and healthcare providers, as well as listings for treatment centers. https://www.rethinkingdrinking.niaaa.nih.gov/

Case Study 

B.P. is a 32-year-old Caucasian man who presents to the emergency department after a motor vehicle accident during which B.P. lost control of his car and drove it into a roadside ditch. There were no other cars on the road at the time, making the accident a one-person collision. B.P. was brought to the hospital by his girlfriend and presented with superficial lacerations and bruising to his face from deployment of the driver’s side airbag and more serious lacerations to his left forearm that were injured by the breaking glass of the driver’s side window. He states that he thinks he may have hit his head on the automobile’s steering wheel before airbag deployment, but then says, “I’m not completely sure about that little detail.”  

B.P.’s vital signs are blood pressure 158/84 mmHg, pulse 78 beats per minute, respirations 16 breaths per minute, and oxygen saturation 95%. His lung fields are clear to auscultation bilaterally, and his cardiovascular exam reveals a regular rate and rhythm without murmurs. Bowel sounds are confirmed in four quadrants via auscultation. Radial, pedal, and dorsal pedal pulses are normal bilaterally. Pupils are sluggish to react to penlight; the patient’s eyes have a glassy appearance. B.P. is oriented to place, but not day or time.  

He can state his name and birthdate without hesitation, but he pauses before stating his complete address and incorrectly states his zip code. When speaking, B.P.’s words are slurred, but his hearing bilaterally is intact. During the musculoskeletal and neurological assessments, B.P. is unable to follow all the instructions the nurse provides and at one point he whines, “Can we stop now? This is super hard and I’m so sleepy. I need to go to bed now.” The patient’s left forearm is red and edematous with two lacerations that are both roughly 1.5 inches in length.  

There are evident shards of glass present in both lacerations and bleeding has slowed significantly since the patient arrived at the hospital. B.P.’s face has several minor red contusions and a couple of superficial lacerations. The patient denies any reports of pain, headache, nausea, or dizziness, and says that he only feels fatigued. 

B.P.’s health history includes chronic hay fever for which he takes over-the-counter antihistamines. He denies any further health issues. The nurse is unable to obtain a detailed social history or family history due to B.P.’s noncompliance. 

After B.P.’s face and left arm are cleaned, and the left arm sutured and bandaged, he is taken for a chest x-ray, which is normal, and a computerized tomography (CT) scan of the head, which shows no intracranial hemorrhage, mass, or stroke. Blood test results reveal folate deficiency, and ALT, AST, MCV, GGT, and CETP levels consistent with heavy alcohol use. Intravenous folate and normal saline are administered during the next several hours, and the patient is consistently monitored for pain and alcohol withdrawal symptoms. As B.P. becomes sober, the nurse initiates the AUDIT questionnaire; B.P. scores a 32. 

When the nurse explains B.P.’s AUDIT score to him, he states, “Yeah, I’m not surprised. I’ve been drinking since I was 13, and my girlfriend keeps telling me that my drinking is getting worse. I just like to have a few to chill after a hard day at work; my job is super stressful. Maybe she’s right. And after tonight, I should probably look into it. These hospital and car bills aren’t going to be cheap.” 

B.P. is discharged with a referral to a psychiatrist for further AUD evaluation and potential treatment. He is also given a couple of brochures about alcohol abuse and in-patient rehabilitation programs. B.P. is encouraged to follow up with his primary care physician for continued care of his injured arm. 

Conclusion

AUD puts individuals at risk for serious health complications, legal problems, and impaired interpersonal relationships. Many alcoholics do not receive appropriate medical care for AUD due to a lack of screening by healthcare providers. Therefore, nurses must use their assessment skills to evaluate patients for AUD and provide them with proper education about the disease, including its long-term effects and complications.

Healthcare screenings for cardiovascular disease and mental health disorders, as well as referrals to community support programs such as Alcoholics Anonymous, help patients take responsibility for their health and recovery.

SSRI Use in Anxiety Disorders

Introduction   

Selective Serotonin Reuptake Inhibitors (SSRIs) are a medication class typically used to treat depression. SSRIs are considered first-line treatment for depression and other psychological disorders, including (2): 

• Major Depressive Disorder 
• Generalized Anxiety Disorder 
• Bulimia Nervosa 
• Bipolar Depression 
• Obsessive-Compulsive Disorder 
• Panic Disorder 

• Premenstrual Dysphoric Disorder 
• Treatment-Resistant Depression 
• Pot-traumatic Distress Disorder 
• Social Anxiety Disorder 

Additional disorders may be treated off-label, including (2): 

• Binge Eating Disorder 
• Body Dysmorphia Disorder 
• Fibromyalgia 
• Premature Ejaculation 
• Paraphilias 
• Autism 
• Raynaud’s Phenomenon 
• Vasomotor symptoms associated with menopause.  

SRRIs remain relatively safe, tolerable, and efficient in treating patients (2). 

Fluoxetine 

The Fluoxetine drug class includes brand names of Prozac, Rapiflux, Sarafem, and Selfemra 

(11). 

Indications 

Fluoxetine is an FDA-approved medication used to treat major depressive, obsessive-compulsive, binge eating, premenstrual dysphoric, and panic disorders. Fluoxetine is also prescribed for bulimia and bipolar depression.  

Off-label uses include social anxiety disorder, adult post-traumatic stress disorder (PTSD), borderline personality disorder, Raynaud phenomenon, and selective mutism (21). 

Mechanisms of Action and Pharmacokinetics 

Fluoxetine blocks the reuptake of serotonin into the presynaptic serotonin neurons. This is accomplished by blocking the reuptake transporter proteins located in the presynaptic terminal. There have been some indications of mild activity at the 5HT2A and 5HT2C receptors. Conversely, there is minimal activity on noradrenergic reuptake (21). 

Fluoxetine produces an activating effect that takes two to four weeks to see antidepressant effects. Fluoxetine actives norfluoxetine, a metabolite produced when cytochrome p450 enzyme acts on it. This indicates that fluoxetine has a high risk for drug-drug interactions that metabolize at the CYP2D6 isoenzyme (21). 

Fluoxetine has a half-life of two to four days. Fluoxetine’s active metabolite, norfluoxetine, has a longer half-life of seven to nine days (21). 

Contraindications and Precautions 

Fluoxetine is contraindicated in patients with (21): 

• Hypersensitivity to fluoxetine or its components 
• Use of monoamine oxidase inhibitors (MAOIs) to treat psychiatric disorders 
  • Prescribers should discontinue MAOIs for > 2 weeks before initiation of fluoxetine 
• Prescription of: 
  • Linezolid 
  • Pimozide 
  • Thioridazine 
  • Tamoxifen 
• History of seizures 
• Elderly patients 
• Suicidal thoughts or ideation 
  • Especially in pediatric patients or those aged 18 to 24 years old 
    • Monitor closely for the first two months of initiating therapy 
• During pregnancy 
  • Use in early pregnancy increases the risk of septal heart defects 
  • After 20 weeks, it is linked with a possible risk for pulmonary hypertension in newborns 
  • This may increase the risk of gestational hypertension and preeclampsia 
• Breastfeeding 
  • Trace amounts found in breast milk 

Precautions should be taken when prescribing Fluoxetine in patients with liver cirrhosis, as this diagnosis reduces clearance of fluoxetine and its active metabolite. This increases the elimination or half-life. Lower or less frequent doses should be considered for these patients (21). 

Adverse Effects and Black Box Warnings 

Fluoxetine’s most common side effects include (21): 

• Insomnia 
• Nausea 
• Diarrhea 
• Anorexia 
• Dry mouth 
• Headache 
• Drowsiness 
• Anxiety 
• Nervousness 
• Yawning 
• Decreased libido 
• Decrease arousal or lubrication 
• Bruising 
• Hyperhidrosis 
• Weight gain or loss 
• Decreased orgasm 
• Muscle weakness 
• Tremors 
• Pharyngitis 

Less common adverse effects include (21): 

• Bleeding 
• Seizures 
• Suicidal ideation and behaviors 
  • Especially in teenagers 

Most adverse effects will appear upon initiation of treatment and should fade with time. It is advised to wait for side effects to subside before changing treatment, as most side effects are dose- and time-dependent.  

If side effects continue after several weeks, dose adjustment then changing medication is recommended (21). 

If insomnia is present, patients should take medication in the early morning (21). 

A Black Box Warning is present for Fluoxetine, as this medication increases suicidal thoughts and behaviors. Individuals prescribed this medication should be closely monitored, especially teenagers as they are more prone to experiencing these severe adverse effects (5). 

Drug Interactions 

Fluoxetine interacts with several medications including (22): 

• Monoamine Oxidase inhibitors 
• Medications that increase serotonin levels 
  • Tricyclic antidepressants (TCAs) 
  • Lithium 
  • Triptan migraine medications 
  • Certain opioids 
  • Other SSRIs 
  • Serotonin and norepinephrine reuptake inhibitors (SNRIs) 
• St John’s Wort 
• Medications that raise the risk of bleeding 
  • Warfarin 
  • Apixaban 
  • Rivaroxaban 
  • Clopidogrel 
  • Prasugrel 
• Pimozide and thioridazine 
• Medications metabolized by certain liver enzymes 
  • Flecainide 
  • Propafenone 
  • TCAs 
  • Benzodiazepines 
  • Antipsychotics 
  • Seizures