Pathophysiology
Joint abnormalities in rheumatoid arthritis
Rheumatoid arthritis is an auotimmune disease, the cause for which is still unknown. It is a systemic (whole body) disorder principally affecting synovial joints.
Chemical mediators (Cytokines) give rise to inflammation of joint synovium. Constitutional symptoms such as fever, malaise, loss of appetite and weight loss are also due to cytokines released in to the blood stream. Blood vessel inflammation (vasculitis) affecting many other organ systems can give rise to systemic complications.
As with most autoimmune disease, it is important to distinguish between the cause(s) that trigger the inflammatory process, and those that permit it to persist and progress.
It has long been suspected that certain infections could be triggers for this disease. The "mistaken identity" theory suggests that an infection triggers an immune response, leaving behind antibodies that should be specific to that organism. The antibodies are not sufficiently specific, though, and set off an immune attack against part of the host. Because the normal host molecule "looks like" a molecule on the offending organism that triggered the initial immune reaction - this phenomenon is called molecular mimicry. Some infectious organisms suspected of triggering rheumatoid arthritis include Mycoplasma, Erysipelothrix, parvovirus B19 and rubella, but these associations have never been supported in epidemiological studies. Nor has convincing evidence been presented for other types of triggers such as food allergies. There is also no clear evidence that physical and emotional effects, stress and improper diet could be a trigger for the disease. The many negative findings suggest that either the trigger varies, or that it might in fact be a chance event, as suggested by Edwards et al [12].
Epidemiological studies have confirmed a potential association between RA and two herpesvirus infections: Epstein-Barr virus (EBV) and Human Herpes Virus 6 (HHV-6). [13] Individuals with RA are more likely to exhibit an abnormal immune response to the Epstein-Barr virus. [14] [15] The allele HLA-DRB1*0404 is associated with low frequencies of T cells specific for the EBV glycoprotein 110 and predisposes one to develop RA. [16]
The factors that allow the inflammation, once initiated, to become permanent and chronic, are much more clearly understood. The genetic association with HLA-DR4 is believed to play a major role in this, as well as the newly discovered associations with the gene PTPN22 and with two additional genes [17], all involved in regulating immune responses. It has also become clear from recent studies that these genetic factors may interact with the most clearly defined environmental risk factor for rheumatoid arthritis, namely cigarette smoking [18] Other environmental factors also appear to modulate the risk of acquiring RA, and hormonal factors in the individual may explain some features of the disease, such as the higher occurrence in women, the not-infrequent onset after child-birth, and the (slight) modulation of disease risk by hormonal medications.
Autoimmune diseases require that the affected individual have a defect in the ability to distinguish foreign molecules from the body's own. There are markers on many cells that confer this self-identifying feature. However, some classes of markers allow for RA to happen. 90% of individuals with RA have the cluster of markers known as the HLA-DR4/DR1 cluster, whereas only 40% of unaffected controls do. Thus, in theory, RA requires susceptibility to the disease through genetic endowment with specific markers and an infectious event that triggers an autoimmune response.
Once triggered, B lymphocytes produce immunoglobins, and rheumatoid factors of the IgG and IgM classes that are deposited in the tissue, this subsequently leads to the activation of the serum complement cascade and the recruitment of the phagocytic arm of the immune response, which further exacerbates the inflammation of the synovium, leading to edema, vasodilation and infiltration by activated T-cells (mainly CD4 in nodular aggregates and CD8 in diffuse infiltrates). Early and intermediate molecular mediators of inflammation include tumor necrosis factor alpha (TNF-α), interleukins IL-1, IL-6, IL-8 and IL-15, transforming growth factor beta, fibroblast growth factor and platelet-derived growth factor. Synovial macrophages and dendritic cells further function as antigen presenting cells by expressing MHC class II molecules, leading to an established local immune reaction in the tissue. The disease progresses in concert with formation of granulation tissue at the edges of the synovial lining (pannus) with extensive angiogenesis and production of enzymes that cause tissue damage. Modern pharmacological treatments of RA target these mediators. Once the inflammatory reaction is established, the synovium thickens, the cartilage and the underlying bone begins to disintegrate and evidence of joint destruction accrues.
Pathophysiology
RA is a chronic, progressive, and disabling disease. Despite intensive research, the cause of RA remains unknown. The pathogenesis of this disease is likely multifactorial, involving autoimmunity and genetic factors; infectious agents also are suspected of having a role. Further details are provided below.
Genetic factors: Family studies reveal that RA has a genetic component; human leukocyte antigen (HLA) is an important genetic factor, and the risk for RA is thought to be associated with a sequence of amino acids within the genetic code of certain individuals.
Autoimmunity: Macrophage-derived cytokines appear to be involved in the induction and perpetuation of the chronic inflammatory processes of the joints seen in RA. High titers of serum rheumatoid factors, or autoantibodies to the Fc portion of the immunoglobulin G (IgG) molecules, are associated with more severe joint disease and with extra-articular manifestations.
Infectious agents: Viral infections such as rubella, Ross River virus, and parvovirus are associated with the development of acute polyarthritis; Chlamydia pneumoniae has been detected in some individuals with RA. However, cause or connection has not been demonstrated(1).
Although the precise mechanism of bone and cartilage destruction in RA is not completely understood, the cytokines IL-1 and TNF-alpha play an important role. These cytokines:
Are abundant in inflamed joints and promote the influx of inflammatory neutrophils and monocytes into the joints
Stimulate cells in the inflamed synovium to produce proteolytic enzymes, including collagenase and stromelysin, that can degrade tissue
Cause systemic manifestations such as malaise and fatigue
Thus, although the initial cause of RA remains unknown, the maintenance and propagation of the disease appear to be related to immunologically mediated inflammatory processes. Hence, interfering with key steps in the inflammatory process would be expected to provide symptomatic relief and to slow disease progression.
Signs and symptoms
Signs and symptoms
While rheumatoid arthritis primarily affects joints, problems involving all other organs of the body are known to occur. Extra-articular ("outside the joints") manifestations occur in about 15% of individuals with rheumatoid arthritis.[3] It can be difficult to determine whether disease manifestations are directly caused by the rheumatoid process itself, or from side effects of the medications commonly used to treat it - for example, lung fibrosis from methotrexate, or osteoporosis from corticosteroids.
[edit] Joints
The arthritis of rheumatoid arthritis is due to synovitis, which is inflammation of the synovial membrane that covers the joint. Joints become red, swollen, tender and warm, and stiffness prevents their use. By definition, RA affects multiple joints (it is a polyarthritis). Most commonly, small joints of the hands, feet and cervical spine are affected, but larger joints like the shoulder and knee can also be involved, differing per individual. Eventually, synovitis leads to erosion of the joint surface, causing deformity and loss of function.[1]
Inflammation in the joints manifests itself as a soft, "doughy" swelling, causing pain and tenderness to palpation and movement, a sensation of localised warmth, and restricted movement. Increased stiffness upon waking is often a prominent feature and may last for more than an hour. These signs help distinguish rheumatoid from non-inflammatory diseases of the joints such as osteoarthritis (sometimes referred to as the "wear-and-tear" of the joints). In RA, the joints are usually affected in a fairly symmetrical fashion although the initial presentation may be asymmetrical.
Hands affected by RA
As the pathology progresses the inflammatory activity leads to erosion and destruction of the joint surface, which impairs their range of movement and leads to deformity. The fingers are typically deviated towards the little finger (ulnar deviation) and can assume unnatural shapes. Common deformities in rheumatoid arthritis are the Boutonniere deformity (Hyperflexion at the proximal interphalangeal joint with hyperextension at the distal interphalangeal joint), swan neck deformity (Hyperextension at the proximal interphalangeal joint, hyperflexion at the distal interphalangeal joint). The thumb may develop a "Z-Thumb" deformity with fixed flexion and subluxation at the metacarpophalangeal joint, and hyperextension at the IP joint.
[edit] Skin
The rheumatoid nodule is the cutaneous (strictly speaking subcutaneous) feature most characteristic of rheumatoid arthritis. The initial pathologic process in nodule formation is unknown but is thought to be related to small-vessel inflammation. The mature lesion is defined by an area of central necrosis surrounded by palisading macrophages and fibroblasts and a cuff of cellular connective tissue and chronic inflammatory cells. The typical rheumatoid nodule may be a few millimetres to a few centimetres in diameter and is usually found over bony prominences, such as the olecranon, the calcaneal tuberosity, the metacarpophalangeal joints, or other areas that sustain repeated mechanical stress. Nodules are associated with a positive RF titer and severe erosive arthritis. Rarely, they can occur in internal organs.
Several forms of vasculitis are also cutaneous manifestations associated with rheumatoid arthritis. A benign form occurs as microinfarcts around the nailfolds. More severe forms include livedo reticularis, which is a network (reticulum) of erythematous to purplish discoloration of the skin due to the presence of an obliterative cutaneous capillaropathy. (This rash is also otherwise associated with the antiphospholipid-antibody syndrome, a hypercoagulable state linked to antiphospholipid antibodies and characterized by recurrent vascular thrombosis and second trimester miscarriages.)
Other, rather rare, skin associated symtoms include:
pyoderma gangrenosum, a necrotizing, ulcerative, noninfectious neutrophilic dermatosis.
Sweet's syndrome, a neutrophilic dermatosis usually associated with myeloproliferative disorders
drug reactions
erythema nodosum
lobular panniculitis
atrophy of digital skin
palmar erythema
diffuse thinning (rice paper skin), and skin fragility (often worsened by corticosteroid use).
[edit] Lungs
Fibrosis of the lungs is a recognised response to rheumatoid disease. It is also a rare but well recognised consequence of therapy (for example with methotrexate and leflunomide). Caplan's syndrome describes lung nodules in individuals with rheumatoid arthritis and additional exposure to coal dust. Pleural effusions are also associated with rheumatoid arthritis.
[edit] Kidneys
Renal amyloidosis can occur as a consequence of chronic inflammation. [4] Rheumatoid vasculitis is a rare cause of glomerular disease in the kidney. Treatment with Penicillamine and gold salts are recognized causes of membranous nephropathy.
[edit] Heart and blood vessels
Possible complications that may arise include: pericarditis, endocarditis, left ventricular failure, valvulitis and fibrosis. The risk of cardiovascular, specifically myocardial infarction (heart attack) or congestive heart failure are greater in individuals with RA. Over 1/3 of deaths of people with RA are directly attributable to cardiovascular death.
[edit] Other
Ocular
Keratoconjunctivitis sicca (dry eyes), scleritis, episcleritis and scleromalacia.
Gastrointestinal and Hematological
Felty syndrome, anemia
Neurological
Peripheral neuropathy and mononeuritis multiplex may occur. The most common problem is carpal tunnel syndrome due to compression of the median nerve by swelling around the wrist. Atlanto-axial subluxation can occur, owing to erosion of the odontoid process and or/transverse ligaments in the cervical spine's connection to the skull. Such an erosion (>3mm) can give rise to vertebrae slipping over one another and compressing the spinal cord. Clumisiness is initially experienced, but without due care this can progress to quadriplegia.
Vasculitis
Vasculitis in rheumatoid arthritis is common. It typically presents as vasculitic nailfold infarcts.
Osteoporosis
Osteoporosis classically occurs in RA around inflamed joints. It is postulated to be partially caused by inflammatory cytokines.
Lymphoma
The incidence of lymphoma is increased in RA as it is in most autoimmune conditions.
Histopatho
There are two popular theories regarding the pathogenesis of rheumatoid arthritis (RA). The first holds that the T cell, through interaction with an - as yet unidentified - antigen, is the primary cell responsible for initiating the disease as well as for driving the chronic inflammatory process. This theory is based upon the known association of RA with class II major histocompatability antigens, the large number of CD4+ T cells and skewed T cell receptor gene usage in the RA synovium. The second theory holds that, while T cells may be important in initiating the disease, chronic inflammation is self-perpetuated by macrophages and fibroblasts in a T-cell independent manner. This theory is based upon the relative absence of activated T cells phenotypes in chronic RA and the preponderance of activated macrophage and fibroblast phenotypesSynovium The synovium, in normal joints, is a thin delicate lining that serves several important functions.
The synovium serves as an important source of nutrients for cartilage since cartilage itself is avascular. In addition, synovial cells synthesize joint lubricants such as hyaluronic acid, as well as collagens and fibronectin that constitute the structural framework of the synovial interstitium.
1. Synovial lining or intimal layer: Normally, this layer is only 1-3 cells thick.
normal synovial lining
In RA, this lining is greatly hypertrophied (8-10 cells thick). Primary cell populations in this layer are fibroblasts and macrophages.
2. Subintimal area of synovium: This is where the synovial blood vessels are located; this area normally has very few cells. In RA, however, the subintimal area is heavily infiltrated with inflammatory cells, including T and B lymphocytes, macrophages and mast cells. The intense cellular infiltrate is accompanied by new blood vessel growth (angiogenesis).
In RA, the hypertrophied synovium (also called pannus) invades and erodes contiguous bone and cartilage. As such, it can be thought of as a tumor-like tissue, although mitotic figures are rare and, of course, metastasis does not occur.
1. CartilageComposed primarily of type II collagen and proteoglycans, this is normally a very resilient tissue that absorbs considerable impact and stress. In RA, its integrity, resilience and water content are all impaired. This appears to be due to elaboration of proteolytic enzymes (collagenase, stromelysin) both by synovial lining cells and by chondrocytes themselves. Polymorphonuclear leukocytes in the synovial fluid may also contribute to this degradative processBoneComposed primarily of type I collagen, invading synovium causes erosion of contiguous bone via release of prostaglandins and proteases by synovial cells and, possibly, by osteoclastsSynovial Cavity Synovial Cavity Normally only a "potential" space with 1-2ml of highly viscous (due to hyaluronic acid) fluid with few cells. In RA, large collections of fluid ("effusions") occur which are, in effect, filtrates of plasma (and, therefore, exudative - i.e., high protein content). The synovial fluid is highly inflammatory. However, unlike the rheumatoid synovial tissue that is infiltrated with lymphocytes and macrophages but not neutrophils, the predominant cell in the synovial fluid is the neutrophil
2. Pathophysiology: Order of changes
1. Synovial Macrophage and fibroblast activation
2. Cytokine production (interleukin, TNF)
3. Lymphoctes infiltrate perivascular areas
4. Synovial thickening (Pannus formation and spread)
5. Neovascularization
6. Local micro-Vasculitis
7. Chondrocyte, Osteoclast, CD4+ Helper activity
8. Endothelial proliferation
9. Joint space narrowing
10. Cytokine release (resulting in fever, Anemia)
Saturday, August 9, 2008
ALCOHOL-RELATED DISORDERS
ALCOHOL-RELATED DISORDERS
DSM-IV
ALCOHOL-INDUCED DISORDERS
303.00 Alcohol intoxication
291.81 Alcohol withdrawal
291.89 Alcohol-induced mood disorder
291.89 Alcohol-induced anxiety disorder
292.81 Intoxication delirium
Alcohol is a CNS depressant drug that is used socially in our society for many reasons (e.g., to enhance the flavor of food, to encourage relaxation and conviviality, for feelings of celebration, and as a sacred ritual in some religious ceremonies). Therapeutically, it is the major ingredient in many OTC/prescription medications. It can be harmless, enjoyable, and sometimes beneficial when used responsibly and in moderation. Like other mind-altering drugs, however, it has the potential for abuse and, in fact, is the most widely abused drug in the United States (research suggests 5% to 10% of the adult population) and is potentially fatal. Frequently, the client in a residential care setting has been using alcohol in conjunction with other drugs. It is believed that alcohol is often used by clients who have other mental illnesses to assuage the pain they feel. The term “dual diagnosis” is used to mean an association between the use/abuse of drugs (including alcohol) and other psychiatric diagnoses. It may be difficult to determine cause and effect in any given situation to determine an accurate diagnosis. However, it is important to recognize when both conditions are present so that the often-overwhelming problems of treatment are instituted for both conditions.
This plan of care for Alcohol related disorders addresses acute intoxication/withdrawal and is to be used in conjunction with CP: Substance Dependence/Abuse Rehabilitation.
ETIOLOGICAL THEORIES
Psychodynamics
The individual remains fixed in a lower level of development, with retarded ego and weak superego. The person retains a highly dependent nature, with characteristics of poor impulse control, low frustration tolerance, and low self-esteem.
Biological
Enzymes, genes, brain chemistry, and hormones create and contribute to an individual’s response to alcohol. The two types of alcohol-related disorders are (1) familial, which is largely inherited, and (2) acquired. A childhood history of attention-deficit disorder or conduct disorder also increases a child’s risk of becoming alcoholic. Certain physiological changes also may cause addiction to alcohol, or alcoholism.
Family Dynamics
One in 12–15 persons has serious problems from drinking. In a dysfunctional family system, alcohol may be viewed as the primary method of relieving stress. Children of alcoholics are 4 times more likely to develop alcoholism than children of nonalcoholics. The child has negative role models and learns to respond to stressful situations in like manner. The use of alcohol is cultural, and many factors influence one’s decision to drink, how much, and how often. Denial of the illness can be a major barrier to identification and treatment of alcoholism and alcohol abuse.
CLIENT ASSESSMENT DATA BASE
Data depend on the duration/extent of alcohol use, concurrent use of other drugs, degree of organ involvement, and presence of other psychiatric conditions.
Activity/Rest
Difficulty sleeping, not feeling well rested
Circulation
Peripheral pulses weak, irregular, or rapid
Hypertension common in early withdrawal stage but may become labile/progress to hypotension
Tachycardia common during acute withdrawal
Ego Integrity
Feelings of guilt/shame; defensiveness about drinking
Denial, rationalization
Reports of multiple stressors; problems with relationships
Multiple stressors/losses (relationships, employment, financial)
Use of substances to deal with life stressors, boredom, etc.
Elimination
Diarrhea
Bowel sounds varied (may reflect gastric complications [e.g., gastric hemorrhage])
Food/Fluid
Nausea/vomiting, food tolerance
Muscle wasting, dry/dull hair, swollen salivary glands, inflamed buccal cavity, capillary fragility (malnutrition)
Generalized tissue edema may be noted (protein deficiencies)
Gastric distension; ascites, liver enlargement (seen in cirrhosis)
Neurosensory
“Internal shakes”
Headache, dizziness, blurred vision, “blackouts”
Psychopathology such as paranoid schizophrenia, major depression (may indicate dual diagnosis)
Level of Consciousness/Orientation: Confusion, stupor, hyperactivity, distorted thought processes, slurred/incoherent speech
Memory loss/confabulation
Affect/Mood/Behavior: May be fearful, anxious, easily startled, inappropriate, silly, euphoric, irritable, physically/verbally abusive, depressed, and/or paranoid
Hallucinations: Visual, tactile, olfactory, and auditory (e.g., picking items out of air or responding verbally to unseen person/voices)
Nystagmus (associated with cranial nerve palsy)
Pupil constriction (may indicate CNS depression)
Arcus senilis, a ringlike opacity of the cornea (normal in aging populations, suggests alcohol-related changes in younger clients)
Fine motor tremors of face, tongue, and hands; seizure activity (commonly grand mal)
Gait unsteady/ataxia (may be due to thiamine deficiency or cerebellar degeneration [Wernicke’s encephalopathy])
Pain/Discomfort
May report constant upper abdominal pain and tenderness radiating to the back (pancreatic inflammation)
Respiration
History of tobacco use, recurrent/chronic respiratory problems
Tachypnea (hyperactive state of alcohol withdrawal)
Cheyne-Stokes respirations or respiratory depression
Breath Sounds: Diminished/adventitious sounds (suggests pulmonary complications [e.g., respiratory depression, pneumonia])
Safety
History of recurrent accidents, such as falls, fractures, lacerations, burns, blackouts, or automobile accidents
Skin: Flushed face/palms of hands, scars, ecchymotic areas, cigarette burns on fingers, spider nevi (impaired portal circulation); fissures at corners of mouth (vitamin deficiency)
Fractures, healed or new (signs of recent/recurrent trauma)
Temperature elevation (dehydration and sympathetic stimulation); flushing/diaphoresis (suggests presence of infection)
Suicidal ideation/attempts (some research suggests alcoholic suicide attempts are 30% higher than national average for general population)
Social Interactions
Frequent sick days off work/school, fighting with others, arrests (disorderly conduct, motor vehicle violations [DUIs])
Denial that alcohol intake has any significant effect on the present condition/situation
Dysfunctional family system of origin; problems in current relationships
Mood changes affecting interactions with others
Teaching/Learning
History of alcohol and/or other drug use/abuse (including tobacco)
Ignorance and/or denial of addiction to alcohol or inability to cut down or stop drinking despite repeated efforts
Large amount of alcohol consumed in last 24–48 hours, previous periods of abstinence/withdrawal
Previous hospitalizations for alcoholism/alcohol-related diseases (e.g., cirrhosis, esophageal varices)
Family history of alcoholism/substance use
DIAGNOSTIC STUDIES
Blood Alcohol/Drug Levels: Alcohol level may/may not be severely elevated depending on amount consumed and length of time between consumption and testing. In addition to alcohol, numerous controlled/illicit substances may be identified in a polydrug screen (e.g., amphetamine, cocaine, morphine, Percodan, Quaalude).
CBC: Decreased (Hb/Hct) may reflect such problems as iron-deficiency anemia or acute/chronic GI bleeding. White blood cell count may be increased with infection or decreased, if immunosuppressed.
Glucose: Hyperglycemia/hypoglycemia may be present, related to pancreatitis, malnutrition, or depletion of liver glycogen stores.
Electrolytes: Hypokalemia and hypomagnesemia are common.
Liver Function Tests: CPK, LDH, AST, ALT, and amylase may be elevated, reflecting liver or pancreatic damage.
Nutritional Tests: Albumin is low and total protein decreased. Vitamin deficiencies are usually present, reflecting malnutrition/malabsorption.
Other Screening Studies (e.g., Hepatitis, HIV, TB): Dependent on general condition, individual risk factors, and care setting.
Urinalysis: Infection may be identified; ketones may be present related to breakdown of fatty acids in malnutrition (pseudodiabetic condition).
Chest X-Ray: May reveal right lower lobe pneumonia (malnutrition, depressed immune system, aspiration) or chronic lung disorders associated with tobacco use.
ECG: Dysrhythmias, cardiomyopathies, and/or ischemia may be present owing to direct effect of alcohol on the cardiac muscle and/or conduction system, as well as effects of electrolyte imbalance.
Addiction Severity Index (ASI): An assessment tool that produces a “problem severity profile” of the client, including chemical, medical, psychological, legal, family/social, and employment/support aspects, indicating areas of treatment needs.
NURSING PRIORITIES
1. Maintain physiological stability during withdrawal phase.
2. Promote client safety.
3. Provide appropriate referral and follow-up.
4. Encourage/support SO involvement in Intervention (confrontation) process.
DISCHARGE GOALS
1. Homeostasis achieved.
2. Complications prevented/resolved.
3. Sobriety being maintained on a day-to-day basis.
4. Ongoing participation in a rehabilitation program/attendance at group therapy (e.g., Alcoholics Anonymous).
5. Plan in place to meet needs after discharge.
This plan of care is to be used in conjunction with CP: Substance Dependence/Abuse Rehabilitation.
NURSING DIAGNOSIS BREATHING PATTERN, risk for ineffective
Risk Factors May Include: Direct effect of alcohol toxicity on respiratory center and/or sedative drugs given to decrease alcohol withdrawal symptoms
Tracheobronchial obstruction
Presence of chronic respiratory problems, inflammatory process
Decreased energy/fatigue
Possibly Evidenced by: [Not applicable; presence of signs and symptoms establishes an actual diagnosis.]
Desired Outcomes Evaluation Criteria— Maintain effective respiratory pattern with
Client Will: respiratory rate within normal range, lungs clear, free of cyanosis and other signs/symptoms of hypoxia.
ACTIONS/INTERVENTIONS RATIONALE
Independent
Monitor respiratory rate/depth and pattern as Frequent assessment is important because toxicity indicated. Note periods of apnea, Cheyne-Stokes levels may change rapidly. Hyperventilation is respirations. common during acute withdrawal phase. Kussmaul respirations are sometimes present because of acidotic state associated with vomiting and malnutrition. However, marked respiratory depression can occur because of CNS depressant effects of alcohol. This may be compounded by drugs used to control alcohol withdrawal symptoms.
Elevate head of bed. Decreases possibility of aspiration; lowers diaphragm, enhancing lung inflation.
Encourage cough/deep breathing exercises and Facilitates lung expansion and mobilization of frequent position changes. secretions to reduce risk of atelectasis/pneumonia.
Auscultate breath sounds. Note presence of Client is at risk for atelectasis related to adventitious sounds (e.g., rhonchi, wheezes). hypoventilation and pneumonia. Right lower lobe pneumonia is common in alcohol-debilitated clients and is often due to aspiration. Chronic lung diseases are also common (e.g., emphysema, chronic bronchitis).
Have suction equipment, airway adjuncts available. Sedative effects of alcohol/drugs potentiate risk of aspiration, relaxation of oropharyngeal muscles, and respiratory depression, requiring intervention to prevent respiratory arrest.
Collaborative
Administer supplemental oxygen if necessary. Hypoxia may occur with CNS/respiratory depression.
Review chest x-rays, pulse oximetry as Monitors presence of secondary complications available/indicated. such as atelectasis/pneumonia; evaluates effectiveness of respiratory effort, identifies therapy needs.
NURSING DIAGNOSIS CARDIAC OUTPUT, risk for decreased
Risk Factors May Include: Direct effect of alcohol on the heart muscle
Altered systemic vascular resistance
Electrical alterations in rate, rhythm, conduction
Possibly Evidenced by: [Not applicable; presence of signs and symptoms establishes an actual diagnosis.]
Desired Outcomes/Evaluation Criteria— Display vital signs within client’s normal range;
Client Will: absence of/reduced frequency of dysrhythmias.
Demonstrate an increase in activity tolerance.
Verbalize understanding of the effect of alcohol on the heart.
ACTION/INTERVENTIONS RATIONALE
Independent
Monitor vital signs frequently during acute Hypertension frequently occurs in acute withdrawal. withdrawal phase. Extreme hyperexcitability accompanied by catecholamine release and increased peripheral vascular resistance raises BP (and heart rate). However, BP may become labile/progress to hypotension. Note: Client may have underlying cardiovascular disease that is compounded by substance withdrawal.
Monitor cardiac rate/rhythm. Document Long-term alcohol abuse may result in irregularities/dysrhythmias. cardiomyopathy/congestive heart failure. Tachycardia is common owing to sympathetic response to increased circulating catecholamines. Irregularities/dysrhythmias may develop with electrolyte shifts/imbalance. All of these may have an adverse effect on cardiac function/output.
Monitor body temperature. Elevation may occur because of sympathetic stimulation, dehydration, and/or infections, causing vasodilation and compromising venous return/cardiac output.
Monitor intake/output. Note 24-hour fluid balance. Preexisting dehydration, vomiting, fever, and diaphoresis may result in decreased circulating volume, which can compromise cardiovascular function. Note: Hydration is difficult to assess in the alcoholic because the usual indicators are not reliable, and overhydration is a risk in the presence of compromised cardiac function.
Be prepared for/assist in cardiopulmonary Causes of death during acute withdrawal stages resuscitation. include cardiac dysrhythmias, respiratory depression/arrest, oversedation, excessive psychomotor activity, severe dehydration or overhydration, and massive infections. Mortality for unrecognized/untreated delirium tremens (DTs) may be as high as 15%–25%.
Collaborative
Monitor laboratory studies (e.g., serum Electrolyte imbalance (e.g., potassium/electrolyte levels). magnesium) potentiates risk of cardiac dysrhythmias and CNS excitability.
Administer medications as indicated: e.g., clonidine Although the use of benzodiazepines is often (Catapres), atenolol (Tenormin); sufficient to control hypertension during initial withdrawal from alcohol, some clients may require more specific therapy. Note: Atenolol and other beta-adrenergic blockers may speed up the withdrawal process and eliminate tremors, as well as lower heart rate, BP, and body temperature, reducing the need for benzodiazepines.
Potassium. Corrects deficits that can result in life-threatening dysrhythmias.
NURSING DIAGNOSIS INJURY, risk for (specify)
Risk Factors May Include: Cessation of alcohol intake with varied autonomic nervous system responses to the suddenly altered state
Involuntary clonic/tonic muscle activity (convulsions)
Equilibrium/balancing difficulties, reduced muscle and hand/eye coordination
Possibly Evidenced by: [Not applicable; presence of signs and symptoms establishes an actual diagnosis.]
Desired Outcomes/Evaluation Criteria— Demonstrate absence of untoward effects of
Client Will: withdrawal.
Experience no physical injury.
ACTIONS/INTERVENTIONS RATIONALE
Independent
Identify stage of alcohol withdrawal, symptoms: Prompt recognition and intervention may halt Stage I is associated with signs/symptoms of progression of symptoms and enhance hyperactivity (e.g., tremors, sleeplessness, nausea/ recovery/improve prognosis. In addition, vomiting, diaphoresis, tachycardia, hypertension). recurrence/progression of symptoms indicates Stage II is manifested by increased hyperactivity need for changes in drug therapy/more intense plus hallucinations and/or seizure activity. treatment.Stage III symptoms include delirium tremens (DTs) and extreme autonomic hyperactivity with profound confusion, anxiety, insomnia, fever.
Monitor/document seizure activity. Maintain patent Grand mal seizures are most common and may be airway. Provide environmental safety (e.g., padded related to decreased magnesium levels, side rails, bed in low position). hypoglycemia, elevated blood alcohol, history of head trauma/preexisting seizure disorder. Note: In absence of previous history of other pathology causing seizure activity, seizures usually stop spontaneously, requiring only symptomatic treatment.
Check deep-tendon reflexes. Assess gait, if possible. Reflexes may be depressed, absent, or hyperactive. Peripheral neuropathies are common, especially in malnourished clients. Ataxia (gait disturbance) is associated with Wernicke’s syndrome (thiamine deficiency) and cerebellar degeneration.
Assist with ambulation and self-care Prevents falls with resultant injury.activities as needed.
Provide for environmental safety when indicated. May be required when equilibrium, hand/(Refer to ND: Sensory/Perceptual alteration eye coordination problems exist.[specify].)
Collaborative
Administer IV/PO fluids with caution, as indicated. Cautious replacement corrects dehydration and promotes renal clearance of toxins while reducing risk of overhydration.
Administer medications as indicated:
Benzodiazepines such as: chlordiazepoxide Commonly used to control neuronal hyperactivity (Librium), diazepam (Valium), clonazepam that occurs as alcohol is detoxified. IV/PO (Klonopin); administration is the route preferred, as intramuscular absorption is unpredictable. Muscle-relaxant qualities are particularly helpful to the client in controlling the “shakes,” trembling, and ataxic quality of movements. Clients may initially require large doses to achieve desired effect, and then the drug(s) may be tapered and discontinued, usually within 96 hours. Note: These agents must be used cautiously in clients with hepatic disease, as the agents are metabolized by the liver.
Oxazepam (Serax); Although less dramatic for control of withdrawal symptoms, this may be the drug of choice in a client with liver disease because of its shorter half-life.
Phenobarbital; Useful in suppressing withdrawal symptoms and is an effective anticonvulsant. Use must be monitored to prevent exacerbation of respiratory depression.
Magnesium sulfate; Reduces tremors and seizure activity by decreasing neuromuscular excitability.
Thiamine. Thiamine deficiency (common in alcohol abuse) may lead to neuritis, Wernicke’s syndrome, and/or Korsakoff’s psychosis.
Nursing Diagnosis Sensory/Perceptual alterations (specify)
May Be Related to: Chemical alteration: Exogenous (e.g., alcohol consumption/sudden cessation) and endogenous (e.g., electrolyte imbalance, elevated ammonia and BUN)
Sleep deprivation
Psychological stress (anxiety/fear)
Possibly Evidenced by: Disorientation in time, place, person, or situation
Changes in usual response to stimuli; exaggerated emotional responses, change in behavior
Bizarre thinking
Restlessness, irritability, apprehension
Desired Outcomes/Evaluation Criteria— Regain/maintain usual level of cognition.
Client Will: Report absence of auditory/visual hallucinations.
Identify external factors that affect sensory-perceptual abilities.
ACTIONS/INTERVENTIONS RATIONALE
Independent
Assess level of consciousness, ability to speak, Speech may be garbled, confused, or slurred. response to stimuli/commands. Response to commands may reveal inability to concentrate, impaired judgment, or muscle coordination deficits.
Observe behavioral responses (e.g., hyperactivity, Hyperactivity related to CNS disturbances may disorientation, confusion, sleeplessness, irritability). escalate rapidly. Sleeplessness is common because of loss of sedative effect gained from alcohol usually consumed prior to bedtime. Sleep deprivation may aggravate disorientation/ confusion. Progression of symptoms may indicate impending hallucinations (Stage II) or DTs (Stage III).
Note onset of hallucinations. Document as Auditory hallucinations are reported to be more auditory, visual, and/or tactile. frightening/threatening to client. Visual hallucinations occur more at night and often include insects, animals, or faces of friends/enemies. Clients are frequently observed picking the air; yelling may occur if client is calling for help from perceived threat (usually seen in Stage III).
Provide quiet environment. Speak in calm, Reduces external stimuli during hyperactive stage. quiet voice. Regulate lighting as indicated. Client may become more delirious when Turn off radio/TV during sleep. surroundings cannot be seen, although some respond better to quiet, darkened room.
Provide care by same personnel whenever possible. Promotes recognition of caregivers and a sense of consistency that may reduce fear.
Reorient frequently to person, place, time, and May reduce confusion/misinterpretation of surrounding environment as indicated. external stimuli.
Avoid bedside discussion about client or topics Client may hear and misinterpret conversation, unrelated to the client that do not include the client. which can aggravate hallucinations.
Provide environment safety (e.g., place bed in low Client may have distorted sense of reality, be position, leave doors in full open or closed position, fearful, or be suicidal, requiring protection from observe frequently, place call light/bell within reach, self-harm.remove articles that can harm client).
Collaborative
Provide seclusion, restraints as necessary. Clients with excessive psychomotor activity, severe hallucinations, violent behavior, and/or suicidal gestures may respond better to seclusion. Restraints are usually ineffective and add to client’s agitation but occasionally may be required for short periods to prevent self-harm.
Monitor laboratory studies (e.g., electrolytes, Changes in organ function may precipitate or magnesium levels, liver function studies, ammonia, potentiate sensory-perceptual deficits. Electrolyte BUN, glucose, ABGs). imbalance is common. Liver function is often impaired in the chronic alcoholic, and ammonia intoxication can occur if the liver is unable to convert ammonia to urea. Ketoacidosis is sometimes present without glycosuria; however, hyperglycemia or hypoglycemia may occur, suggesting pancreatitis or impaired gluconeogenesis in the liver. Hypoxemia and hypercarbia are common manifestations in chronic alcoholics who are also heavy smokers.
Administer medications as indicated, e.g.:
Antianxiety agents (Refer to ND: Anxiety [severe/ Reduces hyperactivity, promoting relaxation/panic]/Fear); sleep. Drugs that have little effect on dreaming may be desired to allow dream recovery (REM rebound) to occur, which has been suppressed by alcohol use.
Thiamine; vitamins C & B complex, multivitamins; Vitamins may be depleted because of insufficient Stresstabs. intake and malabsorption. Vitamin deficiency (especially thiamine) is associated with ataxia, loss of eye movement and pupillary response, palpitations, postural hypotension, and exertional dyspnea.
NURSING DIAGNOSIS NUTRITION: altered, less than body requirements
May Be Related to: Poor dietary intake (replaced by alcohol consumption)
Effects of alcohol on organs involved in digestion (e.g., stomach, pancreas, liver); interference with absorption and metabolism of nutrients and amino acids; and increased loss of vitamins in the urine
Possibly Evidenced by: Reports of inadequate food intake, altered taste sensation, lack of interest in food, abdominal pain
Body weight 20% or more under ideal
Pale conjunctiva and mucous membranes; sore, inflamed buccal cavity/cheilosis
Poor muscle tone, skin turgor
Hyperactive bowel sounds, diarrhea
Third spacing of circulating blood volume (e.g., edema of extremities, ascites)
Presence of neuropathies
Laboratory evidence of decreased red cell count (anemias), vitamin deficiencies, reduced serum albumin level, or electrolyte imbalance
Desired Outcomes/Evaluation Criteria— Verbalize understanding of effects of alcohol
Client Will: ingestion and reduced dietary intake on nutritional status and general well-being.
Demonstrate behaviors, lifestyle changes to regain/maintain appropriate weight.
Maintain stable weight or progressive weight gain toward goal with normalization of laboratory values and absence of signs of malnutrition.
ACTIONS/INTERVENTIONS RATIONALE
Independent
Evaluate presence/quality of bowel sounds. Note Irritation of gastric mucosa is common and may abdominal distension, tenderness. result in epigastric pain, nausea, and hyperactive bowel sounds. More serious effects of GI system may occur secondary to cirrhosis and hepatitis.
Note presence of nausea/vomiting, diarrhea. Nausea and vomiting are often among the first signs of alcohol withdrawal and may interfere with achieving adequate nutritional intake.
Assess ability to feed self. Tremors, altered mentation, or hallucinations may interfere with ingestion of nutrients and indicate need for assistance.
Provide small, easily digested, frequent meals/ May limit gastric distress and enhance intake and snacks, and advance as tolerated. toleration of nutrients. As appetite and ability to tolerate food increase, diet should be adjusted to provide the necessary calories and nutrition for cellular repair and restoration of energy.
Collaborative
Review laboratory tests (e.g., AST, ALT, LDH, Assesses liver function, adequacy of nutritional serum albumin/prealbumin, transferrin). intake; influences choice of diet and need for/ effectiveness of supplemental therapy.
Refer to dietitian/nutritional support team. Useful in establishing and coordinating individual nutritional regimen.
Provide diet high in protein with at least half of Stabilizes blood sugar, thereby reducing risk of calories obtained from carbohydrates. hypoglycemia, while providing for energy needs and cellular regeneration.
Administer medications as indicated, e.g.:
Antacids, antiemetics, antidiarrheal; Reduces gastric irritation and limits effects of sympathetic stimulation.
Vitamins, Replace losses. Note: All clients should receive thiamine. thiamine and vitamins, because deficiencies (clinical or subclinical) exist in most, if not all, clients with chronic alcoholism.
Institute/maintain NPO status as indicated. Provides gastrointestinal rest to reduce harmful effects of gastric/pancreatic stimulation in presence of GI bleeding or excessive vomiting.
NURSING DIAGNOSIS ANXIETY [severe/panic]/FEAR
May Be Related to: Cessation of alcohol intake/physiological withdrawal
Situational crisis (hospitalization)
Threat to self-concept, perceived threat of death
Possibly Evidenced by: Feelings of inadequacy, shame, self-disgust, and remorse
Increased helplessness/hopelessness with loss of control of own life
Increased tension, apprehension
Fear of unspecified consequences; identifying object of fear
Desired Outcomes/Evaluation Criteria— Verbalize reduction of fear and anxiety to an
Client Will: acceptable and manageable level.
Express sense of regaining some control of situation/life.
Demonstrate problem-solving skills and use resources effectively.
ACTIONS/INTERVENTIONS RATIONALE
Independent
Identify cause of anxiety, involving client in the Clients in acute phase of withdrawal may be process. Explain that alcohol withdrawal increases unable to identify and/or accept what is anxiety and uneasiness. Reassess level of anxiety happening. Anxiety may be physiologically or on an ongoing basis. environmentally caused. Continued alcohol toxicity will be manifested by increased anxiety and agitation as effects of medications wear off.
Develop a trusting relationship through frequent Provides client with a sense of humanness, helping contact, being honest and nonjudgmental. Project to decrease paranoia and distrust. Client will be an accepting attitude about alcoholism. able to detect biased or condescending attitude of caregivers.
Inform client what you plan to do and why. Include Enhances sense of trust, and explanation may client in planning process and provide choices increase cooperation/reduce anxiety. Provides when possible. sense of control over self in circumstances where loss of control is a significant factor. Note: Feelings of self-worth are intensified when one is treated as a worthwhile person.
Reorient frequently. (Refer to ND: Sensory/ Client may experience periods of confusion, Perceptual alterations [specify].) resulting in increased anxiety.
Collaborative
Administer medications as indicated, e.g.:
Benzodiazepines: chlordiazepoxide (Librium), Antianxiety agents are given during acute diazepam (Valium); withdrawal to help client relax, be less hyperactive, and feel more in control.
Barbiturates: phenobarbital, or possibly These drugs suppress alcohol withdrawal but secobarbital (Seconal), pentobarbital (Nembutal). need to be used with caution as they are respiratory depressants and REM sleep cycle inhibitors.
Arrange Intervention (confrontation) in controlled The process of Intervention, wherein SOs/family group setting. members, supported by staff, provide information about how the client’s drinking and behavior have affected each one of them, helps the client to acknowledge that drinking is a problem and has resulted in current situational crisis.
Provide consultation for referral to recovery/ Client is more likely to contract for treatment rehabilitation program for ongoing treatment as while still hurting and experiencing fear and soon as medically stable (e.g., oriented to reality). anxiety from last drinking episode. Motivation decreases as well-being increases and person again feels able to control the problem. Direct contact with available treatment resources provides realistic picture of help. Decreases time for client to “think about it”/change mind or restructure and strengthen denial systems.
DSM-IV
ALCOHOL-INDUCED DISORDERS
303.00 Alcohol intoxication
291.81 Alcohol withdrawal
291.89 Alcohol-induced mood disorder
291.89 Alcohol-induced anxiety disorder
292.81 Intoxication delirium
Alcohol is a CNS depressant drug that is used socially in our society for many reasons (e.g., to enhance the flavor of food, to encourage relaxation and conviviality, for feelings of celebration, and as a sacred ritual in some religious ceremonies). Therapeutically, it is the major ingredient in many OTC/prescription medications. It can be harmless, enjoyable, and sometimes beneficial when used responsibly and in moderation. Like other mind-altering drugs, however, it has the potential for abuse and, in fact, is the most widely abused drug in the United States (research suggests 5% to 10% of the adult population) and is potentially fatal. Frequently, the client in a residential care setting has been using alcohol in conjunction with other drugs. It is believed that alcohol is often used by clients who have other mental illnesses to assuage the pain they feel. The term “dual diagnosis” is used to mean an association between the use/abuse of drugs (including alcohol) and other psychiatric diagnoses. It may be difficult to determine cause and effect in any given situation to determine an accurate diagnosis. However, it is important to recognize when both conditions are present so that the often-overwhelming problems of treatment are instituted for both conditions.
This plan of care for Alcohol related disorders addresses acute intoxication/withdrawal and is to be used in conjunction with CP: Substance Dependence/Abuse Rehabilitation.
ETIOLOGICAL THEORIES
Psychodynamics
The individual remains fixed in a lower level of development, with retarded ego and weak superego. The person retains a highly dependent nature, with characteristics of poor impulse control, low frustration tolerance, and low self-esteem.
Biological
Enzymes, genes, brain chemistry, and hormones create and contribute to an individual’s response to alcohol. The two types of alcohol-related disorders are (1) familial, which is largely inherited, and (2) acquired. A childhood history of attention-deficit disorder or conduct disorder also increases a child’s risk of becoming alcoholic. Certain physiological changes also may cause addiction to alcohol, or alcoholism.
Family Dynamics
One in 12–15 persons has serious problems from drinking. In a dysfunctional family system, alcohol may be viewed as the primary method of relieving stress. Children of alcoholics are 4 times more likely to develop alcoholism than children of nonalcoholics. The child has negative role models and learns to respond to stressful situations in like manner. The use of alcohol is cultural, and many factors influence one’s decision to drink, how much, and how often. Denial of the illness can be a major barrier to identification and treatment of alcoholism and alcohol abuse.
CLIENT ASSESSMENT DATA BASE
Data depend on the duration/extent of alcohol use, concurrent use of other drugs, degree of organ involvement, and presence of other psychiatric conditions.
Activity/Rest
Difficulty sleeping, not feeling well rested
Circulation
Peripheral pulses weak, irregular, or rapid
Hypertension common in early withdrawal stage but may become labile/progress to hypotension
Tachycardia common during acute withdrawal
Ego Integrity
Feelings of guilt/shame; defensiveness about drinking
Denial, rationalization
Reports of multiple stressors; problems with relationships
Multiple stressors/losses (relationships, employment, financial)
Use of substances to deal with life stressors, boredom, etc.
Elimination
Diarrhea
Bowel sounds varied (may reflect gastric complications [e.g., gastric hemorrhage])
Food/Fluid
Nausea/vomiting, food tolerance
Muscle wasting, dry/dull hair, swollen salivary glands, inflamed buccal cavity, capillary fragility (malnutrition)
Generalized tissue edema may be noted (protein deficiencies)
Gastric distension; ascites, liver enlargement (seen in cirrhosis)
Neurosensory
“Internal shakes”
Headache, dizziness, blurred vision, “blackouts”
Psychopathology such as paranoid schizophrenia, major depression (may indicate dual diagnosis)
Level of Consciousness/Orientation: Confusion, stupor, hyperactivity, distorted thought processes, slurred/incoherent speech
Memory loss/confabulation
Affect/Mood/Behavior: May be fearful, anxious, easily startled, inappropriate, silly, euphoric, irritable, physically/verbally abusive, depressed, and/or paranoid
Hallucinations: Visual, tactile, olfactory, and auditory (e.g., picking items out of air or responding verbally to unseen person/voices)
Nystagmus (associated with cranial nerve palsy)
Pupil constriction (may indicate CNS depression)
Arcus senilis, a ringlike opacity of the cornea (normal in aging populations, suggests alcohol-related changes in younger clients)
Fine motor tremors of face, tongue, and hands; seizure activity (commonly grand mal)
Gait unsteady/ataxia (may be due to thiamine deficiency or cerebellar degeneration [Wernicke’s encephalopathy])
Pain/Discomfort
May report constant upper abdominal pain and tenderness radiating to the back (pancreatic inflammation)
Respiration
History of tobacco use, recurrent/chronic respiratory problems
Tachypnea (hyperactive state of alcohol withdrawal)
Cheyne-Stokes respirations or respiratory depression
Breath Sounds: Diminished/adventitious sounds (suggests pulmonary complications [e.g., respiratory depression, pneumonia])
Safety
History of recurrent accidents, such as falls, fractures, lacerations, burns, blackouts, or automobile accidents
Skin: Flushed face/palms of hands, scars, ecchymotic areas, cigarette burns on fingers, spider nevi (impaired portal circulation); fissures at corners of mouth (vitamin deficiency)
Fractures, healed or new (signs of recent/recurrent trauma)
Temperature elevation (dehydration and sympathetic stimulation); flushing/diaphoresis (suggests presence of infection)
Suicidal ideation/attempts (some research suggests alcoholic suicide attempts are 30% higher than national average for general population)
Social Interactions
Frequent sick days off work/school, fighting with others, arrests (disorderly conduct, motor vehicle violations [DUIs])
Denial that alcohol intake has any significant effect on the present condition/situation
Dysfunctional family system of origin; problems in current relationships
Mood changes affecting interactions with others
Teaching/Learning
History of alcohol and/or other drug use/abuse (including tobacco)
Ignorance and/or denial of addiction to alcohol or inability to cut down or stop drinking despite repeated efforts
Large amount of alcohol consumed in last 24–48 hours, previous periods of abstinence/withdrawal
Previous hospitalizations for alcoholism/alcohol-related diseases (e.g., cirrhosis, esophageal varices)
Family history of alcoholism/substance use
DIAGNOSTIC STUDIES
Blood Alcohol/Drug Levels: Alcohol level may/may not be severely elevated depending on amount consumed and length of time between consumption and testing. In addition to alcohol, numerous controlled/illicit substances may be identified in a polydrug screen (e.g., amphetamine, cocaine, morphine, Percodan, Quaalude).
CBC: Decreased (Hb/Hct) may reflect such problems as iron-deficiency anemia or acute/chronic GI bleeding. White blood cell count may be increased with infection or decreased, if immunosuppressed.
Glucose: Hyperglycemia/hypoglycemia may be present, related to pancreatitis, malnutrition, or depletion of liver glycogen stores.
Electrolytes: Hypokalemia and hypomagnesemia are common.
Liver Function Tests: CPK, LDH, AST, ALT, and amylase may be elevated, reflecting liver or pancreatic damage.
Nutritional Tests: Albumin is low and total protein decreased. Vitamin deficiencies are usually present, reflecting malnutrition/malabsorption.
Other Screening Studies (e.g., Hepatitis, HIV, TB): Dependent on general condition, individual risk factors, and care setting.
Urinalysis: Infection may be identified; ketones may be present related to breakdown of fatty acids in malnutrition (pseudodiabetic condition).
Chest X-Ray: May reveal right lower lobe pneumonia (malnutrition, depressed immune system, aspiration) or chronic lung disorders associated with tobacco use.
ECG: Dysrhythmias, cardiomyopathies, and/or ischemia may be present owing to direct effect of alcohol on the cardiac muscle and/or conduction system, as well as effects of electrolyte imbalance.
Addiction Severity Index (ASI): An assessment tool that produces a “problem severity profile” of the client, including chemical, medical, psychological, legal, family/social, and employment/support aspects, indicating areas of treatment needs.
NURSING PRIORITIES
1. Maintain physiological stability during withdrawal phase.
2. Promote client safety.
3. Provide appropriate referral and follow-up.
4. Encourage/support SO involvement in Intervention (confrontation) process.
DISCHARGE GOALS
1. Homeostasis achieved.
2. Complications prevented/resolved.
3. Sobriety being maintained on a day-to-day basis.
4. Ongoing participation in a rehabilitation program/attendance at group therapy (e.g., Alcoholics Anonymous).
5. Plan in place to meet needs after discharge.
This plan of care is to be used in conjunction with CP: Substance Dependence/Abuse Rehabilitation.
NURSING DIAGNOSIS BREATHING PATTERN, risk for ineffective
Risk Factors May Include: Direct effect of alcohol toxicity on respiratory center and/or sedative drugs given to decrease alcohol withdrawal symptoms
Tracheobronchial obstruction
Presence of chronic respiratory problems, inflammatory process
Decreased energy/fatigue
Possibly Evidenced by: [Not applicable; presence of signs and symptoms establishes an actual diagnosis.]
Desired Outcomes Evaluation Criteria— Maintain effective respiratory pattern with
Client Will: respiratory rate within normal range, lungs clear, free of cyanosis and other signs/symptoms of hypoxia.
ACTIONS/INTERVENTIONS RATIONALE
Independent
Monitor respiratory rate/depth and pattern as Frequent assessment is important because toxicity indicated. Note periods of apnea, Cheyne-Stokes levels may change rapidly. Hyperventilation is respirations. common during acute withdrawal phase. Kussmaul respirations are sometimes present because of acidotic state associated with vomiting and malnutrition. However, marked respiratory depression can occur because of CNS depressant effects of alcohol. This may be compounded by drugs used to control alcohol withdrawal symptoms.
Elevate head of bed. Decreases possibility of aspiration; lowers diaphragm, enhancing lung inflation.
Encourage cough/deep breathing exercises and Facilitates lung expansion and mobilization of frequent position changes. secretions to reduce risk of atelectasis/pneumonia.
Auscultate breath sounds. Note presence of Client is at risk for atelectasis related to adventitious sounds (e.g., rhonchi, wheezes). hypoventilation and pneumonia. Right lower lobe pneumonia is common in alcohol-debilitated clients and is often due to aspiration. Chronic lung diseases are also common (e.g., emphysema, chronic bronchitis).
Have suction equipment, airway adjuncts available. Sedative effects of alcohol/drugs potentiate risk of aspiration, relaxation of oropharyngeal muscles, and respiratory depression, requiring intervention to prevent respiratory arrest.
Collaborative
Administer supplemental oxygen if necessary. Hypoxia may occur with CNS/respiratory depression.
Review chest x-rays, pulse oximetry as Monitors presence of secondary complications available/indicated. such as atelectasis/pneumonia; evaluates effectiveness of respiratory effort, identifies therapy needs.
NURSING DIAGNOSIS CARDIAC OUTPUT, risk for decreased
Risk Factors May Include: Direct effect of alcohol on the heart muscle
Altered systemic vascular resistance
Electrical alterations in rate, rhythm, conduction
Possibly Evidenced by: [Not applicable; presence of signs and symptoms establishes an actual diagnosis.]
Desired Outcomes/Evaluation Criteria— Display vital signs within client’s normal range;
Client Will: absence of/reduced frequency of dysrhythmias.
Demonstrate an increase in activity tolerance.
Verbalize understanding of the effect of alcohol on the heart.
ACTION/INTERVENTIONS RATIONALE
Independent
Monitor vital signs frequently during acute Hypertension frequently occurs in acute withdrawal. withdrawal phase. Extreme hyperexcitability accompanied by catecholamine release and increased peripheral vascular resistance raises BP (and heart rate). However, BP may become labile/progress to hypotension. Note: Client may have underlying cardiovascular disease that is compounded by substance withdrawal.
Monitor cardiac rate/rhythm. Document Long-term alcohol abuse may result in irregularities/dysrhythmias. cardiomyopathy/congestive heart failure. Tachycardia is common owing to sympathetic response to increased circulating catecholamines. Irregularities/dysrhythmias may develop with electrolyte shifts/imbalance. All of these may have an adverse effect on cardiac function/output.
Monitor body temperature. Elevation may occur because of sympathetic stimulation, dehydration, and/or infections, causing vasodilation and compromising venous return/cardiac output.
Monitor intake/output. Note 24-hour fluid balance. Preexisting dehydration, vomiting, fever, and diaphoresis may result in decreased circulating volume, which can compromise cardiovascular function. Note: Hydration is difficult to assess in the alcoholic because the usual indicators are not reliable, and overhydration is a risk in the presence of compromised cardiac function.
Be prepared for/assist in cardiopulmonary Causes of death during acute withdrawal stages resuscitation. include cardiac dysrhythmias, respiratory depression/arrest, oversedation, excessive psychomotor activity, severe dehydration or overhydration, and massive infections. Mortality for unrecognized/untreated delirium tremens (DTs) may be as high as 15%–25%.
Collaborative
Monitor laboratory studies (e.g., serum Electrolyte imbalance (e.g., potassium/electrolyte levels). magnesium) potentiates risk of cardiac dysrhythmias and CNS excitability.
Administer medications as indicated: e.g., clonidine Although the use of benzodiazepines is often (Catapres), atenolol (Tenormin); sufficient to control hypertension during initial withdrawal from alcohol, some clients may require more specific therapy. Note: Atenolol and other beta-adrenergic blockers may speed up the withdrawal process and eliminate tremors, as well as lower heart rate, BP, and body temperature, reducing the need for benzodiazepines.
Potassium. Corrects deficits that can result in life-threatening dysrhythmias.
NURSING DIAGNOSIS INJURY, risk for (specify)
Risk Factors May Include: Cessation of alcohol intake with varied autonomic nervous system responses to the suddenly altered state
Involuntary clonic/tonic muscle activity (convulsions)
Equilibrium/balancing difficulties, reduced muscle and hand/eye coordination
Possibly Evidenced by: [Not applicable; presence of signs and symptoms establishes an actual diagnosis.]
Desired Outcomes/Evaluation Criteria— Demonstrate absence of untoward effects of
Client Will: withdrawal.
Experience no physical injury.
ACTIONS/INTERVENTIONS RATIONALE
Independent
Identify stage of alcohol withdrawal, symptoms: Prompt recognition and intervention may halt Stage I is associated with signs/symptoms of progression of symptoms and enhance hyperactivity (e.g., tremors, sleeplessness, nausea/ recovery/improve prognosis. In addition, vomiting, diaphoresis, tachycardia, hypertension). recurrence/progression of symptoms indicates Stage II is manifested by increased hyperactivity need for changes in drug therapy/more intense plus hallucinations and/or seizure activity. treatment.Stage III symptoms include delirium tremens (DTs) and extreme autonomic hyperactivity with profound confusion, anxiety, insomnia, fever.
Monitor/document seizure activity. Maintain patent Grand mal seizures are most common and may be airway. Provide environmental safety (e.g., padded related to decreased magnesium levels, side rails, bed in low position). hypoglycemia, elevated blood alcohol, history of head trauma/preexisting seizure disorder. Note: In absence of previous history of other pathology causing seizure activity, seizures usually stop spontaneously, requiring only symptomatic treatment.
Check deep-tendon reflexes. Assess gait, if possible. Reflexes may be depressed, absent, or hyperactive. Peripheral neuropathies are common, especially in malnourished clients. Ataxia (gait disturbance) is associated with Wernicke’s syndrome (thiamine deficiency) and cerebellar degeneration.
Assist with ambulation and self-care Prevents falls with resultant injury.activities as needed.
Provide for environmental safety when indicated. May be required when equilibrium, hand/(Refer to ND: Sensory/Perceptual alteration eye coordination problems exist.[specify].)
Collaborative
Administer IV/PO fluids with caution, as indicated. Cautious replacement corrects dehydration and promotes renal clearance of toxins while reducing risk of overhydration.
Administer medications as indicated:
Benzodiazepines such as: chlordiazepoxide Commonly used to control neuronal hyperactivity (Librium), diazepam (Valium), clonazepam that occurs as alcohol is detoxified. IV/PO (Klonopin); administration is the route preferred, as intramuscular absorption is unpredictable. Muscle-relaxant qualities are particularly helpful to the client in controlling the “shakes,” trembling, and ataxic quality of movements. Clients may initially require large doses to achieve desired effect, and then the drug(s) may be tapered and discontinued, usually within 96 hours. Note: These agents must be used cautiously in clients with hepatic disease, as the agents are metabolized by the liver.
Oxazepam (Serax); Although less dramatic for control of withdrawal symptoms, this may be the drug of choice in a client with liver disease because of its shorter half-life.
Phenobarbital; Useful in suppressing withdrawal symptoms and is an effective anticonvulsant. Use must be monitored to prevent exacerbation of respiratory depression.
Magnesium sulfate; Reduces tremors and seizure activity by decreasing neuromuscular excitability.
Thiamine. Thiamine deficiency (common in alcohol abuse) may lead to neuritis, Wernicke’s syndrome, and/or Korsakoff’s psychosis.
Nursing Diagnosis Sensory/Perceptual alterations (specify)
May Be Related to: Chemical alteration: Exogenous (e.g., alcohol consumption/sudden cessation) and endogenous (e.g., electrolyte imbalance, elevated ammonia and BUN)
Sleep deprivation
Psychological stress (anxiety/fear)
Possibly Evidenced by: Disorientation in time, place, person, or situation
Changes in usual response to stimuli; exaggerated emotional responses, change in behavior
Bizarre thinking
Restlessness, irritability, apprehension
Desired Outcomes/Evaluation Criteria— Regain/maintain usual level of cognition.
Client Will: Report absence of auditory/visual hallucinations.
Identify external factors that affect sensory-perceptual abilities.
ACTIONS/INTERVENTIONS RATIONALE
Independent
Assess level of consciousness, ability to speak, Speech may be garbled, confused, or slurred. response to stimuli/commands. Response to commands may reveal inability to concentrate, impaired judgment, or muscle coordination deficits.
Observe behavioral responses (e.g., hyperactivity, Hyperactivity related to CNS disturbances may disorientation, confusion, sleeplessness, irritability). escalate rapidly. Sleeplessness is common because of loss of sedative effect gained from alcohol usually consumed prior to bedtime. Sleep deprivation may aggravate disorientation/ confusion. Progression of symptoms may indicate impending hallucinations (Stage II) or DTs (Stage III).
Note onset of hallucinations. Document as Auditory hallucinations are reported to be more auditory, visual, and/or tactile. frightening/threatening to client. Visual hallucinations occur more at night and often include insects, animals, or faces of friends/enemies. Clients are frequently observed picking the air; yelling may occur if client is calling for help from perceived threat (usually seen in Stage III).
Provide quiet environment. Speak in calm, Reduces external stimuli during hyperactive stage. quiet voice. Regulate lighting as indicated. Client may become more delirious when Turn off radio/TV during sleep. surroundings cannot be seen, although some respond better to quiet, darkened room.
Provide care by same personnel whenever possible. Promotes recognition of caregivers and a sense of consistency that may reduce fear.
Reorient frequently to person, place, time, and May reduce confusion/misinterpretation of surrounding environment as indicated. external stimuli.
Avoid bedside discussion about client or topics Client may hear and misinterpret conversation, unrelated to the client that do not include the client. which can aggravate hallucinations.
Provide environment safety (e.g., place bed in low Client may have distorted sense of reality, be position, leave doors in full open or closed position, fearful, or be suicidal, requiring protection from observe frequently, place call light/bell within reach, self-harm.remove articles that can harm client).
Collaborative
Provide seclusion, restraints as necessary. Clients with excessive psychomotor activity, severe hallucinations, violent behavior, and/or suicidal gestures may respond better to seclusion. Restraints are usually ineffective and add to client’s agitation but occasionally may be required for short periods to prevent self-harm.
Monitor laboratory studies (e.g., electrolytes, Changes in organ function may precipitate or magnesium levels, liver function studies, ammonia, potentiate sensory-perceptual deficits. Electrolyte BUN, glucose, ABGs). imbalance is common. Liver function is often impaired in the chronic alcoholic, and ammonia intoxication can occur if the liver is unable to convert ammonia to urea. Ketoacidosis is sometimes present without glycosuria; however, hyperglycemia or hypoglycemia may occur, suggesting pancreatitis or impaired gluconeogenesis in the liver. Hypoxemia and hypercarbia are common manifestations in chronic alcoholics who are also heavy smokers.
Administer medications as indicated, e.g.:
Antianxiety agents (Refer to ND: Anxiety [severe/ Reduces hyperactivity, promoting relaxation/panic]/Fear); sleep. Drugs that have little effect on dreaming may be desired to allow dream recovery (REM rebound) to occur, which has been suppressed by alcohol use.
Thiamine; vitamins C & B complex, multivitamins; Vitamins may be depleted because of insufficient Stresstabs. intake and malabsorption. Vitamin deficiency (especially thiamine) is associated with ataxia, loss of eye movement and pupillary response, palpitations, postural hypotension, and exertional dyspnea.
NURSING DIAGNOSIS NUTRITION: altered, less than body requirements
May Be Related to: Poor dietary intake (replaced by alcohol consumption)
Effects of alcohol on organs involved in digestion (e.g., stomach, pancreas, liver); interference with absorption and metabolism of nutrients and amino acids; and increased loss of vitamins in the urine
Possibly Evidenced by: Reports of inadequate food intake, altered taste sensation, lack of interest in food, abdominal pain
Body weight 20% or more under ideal
Pale conjunctiva and mucous membranes; sore, inflamed buccal cavity/cheilosis
Poor muscle tone, skin turgor
Hyperactive bowel sounds, diarrhea
Third spacing of circulating blood volume (e.g., edema of extremities, ascites)
Presence of neuropathies
Laboratory evidence of decreased red cell count (anemias), vitamin deficiencies, reduced serum albumin level, or electrolyte imbalance
Desired Outcomes/Evaluation Criteria— Verbalize understanding of effects of alcohol
Client Will: ingestion and reduced dietary intake on nutritional status and general well-being.
Demonstrate behaviors, lifestyle changes to regain/maintain appropriate weight.
Maintain stable weight or progressive weight gain toward goal with normalization of laboratory values and absence of signs of malnutrition.
ACTIONS/INTERVENTIONS RATIONALE
Independent
Evaluate presence/quality of bowel sounds. Note Irritation of gastric mucosa is common and may abdominal distension, tenderness. result in epigastric pain, nausea, and hyperactive bowel sounds. More serious effects of GI system may occur secondary to cirrhosis and hepatitis.
Note presence of nausea/vomiting, diarrhea. Nausea and vomiting are often among the first signs of alcohol withdrawal and may interfere with achieving adequate nutritional intake.
Assess ability to feed self. Tremors, altered mentation, or hallucinations may interfere with ingestion of nutrients and indicate need for assistance.
Provide small, easily digested, frequent meals/ May limit gastric distress and enhance intake and snacks, and advance as tolerated. toleration of nutrients. As appetite and ability to tolerate food increase, diet should be adjusted to provide the necessary calories and nutrition for cellular repair and restoration of energy.
Collaborative
Review laboratory tests (e.g., AST, ALT, LDH, Assesses liver function, adequacy of nutritional serum albumin/prealbumin, transferrin). intake; influences choice of diet and need for/ effectiveness of supplemental therapy.
Refer to dietitian/nutritional support team. Useful in establishing and coordinating individual nutritional regimen.
Provide diet high in protein with at least half of Stabilizes blood sugar, thereby reducing risk of calories obtained from carbohydrates. hypoglycemia, while providing for energy needs and cellular regeneration.
Administer medications as indicated, e.g.:
Antacids, antiemetics, antidiarrheal; Reduces gastric irritation and limits effects of sympathetic stimulation.
Vitamins, Replace losses. Note: All clients should receive thiamine. thiamine and vitamins, because deficiencies (clinical or subclinical) exist in most, if not all, clients with chronic alcoholism.
Institute/maintain NPO status as indicated. Provides gastrointestinal rest to reduce harmful effects of gastric/pancreatic stimulation in presence of GI bleeding or excessive vomiting.
NURSING DIAGNOSIS ANXIETY [severe/panic]/FEAR
May Be Related to: Cessation of alcohol intake/physiological withdrawal
Situational crisis (hospitalization)
Threat to self-concept, perceived threat of death
Possibly Evidenced by: Feelings of inadequacy, shame, self-disgust, and remorse
Increased helplessness/hopelessness with loss of control of own life
Increased tension, apprehension
Fear of unspecified consequences; identifying object of fear
Desired Outcomes/Evaluation Criteria— Verbalize reduction of fear and anxiety to an
Client Will: acceptable and manageable level.
Express sense of regaining some control of situation/life.
Demonstrate problem-solving skills and use resources effectively.
ACTIONS/INTERVENTIONS RATIONALE
Independent
Identify cause of anxiety, involving client in the Clients in acute phase of withdrawal may be process. Explain that alcohol withdrawal increases unable to identify and/or accept what is anxiety and uneasiness. Reassess level of anxiety happening. Anxiety may be physiologically or on an ongoing basis. environmentally caused. Continued alcohol toxicity will be manifested by increased anxiety and agitation as effects of medications wear off.
Develop a trusting relationship through frequent Provides client with a sense of humanness, helping contact, being honest and nonjudgmental. Project to decrease paranoia and distrust. Client will be an accepting attitude about alcoholism. able to detect biased or condescending attitude of caregivers.
Inform client what you plan to do and why. Include Enhances sense of trust, and explanation may client in planning process and provide choices increase cooperation/reduce anxiety. Provides when possible. sense of control over self in circumstances where loss of control is a significant factor. Note: Feelings of self-worth are intensified when one is treated as a worthwhile person.
Reorient frequently. (Refer to ND: Sensory/ Client may experience periods of confusion, Perceptual alterations [specify].) resulting in increased anxiety.
Collaborative
Administer medications as indicated, e.g.:
Benzodiazepines: chlordiazepoxide (Librium), Antianxiety agents are given during acute diazepam (Valium); withdrawal to help client relax, be less hyperactive, and feel more in control.
Barbiturates: phenobarbital, or possibly These drugs suppress alcohol withdrawal but secobarbital (Seconal), pentobarbital (Nembutal). need to be used with caution as they are respiratory depressants and REM sleep cycle inhibitors.
Arrange Intervention (confrontation) in controlled The process of Intervention, wherein SOs/family group setting. members, supported by staff, provide information about how the client’s drinking and behavior have affected each one of them, helps the client to acknowledge that drinking is a problem and has resulted in current situational crisis.
Provide consultation for referral to recovery/ Client is more likely to contract for treatment rehabilitation program for ongoing treatment as while still hurting and experiencing fear and soon as medically stable (e.g., oriented to reality). anxiety from last drinking episode. Motivation decreases as well-being increases and person again feels able to control the problem. Direct contact with available treatment resources provides realistic picture of help. Decreases time for client to “think about it”/change mind or restructure and strengthen denial systems.
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