A potentially lethal complication of various forms of cancer treatment, TLS occurs when large numbers of neoplastic cells are rapidly killed, resulting in the release of large amounts of potassium, phosphate, and uric acid into the systemic circula-tion. It is most commonly seen in patients with lymphoma, leukemia, or multiple metastatic conditions.19
Although most often associated with the use of chemo-therapeutic medications, biologic agents, and irradiation used in the treatment of malignant disorders, TLS can in rare instances occur spontaneously. The development of TLS has been linked to other pathophysiologic conditions such as elevated WBC counts, large tumors, multiple organ involve-ment by malignancy, and renal insufficiency.19
Pathophysiology
The primary mechanism involved in the development of TLS is the destruction of massive numbers of malignant cells by chemotherapy or radiation therapy (Figure 27-5). Massive skin integrity that indicate impaired tissue or organ
perfu-sion. Particular parameters to include are mental status, BUN and creatine levels, urine output, vital signs, hemodynamic values, cardiac rhythm, arterial blood gas and pulse oximetry values, skin breakdown, ecchymosis, or hematomas.18
The critical care nurse must recognize and support the patient’s vital physiologic functions. Administration of intra-venous fluids, blood products, and inotropic agents to provide adequate hemodynamic support and tissue oxygenation is essential in preventing or combating end-organ damage.
Close monitoring of vital signs, hemodynamic parameters, intake and output, and appropriate laboratory values assists the critical care nurse in administering and titrating appro-priate agents.18
Maintaining Surveillance for Complications
The critical care nurse needs to be vigilant for signs of life- threatening complications such as septicemia, acute myocar-dial infarction, priapism, ischemic stroke, and shock.14 If there are any significant concerns, these must be reported immediately. Other issues that may arise are dehydration, hypoxia, infection, skin and tissue viability, and decreased hemoglobin levels.
Educating the Patient and Family
Even though there is no cure for SCA, the focus of care is prevention. Early in the patient’s hospital stay, the patient and family should be taught about SCA, its etiologies, and treat- ment options available (Box 27-8). Patient and family educa-tion focuses on measures to help prevent painful reoccurring episodes. If the patient smokes, he or she should be encour-aged to stop smoking and be referred to a smoking cessation program. In addition, the importance of continuous medical follow-up should be stressed. While research continues to try to find a cure, nurses must continue to be sensitive to the effects of the disease on the patient and the family as well as the need to be culturally sensitive.20 Collaborative manage-ment of the patient with SCA is outlined in Box 27-9.
TUMOR LYSIS SYNDROME
of patients with TLS is most often caused by complications of renal failure or cardiac arrest.19-21
Hyperuricemia
Hyperuricemia occurs 48 to 72 hours after the initiation of anticancer therapy.19 Tumor cells undergo rapid growth destruction of cells releases large amounts of potassium,
phosphorus, and nucleic acids, leading to severe metabolic disturbances such as hyperuricemia, hyperkalemia, hyper-phosphatemia, and hypocalcemia (Table 27-4). Vomiting, diarrhea, and other insensible fluid losses from fever or tachy-pnea also contribute to these electrolyte disturbances.19 Death
FIG 27-5 Metabolic Abnormalities in Tumor Lysis Syndrome and Clinical Consequences.
AKI, Acute kidney injury. (From Abu-Alfa AK, Younes A. Tumor lysis syndrome and acute kidney injury: evaluation, prevention and management. Am J Kidney Dis. 2010;55[5 suppl 3]:S1.)
Malignant cell lysis
Release of intracellular contents
Potassium
Uric acid Phosphorus
Hyperuricemia Hyperphosphatemia
( calcium)
Crystal deposition
• Uric acid
• Calcium phosphate
Volume depletion Hypotension
Aggravating factors:
• Extrinsic urinary obstruction
• Tumor infiltration of kidney
• Chronic kidney disease
• Congestive heart failure
• Hypotension
• Nephrotoxic medications
• Radiocontrast agents
• Sepsis AKI
Oliguria Anuria Hyperkalemia
Hypocalcemia
Cardiac arrhythmia Cardiac arrest
Fluid overload
Respiratory failure
From Davidson MB, et al. Pathophysiology, clinical consequences, and treatment of tumor lysis syndrome. Am J Med. 2004; 116:546.
ELECTROLYTE PATHOPHYSIOLOGY CLINICAL CONSEQUENCE TREATMENT OPTIONS
Potassium Rapid expulsion of
intracellular K+ into the circulation due to cell lysis
Adverse skeletal and cardiac manifestations (e.g., ventricular dysrhythmias, weakness, paresthesias)
Insulin/glucose, sodium bicarbonate, inhaled beta-agonist, K+-binding resins, dialysis, calcium gluconate Phosphate Release of intracellular
PO4− due to cell lysis May be compounded
by renal dysfunction
Muscle cramps, tetany, dysrhythmias, seizures
Dialysis, phosphate binders
Calcium Precipitation of the
calcium phosphate complex because of the rapid increase in the phosphorous concentration
Muscle cramps, tetany, dysrhythmias, seizures, renal failure (acute nephrocalcinosis)
Calcium gluconate (Treatment should be reserved for those with neuromuscular irritability.)
Uric acid Cell lysis leads to
increased levels of purine nucleic acids into the circulation that are metabolized to uric acid.
Renal failure (uric acid nephropathy)
Hydration, dialysis, xanthine oxidase inhibitors, alkalization of urine, urate oxidase
TABLE 27-4 Electrolyte Abnormalities Encountered in Tumor Lysis Syndrome and Their Clinical Consequences
BUN, Blood urea nitrogen; Cr, creatinine; ECG, electrocardiogram;
PaCO2, partial pressure of carbon dioxide; ↑ increased;
↓ decreased.
DIAGNOSTIC
PARAMETER FINDINGS
Clinical Weight gain, edema, diarrhea, lethargy, muscle cramps, nausea and vomiting, paresthesia,
weakness, oliguria, uremia, seizures Laboratory ↑ Potassium, phosphorus, uric acid,
BUN, Cr
↓ Calcium, creatinine clearance, pH, bicarbonate, PaCO2
Diagnostic Positive Chvostek and Trousseau signs, hyperactive deep tendon reflexes, dysrhythmias, ECG changes
TABLE 27-5 Common Findings in Tumor Lysis Syndrome
and development, and large amounts of nucleic acids are present within them. When therapy is initiated, tumor cell destruction releases nucleic acids, which are metabolized into uric acid. Metabolic acidosis ensues, resulting in crystalliza-tion of the uric acid in the distal tubules of the kidney and leading to obstruction of urine flow. Glomerular filtration rates drop as the kidneys are unable to clear the increasing amounts of uric acid. Consequently, acute kidney injury eventually occurs.22 Acute kidney injury is discussed further in Chapter 20.
Hyperuricemia associated with TLS can be potentiated by several other factors, including elevated uric acid levels before the initiation of therapy. Other causes of increased uric acid production are elevated WBC counts, destruction of WBCs, and enlargement of the lymph nodes, spleen, or liver.19 Hyperkalemia
Hyperkalemia occurs within 6 to 72 hours after the initiation of chemotherapy. This is the most deleterious of all the mani-festations of TLS.19 In addition to the release of nucleic acids, tumor cell destruction also results in the release of potassium.
Renal insufficiency related to hyperuricemia prevents adequate excretion of potassium, and levels rise. The resultant hyperka- lemia may have a profound effect on intracellular and extracel-lular fluid levels.23 Left untreated, hyperkalemia can have devastating consequences, including cardiac arrest and death.19 Hyperphosphatemia and Hypocalcemia
Hyperphosphatemia and hypocalcemia occur 24 to 48 hours after the initiation of therapy.19 Phosphorus levels also rise as a consequence of tumor cell destruction. Calcium ions then bind with the excess phosphorus, creating calcium phosphate salts and bringing about hypocalcemia. These salts precipitate in the kidney tubules, worsening renal insufficiency. Hypo-calcemia causes tetany and cardiac dysrhythmias, which can result in cardiac arrest and death.22,23
Assessment and Diagnosis
Detection and recognition of TLS is accomplished through assessment of clinical manifestations, evaluation of labora- tory findings, and other diagnostic tests. Table 27-5 summa-rizes common findings in TLS.19,21
Clinical Manifestations
Clinical manifestations are related to the metabolic distur-bances associated with TLS.21 The patient’s history reveals an unexplained weight gain after initiation of chemotherapy or radiation therapy. The weight gain is associated with fluid retention due to electrolyte disturbances. Other early signs heralding the onset of TLS include diarrhea, lethargy, muscle cramps, nausea, vomiting, paresthesias, and weakness.20
Physical examination reveals positive Chvostek and Trous-seau signs related to hypocalcemia. Hyperactive deep tendon reflexes indicate hyperkalemia and hypocalcemia.21 Potas-sium and calcium disturbances result in changes that can be seen on the electrocardiogram (ECG), such as peaked or inverted T waves, altered QT intervals, widened QRS com-plexes, and dysrhythmias.19
Laboratory Findings
Laboratory findings demonstrate electrolyte disturbances such as elevated potassium and phosphorus levels and a
decreased calcium level. Uric acid levels are increased. Ele-vated levels of BUN and creatinine and a decreased creatinine clearance also indicate TLS. Metabolic acidosis is confirmed by the presence of decreased pH, bicarbonate levels, and partial pressure of carbon dioxide (PaCO2) on arterial blood gas measurements.20
Medical Management
Medical interventions are aimed at maintaining adequate hydration, treating metabolic imbalances, and preventing life-threatening complications (Table 27-4).20,23
Adequate Hydration
Administration of intravenous fluids may be necessary early in the course of treatment if inadequate hydration exists. The administration of isotonic saline (0.9% normal saline) reduces serum concentrations of uric acid, phosphate, and potas-sium.21 The use of nonthiazide diuretics to maintain adequate urine output may be required. If renal failure occurs, hemo-dialysis should be considered.21
Metabolic Imbalances
Electrolytes and arterial blood gases are closely monitored.
Dietary restrictions of potassium and phosphorus may be necessary. The goals in treating hyperuricemia are to inhibit uric acid formation and to increase renal clearance.23 This can be accomplished through the administration of sodium bicarbonate to increase the pH of the urine to above 7.0, which increases the solubility of uric acid, preventing subse-quent crystallization. Allopurinol administration can also inhibit uric acid formation.21
Life-Threatening Complications
If potassium levels rise dangerously, Kayexalate (sodium polystyrene sulfonate) may be given orally, or if the patient is unable to tolerate oral medications due to nausea and vomit-ing, rectal instillation may be used. If the patient is oliguric, glucose and insulin infusions may be given to facilitate lower-ing the potassium levels. A 10% solution of calcium gluconate may be administered to stabilize cardiac tissue membranes to
levels are disrupted. Insertion of a nasogastric tube is appro-priate if nausea or vomiting occurs. Dietary adjustments are necessary, such as potassium and phosphorus restrictions in the presence of elevated serum levels and providing addi-tional fiber to combat the constipation associated with the administration of antacids.24
Educating the Patient and Family
Education of the patient and family is a primary role of the critical care nurse. All treatments and interventions should be explained before carrying them out, and questions should be answered at a level understandable to the patient and family. Before discharge, potential risk factors and identifica- tion of early signs and symptoms should be reviewed. Col-laborative management of the patient with TLS is outlined in Box 27-11.
prevent life-threatening dysrhythmias.24 Phosphorus-binding antacids can be used for treating hyperphosphatemia. Stool softeners may be necessary to treat the constipation often associated with the administration of these antacids. Calcium gluconate may be required to replace calcium, but it should be used judiciously.19
Nursing Management
Nursing management of the patient with TLS incorporates a variety of nursing diagnoses (Box 27-10). Nursing priorities are directed toward 1) monitoring fluid and electrolytes, 2) providing comfort and emotional support, 3) maintaining surveillance for complications, and 4) initiating patient education.
Monitoring Fluid and Electrolytes
Assessment and continued monitoring of the patient is an important role of the critical care nurse when caring for the patient with TLS. Recognizing critical laboratory changes or development of symptoms and notifying the physician in a timely manner are essential. Insertion of a urinary catheter and maintenance of the intravenous line site are necessary to ensure adequate intake and output. Vital signs should be monitored frequently, and weight should be monitored daily.
Maintaining Surveillance for Complications
Nursing interventions are aimed at preventing complications.
Seizure precautions should be instituted, especially if calcium BOX 27-10 NURSING DIAGNOSES
• Excess Fluid Volume related to renal dysfunction, p. 590
• Decreased Cardiac Output related to alterations in contrac-tility, p. 580
• Anxiety related to threat to biologic, psychologic, and/or social integrity, p. 576
• Ineffective Coping related to a situational crisis and per-sonal vulnerability, p. 599
Tumor Lysis Syndrome
• Facilitate adequate renal function.
• Volume hydration with 0.9% normal saline
• Nonthiazide diuretics
• Treat hyperkalemia.
• Kayexalate
• Glucose and insulin
• Treat hyperuricemia.
• Sodium bicarbonate
• Allopurinol
• Treat hyperphosphatemia.
• Dietary restrictions
• Phosphorus-binding antacids
• Treat hypocalcemia.
• Calcium gluconate
• Maintain surveillance for complications.
• Acute kidney injury
• Cardiac dysrhythmias
• Provide comfort and emotional support.
BOX 27-11 COLLABORATIVE MANAGEMENT Tumor Lysis Syndrome
Brief Patient History
Mr. L is an otherwise healthy, 23-year-old African American man who presents with a week-long history of diarrhea, nausea, and vomiting after attending a barbecue last weekend.
Clinical Assessment
Mr. L is admitted to the critical care unit from the emergency department with hypotension, fever, and leukocytosis.
Diagnostic Procedures
His vital signs are as follows: blood pressure of 65/42 mm Hg, heart rate of 145 beats/min (sinus tachycardia), respiratory rate of 35 breaths/min, and temperature of 102.4° F. His white blood cell count is 25,000/mm3 with 15% bands, lactate level is 7 mmol/L, prothrombin time is 25 seconds, and platelet count is 22,000/mm3. Blood cultures reveal gram-negative bacilli.
Medical Diagnosis
Mr. L is diagnosed with severe sepsis and disseminated intra-vascular coagulation.
Questions
1. What major outcomes do you expect to achieve for this patient?
2. What problems or risks must be managed to achieve these outcomes?
3. What interventions must be initiated to monitor, prevent, manage, or eliminate the problems and risks identified?
4. What interventions should be initiated to promote optimal functioning, safety, and well-being of the patient?
5. What possible learning needs do you anticipate for this patient?
6. What cultural and age-related factors may have a bearing on the patient’s plan of care?
CASE STUDY Patient with Hematologic Disorders and Oncologic Emergencies
13. Linkins LA, et al: Treatment and prevention of heparin-induced thrombocytopenia: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed.: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines, Chest 141(2 Suppl):e495S, 2012.
14. De D: Acute nursing care and management of patients with sickle cell, Br J Nurs 17:818, 2012.
15. Pack-Mabien A, Haynes J Jr: A primary care provider’s guide to preventive and acute care management of adults and children with sickle cell disease, J Am Acad Nurse Pract 21:250, 2009.
16. Porter B, et al: Hematologic and immune problems. In Dunphy L, et al, editors: Primary care: the art and science of advanced practice nursing, ed 3, Philadelphia, 2011, FA Davis.
17. Addis G: Sickle cell disease, part 1: Understanding the condition, Br J Nurs 5:231, 2010.
18. Brown M: Managing the acutely ill adult with sickle cell disease, Br J Nurs 21:90, 2012.
19. Robison J: Metabolic emergencies: tumor lysis syndrome. In Newton S, et al, editors: Oncology nursing advisor: a
comprehensive guide to clinical practice, St. Louis, 2009, Mosby.
20. Tosi P, et al: Consensus conferences on the management of tumor lysis syndrome, Haemtologica 93:1877, 2008.
21. Behl D, et al: Oncologic emergencies, Crit Care Clin 26:181, 2010.
22. Shelton BK: Tumor lysis syndrome. In Chernecky CC, Murphy-Ende K, editors: Acute care oncology, ed 2, St. Louis, 2009, Mosby.
23. Abu-Alfa AK, Younes A: Tumor lysis syndrome and acute kidney injury: evaluation, prevention and management, Am J Kidney Dis 55(5 Suppl 3):S1, 2010.
24. Myers JS: Complications of cancer and cancer treatment. In Langhorne ME, et al, editors: Oncology nursing, ed 5, St. Louis, 2007, Mosby.
REFERENCES
1. Kitchens CS: Thrombocytopenia and thrombosis in disseminated intravascular coagulation (DIC), Hematology Am Soc Hematol Educ Program 2009:240, 2009.
2. Levi M, van der Poll T: Disseminated intravascular
coagulation: a review for the internist, Intern Emerg Med 8:23, 2013.
3. Rote NS, McCance KL: Structure and function of the hematologic system. In McCance KL, et al, editors:
Pathophysiology: the biologic basis for disease in adults and children, ed 7, St. Louis, 2014, Mosby.
4. Castoldi E, Hackeng TM: Regulation of coagulation by protein S, Curr Opin Hematol 15:529, 2008.
5. Gando S: Microvascular thrombosis and multiple organ dysfunction, Crit Care Med 38(Suppl 2):S35, 2010.
6. Blaisdell FW: Causes, prevention, and treatment of intravascular coagulation and disseminated intravascular coagulation, J Trauma Acute Care Surg 72:1719, 2012.
7. Furie B, Furie BC: Mechanisms of thrombus formation, N Engl J Med 359:938, 2008.
8. Shantsila E, et al: Heparin-induced thrombocytopenia.
A contemporary clinical approach to diagnosis and management, Chest 135:1651, 2009.
9. Marques MB: Thrombotic thrombocytopenic purpura and heparin-induced thrombocytopenia: two unique causes of life-threatening thrombocytopenia, Clin Lab Med 29:321, 2009.
10. Warkentin TE: Heparin-induced thrombocytopenia, Hematol Oncol Clin North Am 21:589, 2007.
11. Selleng K, et al: Heparin-induced thrombocytopenia in intensive care patients, Crit Care Med 35:1165, 2007.
12. Donavan JL, et al: An overview of heparin-induced thrombocytopenia, J Pharm Pract 23:226, 2010.
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A P P E N D I X
A
Nursing Management Plans of Care
ACTIVITY INTOLERANCE
Definition: Insufficient physiologic or psychologic energy to endure or complete required or desired daily activities.
Activity Intolerance Related to Cardiopulmonary Dysfunction Defining Characteristics
• Chest pain with activity
• Electrocardiographic changes with activity
• Heart rate is >15 beats/min above baseline with activity for patients on beta-blockers or calcium channel blockers.
• Heart rate remains elevated above baseline 5 minutes after activity.
• Breathlessness with activity
• SpO2 <92% with activity
• Postural hypotension when moving from supine to upright position
• Patient reports fatigue with activity.
Outcome Criteria
• Heart rate is <20 beats/min above baseline with activity and is <10 beats/min above baseline with activity for patients on beta-blockers or calcium channel blockers.
• Heart rate returns to baseline 5 minutes after activity.
• Chest pain with activity is absent.
• Patient reports tolerance to activity.
Nursing Interventions and Rationale
1. Encourage active or passive range-of-motion exercises while the patient is in bed to keep joints flexible and muscles stretched.
2. Teach patient to refrain from holding breath while performing exercises and to avoid the Valsalva maneuver.
3. Encourage performance of muscle-toning exercises at least three times daily, because a toned muscle uses less oxygen when performing work than an untoned muscle.
4. Progress ambulation to increase tolerance to activity.
5. Teach patient to take pulse to determine activity tolerance: Take pulse for a full minute before exercise and then for 10 seconds and multiply by 6 at exercise peak.
6. Consult with physician regarding the administration of fluids to ensure that the patient is hydrated to 24-hour fluid requirements per body surface area (BSA) to increase preload and thereby increase stroke volume and cardiac output.
Activity Intolerance Related to Prolonged Immobility or Deconditioning Defining Characteristics
• Decrease in systolic blood pressure is >20 mm Hg.
• Increase in heart rate is >20 beats/min with postural change.
• Syncope with postural change
• Patient reports lightheadedness with postural change.
Outcome Criteria
• Decrease in systolic blood pressure is <10 mm Hg.
• Increase in heart rate is <10 beats/min with postural change.
• Syncope or lightheadedness is absent with postural change.
• Absence of hypoxemia
• Patient reports tolerance to activity.
Nursing Interventions and Rationale
1. Collaborate with physician regarding patient’s activity level and the need for physical therapy to ensure patient’s safety.
2. Collaborate with physical therapist to develop progressive activity plan for patient to return to prior level of function.
For Patient on Bed Rest
1. Instruct the patient how to perform straight-leg raises, dorsiflexion or plantar flexion, and quadriceps-setting and gluteal-setting exercises to increase muscular and vascular tone.
2. Reposition patient incrementally to avoid syncope:
a. Head of bed to 45 degrees and hold until symptom free b. Head of bed to 90 degrees and hold until symptom free c. Dangle until symptom free
d. Stand until symptom free and ambulate For Patient on Ventilator
1. Collaborate with physician, respiratory care practitioner, and physical therapist regarding patient’s eligibility for early progressive mobility to ensure patient is ready and able to participate.
2. Initiate early progressive mobility program when patient is ready to limit the effects of prolonged immobility.
a. Elevation of the head of the bed b. Turn patient every 2 hours.
c. Perform passive range of motion at least 3 times/day.
d. Progress patient to active range of motion when ready.
e. Place bed in chair position to position patient in upright/
leg-down position.
f. Initiate bed mobility activities such as sitting on the edge of the bed (dangling).
g. Initiate transfer training.
h. Implement pre-gait activities such as standing at the side of the bed and marching in place.
i. Progress patient to ambulation.
3. Monitor patient’s response to activity and discontinue activity if patient shows signs of intolerance to ensure patient safety:
a. Hypoxemia b. Hypotension
c. Dysrhythmias or electrocardiographic changes
ACTIVITY INTOLERANCE—cont’d
ACUTE CONFUSION
Definition: Abrupt onset of reversible disturbances of consciousness, attention, cognition, and perception that develop over a short period of time.
Acute Confusion Related to Sensory Overload, Sensory Deprivation, and Sleep Pattern Disturbance Defining Characteristics
Early Symptoms
• Sudden onset of global cognitive function impairment (hours to days)
• Restlessness, agitation, and combative behavior
• Drowsiness (can lead to loss of consciousness)
• Slurring of speech, inappropriate statements or “word salad,” mumbling, or inappropriate gestures
• Short attention span (needs questions repeated); inability to learn new material
• Disordered sleep/wake cycle
• Disorientation to person, time, place, and situation
• Difficulty in separating dreams from reality (may experience bizarre dreams or nightmares)
• Anger at staff for continued questions about his or her orientation
Later Symptoms
• Symptoms that tend to fluctuate throughout the day and night
• Continuations of early symptoms, which may be more frequent or of longer duration
• Illusions
• Hallucinations
• Extreme agitation (e.g., attempts to climb out of bed, pull out catheters, rip off dressings)
• Calling out in loud voice, swearing, or attempting to bite or hit people who approach patient
Nursing Interventions and Rationale
1. Determine and document the patient’s dominant spoken language, his or her literacy, and the languages in which he or she is literate. Sometimes, people are not literate in their spoken language, or, less commonly, they are literate only in their second language.
2. Determine and document patient’s premorbid degree of orientation, cognitive capabilities, and any sensory/
perceptual deficits.
For Sensory Overload
1. Initiate each nurse/patient encounter by calling the patient by name and identifying yourself by name. This fosters
reality orientation and assists the patient in filtering irrelevant or impersonal conversation.
2. Assess the patient’s immediate physical environment from his or her viewpoint and explain equipment, its sounds, and its therapeutic purpose. Demonstrate audible and visual alarms and explain possible alarm conditions. This
decreases alienation of the patient from the technologic environment and reduces the inherent sense of fear and urgency accompanying alarm conditions.
3. Provide preparatory sensory information by explaining procedures in relation to the sensations the patient will experience, including duration of sensations. Preparatory sensory information enhances learning and lessens anticipatory anxiety.
4. Limit noise levels. Audible alarms cannot and must not be silenced, and many critical but noisy activities must take place in the critical care area. It has been shown, however, that noise levels produced by clinical
personnel exceed those levels designated as acceptable and are often greater than those generated by
technologic devices.
a. Keep staff conversations soft enough that they are inaudible to the patient whenever possible.
b. Assume that everything said at or around a patient’s bedside is intended for that patient’s awareness and that it will be interpreted as pertaining to him or her. As in the discussion that follows, conversations about the patient but not to him or her foster
depersonalization and delusions of reference.
c. Enforce nighttime noise limits.
5. Readjust alarm limits on physiologic monitoring devices as the patient’s condition changes (improves or deteriorates) to lessen unnecessary alarm states.
6. Consider use of headphones and digital music player with patient’s favorite and/or subliminal or classical music. This can effectively filter out assaultive noise of the critical care environment and supplant it with familiar, soothing sounds and rhythms.
7. Modify lighting. Day and night cycles need to be simulated with environmental lighting.
a. Never turn on overhead fluorescent lights abruptly without warning the patient, assisting him or her out of
Continued