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Hepatic Encephalopathy

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Hepatic Encephalopathy
Raven Dunn, SRN
Augusta Technical College
Adult Nursing II
RNSG 2210
Ms. Kandace Chariff, BSN, MSN
July 23, 2012

Table of Contents
Abstract Page 3
Case Study Etiology and Pathophysiology Page 4 Clinical Manifestations Page 5 Diagnostic Findings Page 7 Treatment and Nursing Interventions Page 7 Patient Presentation Page 8
Conclusion Page 9

References Page 10
Appendix I Page 11
Appendix II Page 11
Appendix III Page 12
Appendix IV Page 13
Appendix V Page 13
Appendix VI Page 16

This paper will focus on the clinical manifestations of hepatic encephalopathy and its effects on Mrs. X. She is a 64 year old female who has been an alcoholic for more than 40 years. The constant abuse of alcohol has left her with cirrhosis of the liver. One problem of cirrhosis is the inability of the liver to filter ammonia. When the levels of ammonia build up in the body, it affects various organs and systems. In Mrs. X’s case, it affected her brain. She manifested impaired cognitive abilities as well as physical limitations. This case study will expand on these processes as well as her prognosis and nursing implications.

Hepatic Encephalopathy
Mrs. X is a 64 year old white female and was a functional alcoholic and smoker for more than 40 years. She presented to the E.R. from home with complaints of lethargy, confusion, and decreased mobility. This paper will discuss the clinical manifestations of hepatic encephalopathy and the effects it has had and still do on Mrs. X’s mind, body, and soul. Mosby’s medical dictionary (2007) defines hepatic encephalopathy as:
A neuropsychiatric manifestation of extensive liver damage caused by chronic or acute liver disease. Either endogenous or exogenous waste toxic to the brain is not neutralized in the liver before being shunted back into the peripheral circulation of the blood, or substances required for cerebral function are not synthesized in the liver and therefore are not available to the brain. Commonly, ammonia, a by-product of protein metabolism that is toxic to the brain, is not converted to urea by the liver. The condition is characterized by variable consciousness, including lethargy, stupor, and coma; a tremor of the hands; personality change; memory loss; hyperreflexia; and hyperventilation. Respiratory alkalosis, mania convulsions, and death may occur. The outcome varies according to the pathogenesis of the condition and the treatment. (p. 804)
Etiology and Pathophysiology Despite the frequency with which hepatic encephalopathy occurs, the precise Pathophysiology is not fully defined (Feldman, Friedman & Brandt, 2006). Two major differences cause its development in acute and chronic liver disease. First hepatic insufficiency may result in encephalopathy because of the inability of the liver to detoxify toxic byproducts of metabolism. Second, portal-systemic shunting, in which collateral vessels develop as a result of portal hypertension, allows elements of the portal blood to enter the systemic circulation (Smeltzer, Bare, Hinkle, & Cheever, 2010, p. 1133). Ammonia is considered the major causative factor in the development of encephalopathy. It enters the brain and excites peripheral benzodiazepine-type receptors on astrocyte cells, thus increasing neurosteroid synthesis; this then stimulates gamma-aminobutyric acid (GABA) neurotransmission. GABA causes depression of the central nervous system (Hauser, Pardi, & Poterucha, 2006). Ammonia inhibits neurotransmission and synaptic regulation, producing sleep and behavior patterns indicative of hepatic encephalopathy. There are different causes of increased ammonia levels in the bloodstream. The largest cause is the digestion of dietary and blood protein in the gastrointestinal tract. Other things that can cause hepatic encephalopathy that are not related to ammonia levels are excessive dieresis, dehydration, infections, surgery, fever, and some medications. Serum ammonia is decreased by elimination of protein from the diet and by the administration of antibiotic agents, such as neomycin sulfate, which reduce the number of intestinal bacteria capable of converting urea to ammonia (Smeltzer et al., 2010, p. 1135).
Clinical Manifestations The earliest symptoms of hepatic encephalopathy include minor mental changes and motor disturbances. The patients may appear slightly confused and their sleep and mood patterns may change. The patient tends to sleep all day alternating with periods of insomnia at night. The patient will become difficult to arouse as the ammonia levels rise. Disorientation and confusion will continue to increase and eventually if left untreated hepatic encephalopathy will cause seizures, coma, and then death. As follows will be a table of the four stages of hepatic encephalopathy:
(Smeltzer et al., 2010, table 39-3) Stage 1 | Clinical Symptoms | Clinical Signs and EEG Changes | 1 | Normal level of consciousness with periods of lethargy and euphoria; reversal of day-night sleep patterns | Asterixis; impaired writing and ability to draw line figures. Normal EEG. | 2 | Increased drowsiness; disorientation; inappropriate behavior; mood swings; agitation | Asterixis; fetor hepaticus. Abnormal EEG with generalized slowing. | 3 | Stuporous; difficult to rouse; sleeps most of time; marked confusion; incoherent speech | Asterixis; increased deep tendon reflexes; rigidity of extremities. EEG markedly abnormal. | 4 | Comatose; may not respond to painful stimuli | Absence of asterixis; absence of deep tendon reflexes; flaccidity of extremities. EEG markedly abnormal. |
Assessment and Diagnostic Findings An electroencephalogram (EEG) will show generalized slowing, an increase in the amplitude of brain waves, and characteristic triphasic waves (Smeltzer et al., 2010, p. 1135). The survival rate after a first episode of overt hepatic encephalopathy in patients with cirrhosis is approximately 40% at 1 year. Patients should be referred for liver transplantation after this initial episode (Hauser et al., 2006).
Treatment and Nursing Interventions Medical management of hepatic encephalopathy focuses on identifying and eliminating the precipitating cause if possible, initiating ammonia-lowering therapy, minimizing potential medical complications of cirrhosis and depressed consciousness, and reversing the underlying liver disease, if possible (Smeltzer et al., 2010, p. 1135). Lactulose is administered via mouth, feeding tube, or rectally to reduce serum ammonia levels. It acts by several mechanisms that promote the excretion of ammonia in the stool: (1) ammonia is kept in the ionized state, resulting in a decrease in colon pH, reversing the normal passage of ammonia from the colon to the blood; (2) evacuation of the bowel takes place, which decreases the ammonia absorbed from the colon; and (3) the fecal flora are changed to organisms that do not produce ammonia from urea (Smeltzer et al., 2010, p. 1136). Two or three stools per day are preferred; this is indicative of positive results. Antibiotics such as Neomycin and Xifaxan have been used to reduce levels of ammonia-forming bacteria in the colon (Hauser et al., 2006). Other ways to manage hepatic encephalopathy are: assessing neurological checks frequently, monitoring fluid intake and output and body weight, monitoring of vital signs, checking serum ammonia levels every day, restrict protein intake, and discontinuation of medications that are filtered through the liver. The nurse should maintain a safe environment to prevent injury, bleeding, and infection. The nurse communicates with the patient’s family to inform them about the patient’s status and supports them by explaining the procedures and treatments that are part of the patient’s care (Smeltzer et al., 2010, p. 1136). The nurse is also responsible for teaching the patient self-care and continuing care.
Patient Presentation
Mrs. X was ambulating at home with assistance but upon admission into the facility, she could not stand. These symptoms occurred approximately over a few weeks marked by progressive weakness and confusion. The family attributed these findings to alcohol abuse. She was in the beginning stages of hepatic encephalopathy. The patient was living at home alone but her two daughters and granddaughter would alternate spending the night with her. While in the hospital, physical therapy was ordered and the patient required a two person assist just to stand. Mrs. X was alert and oriented to person, place, time, and situation. She could follow commands and her speech was clear and appropriate. She was unable to ambulate and perform ADLs without assistance at time of discharge so was referred to a skilled rehabilitation facility. She was nearsighted so she required glasses. She had a deficit in taste that was noted because she said food had no taste. She had plus two pitting edema to the lower extremities. Mrs. X had a potassium value of 2.3 mEq/L. According to Smeltzer et al. (2010), some manifestations of hypokalemia related to the heart are dysrhythmias. Mrs. X’s initial echocardiogram revealed an inverted T wave but upon discharge the rhythm was sinus. She had large bowel movements due to the lactulose prescribed. She had a foley catheter to bedside drainage due to decreased mobility and to monitor urine output more accurately due to decreased kidney.

Mrs. X chose to drink herself to near death. She has acquired cirrhosis of the liver after repeatedly counseled by health care professionals to cease. She has been pleaded with by her family members. She chose not to listen. Now she requires around the clock care and is a burden to her family with a disease that could have been avoided. Alcoholism is a real disease and can be treated but only if the individual wants help.

Ackley, B. J., & Ladwig, G. B. (2011). In NURSING DIAGNOSIS HANDBOOK: An Evidence-Based Guide to Planning Care (9th ed.). St. Louis, MO: Mosby Elsevier.
Anderson, D. M., Keith, J., Novak, P. D., & Elliot, M. A. (2007). Mosby’s medical, nursing, & allied health dictionary (6th ed.). St. Louis, MO: Elsevier
Deglin, J. H., Vallerand, A. H., & Sanoski, C. A. (2011). . In P. L. Cleary (Ed.), Davis’s drug guide for nurses (12th ed.). Philadelphia, PA: F.A. Davis Company.
Feldman, M., Friedman, L. S., & Brandt, L. J. (2006). Sleisenger and Fordtran’s gastrointestinal and liver disease: Pathophysiology, diagnosis, and management. Philadelphia, PA:
Hauser, S. C., Pardi, D. S., & Poterucha, J. J. (2006). Mayo Clinic gastroenterology and hepatology board review (2nd ed.). Rochester, MN: Mayo Foundation for Medical Education and Research.
Smeltzer, S. C., Bare, B. G., Hinkle, J. L., & Cheever, K. H. (2010). Assessment and management of patients with hepatic disorders. In Brunner & Suddarth’s textbook of medical-surgical nursing (12th ed., pp. 1133-1137). Philadelphia, PA: Lippincott Williams & Wilkins.
Venes, M.D., M.S.J., D. (2009). Taber’s CYCLOPEDIC MEDICAL DICTIONARY. In A. Biderman, B. G. Fenton, J. Patwell, A. D. Enright, E. Adler, & D. M. Posner (Eds.),

Appendix I
Expected vs. Actual: Client’s demographic data and past medical history Expected | Actual | Cirrhosis occurs with greatest frequency among people with alcoholism. | Patient has been an alcoholic for approximately 30-40 years. | Most patients with cirrhosis are between 40 and 60 years of age. | Mrs. X is 64 years of age. | Twice as many men as women are affected, although, women are at greater risk for development of alcohol-induced liver disease. | Mrs. X is a female diagnosed with cirrhosis. |

Appendix II
Expected vs. Actual: Clinical presentation and physical findings. Expected Presentation | Actual Presentation | The earliest symptoms of hepatic encephalopathy include minor mental changes and motor disturbances. | The chief complaint from the patient and family members was that she could not walk or write. Mrs. X also displayed some confusion that worsened with time. | The patient tends to sleep during the day and has restlessness and insomnia at night. | Mrs. X was sleep during the day and it was reported by the family that she did not sleep the night before. | Asterixis (flapping tremor of the hands) may be seen in stage II encephalopathy. | Mrs. X did not display this feature but did have weakness in hands. | Sometimes, fetor hepaticus, a sweet, slightly fecal odor to the breath that is presumed to be of intestinal origin, may be noticed. | Mrs. X did display this clinical manifestation. |

Appendix III
Expected pharmacotherapy vs. actual pharmacotherapy for a patient with pancreatitis. Expected Pharmacotherapy | Actual Pharmacotherapy | Lactulose is administered to reduce serum ammonia levels. | This medication was administered throughout hospital stay. Directions were 30 milliliters by mouth three times daily. | Intravenous administration of glucose to minimize protein breakdown. | This medication was not ordered. | Administration of vitamins to correct deficiencies. | Folic acid one milligram by mouth daily and thiamine 100 milligram by mouth once daily. | Correction of electrolyte imbalances (especially potassium). | Neutra-Phos by mouth three times daily, magnesium sulfate two grams intravenously over one hour times one dose, K-Dur 20 milliequivalent by mouth three times daily. | Antibiotics may be added such as Xifaxan which has been shown to reduce ammonia-forming bacteria levels. | Xifaxan 550 milligrams by mouth twice daily was ordered. |

Appendix IV
Expected lab values vs. actual lab values from a patient with hepatic encephalopathy. Expected laboratory values | Actual laboratory values | Ammonia is a byproduct of protein digestion by the liver. Excessive serum levels enter the brain and ultimately depress the central nervous system. Normal range is 15-45 mcg/dL | 55 mcg/dL (high) due to severe liver disease | Hemoglobin is an iron-containing protein which delivers oxygen to tissues.Normal range is 11.7-16.1 g/dL | 8.4 g/dL (low) due to cirrhosis of the liver | Hematocrit is the percentage of total blood volume consisting of RBCs.Normal range is 34%-46% | 24.6% (low) due to cirrhosis of the liver | Chloride is produced in the stomach, where it combines with hydrogen to form hydrochloric acid. Normal range is 97-107 mEq/L | 119 mEq/L (high) due to acute renal failure | Albumin is important for the maintenance of fluid balance within the vascular system.Normal range is 3.2-4.6 g/dL | 1.4 g/dL (low) due to liver disease | BUN stands for blood urea nitrogen which is the nitrogenous end product of protein metabolismNormal range is 8-21 mg/dL | 6 mg/dL (low) due to severe liver disease | Creatinine is an endogenous waste product of skeletal muscle that is filtered at the glomerulus, passed through the tubules with minimal change, and excreted in the urine.Normal range is 0.5-1.1 mg/dL | 0.4 mg/dL (low) due to liver disease | Potassium influences both skeletal and cardiac muscle activity.Normal range is 3.5-5.0 mEq/L | 2.3 mEq/L (low) due to alcoholism and nutritional deficits | Sodium has a major role in controlling water distribution throughout the body.Normal range is 135-145 mEq/dL | 121 mEq/L (low) due to hepatic failure |

Appendix V
Medication/Dose | Reason Prescribed | Side Effects | Nursing Interventions | Zoloft (sertraline)50 mg by mouth once daily | Depression | Neuroleptic malignant syndrome, suicidal thoughts, dizziness, drowsiness, fatigue, headache, insomnia, diarrhea, dry mouth, nausea, sexual dysfunction, increased sweating, serotonin syndrome | Assess for suicidal tendencies. Assess for serotonin syndrome. Monitor mood changes. | Duragesic (fentanyl) 100 mcg Apply one patch every 72 hours | Moderate to severe chronic pain | Confusion, sedation, weakness, anorexia, constipation, dry mouth, nausea, vomiting, sweating | Assess type, location, and intensity of pain before and 24 hours after application. Assess blood pressure, pulse, and respirations before and during administration. Assess bowel function routinely. | Megace (megesterol) 400 mg by mouth daily | Treatment of anorexia | Asymptomatic adrenal suppression (chronic therapy) | Assess for swelling, pain, or tenderness in legs. Monitor weight, appetite, and nutritional intake. | Ativan (lorazepam) 0.5 mg by mouth three times daily as needed | Anxiety disorder | Dizziness, drowsiness, lethargy, apnea, cardiac arrest | Assess geriatric patients carefully for CNS reactions. Assess degree and manifestations of anxiety and mental status. | Protonix (pantoprozale) 40 mg by mouth once daily | GERD | Headache, abdominal pain | Assess patient for epigastric or abdominal pain and for frank occult blood in stool, emesis, or gastric aspirate. | Levaquin (levofloxacin) 500 mg IV every 24 hours | Treatment of bacterial infection | Seizures, dizziness, headache, insomnia, arrhythmias, hepatotoxicity pseudomembranous colitis, diarrhea, nausea, anaphylaxis, Stevens-Johnson syndrome | Assess for infection. Obtain specimens for culture and sensitivity before initiating therapy. Observe for signs and symptoms of anaphylaxis. Monitor bowel function. | Folic acid1 mg by mouth once daily | Anemia | Rash, irritability, difficulty sleeping | Assess for signs of megaloblastic anemia.Monitor plasma folic acid levels, hemoglobin, hematocrit, and reticulocyte count before and during therapy | Thiamine 100 mg by mouth once daily | Dietary supplement in patients with alcoholism or cirrhosis | Vascular collapse, angioedema | Assess for signs and symptoms of thiamine deficiency. Assess nutritional status | Enulose (Lactulose) 20g/30ml by mouth three times daily | Adjunct in the management of hepatic encephalopathy | Belching, cramps, distention, flatulence | Adjust dose until patient averages 2-3 soft bowel movements per day.Mix with fruit juice, water, milk, or carbonated citrus beverage to improve flavor. | K-Dur(potassium chloride)20 mEq by mouth 3 times daily | Treatment of potassium depletion | Arrhythmias, abdominal pain, diarrhea, flatulence, nausea, vomiting | Assess for signs and symptoms of hypokalemia.Monitor serum potassium before and during therapy. | Xifaxan(rifaximin)550 mg by mouth twice daily | Help reduce reoccurrence of hepatic encephalopathy | Pseudomembranous colitis | Instruct to complete therapy. | Neutra-Phos(potassium and sodium phosphate)1 pack by mouth 3 times daily | Treatment of phosphate depletion | Arrhythmias, cardiac arrest, diarrhea | Assess for signs and symptoms of hypokalemia.Monitor serum phosphate, potassium, sodium, and calcium levels prior to and throughout therapy. | Magnesium sulfateInfuse 2 gm IV over 1 hour times one dose | Treatment of hypomagnesemia | Diarrhea | Monitor pulse, blood pressure, respirations, and ECG frequently throughout administration.Monitor neurologic status before and throughout therapy. | Toradol(ketorolac)15 mg/0.5ml IV every 6 hours as needed | Short-term management of pain (not to exceed 5 days total for all routes combined) | Drowsiness, GI bleeding, exfoliative dermatitis, Stevens Johnson syndrome, toxic epidermal necrolysis, anaphylaxis | Coadministration with opioid analgesics may have additive analgesic effects and may permit lower opioid doses.Administer undiluted. | Zofran(ondanestron)4mg/2ml IV every 12 hours as needed | Prevention of nausea and vomiting | Headache, constipation, diarrhea | Assess for EPS. |

(Anderson, Keith, Novak, & Elliot, 2005)

Appendix VI
Student: Shannon Miller Instructor: Kandace Chariff, RN, MN
Date: 06/06 /2012
Client Initials: X Age: 64 WT: 48.18 kg HT: 5ft 4 Allergies: NKDA

Medical Diagnosis/Research of Medical Diagnosis

Hepatic Encephalopathy
Mosby’s medical dictionary (2007) defines hepatic encephalopathy as: A neuropsychiatric manifestation of extensive liver damage caused by chronic or acute liver disease. Waste products are not the liver before being circulated back into the blood vessels. Substances required for cerebral function are not synthesized in the liver and are not available to the brain. Ammonia, a by-product of protein metabolism that is toxic to the brain, is not converted to urea by the liver. The condition is characterized by variable consciousness, including lethargy, stupor, and coma; a tremor of the hands; personality change; memory loss; hyperreflexia; and hyperventilation. Respiratory alkalosis, mania convulsions, and death may occur. Treatment includes cleansing enemas, low-protein diet, parenteral hydration with a balanced electrolyte solution, and specific treatment or the underlying cause. (p. 804).
Abnormal Labs Labs | Result | Reason | BUN | 6 mg/dL (low) | Severe liver disease | Creatinine | 0.4 mg/dL (low) | Liver disease | Potassium | 2.3 mEq/L (low) | Alcoholism | Chloride | 119 mEq/L (high) | Acute renal failure | Albumin | 1.4 g/dL (low) | Liver disease | WBC | 11.6 (high) | Leukocytosis | RBC | 2.49 (low) | Nutritional deficit | Hemoglobin | 8.4 g/dL (low) | cirrhosis | Hematocrit | 24.6 % (low) | cirrhosis | Ammonia | 55 g/dL (high) | Hepatic coma |

Surgical Procedures/Treatments
Patient has a history of a cholecystectomy, hysterectomy, and a cervical disk repair.
Reference Appendix V

Support Systems (family, friends, co-workers)
Patient resides with two daughters at different houses. They take turns caring for patient. Upon discharge from hospital, patient will go to skilled nursing home for rehabilitation.
Past Medical History:
Pt has a history of alcohol abuse, lupus, osteoarthritis, osteoporosis, and rheumatoid arthritis. Admitted to drinking and smoking for 30-40 years and quit both substances on 11/11/2011. Denies illicit drug use.

Head to Toe Assessment
VITAL SIGNS: 06/06/2012 Time | Vital Sign | Reading | Intervention if needed | 0800 | TemperatureBlood PressurePulseRespirationsOxygen SatPain level | 98.6° F102/52901898% room air8 (c/o generalized pain) | Toradol 15 mg IV given for pain level of 8. Patient also has Duragesic patch on right chest wall. | 0900 | Pain level reassessed | 3 | No intervention at this time. Pain level did decrease after administration of Toradol. | 1200 | TemperatureBlood PressurePulseRespirationsOxygen SatPain level | 98.7° F110/60881899% room air5 | Reassess vital signs at 1600. |

SKIN: Skin, was intact and cool to the touch. Patient had a 20 gauge peripheral IV in place in the right forearm with no redness, pain, or warmth to touch. Fair turgor. Reddened sacral area. Skin protectant applied. Nurse notified. Adult brief applied.
EENT (ears, eyes, nose and throat): Ears symmetrical in comparison. Hearing intact. No obvious deformities. Pupils reactive to light 3mm. No drainage from nares. Oral mucosa pink and moist. No sores. No swelling in neck.
LOC: (level of consciousness) Pt alert and oriented to person, place, time, and situation. Can follow commands. Speech clear and appropriate.
MUSCULOSKELETAL: Pt unable to ambulate. Limited ROM in upper extremities. Pt requires two person lift with assistance to get out of bed. Unable to stand. Cannot perform ADLs without assistance.
CARDIOVASCULAR: Regular heart rhythm noted. Bilateral radial/pedal pulses normal +2. Capillary response within 3 seconds. Pitting edema +2 to lower extremities.
PULMONARY: Breath sounds clear but diminished bilaterally, unlabored and regular. No secretions or cough. Oxygen via nasal cannula at 2L per minute as needed.
GASTROINTESTINAL: Abdomen soft and nontender. Nondistended. Bowel sounds active and heard in all 4 quadrants. Pt ate 75% of breakfast desired.
NUTRITION: Ate 75 % of breakfast and 25% of lunch. States has no appetite. On Megace for this issue.
GENITOURINARY: bladder nondistended. Foley catheter to bedside drainage. Secured and unclamped. Foley care done. No complaints.

Nursing Diagnosis/NANDA
Nursing Diagnosis/NANDA Definitions
1. Impaired skin integrity r/t physical immobilization AEB inability to move lower extremities (Ackley & Ladwig, 2011)
NOC Outcomes/Plan
The patient skin will regain integrity of skin surface during my shift.
NIC Interventions
1. Assess site of skin impairment and determine cause (Ackley & Ladwig, 2011).
2. Monitor site of skin impairment at least once a day for color changes, redness, swelling, warmth, pain, or other signs of infection. Determine whether the patient is experiencing changes in sensation or pain. Pay special attention to high-risk areas such as bony prominences, skinfolds, the sacrum, and heels (Ackley & Ladwig, 2011).
3. Implement a written treatment plan for topical treatment of the site of skin impairment (Ackley & Ladwig, 2011).

1. The cause of the wound must be determined before appropriate interventions can be implemented. This will provide the basis for additional testing and evaluation to start the assessment process (Ackley & Ladwig, 2011).
2. Systematic inspection can identify impending problems early (Ackley & Ladwig, 2011).
3. A written plan ensures consistency in care and documentation (Ackley & Ladwig, 2011).

Goals & Evaluations
1. Goal met. Pt had reddened sacral area. Protective skin barrier cream applied. Nurse notified. Affected area showed no increase of size at end of my shift.
2. Goal met. Pt has a Braden scale done on admission and has a plan implemented. Has geometric cushion for wheelchair and attends physical therapy five times a week to increase strength and mobility.
3. Goal unmet. Facility has scheduled days for showers but pt did wash perianal areas and face without assistance.
Nursing Diagnosis/NANDA Definitions
2. Risk for impaired oral mucous membranes: risk factors: altered nutrition, inadequate oral care (Ackley & Ladwig, 2011).
NOC Outcomes/Plan
Patient will maintain intact, moist oral mucous membranes that are free of ulceration, inflammation, infection, and debris during my shift (Ackley & Ladwig, 2011).
NIC Interventions A. Inspect the oral cavity at least once daily and note any discoloration, lesions, edema, bleeding, exudates, or dryness (Ackley & Ladwig, 2011). B. Encourage the patient to brush the teeth with a soft toothbrush using fluoride-containing toothpaste at least twice per day (Ackley & Ladwig, 2011). C. Encourage patient to floss once per day or use and interdental cleaner (Ackley & Ladwig, 2011).

Rationales A. Oral inspection can reveal signs of oral disease, symptoms of systemic disease, drug side effects, or trauma of the oral cavity (Ackley & Ladwig, 2011). B. A systematic review found that the toothbrush is the most important tool for oral care. Brushing the teeth is the most effective method for reducing plaque and controlling periodontal disease (Ackley & Ladwig, 2011). C. Floss is useful to remove plaque buildup between the teeth (Ackley & Ladwig, 2011).
Goals & Evaluations A. Goal met. No evidence of lesions, edema, bleeding, exudates, or dryness noted during my shift. B. Goal met. Assisted with brushing teeth during morning care. C. Goal not met. Floss not readily available in hospital.

Nursing Diagnosis/NANDA Definitions
3. High risk for injury related to altered level of consciousness (Ackley & Ladwig, 2011).

NOC Outcomes/Plan
Patient is reoriented to person, place, time, and situation during my shift (Ackley & Ladwig, 2011).
NIC Interventions A. Record vital signs at frequent intervals, depending on patient acuity (every 1-4 hours) (Ackley & Ladwig, 2011). B. Provide safe environment (pad side rails, remove obstacles in room, prevent falls) (Ackley & Ladwig, 2011). C. Be alert for symptoms of anxiety, epigastric fullness, weakness, and restlessness (Ackley & Ladwig, 2011).
A. Provides baseline and evidence of hypovolemia, and hemorrhagic shock (Ackley & Ladwig, 2011). B. Minimizes falls and injury if falls occur (Ackley & Ladwig, 2011). C. May indicate early signs of bleeding and shock (Ackley & Ladwig, 2011).
Goals & Evaluations A. Goal met. Vital signs assessed every 4 hours and within normal limits during my shift. B. Goal met. No fall during morning shift. C. Goal met. No signs of bleeding and shock noted during my shift.
Nursing Diagnosis/NANDA Definitions
4. Risk for a decrease in blood volume that may compromise health (Ackley & Ladwig, 2011).
NOC Outcomes/Plan
Explain actions can take if bleeding occurs during my shift (Ackley & Ladwig, 2011).
NIC Interventions A. Review client history for increased bleeding risk (Ackley & Ladwig, 2011). B. Monitor signs of bleeding in the urine, stool, sputum, and/or vomit. Watch for nosebleeds, any petechiae, purpura, or abnormal bruising (Ackley & Ladwig, 2011). C. Implement safety precautions, such as a falls prevention protocol for a client who has identified falls risk (i.e., history of falls) (Ackley & Ladwig, 2011).
A. Clients with or without a history of gastrointestinal bleeding may be at increased risk for bleeding if they take selective serotonin reuptake inhibitors (SSRIs) such as sertraline (Ackley & Ladwig, 2011). B. Disseminated intravascular coagulation (DIC) is a critical disease state that requires prompt action to avert death. It often results from a systemic infection. Specific signs include petechiae, cyanosis of fingers and nose, and oozing of blood from three unrelated sites. The underlying cause must be treated quickly, along with maintaining homeostasis (Ackley & Ladwig, 2011). C. On admission and as indicated, nurses should assess for falls risk factors that could increase the incidence of bleeding (Ackley & Ladwig, 2011).
Goals & Evaluations A. Goal met. Chart reviewed and patient continued on sertraline regimen. B. Goal met. No signs of bleeding from any orifice during my shift. C. Goal met. No slip socks applied to patient’s feet. Side rails up times three. Call light within reach throughout my shift.
Nursing Diagnosis/NANDA Definitions
5. Chronic confusion r/t chronic organic disorder with increased ammonia levels, substance abuse (Ackley & Ladwig, 2011)
NOC Outcomes/Plan
The patient will have minimal episodes of agitation.

NIC Interventions A. Gather information about the patient’s pre-admission cognitive functioning during initial assessment (Ackley & Ladwig, 2011). B. Assess the patient for signs of depression; insomnia, poor appetite, flat affect, and withdrawn behavior throughout my shift (Ackley & Ladwig, 2011). C. Determine patient’s normal routines and attempt to maintain them during initial assessment (Ackley & Ladwig, 2011).
A. Individuals with a history of cognitive dysfunction are at higher risk for acute confusion (Ackley & Ladwig, 2011). B. Up to 95% of individuals with dementia have some neuropsychiatric problems, with the most common being depression (Ackley & Ladwig, 2011). C. Activities that are designed to be consistent with past routines were effective at providing engagement and interest and enhancing quality of life (Ackley & Ladwig, 2011).
Goals & Evaluations A. Goal unmet. Patient not lucid at the time of interview and no family at bedside. B. Goal met. Patient mood flat at the start of shift. C. Goal unmet. No family at bedside to interview.
Nursing Diagnosis/NANDA Definitions
6. Fatigue r/t malnutrition AEB decreased appetite (Ackley & Ladwig, 2011).
NOC Outcomes/Plan
The patient will describe ways to assess and track patterns of fatigue (Ackley & Ladwig, 2011).

NIC Interventions A. Collaborate with the PCP regarding the appropriateness of referrals to physical therapy for carefully monitored aerobic exercise program and possible physical aids, such as a walker or cane (Ackley & Ladwig, 2011). B. Evaluate adequacy of nutrition and sleep hygiene (napping throughout the day, inability to fall asleep or stay asleep). Encourage the patient to get adequate rest, limit naps, use a routine sleep/wake schedule, avoid caffeine in the late afternoon or evening, and eat a well-balanced diet with at least eight glasses of water a day (Ackley & Ladwig, 2011). C. Collaborate with the primary care practitioner to identify physiological and/or psychological causes of fatigue that could be treated, such as anemia, pain, electrolyte imbalance (Ackley & Ladwig, 2011).
A. An exercise program may reduce fatigue and improve energy in patients. B. A commonly suggested treatment for fatigue is rest, although excessive sleep can aggravate fatigue (Ackley & Ladwig, 2011). C. If etiology for fatigue can be determined, the condition should be treated according to the underlying cause. Depression and anxiety have been significantly correlated with fatigue (Ackley & Ladwig, 2011).
Goals & Evaluations A. Goal met. Patient to be discharged to rehab facility. B. Goal met. No carbonated soft drinks have been supplied to patient during my shift. C. Goat met. Elevated ammonia levels are suspected cause of increased fatigue.

Nursing Diagnosis/NANDA Definitions
7. Risk for aspiration (Ackley & Ladwig, 2011).
NOC Outcomes/Plan
The patient will swallow and digest oral feeding without aspiration.
NIC Interventions A. Monitor respiratory rate, depth, and effort during initial assessment and during vital signs (Ackley & Ladwig, 2011). B. Auscultate lung sounds frequently and before and after feeding; note any new onset of crackles or wheezing (Ackley & Ladwig, 2011). C. Before initiating oral feeding, check patient’s gag reflex and ability to swallow by feeling the laryngeal prominence as the patient attempts to swallow (Ackley & Ladwig, 2011).
A. Signs of aspiration should be detected as soon as possible to prevent further aspiration and to initiate treatment that can be lifesaving (Ackley & Ladwig, 2011). B. Bronchial auscultation of lung sounds was shown to be specific in identifying patients at risk for aspirating (Ackley & Ladwig, 2011). C. A patient can aspirate even with an intact gag reflex (Ackley & Ladwig, 2011).
Goals & Evaluations A. Goal met. Respiratory function assessed every four hours during my shift. B. Goal met. Respiratory function assessed every four hours during my shift. C. Goal met. Gag reflex intact. Assessed before breakfast administered.

Nursing Diagnosis/NANDA Definitions
8. Impaired ability to perform or complete bathing/hygiene activities for self AEB inability to hold a spoon.
NOC Outcomes/Plan
The patient will remain free of body odor and maintain intact skin.
NIC Interventions A. Consider using a prepackaged bath, especially for high-risk clients to avoid patient exposure to pathogen from contaminated bath basin, water source, and release of skin flora into bath water (Ackley & Ladwig, 2011). B. Establish the goal of patient’s bathing as being a pleasant experience, especially for cognitively impaired patients (Ackley & Ladwig, 2011). C. Use patient-centered bathing interventions: plan for patient’s comfort and bathing preferences, show respect in communications, critically think to solve issues that arise, and use a gentle approach (Ackley & Ladwig, 2011).
A. Use of cleansing cloths avoids exposure to bath basins (which are bacterial reservoirs), contaminated tap water, cross-contamination from use of one cloth to bathe the entire body and contamination of sink and surrounding area from bath water disposal (Ackley & Ladwig, 2011). B. Sensations that make bathing pleasant should be used for everyone to avoid behaviors that are symptoms of unpleasant bathing, which are often due to pain (Ackley & Ladwig, 2011). C. Focusing on the patient rather than the task of bathing results in greater comfort and fewer aggressive (defensive) behaviors (Ackley & Ladwig, 2011).
Goals & Evaluations A. Goal met. Bath completed with morning care using prepackaged bath cloths. B. Goal met. Massage used during bath and patient remained calm throughout procedure. C. Goal met. Engaged patient in conversation to try to keep mind off the fact that she was being bathed.


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