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9/30/2017
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A CLINICAL CASE STUDY
MANJU DANIEL, PHD, MSN, APN, FNP-BCMA VANESSA MABAZZA, BSN, RN, CCRN, CNRN
NORTHERN ILLINOIS UNIVERSITY
Patient casePatient Information:Name: OCAge: 63Gender: Female
Chief Complaint:“Feeling terribly weak for the past 24 hours.”
History of present illness (HPI) Resident of skilled nursing facility Morbidly obeseMultiple chronic health conditions Staff found patient to be too sleepyDifficult for staff to wake her up for meals
and ADLS x 1 day Refused CPAP intermittently in last 48 hours
for C/O of suffocation Episodes of snoring, gasping, and apneaCh use of 02 at 2-3 L PRN (current 4 L, O2
sat- 86%)
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Past Medical History: COPD OSA Chronic respiratory failure Hypertension, CHF Anemia, Hyperlipidemia Chronic renal failure (baseline
creatinine 1.5) GERD
Past Surgical History:Total abdominal hysterectomy bilateral salphingo-oophorectomy (TAHBSO)
Other Pertinent History Social Tobacco: Former smoker. Alcohol and Illicit Drugs : No
Preventive: Up to date with vaccination Bed-bound uses bariatric bed Exercise: None
Allergies: NKDA
Current medications COPD:
Fluticasone Propionate 250mcg 1 puff inhale orally every 12 hours
Duoneb every 6 hours PRN Saline nasal spray solution 0.65%- 2 sprays in
both nostrils TID PRN CHF:
Furosemide 40mg dailyMetolazone 5mg daily
CHF/HTN: Metoprolol succinate 25mg daily
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Current medications Anemia:
Ferrous Sulfate TID; Folic Acid daily Vitamin B12 deficiency:
Monthly Cyanocobalamin 1000mcg/mL IM Hyperlipidemia:
Atorvastatin (Lipitor) 20mg daily Constipation:
Colace BID, Miralax Powder daily GERD:
Omeprazole 20 mg daily Other: CRF and D/T diuretics
Kcl 20meq daily
Review of SystemsGeneral:Fatigue, malaise, weak & sleepy
Respiratory: Dyspnea with minimal exertion 02 at 4L O2 via NC during the day CPAP mask at bedtime & during
daytime for naps
Review of Systems (cont.)Cardiovascular: bilateral pedal edema (legs felt
heavy)Musculoskeletal: Generalized weakness Limited ROM on bilateral lower
extremities due to obesity Bed-bound
Hematologic: reports anemiaGenitourinary: NocturiaOther body systems- No concerns
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Vital SignsBP:124/70; T: 97.6F; HR: 72; RR: 31O2 sat: 86% on 4L O2 via nasal
cannula Pain = denies
Height: 5 feet 2 inches (157 cm)Weight: 502 lbsBMI: 91.8 (obese)
Physical ExamGeneral Survey: morbidly obese,
normotensive, calm, appears drowsy and mildly short of breath when talking , on 4L oxygen via nasal cannula, A&O x 2 (name & place only)
Skin: pale pink, warm, normal turgor
Nails: nailbeds pale pink, capillary refill <2 seconds, no clubbing
Mouth: lips and oral mucosa moist and pale pink
Physical Exam (Cont.)Chest/Lungs:
Respirations regular, tachypnea, symmetrical chest expansion
Increased work of breathing with use of accessory muscles
Diminished at bases bilaterally
Vasculature: +1 bilateral pedal edema
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Physical Exam (cont.)Abdomen:obese but unremarkable
Musculoskeletal:BUE: good strength 5/5 BLE: 3/5 strength D/T increased habitus. BUE- ROM: no limitation BLE- ROM: mild limitation D/T increased
habitus Other body systems: unremarkable
DIFFERENTIAL DIAGNOSES?
LABS/DIAGNOSTICS?
Differential Diagnosis: Acute on Chronic Respiratory Failure
SUPPORT REFUTE
• Morbid obesity• H/O CHF (stable)• OSA• GERD• H/O chronic respiratory failure• Drowsiness, fatigue, & weakness• Home use of O2: 4LPM via NC• CPAP- intermittent refusal x 48h• hypoxia• Diminished bibasilar lung sounds• SOB • tachypnea• Dyspnea with exertion• A& O x 2 (name and place)
• (-) cough • (-) wheezing• (-) cyanosis• (-) tachycardia• (-) crackles
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Differential Diagnosis: Obesity Hypoventilation Syndrome
SUPPORT REFUTE
• Obesity• Sleep apnea• CPAP- intermittent refusal x 48 Hr• Tiredness• Fatigue• Sleepiness• Dyspnea with exertion• (+) snoring• (+) gasping during sleep• Nocturia• Confusion: A& O x 2 (name and place)• Signs of right-sided heart failure such as
BLE edema, tiredness
• (-) headache• (-) personality or
mood changes• (-) cyanosis
(Downey III et al., 2017)
Differential Diagnosis: Acute on Chronic Heart Failure
SUPPORT REFUTE
• Hypertension• Hyperlipidemia• H/O CHF• OSA• Fatigue• Weakness• Dyspnea with exertion• Nocturia• Bilateral pedal edema
• (-) change in appetite (usually decreased)
• (-) crackles • (-) JVD• (-) tachycardia• (-) anxiety
(Dumitru, Baker, Windle, & Ooi, 2016)
Differential Diagnosis: COPD Exacerbation
SUPPORT REFUTE
• Former smoker• GERD• H/O CHF• Fatigue• SOB with exertion• Home use of O2: 4LPM via
NC• CPAP • Dyspnea with exertion: use
of accessory muscles • tachypnea• Sedentary lifestyle
• (-) family history• (-) digital clubbing• (-) wheezing• (-) cough• (-) rhonchi
(Mosenifar et al., 2016)
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Differential Diagnosis: Community-Acquired Pneumonia (CAP)
SUPPORT REFUTE
• (+) Comorbid factors• confusion• (+) Dyspnea with
exertion• (+) Fatigue• Tachypnea• malaise• Skilled nursing facility
resident
(Baer et al., 20114)
• (-) cough • (-) fever• (-) sore throat• (-) rales• (-) change in appetite• (-) increase tactile
fremitus • (-) symptoms of
pneumonia/infection
Complete Blood Count (CBC)Component Resulted Value Standard Range
RBCs 3.4 4.2-5.4/CMMHgb 10.3 12-16 g/dLHct 33.2% 37-47%RBC indices
MCV 97.8 80-100 flMCH 30.2 27.0-34.0 pgMCHC 30.9% 32.0-36.0 g/dL (or 32%-36%)RDW 15% 11.3-14.8%
WBCNeutrophilsLymphocytesMonocytesEosinophilsBasophils
78007025520
5000-10,000/mm3 or 5-10 SI units55-70%20-40%
2-8%1-4%
0.5-1.0%
Reticulocyte Count
1% 0.5-2%
Platelet count 182 150,000-400,000/mm3 or 150-400 SI units
(Pagana, Pagana, & Pagana, 2015)
Comprehensive Metabolic Panel (CMP)Result Normal
Albumin 3.5 3.5 – 5 g/dL
Alkaline Phosphatase 61 30 – 120 units/L
Alanine Aminotransferase (ALT) 33 4 – 36 units/L
Aspartate Aminotransferase (AST) 18 0 – 35 units/L
Blood Urea Nitrogen (BUN) 45 10 – 20 mg/dL
Calcium (Ca) 9.5 9.0 – 10.5 mg/dL
Chloride (Cl) 92 98 – 106 mEq/L
Carbon Dioxide (CO2) 41 23 – 30 mEq/L
Creatinine 1.90 0.6 – 1.2 mg/L
(Pagana et al., 2015)
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CMP (cont.)Result Normal
Globulin 3.1 2 - 3.4 g/dL
Glucose 89 70 – 110 mg/dL
Potassium (K) 4.9 3.5 – 5.0 mEq/L
Sodium (Na) 143 136 – 145 mEq/L
Total Bilirubin 0.7 0.3 – 1.0 mg/dL
Total Protein 6.6 6.4 – 8.3 g/dL
eGFR 32 87 – 107 mL/min (female)
Anion Gap 10 8 – 16 mEq/L (if potassium is not used in
the calculation)(Pagana et al., 2015)
Brain Natriuretic Peptide (BNP) –Result: 2509 (< 100pg/mL)
Troponin I –Result: 0.016 (< 0.03 ng/mL)
Electrocardiogram (EKG) –Normal sinus rhythm, Rate 70, normal intervals2D Echo -
Result: enlarged RV & LV indicating mild diastolic dysfunction, EF = 50%, no wall motion abnormality
Chest X-ray –Mild cardiomegaly and pulmonary vascular congestion
Impression: Mild CHFU/A–Unremarkable
(Pagana et al., 2015)
Other labs
Arterial Blood Gas (ABG) –with BiPap FiO2 40%, inspiratory pressure 10.0/ expiratory pressure 5.0
pH = 7.30 (7.35-7.45)pCO2 = 83 (35-45 mmHg)pO2 = 126 (80-100 mmHg)HCO3 = 37 (21-28 mEq/L)O2 saturation = 98 (95%-100%)Base excess = 13.5 (-2.0– +2.0 mEq/L)Total hemoglobin = 9.9 (11.7-17.7 g/dL)Oxyhemoglobin = 96.9 (85%-100%)Carboxyhemoglobin = 2.2 (0.0–1.5%)Methemoglobin = 0.3 (0.0–1.5%)
(Pagana et al., 2015)
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Final Diagnosis:
Acute on Chronic Respiratory Failure
r/t
Obesity Hypoventilation Syndrome (OHS)
aka
Pickwickian Syndrome
Obesity Hypoventilation Syndrome (OHS) OHS is characterized by: Obesity (31% prevalence) Day time hypoventilation (difficulty getting rid of
carbon dioxide) OSADaytime symptoms:
Sleepiness Lack of energy Breathlessness
Nighttime symptoms: Loud and frequent snoring during sleep And/or breathing pauses
(Dabal and Bahammam, 2009)
OHS (cont.1) In this case, main contributing factors: Obesity Poorly managed OSA R/T Obesity Refusal to wear CPAP as recommended
OHS patients may have: Apnea and sleep hypoventilation with
hypercapnia
Although responsive but c/o dyspnea, fatigue, weakness, drowsiness, and confusion are indications that she was experiencing anAcute hypercapnic respiratory failure
(Dabal and Bahammam, 2009)
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OHS (cont.2)
Acute hypercapnic respiratory failure is further validated by:CMP result- elevated CO2ABG results- respiratory acidosis
Low pH Elevated pCO2 Elevated carboxy- hemoglobin levels
OHS (cont. 3)
Evidence: even transient reductions of ventilation in OSA can produce acute hypercapnia during the
period of low ventilation Evidence: OSA- not directly attributed to
underlying cardio-respiratory disease So less contributing existing conditions were: COPD H/O chronic respiratory failure
(Dabal and Bahammam, 2009)
(Kaynar et al., 2016; National Heart, Lung, and Blood Institute, 2011)
OHS- Respiratory Failure (cont. 3)
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Pathophysiology of OHS Etiology: Exact cause is not known, however
- No correct signals by brain for effective breathing- Fat-producing hormones resulting to ineffective breathing- Extra weight placed on chest makes breathing more difficult
Daytime hypoventilation leads to: Reduced sensitivity to rising levels of PaCO2 Leptin resistance Interaction between the two leads to OHS
Obesity puts extra mechanical load on respiratory system : Leading to its restriction and subsequent respiratory
failure(Dabal and Bahammam, 2009) (Kaynar et al., 2016; National Heart, Lung, and Blood Institute, 2011)
Pathophysiology of OHS Respiratory failure can:
Either result in reduced capacity for ventilation Or result from an increased demand for
ventilation Both
3 processes in respiration: Transfer of O2 across alveolus Transport of oxygen to tissues Removal of CO2 from blood into the alveolus to be
exhaled
(Dabal and Bahammam, 2009) (Kaynar et al., 2016; National Heart, Lung, and Blood Institute, 2011)
Hypoxemic (O2 failure) RF :• From V/Q mismatch and shunt
• These processes results to widening of the alveolar-arterial PO2 gradient
• VQ mismatch is the most common cause of hypoxemia
• Shunt is the persistence of hypoxemia despite 100% O2 inhalation.
Hypercapnic (ventilatory failure) RF: • When PaCO2 increases due to
decrease in ventilation > 4-6L/min.
(Kaynar et al., 2016; National Heart, Lung, and Blood Institute, 2011)
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OHS Management In this case- RF was mainly because of
hypoventilation (Obesity hypoventilation syndrome (OHS)
Hypercapnia Hypoxemia
Main treatment focus: A. Noninvasive ventilation (NIV)
positive pressure ventilation CPAP (continuous positive airway pressure) BIPAP (bi-level positive airway pressure)Properly fit mask: adequate effect
NIV recommended if: Resp. acidosis with arterial blood Ph <7.35 OR PaC02
> 45mm of Hg Persistent hypoxemia with supplemental 02
OHS Management B. Controlled oxygen therapy
Long-term administration of oxygen (> 15 hours per day) to patients with chronic respiratory failure increases survival in patients with severe resting hypoxemia
02 is recommended if with arterial hypoxemia (SP02 less than 88% or Pa02 <55 mmHg)
Target saturation of 88% to 92% in acute hypercapnic respiratory failure (nasal cannula or mask)
Titrate to keep it SP02 >90% with health provider being aware of changes
C. Weight loss management (a future intervention) Bariatric surgery such as gastric bypass
OHS management (Cont.)In this case, BiPap settings were changed to FiO2 35%, inspiratory pressure 12.0/ expiratory pressure 8.0.
Repeat ABGs were: pH = 7.38 (7.35-7.45) pCO2 = 71 (35-45 mmHg) pO2 = 77 (80-100 mmHg) HCO3 = 28 (21-28 mEq/L) O2 saturation = 96 (95%-100%) Base excess = 1.5 (-2.0–2.0 mEq/L) Total hemoglobin = 10.4 (11.7-17.7 g/dL) Oxyhemoglobin = 95.9 (85%-100%) Carboxyhemoglobin = 1.0 (0.0–1.5%) Methemoglobin = 0.3 (0.0–1.5%)
(Pagana et al., 2015)
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Other: GOLD 2017 Guidelines for COPD Classification Severity per airflow limitation (Spriometrically)
Gold 1 (Mild): FEV1 > 80% of predicted Gold 2 (Moderate): 50% < FEV1 <80% of predicted Gold 3 (Severe): 30% < FEV1 <50% of predicted Gold 4 (Very severe): FEV1 <30% of predicted
Modified British Medical Research Council (mMRC): per Dyspnea Grade 0: Breathless with strenuous exercise Grade 1: Breathless when hurrying or walking up a slight hill Grade 2: Breathless makes walk slower than same age
people or have to stop for breath when walking on own pace Grade 3: stop for breath when walking about 100 meters or
after a few minutes Grade 4: Too breathless to leave house, when dressing or
undressing
CAT Assessment: scale of 0-40 (based on cough, chest tightness, breathlessness, activity tolerance and sleep)
GOLD Guidelines: COPD Pharmacological Management
2017 Global Initiative for Chronic Obstructive Lung Disease, Inc
Class A- Bronchodilator, SABA PRN or on a regular basis (LABA preferred over SABA)Class B- LAMA or LABA and if Persistent symptoms- bothClass C- LAMA, if further Exacerbation- (LAMA & LABA) or
(LAMA & ICS) Class D-Same as C; if Persistent and exacerbation- triple: LAMA, LABA, & ICS); Further exacerbation: if FEV₁ < 50%-consider Roflumilast (dalirespt- PDE4 inhibitor); if smoker -consider macrolide2017 Global Initiative for Chronic Obstructive Lung Disease, Inc
GOLD Guidelines: COPD Management (Cont.) Bronchodilators
Beta agonists-SABA( Albuterol, Proair)LABA (Salmeterol, Formoterol, Olodaterol, Brovana)
LABA is preferred over SABA unless occasional dyspnea Maintenance therapy: switching to LABA
recommended SABA with SAMA- as initial bronchodilators to treat an
acute exacerbation; Combination superior compared to either medication alone
Anti-muscarinic drugs SAMA (Atrovent)- more in duoneb (atrovent and
albuterol) LAMA (Spiriva , Tudorza, Ellipta)- Mod, severe, very
severe Methyxanthine (Theophylline)- controversy about
exact effect and increased side effect profile
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GOLD 2017: Anti-inflammatory agents ICS Corticosteroids: In combination with LABA
Moderate, Severe, very severe COPD Advair (salmateorol & fluticasone) Symbicort (formoterol & budesonide)Improve lung function; Reduce exacerbation
Systemic corticosteroids: Oral Prednisone
Acute management of exacerbations of COPD
Not in chronic daily treatment in COPD Improve lung function (FEV1)Shorten recovery time Duration of therapy no more than 5-7 days
GOLD 2017: Anti-inflammatory agents (Cont.) Phosphodiesterase-4 (PDE4) inhibitors:
(Roflumilast or daliresp) Severe, very severe COPD & h/o
exacerbationsReduces moderate and severe exacerbations For maintenance along with ICS in
combination with LABA
Antibiotics – Macrolides (azithromycin and erythromycin)Regular use of macrolide antibiotics may
reduce exacerbation over one yearRisk of drug resistance Hearing impairment
GOLD 2017 Guidelines: COPD Management (Cont.) Oxygen Therapy
With severe chronic resting hypoxemia- long-term oxygen therapy is recommended (( sa02 <88% or Pa02 <55)
Titrate to keep it SP02 >90% Stable COPD with resting or exercise-induced moderate
desaturation, long-term oxygen should not be prescribed routinely
Non invasive ventilation CPAP/BIPAP In exacerbation of COPD COPD with severe chronic hypercapnia (our patient) COPD with acute respiratory failure
Interventional treatments Lung volume reduction Lung transplantation
Other: Pneumococcal vaccine AND manage GERD
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COPD Management for OC In her case of mild COPD- plan was to:Discontinue Fluticasone Inhaler
250mcg, 1 puff every 12 hours
Started Symbicort (formoterol & budesonide), 2 inhalations every 12 hours, according to GOLD Guidelines
To continue Duoneb every 6 hours PRN for shortness of breath
Management of other conditions: Problem: Acute on Chronic Heart Failure
Continue: Metolazone, increased furosemide to 40 mg BID (40 mg IV q 12h for 2 days), metoprolol
Problem: Acute on Chronic Renal Failure Patient voiding adequately H/o chronic renal failure with baseline creatinine of
1.5. Current elevated BUN at 45 and creatinine at 1.9. Nephro consult, goal to bring her creatinine back
to her baseline by increasing lasix to 40mg BID Discontinue KCL due to normal level & elevated
creatinine. Problem: Anemia
Iron deficiency- Continue TID Feso4 TID and daily folic acid
Vitamin B12 deficiency – continue monthly cyanocobalamin injections
Patient Education Avoiding risk factors for respiratory failure and COPD
exacerbation (tobacco cessation in smokers; avoid second hand smoke).
Early recognition and early treatment initiation to prevent complications of respiratory failure
Risks of O2 toxicity and CO2 narcosis Encourage use of incentive spirometer. Pulmonary rehab
helps decrease severity and improve quality of life. Routine physical activity - 150 min of moderate-intensity
aerobic activity per week
Proper technique for inhaler and proper mask fit Proper posture- e.g. sitting posture with a forward-leaning
Stress lifelong adherence to treatment plan Coping strategies, social support and counseling Prepare for emergencies (Kaynar et al., 2016; National Heart, Lung, and Blood Institute, 2011; Rafiq et al., 2015)
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Follow-Up To use an inter-disciplinary approach Follow-up with PCP RT management Consult with pulmonary specialist Consult with nephrologist for renal failure
management Consult with cardiologist for management of
CHF Consult PT and OT for rehabilitation. Serial lab tests for comparison and to see
improvement (CBC, BMP, BNP 2 days after IV lasix ). (Kaynar et al., 2016; National Heart, Lung, and Blood Institute, 2011)
References Agency for Healthcare Research and Quality. (2016). BTS/ICS guideline for
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American Thoracic Society.(2014). Obesity hypoventilation syndrome. American Respiratory Critical Care Journal,189, p15-p16.
Baer, S. L., Colombo, R. A., Vazquez, J. A., Talavera, F., Sanders, C. V., & Bronze, M. S. (2016). Community-acquired pneumonia (CAP). Retrieved from http://emedicine.medscape.com/article/234240-overview#showall
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Dumitru, I., Baker, M. M., Windle, M. L., & Ooi, H. H. (2016). Heart failure. Retrieved from http://emedicine.medscape.com/article/163062-overview#showall
References (cont.) Global Initiative for Chronic Obstructive Lung Disease, Inc.(2017). Pocket guide to COPD diagnosis,
management, and prevention: A guide for health care professionals. Retrieved from www.goldcopd.org
Healthy People 2020. (2017). Respiratory diseases. Retrieved from https://www.healthypeople.gov/2020/topics-objectives/topic/respiratory-diseases
Kaynar, A. M., Sharma, S., & Pinsky, M. R. (2016). Respiratory failure. Retrieved from http://emedicine.medscape.com/article/167981-overview#showall
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(2016). Chronic obstructive pulmonary disease (COPD). Retrieved from http://emedicine.medscape.com/article/297664-overview#showall
National Heart, Lung, and Blood Institute. (2011). What is respiratory failure? Retrieved from https://www.nhlbi.nih.gov/health/health-topics/topics/rf
Pagana, K. D., Pagana, T. J., & Pagana, T. N. (2015). Mosby’s diagnostic and laboratory test reference (12th ed.). St. Louis, MO: Mosby.
Rafiq, M., Proctor, A., McDermott, C., & Shaw, P. (2015). Screening for respiratory failure in ALS using clinical questioning, respiratory function tests and transcutaneous carbon dioxide: Which is the better tool? Journal of Neurology, Neurosurgery & Psychiatry, 86(11), e4.54. Retrieved from http://jnnp.bmj.com/content/86/11/e4.54
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