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PULMONARY ISSUES IN SPINAL CORD INJURIES

Andrew Zadoff MD, FCCP Medical Director ICU and Respiratory Therapy, Shepherd Center Atlanta Pulmonary Associates . PULMONARY ISSUES IN SPINAL CORD INJURIES. Health Impact of Pulmonary Problems in SCI*. 80% of deaths in cervical injuries are 2 0 to pulmonary problems.

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PULMONARY ISSUES IN SPINAL CORD INJURIES

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  1. Andrew Zadoff MD, FCCP Medical Director ICU and Respiratory Therapy, Shepherd Center Atlanta Pulmonary Associates PULMONARY ISSUES IN SPINAL CORD INJURIES

  2. Health Impact of Pulmonary Problems in SCI* 80% of deaths in cervical injuries are 20 to pulmonary problems. 50% of these deaths are 20 to pneumonia. As expected, pre-existing lung disease, smoking history, level of SCI, and other nonpulmonary problems related to trauma contribute to respiratory complications. * J Spinal Cord Med.2007;30:309-18

  3. Financial Importance Respiratory complications are the most common cause of morbidity and mortality: an incidence of 36- 83%.1 Respiratory complications increase length of stay and cost. Mechanical ventilation, pneumonia, need for surgery, and the use of a tracheostomy explain nearly 60% of hospital costs.2 1. J Spinal Cord Med. 2007; 30: 309-18 2. Chest. 2002; 121: 1548-54

  4. PREVIEW ACUTE RESPIRATORY ISSUES PULMONARY PHYSIOLOGY VENTILATION AND VENTILATORS WEANING SECRETION CONTROL OTHER ICU ISSUES

  5. Clinical Problem #1 A 17 yo man suffered a C6 fracture dislocation a with resultant C5-6 ASIA A spinal injury after diving into a swimming pool. No LOC and he reports no sense of drowning – friends were at poolside. 2 days after injury mild LLL atelectasis is noted on AM CXR. He notes some dyspnea. ABG 7.38/ 41/ 65 on 2L N/C. Respiratory RX started. Day 3 routine AM CXR shows complete atelectasis on left side. ABG is about the same. What would you do about his respiratory status?

  6. PHYSIOLOGY AND LOSS OF FUNCTION Loss of function is predictable if extent of injury is known. Complications may be predictable and potential harm to the patient can be anticipated and prevented. Recovery of lung function may be predictable.

  7. ACUTE RESPIRATORY ISSUES Acute neurogenic pulmonary edema Hemodynamic instability, i.e., bradycardia, hypotension, hypothermia – spinal shock Unstable cervical spine/ risk of worsening neurologic injury Inspiratory difficulty, loss of respiratory musculature, flail physiology

  8. ACUTE RESPIRATORY ISSUES Aspiration risks Direct injury to the airway Secondary injury to the airway, i.e., ETT and tracheostomy complications, esophageal fistulae to the airway

  9. ACUTE RESPIRATORY ISSUES Loss of cough ability secondary to the loss of expiratory muscles Inability to generate high expiratory pressures secondary to ETT’s or trachs Pain, pain meds, and sedation issues Restrictive lung physiology Brain injuries, ability to follow commands

  10. PARASYMPATHETHIC TONE “Increased” tone with injuries above the T1 level Bronchoconstriction, narrowing of the airways Increased bronchial gland secretion Increased mucus production Increased viscosity of the mucus

  11. ACUTE RESPIRATORY ISSUES • For high injuries, ~40 – 60%* of patients will develop atelectasis usually in the left lower lung. • Pneumonia is common in acute spinal injuries. In the first 3 – 5 days, it will usually be typical community organisms: strep pneumonia, staph aureus, H. Influenza, Moraxella. After 5 days hospital acquired organisms will be more common. • Anaerobic infections will be < 15% of causes. *J Spinal Cord Med 2007;30:309 - 18

  12. LATE RESPIRATORY ISSUES* Restrictive lung physiology may limit cough and increase risk of pneumonia Sleep apnea-prevalence 22-62% Natural loss of lung function over time Pre- existing lung disease Blunted respiratory drive or reduced CO2 sensitivity * Resp Physiology and Neurobiology 166(2009):129-41

  13. PULMONARY PHYSIOLOGY

  14. Chest 1994

  15. PULMONARY NERVES AND MUSCLES - INSPIRATORY Diaphragm- the major respiratory muscle, 80% of quiet breathing, a smaller % for active breathing Works by descending, increasing negative inspiratory pressure, lateral expansion of the rib cage Controlled by cervical nerves C3, 4, and 5 (“ C3,4,5 keep the diaphragm alive”)

  16. PULMONARY NERVES AND MUSCLES - INSPIRATORY The intercostal muscles stabilize the chest wall and cause lateral expansion of the mid and upper rib cage. The intercostal muscles include internal (expiratory) and external (inspiratory) muscles. The thoracic spine innervates the intercostal muscles, T1-T7

  17. PULMONARY NERVES AND MUSCLES - INSPIRATORY The spinal accessory nerves, cranial nerve XI , innervates the accessory muscles of respiration, the scalene, sternocleidomastoid, and trapezius. These muscles pull up the upper chest “opposes” the diaphragm.

  18. Chest 1994

  19. PULMONARY - NERVES AND MUSCLES - EXPIRATORY The major cough muscles are the abdominal muscles (the rectus and transverse abdominis and external/internal obliques), the internal (expiratory) intercostals, and the clavicular portion of the pectoralis major (C5-7). Innervation of the abdominal m. is by the lower thoracic spine.

  20. Clinical Problem #2 A 27yo woman C4 complete injury (MVA) comes to your ICU intubated. CXR shows mild atelectasis at the bases. Past medical history discloses no medical or surgical history. What are your ventilator settings?

  21. Clinical Problem #3 A 27yo woman C4 complete injury (MVA) comes to your ICU intubated. CXR shows mild atelectasis at the bases. Past medical history discloses no medical or surgical history. 2 days later atelectasis is mildly more pronounced. ABG shows 7.43/38/65 on assist control rate 10, tidal volume 650, PEEP 5, Fi02 50. What are your ventilator orders now?

  22. VENTILATORS & VENTILATION

  23. Ventilation and the Airway Early tracheostomy if appropriate Monitor cuff pressures, ideally less than 20cm pressure Cuff leaks, assisted devices to allow speech

  24. VENTILATION High volume ventilation to prevent atelectasis but…. Keep peak airway pressure < 35cm H2O Anticipation of recovery: realism, defining target parameters such as vital capacity, minute ventilation, secretion control

  25. Time of Admission Initial evaluation and physical exam Vital capacity (Vc) and negative inspiratory force (NIF) ABG Routine cultures, if indicated EKG

  26. Time of Admission High volume ventilation, low PEEP Unplugging the airways: aggressive lavage usually with sodium bicarbonate, suctioning. Avoid in-line suction. If appropriate: quad or assist cough; inexsufflation; vibratory devices- vests, CPT; bronchoscopy; etc

  27. WEANING

  28. Weaning Parameters P1 Max - maximal inspiratory pressure Spontaneous breathing trials Respiratory protocols - therapist driven protocols

  29. WEANING PARAMETERS Tidal volume, vital capacity, minute ventilation, respiratory rate, negative inspiratory force, maximal inspiratory pressure CROP Index = (Cdyn X P I max X PaO2/ PAO2) / rate Rapid Shallow Breathing Index = frequency/ tidal volume in breaths/min/L

  30. WEANING PARAMETERS Tidal volume > 5cc/ kg Vital capacity > 10cc/ kg Minute ventilation < 10L / min or < 2X normal Respiratory rate < 30/ min CROP index > 13 Rapid shallow breathing index < 100

  31. WEANING At Shepherd Center, weaning is begun when vital capacity is approximately 8ml/kg and secretions are under control. Tracheostomy is usually safer and maintains airway control CPAP/PS trials are used rather than SIMV weaning Time is on our side

  32. SECRETION CONTROL High tidal volume ventilation Sodium bicarbonate, inhaled bronchodilators Turning modalities, tilt and turn beds Inexsufflation CPT vest Quad cough / assisted cough IPPB Intermittent percussive ventilation/ IPV

  33. INFECTIONS Minimize (optimize) antibiotic use Reduce antibiotic use to specific organism Hand washing, alcohol cleansers, isolation gowns, gloves, oral care The payoff- low incidence of C. difficile and ventilator associated pneumonias (VAP)

  34. LONG TERM ISSUES Identifying care providers prior to discharge, home and physician care For trach and home ventilator patients, family training, the “what if”s of problem solving, the “AMBU is your friend” speech Sleep study evaluation (polysomnography) if there is any question Appropriate vaccinations

  35. SHEPHERD DATA WEANING STATISTICS 2007, 2008

  36. Weaning at Shepherd Total vents 83 95 Home with vent 15(18%) 22(22%) C-1, C-2 3/7 3/12 -/27 C-3 4/6 2/6 8/21 C-4 22/25 22/27 23/24 Compiled by Wendy Fritz, RRT 2007 2008 Weaned/total weaned/total 2007/2008 Avg # days

  37. Weaning at Shepherd2007 2008 C-5 thru 7 22/25 24/26 16/13 T-1 thru 12 6/6 15/18 18/20 Rancho 1 thru 5 10/13 5/6 7/12 Age of non-weans 2007: 77, 34, 61, 46, 31, 35, 31, 19, 59, 58, 52 2007/2008 Weaned/Total Weaned/Total Avg # days

  38. OTHER MEDICAL ISSUES

  39. Hospital-acquired and Ventilator-associated Pneumonia 1, 2 VAP makes up 1/3 of total nosocomial infections in the ICU- the most common 10- 20% of pts ventilated >48hrs Mortality rate 10- 50%, a doubling of mortality rate, depending on population and organism Length of stay increases a mean of 6.1 d 1. Chest 2006; 130:597- 604 2. Am J Respir Crit Care Med 2005; 171:388- 416

  40. Hospital-acquired and Ventilator-associated Pneumonia Extra costs up to $40,000 per patient Early onset HAP/VAP less than 4 days usually represents community organisms, i.e., antibiotic sensitive Late onset HAP/VAP greater than 5 days usually composed of MDR organisms Health care related pneumonia- considered MDR unless otherwise proven

  41. Hospital-acquired and Ventilator-associated Pneumonia The usual organisms to be considered for empiric antibiotic: MRSA, Pseudomonas, Acinetobactor, other MDR organisms common to your facility. Decide if criteria are met for pneumonia: blood cultures, tracheal aspirate culture, abnormal CXR, worsening oxygenation, fever, elevated WBC’s.

  42. Hospital-acquired and Ventilator-associated Pneumonia Tracheal cultures can include endotracheal aspirate (106 cfu’s), BAL sample (104-105), blind mini-BAL(103), and protected brush(103). This can include quantitative or semi-quantitative colony counts. Surveillance cultures may not be helpful for antibiotic choice.1,2 Am J Respir Crit Care Med 2002;165:41-46 35% correct Chest 2005;127:589 83% correct

  43. MODIFIABLE RISK FACTORS for VAP Re-intubation; cuff pressure > 20cm; possibly oral vsnasotracheal; subglottic suctioning; watching for condensate in vent circuits; oral care Semirecumbent positioning 35-400 Enteral feeding is probably better than parenteral nutrition.

  44. MODIFIABLE RISK FACTORS for VAP Ulcer prophylaxis- The better the ulcer prophylaxis (higher pH), the higher the risk of VAP. The best agent for both protection is ____? Blood transfusion may increase risk. Tight glucose control may reduce risk. Sedation vacations and avoidance of paralytics may help.

  45. Hospital-acquired and Ventilator-associated Pneumonia - Antibiotics Know the common bacteria and best pick empiric antibiotic choice. Simplify antibiotics when cultures return. Don’t continue gorillacillin if you don’t need it. Most pneumonias will respond clinically in 5- 6 days; fever, WBC’s, etc, but X-ray resolution is much slower. Don’t use X-ray resolution as a criteria for stopping Ab’s

  46. Hospital-acquired and Ventilator-associated Pneumonia - Antibiotics • Duration of antibiotics- Place stop dates when starting drugs. It can be changed later if need be. • Antibiotics for 7-8 days with clinical response except Pseudomonas or Acinetobacter (~14d), or possibly MDR organism • Prolonged antibiotics are not associated with better outcomes but are associated with complication.

  47. Clostridium Difficile-Associated Diarrhea (CDAD) CDAD – 6% incremental increase risk of death among critically ill patients 1 Probably does not increase mortality rate in pts with prolonged ventilation >96h Increased length ~ 6 days 2 Total costs increased ~ $10,000 2 1 Chest 2007; 132: 418-24 2 Chest 2009; 136: 752- 8

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