ED Management of Status Asthmaticus

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ED Management of Status Asthmaticus ED Management of Status Asthmaticus ELLIOT MELENDEZ, MD INTERIM CHAIR, DIVISION OF PEDIATRIC CRITICAL CARE JOHNS HOPKINS ALL CHILDREN’S HOSPITAL No conflicts of interest Or financial disclosures Objectives Epidemiology/Prevalence ED asthma mgmt ¡ Primary ED therapies ¡ Core thoughts in asthmatic respiratory failure ÷ Non-invasive ventilation ÷ Intubation and mechanical ventilation strategies Definition Status Asthmaticus ¡ wheezing that does not improve after initial doses of bronchodilators Pathophysiology Asthma is primarily an inflammatory disease Smooth muscle Airway spasm edema Mucous plugging Asthma: “A Public Health Issue” Everyday: ¡ 40,000 miss school or work ÷#1 cause of school absenteeism in children 5,000 go the ER Asthma: “A Public Health Issue” Everyday ¡ 1,000 are admitted ÷44% are children ÷3rd cause of admission in < 15yrs ÷Average LOS 3 days ¡ 11 people die Asthma in Children Most common chronic condition in children More common in children than in adults ¡ 7-10% vs. 3-5% ¡ 5 million asthma sufferers are < 18 years Risk Factors for Mortality Psychosocial risk factors ¡ Poor access to health care ¡ Denial of severity, noncompliance, psychiatric disorder, family dysfunction, low socioeconomic status Difficult to assess ¡ 39% of children in Australia had no identifiable preventable risk factor Historical Risk Factors for Fatal Asthma B-agonist overuse ¡ >2 MDI/mo Previous severe, unexpected, or rapid deterioration Attacks precipitated by food Prior intubation/ICU admission > 2 hosp in past year > 3 ED visits in past year Clinical Presentation Cough and wheezing Increased work of breathing ¡Tachypnea ¡Retractions Anxiety and Restlessness Hypoxia Viral prodrome/trigger Pulsus paradoxus Normal inspiratory drop in SBP is < 5 mmHg Pulsus Paradoxus = exaggeration of this response to > 10 mmHg ¡ Occurs in asthma due hyperinflation and greater negative intrathoracic pressures during inspiration Pulsus paradoxus may be absent in patients who are fatiguing and cannot generate large negative pleural pressures Life Threatening Asthma Signs of Impending Failure Significant distress with minimal or no wheezing ¡ “No air movement” Decreased of level of consciousness or agitation Inability to speak in full sentences Inability to lay down Central cyanosis, diaphoresis, inability to lie down Initial Management Beta agonist Steroids Oxygen, if hypoxic Inhaled Beta agonist Inhaled albuterol is the mainstay of asthma therapy ¡ Binds Beta-2 receptors in the smooth muscle of airways, leading to vasodilation ¡ Initially, 3 doses should be given with ipratropium Addition of Ipratropium Bromide to Albuterol Schuh et al. J of Peds, 1995 ¡ Reduced admission when used in most severe asthmatic children Qureshi et al. NEJM 1998 ¡ Prospective double blind trial ¡ 28.7% reduction in hospitalization in severe asthmatic children (52.6% vs. 37.5%) ¡ Ipratropium with 2nd and 3rd dose ¡ Number to treat to reduce 1 admission: 6.6 Corticosteroids Administer as soon as possible after 1st albuterol ¡ Onset of action in 2-4 hrs ¡ PO vs IV à no difference ÷ IV preferred in those with delayed gastric emptying, emesis, or in critically ill ¡ Any steroid is good! ÷ Just account for relative potency and duration of action Continuous Inhaled Albuterol Consider if wheezing/resp distress despite 3 albuterol/ipratropium nebs +/- magnesium ¡ Reduces hospitalization when compared to intermittent dosing in ED ÷ CA Camargo et al. The Cochrane Database of Systematic Reviews, 2003 IV Magnesium Sulfate When given with initial nebs in ED, reduces hospitalization ¡ Blocks Ca channel A meta-analysis of 5 studies showed favorable effect on reduction of hospitalization ¡ Cheuk et al, Arch Ds Child 2005 Can cause hypotension with rapid infusion ¡ Premedicate with NS 20 mL/kg When Inhaled Albuterol Fails Treat systemically Intramuscular beta-agonist (ie. terbutaline/epinephrine) ¡ Works within 5 minutes, terb peaks 30-60 min ¡ Consider IM epinephrine if potential for anaphylaxis ¡ Follow with inhaled albuterol Continuous IV terbutaline ¡ Titrated to work of breathing or wheezing IV Beta-agonist Decreased hospitalization and earlier discharge in children if given IV Salbutamol ¡ GJ Brown et al, Randomised trial of intravenous salbutamol in early management of acute severe asthma in children. The Lancet, 1997 Small study, randomization not even Side Effects of Beta Agonists Tachycardia à SVT Hypokalemia à prolonged QTc IV administration ¡ Systolic hypertension (beta 1) ¡ Diastolic hypotension (beta 2) Cardiac Toxicity of IV Beta-agonist Previous studies showed patients on IV terbutaline can have biomarkers consistent with myocardial injury Chiang VW, et al. Cardiac toxicity of intravenous terbutaline for the treatment of severe asthma in children: a prospective assessment. J of Pediatrics, 2000 ¡ Troponin elevated in 10% ¡ CK elevated in 62%, CK-MB elevated in 10%, none with elevations in troponin ¡ 20 (69%) with ECG changes consistent with ischemia Cardiac Toxicity Chiang et al. Troponin elevation occurred only in patients with > 72hrs on terbutaline AND mechanically ventilated 19/20 had EKG changes prior to terbutaline No clinically significant cardiac toxicity recognized Helium-Oxygen Heliox (70% helium, 30% oxygen) is well- established in alleviating respiratory distress from upper-airway obstruction Improves aerosol delivery ¡ Lowered density of gas reduces resistance during turbulent flow with more distal delivery of gases/meds Heliox Reduces turbulent flow thus ¡ Requires 60-80% mixture to be efficacious which limits its use in hypoxic patients No data that Heliox prevents intubation. ¡ Some consider use as a bridge as intubation equipment is being prepared Heliox in Asthma Carter et al. Chest 1996 ¡ 11 cases where Heliox used in mild to moderate asthma exacerbation – no benefit. Ho et al. Chest 2003. Meta-analysis ¡ Small improvement in PEFR % predicted in severe exacerbation when used early, but no difference after 1hr of therapy Rodrigo et al. 2003 Cochrane review ¡ No evidence to support use Heliox in Asthma Some consider use as a bridge as intubation equipment is being prepared or in hopes of preventing intubation Insufficient data that Heliox prevents intubation, improves length of stay, or mortality “The Critically Ill Asthmatic” “Just Intubate the patient!” Rates of Intubation in Asthma Roberts et al, Crit Care Med 2002; 30(3): 581-585 Intubating the Asthmatic No clear data on indications for intubation. ¡ Many studies have looked at clinical appearance/concern for “fatigue”. Avoid, if possible, unless clear respiratory failure or impending arrest, altered mental status Intubating the Asthmatic > 50% complications occur around intubation!!! Intubating the Asthmatic Complications Cardiac arrest ¡ Lung hyper-expansion limits cardiac output from poor filling Pulmonary leak syndromes due to air trapping ¡ Pneumothorax, pneumomediastinum, subcutaneous emphysema ¡ From airway obstruction or aggressive bag-ETT ventilation. Intubating the Asthmatic Complications Hypotension (multifactorial) ¡ Positive pressure decreases venous return ÷ Direct atrial compression ÷ Worsened hyperinflation due to insufficient time for exhalation ¡ Relative hypovolemia ¡ Beta 2 agonist effect on peripheral smooth muscle ¡ Augmentation with sedatives and muscle relaxation Intubating the Asthmatic Premedication Atropine/Glycopyrrolate ¡ To diminish secretions (especially if planning to use Ketamine) Lidocaine ¡ Reported in adult literature to all help smooth muscle relaxation ¡ No clinical data Intubating the Asthmatic Premedication IV Fluid Bolus prior to intubation ¡ To support intravascular volume Start Dopamine 3 mcg/kg/min or in-line ¡ To support cardiac output Intubating the Asthmatic Sedation/Analgesia Ketamine - recommended as sedative of choice ¡ Bronchodilatory effects as NE release ¡ The added benefit is questionable in the patient already on IV beta agonist ¡ Side Effects: Laryngospasm, secretions, tachycardia Intubating the Asthmatic Provide adequate sedation and analgesia pre- intubation ¡ Large changes in intrathoracic pressure can lead to leak syndromes Neuromuscular blocker of choice ¡ Avoid Cisatracurium and Atracurium – histamine release Once Intubated Avoid hyperventilation ¡ Ventilation strategy needs to take into account the prolonged expiratory phase needed for exhalation. ¡ Thus, low resp rate needed to allow time to exhale Ventilator Mgmt in Asthma PEEP 3-5 cmH20 to allow alveolar collapse/exhalation Tidal volumes 5-7 mL/kg Permissive hypercapnia ¡ Accepted at lower pH than in other lung diseases/ARDS ÷ pH as low as 7.15 okay. ÷ If pH < 7.15, treat with NaHCO3 or THAM Low RR to decrease hyperinflation and promote exhalation, typically 10-12 Why lower Respiratory Rate? Flow Curve Noninvasive Positive Pressure (NIPPV) Positive pressure: ¡ Keeps small airways patent, decreases bronchiolar collapse on exhalation ¡ Supports fatigued resp muscles Avoids complications associated with intubation ¡ Allows spontaneous breathing ¡ Preserves upper airway function, including cough and swallowing BiPAP in asthma Pre/Post Thill et al, PCCM 2004 AM = accessory muscle use W = wheezing score D = dyspnea score T = Total asthma score BiPAP in ED Asthma Williams et al, Intensive Care Medicine 2011 Continuous albuterol and placed in ED obs unit BiPAP initiated in addition to other therapies ¡ 64/71 kids were able to come off BiPap in ED and not get admitted to ICU ¡ Some able to come off terbutaline Summary
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