Basic Asthma Management (Coreem)

Definition: An episode of wheezing, chest tightness or coughing resulting from variable airflow obstruction that is reversible. Underlying exacerbations is a chronic inflammatory disorder of the airways.

Epidemiology:

• 1 million Americans suffer from asthma
• 75 million ED visits/year
• 456,000 hospitalizations in the US (Akinbami 2011)

Pathophysiology:

• Stimuli (allergen and non-allergen) induce bronchoconstriction
• Bronchoconstricting stimuli result in edema, inflammation, airway smooth muscle hypertrophy and mucous production.
• Long-term permanent structural airway remodeling can develop
• Airway inflammation limiting airflow is the common final pathway

Symptoms:

• Wheezing
• Cough
• Dyspnea
• Chest tightness
• Shortness of Breath

Physical Exam

• Wheezing
• Tachypnea
• Tachycardia
• Retractions
• Use of accessory respiratory muscles
• Speaking in short sentences

Immediate Management:

Basics: ABCs with a focus on breathing. Supplementary O2 typically not needed in mild to moderate exacerbations.

Inhaled Beta2 Agonist (i.e. albuterol)

• Mechanism: Stimulate beta2 receptors in lungs leading to bronchodilation
• Nebulized albuterol solution
  • Dose:5 mg every 10-20 min
  • Can be paired with an inhaled anticholinergic
• Albuterol metered-dose inhaler (MDI)
  • Equally effective to nebulized solution in mild exacerbations (Newman 2002, Cates 2013)
  • Dose: 6-12 puffs every 10-20 min
• Side effects: tachycardia (beta1 stimulation), tremors, lactic acidosis (Lewis 2014)

Inhaled Anticholinergic (i.e. Ipratropium)

• Mechanism: Override smooth muscle constriction and secretory consequences of parasympathetic nervous system. Block reflex bronchoconstriction.
• Dose: 0.5 mg every 10-20 min (up to 3 doses)
• Impact: In combination with beta2 agonist, may avoid hospitalization in up to 1 in 11 treated patients (Plotnick 1998).

Systemic Corticosteroids

• Mechanism: Inhibit recruitment of inflammatory cells and mediators.
• Route: Evidence suggests that oral and intravenous corticosteroids are equally efficacious in patients with mild to moderate asthma exacerbations
• Dose
  • Prednisone: 1 mg/kg (typically up to 60 mg) PO
  • Methylprednisolone sodium: 125 – 250 mg IV or IM
  • Dexamethasone: 10-20 mg PO
• Impact: Numerous studies have shown reductions in admission rates as a result of systemic corticosteroid use in the ED (Rowe 1992). The majority of patients presenting to an ED for asthma exacerbation should receive systemic steroids.

Magnesium 

• Mechanism: Bronchial smooth muscle relaxation
• Dose: 1-2 g over 30-60 min
• Impact: Modest decrease in hospital admission rate in patients refractory to standard management (Levy 2014)
• Reserved for moderate to severe exacerbations

Special Populations: Pregnancy

• Acute asthma exacerbations should be treated the same in pregnant patients as in nonpregnant patients.
• Fetal monitoring should be considered for patients with moderate to severe exacerbations in the 3rd

Diagnostics: Asthma is a clinical diagnosis and patients with mild to moderate exacerbations rarely need any testing in the ED. Diagnostic tests may be useful in patients with asthma that is refractory to standard management as detailed above or if an alternate cause of symptoms is suspected.

Pulmonary Function Tests (PFTs)

• Measure forced expiratory volume in 1 second (FEV1) or peak expiratory flow rate (PEFR)
• Most helpful when patient knows their baseline performance

Chest Radiography

• The majority of patients with asthma exacerbations that are typical for them do not need a chest X-ray performed.
• Consider X-ray in patients with more severe symptoms or those that do not resolve with standard treatment.

Lab Studies

• Rarely useful in mild to moderate (or even in severe) asthma exacerbations.
• Leukocytosis common as a result both of stress as well as steroid use
• Arterial Blood Gas
  • Do not correlate with clinical outcomes
  • Critical ABG data points (O2, CO2) can be obtained by other means (Pulse oximetry for O2, VBG for CO2)

Disposition

• Relapse after ED visits is common (up to 11% at 3 days) (Rosen’s 2014)
• Admission
  • Incomplete response based on overall clinical picture or PFTs (< 70% improvement)
  • Significant comorbidities
• Discharge
  • Airway inflammation continues after discharge and can take days to improve
  • Medications
    • Beta agonist inhaler (and demonstration of proper use). Consider giving all patients a spacer device as this improves drug delivery and thus efficacy.
    • Steroids
      • Short burst steroid treatment with prednisone for 5 days (no taper needed)
      • Dexamethasone – 2 doses on days 1 and 2 shown to be non-inferior to 5 days of prednisone in one small study (Kravitz 2011)
    • Follow-up
      • Patients should contact their physician in 3-5 days and have follow-up arranged in 1-2 weeks
      • Consider referral to an asthma specialist in patients with frequent exacerbations, frequent ED visits or frequent rescue inhaler use.

Take Home Points

• First line treatment for asthma exacerbations is inhaled beta agonists, inhaled anticholinergics and systemic corticosteroids.
• The majority of patients presenting to the ED with asthma exacerbations should be started on short-burst corticosteroids to control inflammation and prevent admission and relapse.
• Diagnostic testing is not required for the majority of patients with asthma exacerbations.

References:

1. Nowak RM, Tokarski GF: Asthma in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 73: p 941-58
2. Akinbami LJ et al. Asthma prevalence, health care use, and mortality: United States, 2005-2009. Natl Health Stat Report 2011; 32:1-14. Link
3. Newman KB et al. A comparison of albuterol administered by metered-dose inhaler and spacer with albuterol by nebulizer in adults presenting to an urban emergency department with acute asthma. Chest 2002; 121: 1036-41. PMID: 11948030
4. Cates CJ et al. Holding chambers (spacers) versus nebulisers for beta-agnonist treatment of acute asthma (Review). Cochrane Database Syst Rev 2013. PMID: 24037768
5. Lewis LM et al. Albuterol administration is commonly associated with increases in serum lactate in patients with asthma treated for acute exacerbations of asthma. Chest 2014; 145(1): 53-9. PMID: 23949578
6. Plotnick LH, Ducharme FM. Should inhaled anticholinergic be added to B2 agonists for treating acute childhood and adolescent asthma? A systematic review. BMJ 1998; 317: 971-7. PMID: 9765164
7. Rowe BH et al. Effectiveness of steroid therapy in acute exacerbations of asthma: a meta-analysis. Am J Emerg Med 1992; 10: 301-10 PMID: 1535500
8. Levy Z, Slesinger TL. Does intravenous magnesium reduce the need for hospital admission among adult patients with acute asthma exacerbations. Ann Emerg Med 2014. PMID: 25128007
9. Kravitz J et al. Two days of dexamethasone versus 5 days of prednisone in the treatment of acute asthma: a randomized controlled trial. Ann Emerg Med 2011; 58: 200-4. PMID: 21334098

This post was initially posted at coreem. Shared with permission. 

Life-Threatening Asthma (Coreem)

Background: Acute severe asthma or status asthmaticus refers to an episode of bronchoconstriction that is unresponsive to standard management. Patients with acute severe asthma will present with significant respiratory distress and it is critical to rapidly treat them to avoid significant morbidity and mortality. Patients will present with tachypnea, retractions, diaphoresis, ability to only speak 1-2 words at a time, abdominal breathing, cold extremeties. and wheezing (although the most severe may have a “quiet chest” indicating the absence of any significant air entry).

Immediate Management:

There are three main goals of immediate management of the severe asthma exacerbation:

1. Stave off intubation while your medications have time to act. Intubation is associated with increased morbidity and mortality.
2. Maximize pre-intubation parameters in case the patient doesn’t turn around and intubation is required.
3. Reverse bronchoconstriction to decrease work of breathing and prevent respiratory failure from exhaustion of respiratory muscles.

Basics: ABCs, IV, supplemental O2. Patient should be provided with all of the therapies used in mild to moderate asthma exacerbations but will require more aggressive management

Oxygenation + Respiratory Support

• Hypoxia only occurs late in a patient with a severe asthma exacerbation. Do not wait for hypoxia before supplying supplemental O2.
• Standard Nasal Cannula – Turn up to 15-20 L/min
• High-Flow Nasal Cannula (HFNC)
  • Allows for increased flow (40-60L/min of humidified O2 
  • May be difficult to administer nebulizer treatments via facemask does not fit over HFNC
• Non-Rebreather with Beta-Agnoist Reservoir
• Non-invasive Positive Pressure Ventilation (NIPPV)
  • Decreases work of breathing and improves gas exchange
  • The evidence demonstrating a benefit to NIPPV is limited but available studies do not show substantial adverse events (Pollack 1995, Soroksky 2003, Lim 2012). These studies did not include the sickest subset of patients with asthma
  • Bilevel Positive Airway Pressure (BPAP) preferred over Continuous Positive Airway Pressure (CPAP)
    • Difference in inspiratory (IPAP) and expiratory (EPAP) pressure aids in increasing tidal volume delivered
    • Start at IPAP 10 mm Hg, EPAP 5 mm Hg (or less) and titrate IPAP up (Typically no need to increase EPAP).

Intravenous Fluids

• Patients with severe asthma exacerbations have enormous insensible losses from increased respirations and work of breathing.
• Lung hyperinflation decreases pulmonary venous return, which can lead to hypotension. This is exacerbated by mechanical ventilation as the patient converts from negative pressure ventilation to positive pressure ventilation thus increasing intrathoracic pressure which can further decrease venous return.
• Aggressive IV fluids (30 cc/kg) should be given early to replete intravascular volume.

Epinephrine

• Epinephrine is a non-selective beta agonist that causes bronchodilation, vasoconstriction, increased cardiac contractility and increased heart rate
• Patients with severe asthma may have minimal benefit from inhaled beta agonists (i.e. albuterol) due to severe bronchoconstriction limiting delivery of medication to distal bronchioles.
• Intramuscular (IM) / Subcutaneous(SQ) Epinephrine
  • Dose: 300-500 mcg
  • Limited evidence demonstrates minimal significant side effects at this dose (Cydulka 1988)
• Intravenous (or Intraosseous) Epinephrine
  • More rapidly reaches target tissue than IM/SQ especially if patient hypotensive
  • Has effect of bronchodilation as well as vasoconstriction, which can reduce airway edema (Grandordy 1995)
  • Dose: 1 – 5 mcg/min and titrate to effect
  • Multiple retrospective studies demonstrate minimal adverse events with IV epinephrine (Smith 2003, Putland 2006)
• Contraindications: Epinephrine can theoretically cause uterine vasoconstriction and should be used with caution in pregnant patients.
• Terbutaline
  • Selective, parenteral beta 2 agonist that causes bronchodilation without effecting heart rate or cardiac output
  • Subcutaneous (SC) Terbutaline: 0.5 mg SC every 4 hours

Magnesium

• Mechanism: Bronchial smooth muscle relaxation
• Impact:
  • Modest decrease in hospital admission rate in patients refractory to standard management (Levy 2014). However, the sickest subset of patients were excluded from this study
  • The 3Mg trial (Goodacre 2013) demonstrated only a weak benefit to IV Magnesium in severe asthma however, this study did not include patients with life-threatening asthma.
  • In the absence of robust evidence, it is reasonable to administer magnesium to severe asthma exacerbations as there are minimal side effects of the drug and a potential for benefit
• Dose: The dose in severe asthma is not established. 2 g IV over 15 minutes is a reasonable first dose and this may be repeated

Heliox

• Mechanism: Improved laminar flow of inhaled has which may allow better airflow through the constricted airways; allows better gas exchange and transport of medications to flow down to distal airways and alveoli
• A mixture of helium and oxygen(multiple possible rations – 60:40, 70:30, 80:20). Only give the minimum FiO2 necessary to achieve goal O2saturation
• Evidence of utility limited but has not been extensively studied in the sickest subset of asthmatic patients and may still be beneficial in this group.
• Heliox may be used both via NIPPV and mechanical ventilator
• Limitation: If patient markedly hypoxic, may not give an adequate amount of FiO2.

Intubation

• Only about 2% of asthma exacerbations require intubation with 10-30% of those admitted to the ICU requiring invasive ventilation (Rosen’s 2014)
• Intubation is an inherently dangerous intervention in asthma because it does not fix the underlying problem (bronchoconstriction) and can cause dynamic hyperinflation (see below under ventilation), and rapid acidosis if respiration is not matched during RSI or post-intubation
• There is no specific vital sign, lab value or other diagnostic test result, which determines the necessity for intubation. The decision to intubate is based on a number of factors including the patients overall appearance, work of breathing, perceived ability to maintain their effort of breathing, mental status etc.
• Prior to intubation, be sure to maximize pre-oxygenation and intravascular volume
• Delayed Sequence Intubation (RSI)
  • Procedural sedation (with dissociative dose ketamine) for the procedure of pre-oxygenation
  • Useful in patients who have significant hypoxia/hypercarbia despite resuscitation and do not tolerate NIPPV to aid in pre-oxygenation
  • See the EMCrit website for full details on the procedure
• Rapid Sequence Intubation (RSI) Medications
  • There is no optimal set of agents for RSI in the severe asthmatic
  • Ketamine
    • Preferred agent because it is relatively hemodynamically stable and it has bronchodilatory properties.
    • Dose: 1-2 mg/kg
  • Paralytic
    • Common options are rocuronium and succinylcholine
    • Rocuronium offers the advantage of longer paralysis which avoids vent asynchrony early in management

Mechanical Ventilation

• Appropriate mechanical ventilation relies on ensuring that the patient has an adequate time to fully expire the delivered breath and avoid hyperinflation
• Permissive Hypercapnea: Decreasing respiratory rate and allowing PaCO2 to rise to supranormal levels.
  • This strategy avoids breath stacking which leads to hyperinflation
  • Hyperinflation leads to increased airway pressures and can lead the development of a tension pneumothorax
  • Hyperinflation can also lead to marked decrease in venous return leading to decreased cardiac output and cardiac arrest
  • Hyperinflation leads to increased pulmonary vascular resistance and right ventricular dysfunction
• Post-intubation meds (A full discussion of post-intubation care will appear in a future post)
  • Analgesia
    • Fentanyl (1-2ug/kg/hr) preferred over morphine or hydromorphone as it has minimal histamine effects
  • Sedation Options: Ketamine, propofol
  • Consider short-term paralysis if difficulty ventilating the patient
• Initial Ventilator Settings
  • RR: 6-10 breaths/min
  • VT: 6-8 ml/kg (ideal body weight
  • PEEP: 0-5 cm H2O
  • FiO2: Minimum necessary to maintain O2 sat > 93%
  • Inspiratory Flow Rate: (suggest 100-120 L/min)
• Check Plateau Pressures and maintain at < 30 mm Hg
  • Plateau pressure reflects the pressure experienced by alveoli
  • Maintaining Pplat < 30 mm Hg helps to avoid alveolar damage
  • If plateau pressure is > 30 mm Hg, consider lowering the RR and VT.

Mechanical ventilation does not fix the underlying bronchoconstriction. Be sure to continue maximal medical management.

Trouble Shooting the Ventilator

• Hemodynamic instability and hypoxia after intubation and mechanical ventilation are common and life-threatening. Rapid recognition of the underlying problem and treatment are critical
• DOPES Mnemonic – describes the most common causes of instability
  • Displacement of the endotracheal tube (ETT)
    • Direct visualization with laryngoscope preferred (US confirmation another option)
  • Obstruction of the endotracheal tube
    • Pass ETT suction catheter
  • Pneumothorax (tension)
    • Lung POCUS for lung sliding
    • Empiric needle decompression or finger thoracostomy
  • Equipment failure
    • Disconnect the vent and deliver manual BVM breaths
  • Stacked Breaths
    • Forcibly exhale patient (gently push down on anterior chest wall with two hands until no further exhalation detected)

Trouble Shooting – Severe Acidemia 

• A pH < 7.15 can lead to physiologic issues
• Check plateau pressure and if < 30 mm Hg, consider increasing ventilation (increase RR/TV)
• Invasive Treatment
  • Inhaled Anesthetics (i.e. sevoflourane)
  • Veno-Venous (VV) ECMO

Take Home Points

• Consider parenteral epinephrine in patients with severe asthma exacerbations as inhaled beta agonists are unlikely to penetrate into the distal airways.
• Intravenous epinephrine is life-saving and safe when used appropriately.
• Use NIPPV and high-flow nasal cannula to appropriately pre-oxygenate patients and avoid critical desaturations during intubation.
• Use a strategy of permissive hypercapnea for mechanical ventilation to avoid breath stacking, hyperinflation and high airway pressures. Aim for plateau pressures < 30 mm Hg.
• Use the DOPES mnemonic to troubleshoot hemodynamic instability after initiation of mechanical ventilation.

Read More:

EMCrit Podcast 15: The Severe Asthmatic

EMCrit Podcast 16: Coding Asthmatic, DOPES and Finger Thoracostomy

REBELCast: The Crashing Asthmatic

References:

Pollack CV et al. Treatment of acute bronchospasm with beta-adrenergic agonist aerosols delivered by a nasal bilevel positive airway pressure circuit. Ann Emerg Med 1995; 26(5): 552-7. PMID: 7486361

Soroksky A et al. A pilot prospective, randomized, placebo-controlled trial of bilevel positive airway pressure in acute asthmatic attack. Chest 2003; 123: 1018-25. PMID: 12684289

Lim WJ et al. Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane Database Syst Rev 2012. PMID: 23235608

Cydulka R et al. The use of epinephrine in the treatment of older adult asthmatics. Ann Emerg Med 1988; 17(4): 322-6. PMID: 3354935

Grandordy BM et al. The effect of intravenous phenylephrine on airway calibre in asthma. Eur Respir J. 1995;8:624-631. PMID: 7664864

Smith D et al. Intravenous epinephrine in life-threatening asthma. Ann Emerg Med 2003; 41(5): 706-711. PMID: 12712039

Putland M et al. Adverse events associated with the use of intravenous epinephrine in emergency department patients presenting with severe asthma. Ann Emerg Med 2006; 47(6): 559-564. PMID: 16713785

Levy Z, Slesinger TL. Does intravenous magnesium reduce the need for hospital admission among adult patients with acute asthma exacerbations. Ann Emerg Med 2014. PMID: 25128007

Goodacre S et al. Intravenous or nebulized magnesium sulphate versus standard therapy for severe acute asthma (3Mg trial): a double-blind, randomised controlled trial. Lancet Respir Med 2013; 1: 293-300. PMID: 24731521

Nowak RM, Tokarski GF: Asthma in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 73: p 941-58

This post was intially posted at coreem. Shared with permission. 

Acute Bronchiolitis

Bronchiolitis is a common LRTI in ≤2 years age group and it is also one of the the leading cause for hospitalization in infants. The most common bus associated with bronchiolitis is RSV (other possible agents are human metapneumovirus, adenovirus, influenza, rhinovirus, and parainfluenza viruses. Following an episode, cough may persist for up to 3 weeks. 

Pathophysiology
The viral infection in bronchiolitis causes inflammation of the lower respiratory tract leading to edema, necrosis, increased mucus production and bronchospasm eventually causing  air trapping, atelectasis, and hyperinflation of the lower airways and increased work of breathing. 

Symptoms
The peak of symptoms is often between the third and fifth day after onset

• Coughing. 
• Rhinorrhea, tachypnea
• Wheezing and Crackles 
• Use of accessory muscles and subcostal and intercostal retractions
• Nasal flaring
• Low grade fever 
• Irritability, cyanosis, and poor feeding
• Apnea in infants
• Dehydration due to increased insensible losses

Risk Factors for severe disease

• Chronic Lung Disease
• Age < 3moths
• Premature Birth
• Congenital Heart Disease
• Immunodeficiency 
• Neuromuscular Disorders

Diagnosis

• Bronchiolitis is a clinical diagnosis. 
• No lab tests are useful 
• Blood tests and CXR: indicated only if other diagnoses need to be excluded or in cases of severe disease (high O2 requirement)

Differential Diagnosis

• Asthma
• Pneumonia
• Foreign Body
• Cystic Fibrosis

Treatment 

• Oxygen Target oxygen saturation of >92%.
• Instillation of saline into the nares followed by suctioning
• Frequent and smaller feeds to prevent dehydration
• Caretakers should use frequent hand washing to minimise spread

Controversial Treatment Options:

• Bronchodilators do not offer any clear benefits and thus should not be given routinely.
• Inhaled epinephrine should be considered only in severe disease
• Steroids do not provide any benefit if used alone. However, current guidelines do advocate consideration for steroid use in combination with epinephrine in the treatment of bronchiolitis.
• Nebulized Hypertonic Saline: Mixed evidence and not recommended for routine use. It improve mucociliary clearance by loosening mucous plugs through osmotic draw of fluid from submucosal and adventitial spaces. 
• Ventilatory Support: Noninvasive ventilation may prevent intubation. 
• Heliox: Heliox does not affect the rates of intubation or mechanical ventilation or length of intensive care admission

Admit if:

• Risk Factors for severe disease
• Premature birth
• Persistent symptoms despite therapy
• Dehydration, 
• Spo2 <90% on room air)
• Episodes of apnea 

Take Home: 

• Bronchiolitis affects <2year age group and RSV is the most common bug.
• Supportive Care and Hydration is the key
• Most treatment modalities are controversial and thus are not recommend for routine use. Consider using in rapidly deteriorating

References and Further Reading:

1. Fernandes R, Bialy L, Vandermeer B, et al: Glucocorticoids for acute viral bronchiolitis in infants and young children. Cochrane Database Syst Rev 6: CD004878, 2013. [PMID:23733383]
2. Ralston SL, Lieberthal AS, Meissner HC, et al: Clinical practice guideline: the diagnosis, management, and prevention of bronchiolitis. Pediatrics 134: e1474, 2014. [PMID: 25349312]
3. http://pediatrics.aappublications.org/content/early/2014/10/21/peds.2014-2742
4. https://www.nice.org.uk/guidance/ng9/chapter/1-Recommendations#management-of-bronchiolitis 
5. http://pedemmorsels.com/bronchiolitis-seriously-what-should-i-do/

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

  

Salbutamol induced hyperlactaemia

Case

24/F with a history of Asthma presented to the ED complaining of shortness of breath that progressively got worse over the past couple of days in-spite-of increased use of inhalers. She has been intubated twice before due to asthma exacerbations. She never smoked and denied having any pets. 

In the ED, she received prednisone and multiple doses of albuterol nebulizations. Physical exam showed mild distress, BP 110/70, PR 110/min RR 28/min. She was able to talk in full sentences and was saturating 100% on 2 liters. Her best peak flow was reportedly 400, and she only did 150. She had bilaterally decreased air entry and significant expiratory wheezing. 

ABG on arrival showed a lactate level of 3 with a peak flow of 220. With treatment, in spite of an improvement in her peak flow to 300, she looked more tachypneic and lactate level increased to 5.5. Rest of the labs and CXR were normal.

Discussion

Salbutamol/ Albuterol is a β2 agonist used for bronchodilation in asthma. Salbutamol causes lactic acidosis by a combination of factors, but the exact etiology remains unclear. It is probably due to its metabolic effects. By creating a hyperadrenergic state it enhances glycogenolysis and gluconeogenesis, leading to more glucose, enhanced glycolysis, and pyruvate production. At the same time, enhanced lipolysis and increased free fatty acids inhibit pyruvate dehydrogenase enzyme, preventing pyruvate from entering the Krebs cycle. This causes pyruvate reduction to lactate.

Reports of lactic acidosis induced by high dose beta agonists used for tocolysis and bronchodilation have been described in obstetric and asthmatic patients. 

What are the types of Lactic Acidosis?

Type A Lactic Acidosis occurs when oxygen delivery to the tissues is compromised. 

Type B Lactic Acidosis occurs when either lactate production is increased or lactate removal is decreased without obvious oxygen delivery problems. It occurs due to increase in both endogenous and exogenous catecholamines. Enhanced β2 receptor activation leads to increased glycogenolysis, gluconeogenesis, lipolysis and ultimately to increased conversion of pyruvate to lactic acid. Concurrent corticosteroid use may enhance the beta receptor sensitivity further potentiating the lactic acidosis. 

Conditions associated with type B lactic acidosis include inborn errors of metabolism (pyruvate dehydrogenase deficiency), systemic disorders (liver failure), and medications (ethanol, metformin, and corticoids). It has also been postulated that endogenous (distress) or exogenous (drugs) adrenergic stimulation may be associated with increased conversion of pyruvate to lactate. 


What are the common blood gas findings in Acute Asthma?
The common metabolic disturbances seen during an acute attack are respiratory alkalosis, followed by respiratory acidosis as patients get tired of breathing.


What are the possible causes of lactic acidosis in Asthma?
1. Pulsus paradoxus and intrinsic PEEP decrease cardiac output and venous return
2. Production of lactate by overworked respiratory muscles
3. Hyperadrenergic State (Beta 2 agonist-induced)


Why is it important for us to know about this?

Albuterol induced lactic acidosis creates a paradoxical situation where there is enhanced bronchodilation but worsening tachypnea as a result of compensation for metabolic acidosis. Acidosis results in hyperventilation which could be mistaken for poor response to treatment. Physicians might misinterpret this situation as worsening respiratory failure and give more albuterol, creating a vicious cycle and ultimately leading to respiratory failure. 

Serial peak flow measurements and examination is the ideal way to identify this situation.

Take Home:
While treating asthmatic patients for severe bronchospasm, when lungs sound clear following treatment but tachypnea persists, suspect albuterol-induced hyperlactatemia. 


References:

1. Dodda, Venkata R., and Peter Spiro. "Can albuterol be blamed for lactic acidosis?." Respiratory care 57.12 (2012): 2115-2118.
2. Stratakos G, Kalomenidis J, Routsi C, Papiris S, Roussos C. Transient lactic acidosis as a side effect of inhaled salbutamol. Chest. 2002 Jul;122(1):385-6
3. Stratakos G, Kalomenidis J, Routsi C, Papiris S, Roussos C: Transient lactic acidosis as a side effect of inhaled salbutamol. Chest 2002; 122: 385–6Stratakos, G Kalomenidis, J Routsi, C Papiris, S Roussos, C 
4. Prakash S, Mehta S: Lactic acidosis in asthma: Report of two cases and review of the literature. Can Respir J 2002; 9: 203–8Prakash, S Mehta, S 

Author:

              

     Lakshay Chanana

     @EMDidactic