Aspiration Pneumonia and Pneumonitis

Aspiration pneumonia (infection occurring from the exposure) results from the swallowing of colonized oropharyngeal contents into the lower respiratory tract with subsequent inflammation and infection. 

Aspiration pneumonitis (Mendelson's syndrome) is from exposure of sterile gastric contents into the lower respiratory tract. This results in a rapid chemical pneumonitis due to irritation of the pulmonary tissues from the acidic material. 

Approximately half of the healthy adults aspirate small amounts oropharyngeal secretions during sleep. Sterile pneumonitis and aspiration pneumonia are difficult to distinguish from one another, even with bronchial lavage. 

Risk Factors for Aspiration

• Reduced Consciousness (EtOH, Drugs, Procedural Sedation, GA)
• Neurologic (Stroke, Seizure, TBI, Dementia, Chronic Neurologic Conditions)
• Oropharyngeal (Poor oral hygiene, Intubation)
• GI (GERD, Esophageal dysmotility, Oral/NG Tube feeding)

About one third of those who aspirate have “silent aspiration” without evidence of cough or gagging. 

Pathophysiology 

• Inflammation (peaks in 4 to 6 hours) --> Increase capillary permeability 
• These reactions may manifest clinically as a cough, pleuritic chest pain, fever, and radiographic findings. 

Typical bacterial species involved in aspiration pneumonia

• S. pneumoniae
• S. aureus
• H. influenzae
• Enterobacteriaceae in community-acquired aspiration pneumonia.

Hospital Acquired Aspiration - P. aeruginosa and gram-negative organisms

Antibiotic therapy for aspiration pneumonia should include coverage for anaerobic organisms.

Presentation

The clinical symptoms of aspiration pneumonia include fever, dyspnea, and productive cough. Patients may show up tachycardia, tachypnea, rales.  Other symptoms of systemic infection in the elderly and debilitated may be present, including a change in mental status, lethargy, and nausea or vomiting.

Witnessed aspiration is a key feature in the diagnosis of aspiration pneumonitis or pneumonia. Typically those with noninfectious aspiration are younger, and the aspiration is witnessed. These patients will present giving a history of aspiration and coughing immediately afterward. 

“Silent aspirators” are typically older and have a chronic neurologic disorder and will present with a cough or fever or general malaise. Historical features that suggest silent aspiration include general debility, recurrent cough, hoarseness, or dysphagia. 


Diagnosis

• CXR usually shows unilateral focal or patchy consolidations in the dependent lung segments (Right lower lobe is the most common in upright aspiration) 
• CT Scan

Initial CXR if done too early in the course may not show any changes

http://www.svuhradiology.ie/case-study/aspiration-pneumonia/

Recumbent Aspiration typically involves posterior portions of the upper lobes and the upper portions of the lower lobes
Upright Aspiration typically involves the most dependent portions i.e. basal segments of the lower lobes. 

Treatment
Large volumes aspiration may require suctioning of the tracheobronchial tree or bronchoalveolar lavage to clear the airway. Bronchodilators aid aspiration-induced bronchospasm.

• Community-Acquired Aspiration (S. aureus, S. pneumoniae, and H. influenzae) - Use Co-Amoxiclav or Levofloxacin
• Suspected MRSA - Add Vancomycin or Linezolid
• Patients with severe periodontal disease, putrid sputum, or lung abscess - Give piperacillin-tazobactam. 

Clinically well-appearing patients with normal gas exchange are candidates for possible discharge with instructions to return if they experience worsening symptoms. Those with significant comorbidities need to get admitted for observation and Antibiotics. 

Further reading

1. Kikuchi R, Watabe N, Komino T, et al: High incidence of silent aspiration in elderly patients with community acquired pneumonia. Am J Respir Crit Care Med 150: 251, 1994. 
2. Marik PE: Aspiration pneumonitis and aspiration pneumonia. N Engl J Med 344: 665, 2001. 

Posted by:

              

     Lakshay Chanana

     

     ST4 Trainee

     Royal Infirmary of Edinburgh
     Department of Emergency Medicine

     Edinburgh
     Scotland

     @EMDidactic

Pulmonary Hypertension

Introduction

Pulmonary vascular system is a high-flow, low-resistance circuit. Normal pulmonary arterial systolic pressures range from 15 to 30 mm Hg, whereas diastolic pulmonary arterial pressures range from 4 to 12 mm Hg and Pulmonary hypertension is defined as a mean pulmonary arterial pressure >25 mm Hg at rest or >30 mm Hg during exertion.

Although echocardiography can estimate pulmonary arterial pressure in a patient with suspected pulmonary hypertension, definitive diagnosis requires right heart catheterization. The World Health Organization classifies pulmonary hypertension into five categories based on cause and response to treatment:

Accurate classification of pulmonary hypertension is key to directing treatments. Regardless of the cause, patients with pulmonary hypertension have high morbidity and mortality rates.

Pathophysiology

Endothelial dysfunction results in an imbalance between endogenous vasodilators and vasoconstrictors with net effect leading to vasoconstriction and formation of in situ thrombi. Other pathologic processes include alterations in microvascular permeability, abnormal hypoxic vasoconstriction, microvascular thrombosis, and the formation of plexiform lesions, leading to vascular remodeling. 

Ultimately, these abnormalities result in sustained elevations of pulmonary vascular resistance and impairment of pulmonary blood flow leading to RV dilatation and poor contractility. With progressive RV dilation, the intraventricular septum is displaced toward the left ventricle. This displacement inhibits left ventricular filling and ultimately impairs cardiac output and systemic perfusion.

Clinical Presentation 

• Symptoms can be non-specific which often leads to delayed diagnosis
• Dyspnea, fatigue, chest pain, near syncope, syncope, exertional lightheadedness
• Orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema

The physical examination is often normal in the early stages of pulmonary hypertension.

Late signs include a holosystolic tricuspid regurgitation murmur, jugular venous distention, hepatomegaly, ascites, and lower extremity edema

Diagnosis 

ECG: The most common ECG abnormality seen in pulmonary hypertension patients is right axis deviation. Additional findings associated with pulmonary hypertension include an R/S ratio >1 in lead V1, an R/S ratio<1 in leads V5 and V6, a qR complex in lead V1, an S1Q3T3, right atrial enlargement in the inferior leads, and an incomplete or complete right bundle branch block. The most common dysrhythmias in patients with pulmonary hypertension are atrial fibrillation, atrial flutter, and atrioventricular nodal reentrant tachycardia.

B-type natriuretic peptide and N-terminal B-type natriuretic peptide are often elevated  Elevations in troponin from myocardial ischemia or a strain-induced leak can be seen.

CXR: Common abnormalities associated with pulmonary hypertension include enlargement of the right atrium, RV, and hilar pulmonary arteries. 

TTE: Transthoracic echocardiography is the best initial diagnostic test to assess pulmonary hypertension in the ED. It allows estimation of the pulmonary artery systolic pressure and detection of decreased RV function, right atrial hypertrophy right ventricular hypertrophy and leftward deviation of the intraventricular septum.

Treatment 

No consensus guidelines exist for the management of critically ill patients with pulmonary hypertension in the ED. The mainstays of ED therapy include:

1. Supplemental oxygen (Target SpO2 >90%)

2. Optimizing intravascular volume, augmenting right ventricular function, maintaining coronary artery perfusion, and decreasing right ventricular afterload 

Treatments caveats:

• Intubation: In patients with severe pulmonary hypertension, intubation and venti- lation can cause rapid cardiovascular collapse due to increased intrathoracic pressure from positive-pressure ventilation and effects of sedative medications on right ventricular function and systemic vascular resistance. Adjust the respiratory rate to avoid hypercapnia, which can increase pulmonary vascular resistance, pulmonary artery pres- sure, and RV strain.
• Fluids in RV Failure: Volume overload can cause RV dilation, displacing the intraventricular septum, impairing left ventricular output, and ultimately compromising tissue perfusion.3 For patients who are hypovolemic, give serial boluses of an isotonic crystalloid solution in 250- to 500-mL aliquots with close monitoring.
• RV Dysfunction: Dobutamine is preferred inotrope of choice. Avoid doses>10 micrograms/kg/min, because large doses can increase pulmonary vascular resistance and cause tachydysrhythmias and hypotension. For patients unable to tolerate dobutamine, milrinone is an alternative. Higher doses of milrinone can cause hypotension.
• RCA Perfusion: For the hypotensive pulmonary hypertension patient, use a vasopressor to increase aortic root pressure and maintain RCA perfusion. Norepinephrine is recommended for this purpose. Avoid high doses of nor- epinephrine because it can increase pulmonary vascular resistance and impair right ventricular output.
• RV Afterload reduction: These medications are rarely used in ED setting. Reducing right ventricular afterload with pulmonary vasodilators is a critical component in the management of stable patients with pulmo- nary hypertension. The most commonly used pulmonary vasodilators are prostanoids, endothelin receptor antagonists, and phosphodiesterase-5 (PDE-5) inhibitors. These medications are used primarily in the treatment of patients with pulmonary arterial hypertension. 

Prostanoids (epoprostenol, treprostinil, and iloprost) are potent vasodilators and are the initial treatment of choice in patients with pulmonary arterial hypertension and right ventricular failure. These medications have antiplatelet and antiproliferative properties.

Endothelin receptor antagonists (Currently not used for critically ill ED patients) are administered orally and increase exercise capacity, improve hemodynamics, and can delay the time to clinical worsening in pulmonary hypertension patients. Drugs: bosentan and ambrisentan. 

PDE-5 inhibitors (Currently not used for critically ill ED patients) sildenafil and tadalafil are approved for use in patients with pulmonary hypertension. They are administered orally, seeking to improve hemodynamics and exercise capacity in patients with pulmonary arterial hypertension.

Pulmonary HTN patients presenting to ED are often critically ill and require HDU/ICU level care. Therefore, almost all of them require admission with expert input. 

Posted by:

              

     Lakshay Chanana

     

     ST4 Trainee

     Royal Infirmary of Edinburgh
     Department of Emergency Medicine

     Edinburgh
     Scotland

     @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

                                                        

 

NIV: What’s the big deal about that big mask?

A patient struggling for that ‘satisfying, good, deep breath’ and failing at every attempt is not an uncommon sight in the ED. Shortness of breath/breathlessness is one of the major presentations in the EDs all around the world. The diverse etiologies and the potential complications due to long periods of breathlessness makes it a time critical symptom requiring early intervention. 

Non-invasive ventilation is one of the important modalities of managing a patient with shortness of breath when indicated. Let us review some of the important points about non-invasive ventilation.

So, what is NIV?

It’s a method of giving ventilatory support/delivering oxygen to a patient with respiratory distress using a positive pressure mask so that invasive methods like endotracheal intubation is postponed or avoided.

What are the types of NIV?

There are 2 modes of NIV: CPAP (Continuous Positive Airway Pressure) and BPAP (Bilevel Positive Airway Pressure). BPAP has IPAP and EPAP (I-Inspiratory, E-Expiratory)

Terminology:

In general,
Type 1 RF requires CPAP type of NIV.

Type 2 RF requires BPAP type of NIV.

PEEP=EPAP=CPAP i.e. they all mean the same!

So you can say in Type 1 RF(Hypoxic failure), the pressure we provide is PEEP or just EPAP or CPAP. 

For Type 2 RF (Hypercapnic), we provide IPAP as well as EPAP. IPAP is greater than EPAP, PS (Pressure Support is the difference between IPAP and EPAP). For instance if IPAP = 15 and EPAP is 10 then PS = 15-10 i.e. 5cm H2O. 

A BPAP machine can be used as a CPAP machine if you set EPAP=IPAP i.e. you deliver the same pressure during inspiration as well as expiration.

Did you just say BPAP instead of BiPAP?

Yes! If you know that ‘Xerox’ is a trademark/brand while ‘photocopy’ is the actual terminology, you got this one right as well. BiPAP and BIPAP are actually trademarked modes of Bilevel Positive Airway Pressure (BPAP). (Apple fanboys can however use the i :-P)

CPAP:

• Found to be more useful in reducing the need for intubation and reducing the mortality in patients with acute cardiogenic pulmonary edema. 
• A fixed positive pressure is delivered throughout the respiratory cycle without any change during inspiration or expiration. The pressure required can be set on the machine and is measured in cmH₂O.  
• Commonly used pressures range 5-15cm of H₂O. (5-8cm of H2O is a reasonable starting pressure)
• O₂ can be titrated depending upon the SpO2, PaO2.

BPAP:

• Found more effective in acute exacerbation of COPD.
• Different pressures are used during inspiration (IPAP) and expiration (EPAP).
• The commonly used initial settings are EPAP: 3-6 and IPAP: 8-12 with supplemental oxygen of 3-5liters/min.
• The pressure can be adjusted depending upon the clinical condition of the patients and /or values of PaO2, PCO2 and SpO2. 
• To treat persistent hypercapnia increase IPAP by 2cms at a time. To treat persistent hypoxia, increase IPAP and EPAP by 2cms at a time.
• The maximum EPAP/IPAP is 25/15cmH₂0.
• Many comparative studies have demonstrated no significant difference between two modes of NIV when used for either for pulmonary edema or COPD.
• So, just in case the nurse asks you “we do not have a BPAP machine but there’s an old CPAP machine, will that be okay?” the answer should be “Yes!” irrespective of the etiology! (Most modern machines can deliver both CPAP and BPAP)

In whom do we put it on?

• In patients with respiratory failure/respiratory distress (e.g COPD and Acute Pulmonary Edema) without any contraindications.
• Although there’s no clear consensus regarding the indications for the use of NIV, when there are no contraindications, many patients with dyspnea may be suitable candidates for NIV. (Asthma, ARDS, Neuromuscular disease, Chest trauma, Cystic Fibrosis)
• To facilitate extubation in patients with COPD who have failed weaning attempts.
• ‘Do-not-intubate (DNI) patients’    
• Obstructive Sleep Apnea (OSA) – CPAP is commonly used in the night.

Contraindications for the use of NIV:

•    Patients who require immediate endotracheal intubation.
•    Decreased level of consciousness.
•    Inability to fix/position the mask due to past facial surgery.
•    Excessive secretions, vomiting and risk of aspiration.
•    Uncooperative patient.
•    Lack of staff trained/experienced in operating and monitoring the device and        patient the patient on NIV.
•    Hemodynamically unstable patient.
•    Severe hypoxia and/or hypercapnia: PaO2/FiO2 ratio<200mmHg, PaCO2 >      60mmHg.
•    Gastrointestinal bleeding.

How does it work?

Alveolar recruitment + increased of FiO2 à Reverse hypoxia.

Improves airflow by, Stenting of closed/obstructed airways à Decreases atelectasis or lung collapse à Improves pulmonary compliance à reduces the work of breathing.

The difference between EPAP and IPAP is called pressure support, which augments ventilation and reduces the work of breathing.

Addition of positive pressure to the thoracic compartment also reduces the preload and afterload à Improvement of patients with cardiogenic pulmonary edema.

How to monitor a patient on NIV?  What do I look for?

Once the patient is on NIV, patient has to be monitored closely.

Be prepared for the RSI in case NIV fails. Keep equipment ready and make sure they are working. Involve senior on the shift. Notify anesthesia if necessary.

Parameters to be looked for which are suggestive of NIV failure include:

•   Intolerance to NIV: Restless and irritable, asynchronous breathing with ventilator.
•   Increased secretions, vomiting patient.
•   Altered mental status.
•   Increasing dyspnea/respiratory distress despite optimum settings. (RR>35-40)
•   Persistent hypoxia despite supplemental oxygen.
•   Hemodynamic instability.
•   Worsening blood gases.

Other important things to be taken care of when patient is on NIV

• Explain the patient what NIV is and how air is delivered with pressure. Just forcing that nasty mask on patient’s face without explaining anything would make an already anxious patient more anxious and you will most probably end up with an uncooperative patient and failed NIV.
• Make sure that the mask is of appropriate size and well fitting. An Ill-fitting mask will result in air leak and NIV will be ineffective.  – Dealing with the big mask is indeed a big deal!
• Face Mask is proffered over nasal mask in the ED.
• Use cotton over the nasal bridge/forehead (pressure points) to avoid pressure sores.
• Sitting position / Head end elevation
• Follow up with a blood gas within 30-60 minutes .
• Have an alternative plan for NIV failure. Be prepared for Intubation.
• Be very cautious if you have to use analgesics that are known to cause sedation.

Complications of NIV:

•   Gastric distension
•   Failure of NIV
•   Aspiration (rare)
•   Hypotension with higher pressures (infrequent)
•   Barotrauma (rare)
•   Pressure ulcers over the face.
•   Oral and nasal dryness à Irritation.

Take home points:

•   Consider NIV ASAP in eligible patients (Timing is important).
•   EPAP=CPAP=PEEP, IPAP > EPAP and PS = IPAP-EPAP.
•   Reassure, use an appropriately sized mask .
•   Have a definitive plan for failed   NIV.

       Author:

      Dr. Apoorva Chandra

      Resident – Emergency Medicine 

      Apollo health city

      Hyderabad, India

      @apoorvamagic on twitter 

      Email: apoorvamagic@gmail.com

References and further reading/listening/viewing:

1. http://www.draeger.com/sites/assets/PublishingImages/Segments/Hospital-US/A_Breath_Ahead/02_Contemporary_Clinical_Practice/NIV-FAQs.pdf
2. http://www.ebmedicine.net/topics.php?paction=showTopic&topic_id=271
3. http://bja.oxfordjournals.org/content/early/2013/04/04/bja.aet070.full
4. Ventilation Literature Summaries http://lifeinthefastlane.com/ccc/ventilation-literature-summaries/
5. EMCrit Podcast 19 – Non-Invasive Ventilation: http://emcrit.org/podcasts/niv/
6. BiPAP part 1 on YouTube by David Gibson:  https://www.youtube.com/watch?v=UXWa1r3hEoM
7. BiPAP part 2: https://www.youtube.com/watch?v=gewxf3FopOY
8. British thoracic society guidelines: https://www.brit-thoracic.org.uk/guidelines-and-quality-standards/non-invasive-ventilation-(niv)/
9. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3042478/
10. Oxford handbook of emergency medicine: Page no. 109 (section on COPD).