Category: Breathing

COPD (2024)

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by Noura Aldosari & Omar Ghazanfar

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You Have A New Patient!

A 67-year-old male arrives at the emergency department with increasing shortness of breath over the past 2 days. He has a 50-pack-year smoking history and a prior diagnosis of chronic obstructive pulmonary disease (COPD). On arrival, he appears fatigued and slightly cyanotic. Vitals: HR 110 bpm, BP 145/85 mmHg, RR 30 breaths/min, SpO2 84% on room air, and temperature 37.3°C. He uses accessory muscles to breathe, and auscultation reveals diffuse expiratory wheezes.

The image was produced by using ideogram 2.0

What Do You Need To Know?

Importance

It is important to learn about Chronic Obstructive Pulmonary Disease (COPD) in the emergency department because COPD exacerbations are a common and potentially life-threatening presentation that requires prompt recognition and management. Emergency providers must quickly identify signs of respiratory distress, understand the appropriate interventions, such as oxygen therapy, bronchodilators, and steroids, and be able to differentiate COPD from other respiratory conditions. Effective and timely treatment can prevent further deterioration, reduce hospital admissions, and improve patient outcomes. Additionally, understanding COPD allows for better patient education on prevention and follow-up care, ultimately reducing the risk of recurrent exacerbations.

Epidemiology

COPD affects approximately 390 million individuals globally and is the third leading cause of death worldwide [1]. In the United States alone, COPD impacts over 16 million individuals, and many cases remain undiagnosed [2]. The prevalence of COPD is strongly associated with smoking, environmental exposures, and aging. However, occupational hazards and indoor air pollution, such as biomass fuel exposure, are significant risk factors in low and middle-income countries. COPD prevalence increases with age, with the highest incidence among individuals over 65 years. A meta-analysis was done and showed that 12.64% of people aged 40 and older had COPD with similar prevalence between males and females [3].

Pathophysiology

COPD is characterized by persistent respiratory symptoms and airflow limitation caused by airway and/or alveolar abnormalities due to chronic exposure to noxious particles or gases [4]. Inhaled irritants, such as cigarette smoke or biomass fuel, trigger exaggerated airway inflammation, mucus hypersecretion, and structural remodeling. Neutrophils, macrophages, and CD8+ T lymphocytes release proteases and cytokines that cause tissue damage [5]. Protease activity, particularly from neutrophil elastase, destroys elastic fibers in alveolar walls, resulting in emphysema and airflow limitation.
Repeated inflammation also induces goblet cell hyperplasia, fibrosis, and smooth muscle hypertrophy, narrowing airways and increasing resistance to airflow [6]. These processes clinically manifest as chronic cough, sputum production, and dyspnea. Spirometry measures expiratory airflow limitation, with reductions in forced expiratory volume in 1 second (FEV1) and the FEV1/forced vital capacity (FVC) ratio.

Medical History

A thorough medical history is important when evaluating a patient with COPD, especially during an exacerbation. Symptoms include dyspnea, which often worsens over hours to days, increased sputum production, and changes in sputum color that may suggest infection.1 Other symptoms include wheezing, chest tightness, fatigue, and reduced tolerance to exercise. It is important to ask about the onset, timing, exacerbating factors (infections, exposure to pollutants, medication non-adherence), and relieving factors (use of bronchodilators).

Ask about risk factors such as smoking history, occupational/environmental exposures, and previous exacerbations requiring hospitalizations. Also, ask about medications, including prior use of short-acting beta-agonists (SABAs), inhaled corticosteroids, long-acting bronchodilators, and home oxygen therapy.

Allergies should also be noted. Red flags that indicate worse outcomes include severe baseline dyspnea, frequent exacerbations, altered mental status, and signs of respiratory fatigue, such as inability to complete sentences or accessory muscle use. Ask about the patient’s medical history, including cardiovascular disease, diabetes, or pulmonary infections [7,8].

Physical Examination

Physical Examination The physical exam should prioritize a thorough assessment of the patient’s cardiorespiratory status [9]:

  1. Vital Signs: Pay attention to tachypnea, tachycardia, and hypoxemia.
  2. Respiratory Findings:
    • Air movement and wheezing
    • Be cautious: The absence of wheezing may indicate reduced airflow rather than an absence of obstruction.
  3. Cyanosis: Indicates significant hypoxemia.
  4. Mental Status: Confusion or lethargy suggests worsening respiratory failure.
  5. Other Signs: Fever may point to an infectious cause

Indicators of Severe Exacerbation

  • Use of accessory muscles during breathing.
  • Inability to lie flat or in a tripod position to optimize breathing.
  • Speaking only one or two words between breaths due to dyspnea.

Red Flags: Impending Respiratory Failure Be alert for these critical signs requiring immediate intervention:

  • Bradycardia or other dysrhythmias.
  • Cyanosis indicates severe hypoxemia.
  • Marked reduction in mental status, such as confusion or drowsiness.
  • Loss of respiratory effort is a concerning sign that indicates a possible pre-arrest state [9].

Alternative Diagnoses

It is crucial for an emergency physician to consider the broad differentials to dyspnea during the initial and ongoing evaluation, including bedside treatments and the plans that follow [10-14]. It is important to acknowledge that patients with COPD can have concurrent comorbid conditions, including other cardiopulmonary diseases.

The emergency physician should suspect COPD in patients with symptoms including shortness of breath, wheezing, and chronic cough with sputum production. In addition, COPD patients have known risk factors, including smoking and environmental exposures that include working in areas with smoke production, and that is when it is important to have adequate history-taking skills. History-taking will give us a better understanding of the patient’s chronic dyspnea with declining pulmonary function, especially on exertion.

When a patient presents with acute dyspnea, one can classify the etiologies based on the organ systems. HEENT causes include angioedema, anaphylaxis, foreign body, and deep neck infections. If a patient presents with acute dyspnea after a motor vehicle accident, then it is plausible to consider rib fractures and lung contusion. Since our chapter focuses on COPD, we can consider cardiopulmonary cases of acute dyspnea. Pulmonary causes are asthma exacerbation, pulmonary embolism, pneumothorax, pulmonary infections, ARDS, and hemorrhage. Cardiac causes consist of acute coronary syndrome, acute decompensated heart failure, flash pulmonary edema, cardiomyopathies, arrhythmia, valvular pathologies, and cardiac tamponade.

Patients with COPD can often present with wheezing, which should not be confused with other causes. When a patient presents to you with wheezing, this suggests that there is an obstruction below the tracheal level. This obstruction occurs in asthma, foreign body, anaphylaxis, and pulmonary edema, also known as a cardiac wheeze [10-14].

The emergency physician should also be mindful of the severity of COPD exacerbation. In some cases, patients deteriorate rapidly, and urgent intervention is warranted. COPD patients can present with other conditions, as mentioned above.

Acing Diagnostic Testing

There are bedside, laboratory, and imaging tests that aid in the evaluation and management of patients with respiratory distress, particularly those with suspected or known COPD exacerbations. 

Bedside Tests

  1. Pulse Oximetry [15]
    • Assesses oxygenation status in real-time.
    • Indicated in patients presenting with dyspnea or suspected hypoxemia.
    • SpO₂ <88% indicates the need for supplemental oxygen. However, hyperoxia (SpO₂ >92%) should be avoided in COPD to prevent worsening hypercapnia.
  2. Arterial Blood Gas (ABG) [16]
    • Evaluates ventilation (PaCO₂), oxygenation (PaO₂), and acid-base status.
    • Indicated in severe dyspnea, altered mental status, or suspected respiratory failure.
    • Acidosis (pH <7.35) and hypercapnia (PaCO₂ >45 mmHg) confirm significant respiratory compromise.
  3. Capnography [17]
    • Provides continuous monitoring of end-tidal CO₂ levels.
    • This is for patients on mechanical ventilation or receiving non-invasive ventilation (NIV).
    • High end-tidal CO₂ suggests hypoventilation, while decreasing levels may indicate respiratory improvement.

Laboratory Tests

  1. Complete Blood Count (CBC)
    • This is for patients with fever, purulent sputum, or systemic symptoms.
    • An elevated white blood cell (WBC) count may suggest bacterial infection, a common trigger for exacerbations.
  2. C-Reactive Protein (CRP) and Procalcitonin [18]
    • Indications: Differentiating bacterial vs. viral triggers.
    • Interpretation: Elevated CRP and procalcitonin levels support bacterial infection as the underlying cause of exacerbation.
  3. B-Type Natriuretic Peptide (BNP) [19]
    • Differentiates COPD exacerbation from acute decompensated heart failure.
    • For patients presenting with dyspnea and peripheral edema.
    • High BNP levels (>400 pg/mL) may indicate heart failure, while normal levels mainly suggest pulmonary etiology.
  4. Electrolytes
    • Identifies metabolic disturbances, such as hypercapnic acidosis.
    • For all patients with severe COPD exacerbations or on chronic diuretics.
    • Low bicarbonate (HCO₃⁻) levels can reflect chronic compensation in hypercapnia.

Imaging

  1. Chest X-Ray (CXR) [20]
    • Rules out alternative or concurrent diagnoses, such as pneumonia, pneumothorax, or pulmonary edema.
    • This is for patients with fever, chest pain, or unilateral lung findings on auscultation.
    • Consolidation suggests pneumonia; hyperinflation and flattened diaphragms are consistent with COPD. A visible pleural line indicates pneumothorax.
  2. Computed Tomography (CT) Scan [21]
    • Identifies pulmonary embolism (PE) or atypical infections.
    • Consider CT for patients with high clinical suspicion of PE (e.g., sudden dyspnea, pleuritic chest pain) or non-resolving symptoms after standard treatment.
    • Pulmonary artery filling defects confirm PE. CT also provides detailed imaging for complex pneumonic infiltrates.
  3. Ultrasound [22]
    • Bedside evaluation for pleural effusions or cardiac function.
    • It is helpful in patients with dyspnea with suspected heart failure or pleural pathology.
    • Positive B-lines indicate pulmonary edema; pleural effusions appear as anechoic regions.

Risk Stratification

Frequent exacerbations (>2/year) and prior ICU admissions are associated with a higher mortality risk in patients, particularly those with comorbidities like cardiovascular disease and diabetes, which further worsen prognosis [23,24]. On physical examination, signs such as tachypnea (>30 breaths/min), accessory muscle use, cyanosis, and altered mental status strongly indicate severe respiratory distress [15]. Diagnostic testing, including arterial blood gas (ABG) analysis, reveals that acidosis (pH <7.35) and hypercapnia (PaCO₂ >45 mmHg) are predictive of ventilatory failure [25]. Imaging studies, such as chest X-rays, play a critical role by identifying conditions like pneumonia or pneumothorax that necessitate urgent medical intervention [20].

Risk Stratification Tools

  1. DECAF Score (link mdcalc)
    • Includes dyspnea, eosinopenia, consolidation, acidosis, and atrial fibrillation. Higher scores predict in-hospital mortality [26].
  2. BAP-65 Score (link mdcalc)
    • Evaluates hypotension, acidosis, pulse >110 bpm, and age ≥65 years to predict ICU need and mortality [27].

Management

Initial Stabilization: The ABCDE Approach

  1. Airway
    • Assessment: Evaluate airway patency and signs of obstruction.
    • Intervention: Patients with severe respiratory distress may require endotracheal intubation if non-invasive ventilation (NIV) fails or they are unable to protect their airway.
  2. Breathing
    • Assessment: Check respiratory rate, oxygen saturation, and work of breathing.
    • Intervention: Provide supplemental oxygen targeting SpO₂ levels between 88% and 92%. Non-invasive ventilation (e.g., BiPAP) is the preferred first-line treatment for hypercapnic respiratory failure or severe dyspnea. NIV reduces intubation rates and mortality [9].
  3. Circulation
    • Assessment: Assess heart rate, blood pressure, and perfusion.
    • Intervention: Establish IV access and administer fluids judiciously, particularly in hemodynamically unstable patients.
  4. Disability
    • Assessment: Monitor neurological status for signs of hypoxia or hypercapnia (e.g., confusion, agitation).
    • Intervention: Correct hypoxemia and hypercapnia promptly to prevent further deterioration [9].
  5. Exposure
    • Assessment: Perform a thorough examination to identify underlying triggers (e.g., infections, pneumothorax).
    • Intervention: Obtain chest imaging to evaluate for pneumonia, pneumothorax, or other contributing factors [9].

Medications

The management of COPD exacerbations often includes a combination of pharmacological treatments tailored to address airway obstruction, inflammation, and potential infections. Key medications include bronchodilators like albuterol and ipratropium to relieve bronchospasm, corticosteroids such as prednisone to reduce inflammation, and magnesium sulfate for severe bronchospasm. Antibiotics are considered when infection is suspected. Each drug requires careful dosing and monitoring, with specific precautions based on patient factors and pregnancy category [15].

Albuterol (Nebulizer):

  • Dose: 2.5 mg
  • Frequency: Every 20 minutes as needed
  • Maximum Dose: 10 mg/hour
  • Pregnancy Category: C
  • Cautions/Comments: Monitor for tachycardia and tremors.

Ipratropium (Nebulizer):

  • Dose: 500 mcg
  • Frequency: Every 6 hours
  • Maximum Dose: Not applicable
  • Pregnancy Category: B
  • Cautions/Comments: Use in combination with albuterol for synergistic effects.

Prednisone (Oral):

  • Dose: 40-60 mg
  • Frequency: Once daily
  • Maximum Dose: Not applicable
  • Pregnancy Category: C
  • Cautions/Comments: Use cautiously in diabetic patients.

Magnesium Sulfate (IV):

  • Dose: 2 g
  • Frequency: Single dose
  • Maximum Dose: 2 g
  • Pregnancy Category: C
  • Cautions/Comments: Consider in severe cases with bronchospasm.

Antibiotics:

  • Dose: Based on local guidelines
  • Frequency: Per protocol
  • Maximum Dose: Not applicable
  • Pregnancy Category: Varies
  • Cautions/Comments: Initiate if infection is suspected.
  •  

Procedural Interventions

In the management of acute COPD exacerbations, advanced interventions play a crucial role in stabilizing respiratory function and addressing underlying complications. Non-invasive ventilation (NIV) is a first-line strategy for patients with hypercapnic respiratory failure or persistent hypoxemia, offering improved gas exchange and reducing the likelihood of intubation [15]. For patients who do not respond to NIV or have contraindications, endotracheal intubation with lung-protective ventilation strategies becomes necessary to manage severe respiratory distress while minimizing barotrauma [15]. Additionally, imaging modalities such as chest X-rays or ultrasounds are essential for identifying structural abnormalities like pneumonia or pneumothorax, ensuring comprehensive evaluation and treatment [15].

Special Patient Groups

Pediatrics

Although COPD is primarily an adult disease, children with chronic respiratory conditions, such as bronchopulmonary dysplasia or severe asthma, may exhibit symptoms resembling COPD exacerbations.

  • Clinical Differences:
    • Symptoms may mimic asthma exacerbations, presenting as wheezing and breathlessness.
    • Pulmonary function tests are often challenging to interpret in younger children.
    • A history of prematurity or recurrent lower respiratory tract infections may predispose children to COPD-like symptoms.
  • Management Implications:
    • Employ pediatric-specific dosing for bronchodilators and corticosteroids.
    • Avoid overuse of systemic steroids due to potential risks, such as growth suppression and adrenal insufficiency [15].

Geriatrics

The elderly population often presents unique challenges in COPD exacerbations due to comorbidities and altered physiological responses.

  • Clinical Differences:
    • Exacerbations may manifest atypically, such as confusion or lethargy, rather than standard respiratory symptoms.
    • Comorbidities, including heart failure and frailty, complicate diagnosis and treatment.
    • There is an increased risk of medication side effects, including corticosteroid-induced hyperglycemia and osteoporosis.
  • Management Implications:
    • Emphasize non-pharmacological interventions, such as pulmonary rehabilitation.
    • Closely monitor for potential drug interactions and side effects [28].

Pregnant Patients

Pregnant individuals with COPD exacerbations face unique clinical challenges stemming from physiological changes and fetal considerations.

  • Clinical Differences:
    • Increased respiratory rate and reduced functional residual capacity may exacerbate symptoms.
    • Exacerbations pose risks to maternal and fetal health, including preterm labor and fetal growth restriction.
  • Management Implications:
    • Prioritize non-teratogenic medications, such as inhaled corticosteroids and short-acting beta-agonists.
    • Monitor maternal oxygen saturation to ensure adequate fetal oxygenation [29].

When To Admit This Patient

Indications for Hospital Admission

Hospitalization is indicated for patients with any of the following:

Severe Symptoms:

  • Marked dyspnea interfering with daily activities.
  • Respiratory rate >30 breaths/min, use of accessory muscles.
  • Cyanosis or signs of hypoxemia (oxygen saturation <90% despite supplemental oxygen) [15,30].

Hemodynamic Instability:

  • Hypotension or signs of poor perfusion (e.g., confusion, altered mental status) [31].

Failure of Outpatient Management:

  • Lack of improvement or worsening symptoms despite appropriate outpatient therapy, including bronchodilators, corticosteroids, and antibiotics [32].

Comorbidities:

  • Exacerbations complicated by comorbid conditions such as congestive heart failure, diabetes mellitus, or arrhythmias [33].

Acute Respiratory Failure:

  • Arterial blood gases (ABGs) showing PaO2 <60 mmHg or PaCO2 >50 mmHg with pH <7.35 [16].

High-Risk Features:

  • Frequent exacerbations (e.g., ≥2/year) [11, 23].
  • Recent hospitalizations for COPD exacerbation [11, 23],
  • Advanced COPD with significant functional limitations (e.g., home oxygen use) [15].

ICU Admission Criteria [30,34,35]

Intensive care unit (ICU) management is required if:

  • Non-invasive ventilation (NIV) fails, or mechanical ventilation is necessary.
  • Life-threatening hypoxemia or severe hypercapnia.
  • Persistent hemodynamic instability.

Criteria for Safe Discharge [32,33,36]

Patients can be discharged or managed on an outpatient basis if:

  • Symptoms are mild and improving with therapy [15,30]
  • No significant hypoxemia or hypercapnia (oxygen saturation ≥90%, stable ABGs).
  • No significant comorbidities or recent hospitalizations.
  • The patient has a reliable social support system and access to follow-up care.

Follow-Up Recommendations [8,15,37]

Patients managed as outpatients should have the following:

  • Clear instructions for medication use (e.g., short-acting bronchodilators, oral corticosteroids, antibiotics if indicated).
  • A follow-up appointment within 2 weeks.
  • Education on recognizing warning signs of worsening symptoms.

Discharge Information [15,34,35]

Before sending a patient home, provide:

  • A detailed medication plan, including proper inhaler technique.
  • Instructions on the duration of oral corticosteroid and antibiotic therapy.
  • Education on lifestyle modifications (e.g., smoking cessation, pulmonary rehabilitation).

Safety-Netting Measures [30,33]

  • Clear guidance on when to seek medical attention (e.g., worsening dyspnea, fever, confusion).
  • Contact information for emergency services and primary care provider.

Closing Loops [31,32,36]

  • Arrangements for follow-up appointments and pulmonary function testing.
  • Discuss long-term COPD management strategies, such as home oxygen therapy or vaccinations (influenza, pneumococcal).
  • Confirm that the patient understands the discharge instructions and can to prescribed medications.

Revisiting Your Patient

The management of the patient who presented with a COPD exacerbation followed a structured approach. Oxygen therapy was initiated, targeting SpO₂ levels of 88–92% using a nasal cannula or a Venturi mask, with BiPAP considered for cases of persistent hypoxemia or hypercapnic respiratory failure. Medications included nebulized bronchodilators, such as albuterol (2.5 mg) combined with ipratropium (0.5 mg), which were administered every 20 minutes for the first hour. Systemic steroids, like oral prednisone (40 mg) or IV methylprednisolone, were given as needed. Empiric antibiotics, such as doxycycline or amoxicillin-clavulanate, were started when an infection was suspected. Diagnostics involved chest X-rays, arterial blood gas analysis, a complete blood count (CBC), and electrolyte evaluation, with an ECG performed due to concerns about potential cardiac involvement. Continuous monitoring of SpO₂, respiratory rate, and ABG was conducted to track the patient’s progress. Regarding disposition, the patient was admitted due to severe hypoxemia and hypercapnia, with plans for outpatient follow-up scheduled within 1–2 weeks after discharge. Finally, the patient received education, including smoking cessation support and instructions on proper inhaler use, to reduce the risk of future exacerbations.

Authors

Picture of Noura Aldosari

Noura Aldosari

Emergency medicine resident at Cleveland Clinic Abudhabi. Interested in neurocritical and trauma resuscitation. Rotated in the neurocritical ICU department of Brigham and Women's Hospital (Harvard University) and worked in a research lab to detect genes involved in the pathophysiology of glioblastoma in Virginia University. Outside of medicine, I am a musician where I play the guitar and I cook.

Picture of Omar Ghazanfar

Omar Ghazanfar

Dr Omar Ghazanfar is the Medical Director HIMS and Emergency Physician Cleveland Abu Dhabi.Dr Ghazanfar has a keen interest in research and is part of the IFEM research committee as well as the scientific committee for ESEM. He is triple board certified with boards in Emergency and Disaster Medicine as well as Medical Quality. He has also completed an MBA.

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References

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  3. Al Wachami N, Guennouni M, Iderdar Y, et al. Estimating the global prevalence of chronic obstructive pulmonary disease (COPD): a systematic review and meta-analysis. BMC Public Health. 2024;24(1):297. Published 2024 Jan 25. doi:10.1186/s12889-024-17686-9
  4. MacNee W. Pathology, pathogenesis, and pathophysiology. BMJ. 2006;332(7551):1202-1204.
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  9. Long B, Rezaie SR. Evaluation and Management of Asthma and Chronic Obstructive Pulmonary Disease Exacerbation in the Emergency Department. Emerg Med Clin North Am. 2022;40(3):539-563. doi:10.1016/j.emc.2022.05.007
  10. BMJ Best Practice. Chronic obstructive pulmonary disease (COPD) – History and exam. BMJ Best Practice. Accessed December 18, 2024. https://bestpractice.bmj.com/topics/en-us/7/history-exam
  11. National Heart, Lung, and Blood Institute. COPD Causes and Risk Factors. NHLBI. Accessed December 18, 2024. https://www.nhlbi.nih.gov/health/copd/causes
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  16. Tan HL, Ong CY, Foo LL, et al. High-flow nasal cannula oxygen therapy versus non-invasive ventilation in acute exacerbations of COPD with moderate hypercapnic respiratory failure: A randomized controlled non-inferiority trial. 2024;165(4):789-798. doi:10.1016/j.chest.2024.02.276.
  17. Schreiber A, Berthelsen PG, Hess D. Monitoring carbon dioxide during acute respiratory failure. 2013;143(3):741-750. doi:10.1378/chest.12-2305.
  18. van Vugt SF, Verheij TJ, de Jong PA, et al. Procalcitonin, CRP levels, and the bacterial etiology of pneumonia. J Clin Microbiol. 2013;51(8):2662-2665. doi:10.1128/JCM.00330-13.
  19. Mueller C, Scholer A, Laule-Kilian K, et al. Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea. N Engl J Med. 2004;350(7):647-654. doi:10.1056/NEJMoa031681.
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  33. GOLD Teaching Slide Set. Global Initiative for Chronic Obstructive Lung Disease. 2024. https://goldcopd.org/2024-gold-report/
  34. Lindenauer PK, et al. Association of corticosteroid dose and route of administration with risk of treatment failure in acute exacerbation of chronic obstructive pulmonary disease. JAMA. 2010;303(23):2359-2367. doi:10.1001/jama.2010.796.
  35. Quon BS, Gan WQ, Sin DD. Contemporary management of acute exacerbations of COPD: a systematic review and meta-analysis. Chest. 2008;133(3):756-766. doi:10.1378/chest.07-0822.
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  37. Vollenweider DJ, Frei A, Steurer-Stey CA, Garcia-Aymerich J, Puhan MA. Antibiotics for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2018;10:CD010257. doi:10.1002/14651858.CD010257.pub2.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Bronchial Foreign Body Aspiration (2024)

~ iEM Education Project Team ~ Leave a comment

by Elhaitham Ahmed & Khalifa Alqaydi

Authors
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You have a new patients!

Patient 1

A 72-year-old male was brought from an inpatient stroke rehabilitation center to the emergency department for a cough lasting the past ten days. Along with the cough, the patient was noted to have blood-tinged sputum, which is sometimes foul-smelling. His vital signs are as follows: temperature of 38.4°C, blood pressure of 138/78 mmHg, heart rate of 103 bpm, respiratory rate of 26 breaths/min, and oxygen saturation of 93% on room air. On physical examination, the patient exhibits tachypnea, dullness on percussion, bronchial breathing, egophony, and increased vocal fremitus upon examining the right side of his lung.

The image was produced by using ideogram 2.0.

Patient 2

Thirty minutes later, the nurse calls you regarding a 5-year-old boy brought in by his mother, presenting with stridor and an ongoing cough. The mother mentions that she found her child playing with her wallet while she was in the next room and discovered him in this condition. The child is tachypneic, saturating at 90% on room air with subcostal retractions. Examination of the right lung revealed wheezing with decreased air entry.

a-photo-of-a-5-year-old-male-patient-(the image was produced by using ideogram 2.0)

What do you need to know?

Importance

Tracheobronchial foreign body aspiration (FBA) can be a potentially life-threatening event. FBA in children may be suspected based on a choking episode if such an episode is witnessed by an adult or remembered by the child. In contrast, the clinical presentation of unwitnessed FBA may be subtle, requiring careful review of the history, clinical assessment, and judicious use of radiography and bronchoscopy for diagnosis. Flexible and rigid bronchoscopy have become the cornerstone of both diagnosis and treatment in patients with suspected airway foreign bodies, which are most commonly seen in patients with FBA [1].

Epidemiology

FBA is more common in children than in adults. Data from the National Security Council report that approximately 80 percent of cases occur in patients younger than 15 years of age, with the remaining 20 percent presenting in those older than 15 years. Overall, death from FBA is the fourth leading cause of accidental home and community deaths in the United States, with over 5,000 fatal episodes of FBA reported during 2015. Death from FBA peaks in children under 1 year old and in adults over 75 years [2].

Pathophysiology

In children, nuts, seeds, and other organic material account for the majority of foreign bodies. However, in adults, the nature of inhaled objects is highly variable, ranging from organic to inorganic material. The type of foreign body significantly impacts the degree of tissue reaction in the airway. For example, some inorganic materials, such as metal or glass items, may cause little tissue inflammation but can result in direct airway injury if they are sharp. In contrast, some organic materials, such as nuts and a variety of pills, can cause significant inflammation, granulation tissue formation, and airway stenosis. Aspirated organic material can also expand from airway moisture, worsening obstruction. Aspiration of medications in pill form, such as iron tablets, aspirin, and potassium chloride, can also cause severe airway inflammation and ulceration [2].

Medical History

Clinical presentation can range from chronic nonspecific respiratory complaints to acute airway obstruction. In most cases of aspiration, the presence of a foreign body can be suspected after a thorough history. Patients with airway foreign bodies may present with noisy breathing, inspiratory stridor, rhonchi, vomiting, changes in voice, and hemoptysis [3]. Some patients may report a history known as penetration syndrome, which includes a choking sensation accompanied by wheezing and coughing. Coughing may not completely expel the foreign body but may instead cause its impaction in the subglottic region. Therefore, coughing after suspected aspiration should prompt a search for a foreign body, even if symptoms improve [4].

In pediatric patients with suspected foreign body aspiration, the sudden onset of choking or intractable cough associated with wheezing and respiratory distress occurs in more than 63% of cases [5,6]. In addition to coughing and choking, stridor is a frequent symptom. The absence of early coughing and choking is associated with delayed diagnosis and chronic presentations, such as recurrent pneumonia [4]. The sudden onset of dyspnea and odynophagia may indicate an impacted subglottic object. If the object is sharp and thin, the emergency clinician should suspect embedding between the vocal cords or in the subglottic region, resulting in partial obstruction [7].

Other components of the history can assist in diagnosing and characterizing foreign bodies in patients with aspiration of nonfood objects. Many types of items may be aspirated by children exploring their environment. Another at-risk population includes individuals who habitually store small items in their mouths for quick access; examples include construction workers (nails) and seamstresses (pins). The presentation of patients with a retained airway foreign object may involve only infectious complications. A foreign object can lead to a retropharyngeal abscess. Patients with atypical or recurrent pneumonia may have pulmonary infections caused by the persistence of a foreign object serving as a focus of infection [6].

Physical Examination

Physical findings depend on the degree of airway obstruction and the duration of the object’s presence. Depending on the size and location of the foreign body, the examination may reveal a normal patient, one with cyanosis and respiratory arrest, or any condition between these two extremes. Patients may exhibit stridor or hoarseness with upper airway foreign objects, and intercostal or sternal retractions may be observed in patients with high-grade obstruction caused by tracheal foreign bodies [8]. Hypoxemia may be present; however, normoxia does not rule out the presence of a foreign body. Patients with secondary infections may present with fever.

Oropharyngeal examination may reveal a foreign body posteriorly or donor sites of fractured teeth. The examination should also include a search for fractured or missing dental prostheses. Oropharyngeal examination can often be supplemented by indirect or direct laryngoscopy or nasopharyngoscopy, but these procedures should be performed only if the procedural stress does not pose an undue risk of airway compromise.

Coughing may result from local irritation caused by bronchial foreign bodies. Localized or apparently generalized wheezing is frequently auscultated in patients with lower respiratory tract foreign bodies [9]. Complete obstruction of a mainstem bronchus may result in absent ipsilateral breath sounds; however, breath sounds can sometimes be transmitted across the thorax, and the only physical abnormality may be asymmetric chest rise. Occasionally, a foreign body acts as a one-way valve, allowing air into the lung during inspiration but preventing its exit during expiration. The affected lung becomes hyperexpanded, which may be detected as hyper-resonance on percussion [6].

Alternative Diagnoses

The selected differential diagnoses for airway foreign bodies include anaphylactic reactions, acute pharyngitis, acute epiglottitis, retropharyngeal abscess, neck tumors, pulmonary carcinomas, pneumonia, bronchitis, bronchiolitis, and tuberculosis.

Acing Diagnostic Testing

Imaging should not delay intervention in cases of suspected acute asphyxiation but is indicated for stable patients [10].

Findings on imaging depend on the type and location of the material aspirated and the time elapsed. In practice, plain films of the neck and chest are often performed simultaneously and can be followed by site-specific CT if suspicion remains. The majority of foreign bodies are radiolucent and not easily identified on plain film. If obstruction of the upper airway (oropharynx and upper trachea) is suspected, initial imaging should include anterior-posterior and lateral soft tissue views of the neck [11]. If these tests are negative and suspicion for FBA persists, further imaging with CT may be indicated. When FBA of the lower airways (below the vocal cords) is suspected, a chest radiograph should be the initial radiographic test to look for an obvious radiopaque airway lesion. Negative scans may prompt further evaluation with CT. The reported sensitivity of chest radiography is approximately 60 to 80 percent in children, and clinical experience suggests similarly poor sensitivity in adults [12].

Given its widespread availability, flexible bronchoscopy is often the diagnostic procedure of choice for non-life-threatening FBA in adults, particularly in cases involving smaller foreign bodies in the lower airway. Flexible bronchoscopy allows precise identification and localization of foreign bodies and facilitates the selection of instruments necessary for retrieval [13]. Additionally, flexible bronchoscopy enables removal of the foreign body during the diagnostic procedure if the operator is skilled in these techniques. Standard diagnostic or therapeutic flexible bronchoscopes are usually adequate for the management of FBA in adults [6].

Risk Stratification

Risk factors in adults include loss of consciousness due to trauma, drug or alcohol intoxication, or anesthesia. Additional risk factors in older adults include age-related slowing of the swallowing mechanism, medication use (impairing cough and swallowing), stroke-related dysphagia, and various degenerative neurologic diseases such as Alzheimer’s or Parkinson’s disease [2].

Management

In a conscious adult, data support the efficacy of chest thrusts, back blows or slaps, blind finger sweeps, and abdominal thrusts in relieving complete foreign body airway obstruction [6, 14]. In cases of life-threatening asphyxiation, initial support should focus on treating airway obstruction and respiratory failure. Once the airway is secured, a laryngoscopic evaluation of the oropharynx should be performed immediately to diagnose and retrieve a supraglottic or glottic foreign body. If a foreign body is not seen, rigid bronchoscopy is generally the procedure of choice for suspected asphyxiating foreign bodies located in the trachea or major bronchi. In patients with non-life-threatening FBA, flexible bronchoscopy is typically performed [15].

When large foreign bodies completely or almost completely obstruct major upper airways (glottis, supraglottis, trachea), it is critical to ensure the patient is oxygenated and the airway is secured [16]. Support measures may include bag-valve-mask ventilation and endotracheal intubation. If ventilation is unsuccessful, an emergent cricothyrotomy or tracheotomy may be required if the foreign body is suspected to be above the vocal cords. Once the airway is secured, immediate inspection of the oropharynx (glottis, supraglottis) is indicated, as one-third of FBA cases presenting as acute asphyxiation are located in the supraglottis. Retrieval of the foreign body with Magill forceps can be safely performed using direct laryngoscopy (glottis, supraglottis) or with smooth or alligator forceps during rigid or flexible bronchoscopy (large central foreign body in the trachea or major bronchus) [17].

The choice of procedure for foreign body removal depends on the type of presentation, characteristics of the inhaled foreign body, its location, the duration it has been in the airway (if known), and local expertise. Anti-inflammatories and antibiotics are not routinely administered to patients with suspected or documented FBA. Antibiotics are indicated only in cases of clinically, radiologically, or microbiologically documented respiratory tract infections. However, their use should not delay foreign body extraction, even if pneumonia or sepsis is suspected [2].

Figure 1 - Approach to Upper Airway Foreign Body. Original Image can be found here: White JJ. Upper Airway Foreign Bodies: Emergency department presentation, Evaluation and Management. emDOCs.net - Emergency Medicine Education. April 12, 2021. Accessed May 9, 2023. http://www.emdocs.net/upper-airway-foreign-bodies-emergency-department-presentation-evaluation-and-management/.

Special Patient Groups

In the pediatric age group, moderate or high suspicion of FBA is suggested by any of the following:

  • Witnessed FBA, regardless of symptoms.
  • History of choking, with any subsequent symptoms or suspicious characteristics on imaging.
  • A young child with suggestive symptoms without another explanation, especially if there are suspicious characteristics on imaging. Suspicious symptoms include cyanotic spells, dyspnea, stridor, sudden onset of cough or wheezing (often focal and monophonic), and/or unilaterally diminished breath sounds.

The tracheobronchial tree should be examined in all cases with moderate or high suspicion of FBA, using rigid bronchoscopy (or, in some cases, computed tomography [CT]). On occasion, the adjunctive use of a flexible bronchoscope may be helpful. Normal chest radiographs are not sufficient to rule out FBA [19], primarily because most foreign bodies are radiolucent. Morbidity and mortality may increase if bronchoscopic evaluation is delayed.

When To Admit This Patient

Most patients improve clinically following FBA removal. Those with imaging abnormalities should undergo follow-up imaging six weeks to three months after extraction to confirm resolution. Patients presenting with a delayed presentation and belonging to high-risk groups should be admitted for management of complications and FBA retrieval and removal.

Revisiting Your Patients

The elderly patient, given his history of a recent stroke and being in a rehabilitation center, is at risk of FBA. His presentation with chronic cough and fever raises suspicion of pneumonia; however, the emergency medicine clinician should maintain a broad differential diagnosis based on further history, including foul-smelling sputum and nursing staff observations of difficulty swallowing and previous admissions for pneumonia. Such delayed presentations of FBA can occur in this age group. The patient’s management began with initial stabilization using oxygen support, along with workup for infection. Imaging modalities started with a chest plain film, which showed right lower lobe opacities but no clear foreign body. With suspicion for FBA still high, a chest CT scan was performed and revealed evidence consistent with FBA. The patient was started on broad-spectrum antibiotics, and bronchoscopy was scheduled as the definitive management for FBA. Follow-up bronchoscopy identified distal fragments of nuts impacted in the right lower lobe bronchus.

In the pediatric patient, the presentation is more acute and requires securing the airway. After placing the patient on a non-rebreather mask with 15L of oxygen, his saturation improved to 100%. Given the history of playing with a wallet, suspicion of coin aspiration was considered. A chest radiograph with posteroanterior and lateral views was performed, showing a rounded radiopaque structure in the right main bronchus. Airway support and supplemental oxygen should be provided until bronchoscopy is performed and the coin is retrieved.

Authors

Picture of Elhaitham Ahmed

Elhaitham Ahmed

Zayed Military Hospital, AbuDhabi

Picture of Khalifa Alqaydi

Khalifa Alqaydi

Zayed Military Hospital, AbuDhabi

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References

  1. Ruiz, F.E. (2022) Airway foreign bodies in children, UpToDate. Available at: https://www.uptodate.com/contents/airway-foreign-bodies-in-children?search=airway+foreign+bodies+in+children&source=search_result&selectedTitle=1~83&usage_type=default&display_rank=1 (Accessed: 08 May 2023).
  2. Shepherd, W. (2023) Airway foreign bodies in adults, UpToDate. Available at: https://www.uptodate.com/contents/airway-foreign-bodies-in-adults?search=adult+forign+body+&source=search_result&selectedTitle=3~150&usage_type=default&display_rank=3 (Accessed: 08 May 2023).
  3. Bajaj D, Sachdeva A, Deepak D. Foreign body aspiration. J Thorac Dis. 2021;13(8):5159-5175. doi:10.21037/jtd.2020.03.94
  4. Dabu J, Lindner M, Azzam M, et al. A Case of Chronic Cough and Pneumonia Secondary to a Foreign Body. Case Rep Med. 2017;2017:3092623. doi:10.1155/2017/3092623
  5. Mîndru DE, Păduraru G, Rusu CD, et al. Foreign Body Aspiration in Children-Retrospective Study and Management Novelties. Medicina (Kaunas). 2023;59(6):1113. Published 2023 Jun 9. doi:10.3390/medicina59061113
  6. Goodloe JM, Soulek J. Foreign Bodies . In: Rosen’s Emergency Medicine Concepts and Clinical Practice. 10th ed. Elsevier; 2023:666-681.
  7. Hazra TK, Ghosh AK, Roy P, Roy S, Sur S. An impacted meat bone in the larynx with an unusual presentation. Indian J Otolaryngol Head Neck Surg. 2005;57(2):145-146. doi:10.1007/BF02907672
  8. Swanson KL, Edell ES. Tracheobronchial foreign bodies. Chest Surg Clin N Am. 2001;11(4):861-872.
  9. Kazmerski T, Dedhia K, Maguire R, Aujla S. Chronic Esophageal Foreign Body Presenting as Wheezing and Cough in a Toddler. Pediatr Allergy Immunol Pulmonol. 2014;27(3):151-153. doi:10.1089/ped.2014.0370
  10. White JJ, Cambron JD, Gottlieb M, Long B. Evaluation and Management of Airway Foreign Bodies in the Emergency Department Setting. J Emerg Med. 2023;64(2):145-155. doi:10.1016/j.jemermed.2022.12.008
  11. António P, Raffaella C, Luigia R. Plain Film and MDCT Assessment of Neck Foreign Bodies. 2014;1007/978-88-470-5406-6_1.
  12. Svedström E, Puhakka H, Kero P. How accurate is chest radiography in the diagnosis of tracheobronchial foreign bodies in children?. Pediatr Radiol. 1989;19(8):520-522. doi:10.1007/BF02389562
  13. Turk D, Moslehi MA, Hosseinpour H. Role of Flexible Fiberoptic Bronchoscopy in the Diagnosis and Treatment of Pediatric Airway Foreign Bodies: A 5-Year Experience at a Tertiary Care Hospital in Iran. Tanaffos. 2022;21(3):354-361.
  14. Pavitt MJ, Swanton LL, Hind M, et al. Choking on a foreign body: a physiological study of the effectiveness of abdominal thrust manoeuvres to increase thoracic pressure. Thorax. 2017;72(6):576-578. doi:10.1136/thoraxjnl-2016-209540
  15. Bodart E, Gilbert A, Thimmesch M. Removal of an unusual bronchial foreign body: rigid or flexible bronchoscopy?. Acta Clin Belg. 2014;69(2):125-126. doi:10.1179/2295333714Y.0000000006
  16. Davis RJ, Stewart CM. Complete Glottic Obstruction by an Unusual Foreign Body. Otolaryngol Head Neck Surg. 2019;160(5):935-936. doi:10.1177/0194599818824298
  17. Singh GB, Aggarwal D, Mathur BD, Lahiri TK, Aggarwal MK, Jain RK. Role of magill forcep in retrieval of foreign body coin. Indian J Otolaryngol Head Neck Surg. 2009;61(1):36-38. doi:10.1007/s12070-009-0031-7
  18. White Upper Airway Foreign Bodies: Emergency department presentation, Evaluation and Management. emDOCs.net – Emergency Medicine Education. April 12, 2021. Accessed May 9, 2023. http://www.emdocs.net/upper-airway-foreign-bodies-emergency-department-presentation-evaluation-and-management/.
  19. Pinto A, Scaglione M, Pinto F, et al. Tracheobronchial aspiration of foreign bodies: current indications for emergency plain chest radiography. Radiol Med. 2006;111(4):497-506. doi:10.1007/s11547-006-0045-0

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Fundamentals of Pediatric Advanced Life Support (2024)

~ iEM Education Project Team ~ Leave a comment

by Burak Çakar & Ayça Koca

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Introduction

Pediatric cardiac arrest (CA) is a rare but critical event associated with high mortality and significant risk of severe sequelae [1,2]. Unlike in adults, respiratory causes are the primary contributors to CA in children. Hypoxia and bradycardia can lead to cardiopulmonary failure, which may ultimately progress to CA.

Common causes of pediatric CA include infections (e.g., pneumonia, sepsis), trauma, asphyxia, seizures, asthma, suffocation, and sudden infant death syndrome [2]. Clinical signs of cardiopulmonary arrest include respiratory arrest, absence of a palpable pulse, muscle flaccidity, unresponsiveness, cyanosis or other discoloration, and dilated pupils. Recognizing and promptly addressing these signs is crucial for improving outcomes.

Recognition of a Critically Ill Child

Early recognition of a critically ill child is essential to implementing timely interventions that may prevent progression to CA [3]. Abnormal vital signs, relative to age-specific norms, are often the most reliable indicators of impending arrest.

Pediatric Early Warning Scores (PEWS) are recommended as a systematic tool to identify children at risk of clinical deterioration [4]. PEWS evaluates three domains: behavior, cardiovascular function, and respiratory status [5]. It incorporates vital findings such as respiratory rate, heart rate, blood pressure, oxygen saturation, temperature, level of consciousness, and capillary refill time [6]. 

Monitoring Vital Signs in Children

It is essential to recognize abnormal vital signs for early recognition of pediatric deterioration.

Blood Pressure

Systolic Hypotension is defined as a systolic blood pressure below the 5th percentile for age. The threshold for concern is when the systolic blood pressure is <70 mmHg + (2x the child’s age in years).

Respiratory Rate

Tachypnea: A respiratory rate exceeding 60 breaths per minute indicates tachypnea.
Decreased Respiratory Rate: A reduction in respiratory rate in a previously tachypneic patient could signal either improvement or fatigue. Fatigue in this context could precede respiratory failure, particularly if it occurs in conjunction with other signs of decompensation.

Temperature

Fever significantly affects physiology. For every 1°C increase in body temperature:

  • The heart rate increases by approximately 10 beats per minute.
  • The respiratory rate increases by 2 to 5 breaths per minute.

End-Tidal Carbon Dioxide (EtCO2)

Changes in EtCO2 levels are critical indicators of respiratory status. A progressive increase or decrease in EtCO2 levels can signal impending desaturation and respiratory failure.

Assessment

Given the poor outcomes associated with pediatric CA, the emphasis must be on early recognition of pre-arrest states. Identifying signs of impending respiratory failure and shock, regardless of their underlying cause, should be a primary focus [4].

Findings Preceding Cardiopulmonary Arrest

Key findings preceding cardiopulmonary arrest are categorized as follows:

  1. Airway: Signs include stridor, drooling, and retractions, which indicate significant airway obstruction or distress.

  2. Breathing: Irregular respiration, bradypnea, gasping respirations, and cyanosis are warning signs of severe respiratory compromise.

  3. Circulation: Indicators such as a capillary refill time greater than 5 seconds, bradycardia, hypotension, cool extremities, weak central pulses, and the absence of peripheral pulses suggest circulatory failure.

  4. Disability: An altered level of consciousness and decreased responsiveness point toward significant neurological impairment, often accompanying or preceding arrest.

Initial Assessment

The initial assessment begins with a first impression of the child’s general appearance, breathing pattern, and circulatory status. During the primary assessment, the ABCDE approach is followed, with immediate interventions performed at each step when abnormalities are identified. Initial management focuses on supporting airway, breathing, and circulation [7].

The clinician should rapidly assess the following:

Airway

  • Assess for patency (open, requiring maneuvers/adjuncts, partially or completely obstructed)
  • Perform cervical spine stabilization for injured children.
  • Provide 100% inspired oxygen, clear the airway (e.g., suction), apply airway maneuvers, and insert airway adjuncts if the child is unconscious.
  • Initiate chest compressions immediately if the child is unresponsive and shows no signs of life.
  •  

 Breathing

  • Evaluate respiratory rate, effort, tidal volume, lung sounds, and pulse oximetry.
  • Assist ventilation manually for patients unresponsive to basic airway maneuvers or exhibiting inadequate respiratory effort.
  • Monitor oxygenation and ventilation using pulse oximetry and ETCO₂.
  • Administer appropriate medications based on the cause of respiratory distress (e.g., albuterol for status asthmaticus, inhaled racemic epinephrine for croup).
  • Consider intubation when necessary, ensuring 100% oxygen delivery via a non-rebreather mask. Apply positive pressure ventilation with a bag-valve-mask (BVM) in cases of respiratory failure.

Circulation

  • Assess skin color and temperature, heart rate and rhythm, blood pressure, peripheral and central pulses, and capillary refill time.
  • Control hemorrhage in injured children.
  • For circulation deficiencies, monitor heart rate and rhythm, and establish vascular access for volume resuscitation or medication administration.

Disability

  • Evaluate neurological status and level of consciousness using the AVPU scale (Alert, Voice, Pain, Unresponsive) and the Glasgow Coma Scale (GCS) for trauma patients.
  • Assess pupil size and reactivity to light.
  • Check for hypoglycemia using rapid bedside glucose testing or by observing the response to empiric dextrose administration.

Exposure

  • Examine for skin findings, fever or hypothermia, and evidence of trauma.

Secondary and Tertiary Assessments

  • The secondary assessment involves a detailed head-to-toe physical examination, supplemented with a medical history.
  • The tertiary assessment focuses on identifying the underlying causes of trauma, illness, or infection through ancillary studies.

Respiratory Distress and Failure

Respiratory distress and failure are common precursors to CA in children. Early recognition of breathing difficulties is essential to improving clinical outcomes.

Respiratory distress is characterized by tachypnea, nasal flaring, retractions, and the use of accessory muscles. Additional signs include agitation, hypoxia, and abnormal breath sounds, such as stridor or wheezing. If not promptly addressed, these findings can progress to a decreased respiratory rate, respiratory fatigue, and eventual respiratory arrest.

Bradycardia

In children, bradycardia is often secondary to hypoxia. A heart rate slower than the age-appropriate normal range is indicative of bradyarrhythmia. Management focuses on optimizing oxygenation and ventilation through basic airway maneuvers.

If the heart rate remains below 60 beats per minute despite adequate oxygenation and ventilation, chest compressions should be initiated. Epinephrine (0.01 mg/kg) should be administered every 3–5 minutes. For bradycardia caused by increased vagal tone or primary atrioventricular block, atropine (0.02 mg/kg; maximum single dose 0.5 mg) is recommended [7].

Tachycardia

Tachycardia refers to a heart rate that exceeds the normal range for a child’s age, considering other factors such as physical activity or fever. The management of tachycardias depends on the child’s hemodynamic condition and rhythm [7].

Pulseless Arrest

Pediatric CAs are typically the result of cardiopulmonary distress, failure, or shock. When a child has no palpable pulse and is unresponsive, cardiopulmonary resuscitation (CPR) should be initiated.

A child with pulseless arrest will present as apneic and may exhibit gasping respirations. The rhythms associated with pulseless arrest include [2]:

Shockable rhythms: Ventricular fibrillation (VF), pulseless ventricular tachycardia (pVT).

Ventricular Fibrillation

Ventricular Tachycardia

Unshockable rhythms: Asystole, pulseless electrical activity (PEA).

Asystole

Pulseless Electrical Activity (PEA)

During CPR, reversible causes of PEA should be actively identified and addressed. The mnemonic 6H5T is useful for recalling these potential causes [2]:

  • 6 H’s:
    • Hydrogen ion (acidosis)
    • Hypoxia
    • Hypovolemia
    • Hypo- or hyper -kalemia, -calcemia, -magnesemia
    • Hypoglycemia
    • Hypo- or hyperthermia
  • 5 T’s:
    • Tension pneumothorax
    • Tamponade
    • Thrombosis (cardiac)
    • Thrombosis (pulmonary)
    • Toxic agents

By addressing these potential causes, advanced life support providers can significantly improve the likelihood of successful resuscitation.

Resuscitation

An effective resuscitation team is critical to the successful management of pediatric advanced life support (PALS). The team must perform multiple tasks simultaneously, including airway management, ventilation, vascular access, medication preparation and administration, chest compressions, monitor/defibrillator operation, recording/timing, and overall leadership.

The team leader plays a pivotal role by assigning tasks, directing team members, and modeling exemplary teamwork. In addition to medical expertise and resuscitation skills, the team must demonstrate effective communication. Key elements of effective team dynamics include:

  • Closed-loop communication
  • Clear messages
  • Defined roles and responsibilities
  • Knowing and communicating one’s limitations
  • Knowledge sharing
  • Constructive interventions
  • Reevaluation and summarization
  • Mutual respect [8]

Initiation of CPR

Timely recognition of CA, prompt initiation of high-quality chest compressions, and ensuring adequate ventilation are crucial for improving outcomes [2].

Healthcare providers should begin chest compressions promptly in any child who is unresponsive, not breathing normally, and has no signs of circulation [7, 9]. Pulse checks may be performed but should not delay the initiation of CPR for more than 10 seconds [10, 11]. Pulse palpation alone is unreliable in determining the need for compressions or confirming CA.

Since respiratory-related CA is more common in infants and children than primary cardiac causes, ensuring adequate ventilation during resuscitation is essential [2]. The recommended sequence for CPR is compressions-airway-breathing (CAB) [12].

High-quality CPR enhances blood flow to vital organs and increases the likelihood of return of spontaneous circulation (ROSC). The five key components of high-quality CPR are [2, 13]:

  • Optimal chest compression rate
  • Sufficient chest compression depth
  • Minimal interruptions in compressions
  • Complete chest recoil between compressions [7, 14]
  • Avoidance of excessive ventilation

Components of High-Quality CPR

  • Compression Rate: 100–120 compressions per minute [15–18].
  • Compression Depth:
    • At least one-third of the anterior-posterior diameter of the chest:
      • 4 cm for infants
      • 5 cm for children
      • 5–6 cm for adolescents who have reached puberty [7, 19].
    • Allow complete chest recoil after each compression.
    • Use 100% oxygen with a bag-valve-mask (BVM) during CPR.
    • Compression-Ventilation Ratios:
      • 30:2 for single rescuers.
      • 15:2 for two rescuers [7, 20].

To prevent fatigue and ensure adequate compressions, switch the person performing compressions at least every 2 minutes or sooner if necessary [7].

CPR Technique

For Infants

Single Rescuer: Use two fingers (Figure 1) or two thumbs below the nipple line (lower half of the sternum but one-finger width above the xiphisternum) [21–24].

Figure 1. Two-finger compressions

Two Rescuers: Use the two-thumb encircling hands technique (Figure 2) [25–29].

Figure 2. Thumb-encircling hands compression

If the recommended depth cannot be achieved, use the heel of one hand (Figure 3) [2, 18, 30, 31].

Figure 3. Compression with the heel of one hand

For children older than 1 year

Use either one-handed or two-handed CPR.

Perform chest compressions on a firm surface. Use a backboard or activate the bed’s “CPR mode” if available [32–35].

The Airway

Unless a cervical spine injury is suspected, the head tilt-chin lift maneuver is recommended to open the airway [36]. In trauma patients with suspected cervical spinal injury, the jaw thrust maneuver should be used. If the jaw thrust is ineffective, the head tilt-chin lift may be performed, even in cases of suspected cervical spine injury [2].

Use 100% oxygen delivered via bag-valve-mask (BVM) during CPR.

Advanced Airway Interventions During CPR

Bag-mask ventilation (BMV) is effective for most patients but requires pauses in chest compressions and carries risks of aspiration and barotrauma [2]. Advanced airway interventions, such as supraglottic airway (SGA) placement or endotracheal intubation (ETI), improve ventilation, reduce aspiration risks, and enable uninterrupted chest compressions. However, these procedures require specialized equipment and trained providers, and may be challenging for those inexperienced in pediatric intubation [2]. BMV is more reliable than advanced airway interventions during out-of-hospital pediatric CA [37–39].

For patients with advanced airway, ventilations should be asynchronous. Exceeding recommended ventilation rates can compromise hemodynamics and lower systolic blood pressure [40].

Ventilations should be tailored to age:

  • 25 breaths/min (infants)
  • 20 breaths/min (>1 year)
  • 15 breaths/min (>8 years)
  • 10 breaths/min (>12 years) [7].

Capnography should be used to confirm endotracheal tube placement and monitor for ROSC. However, ETCO₂ should not be used as a definitive quality indicator or target during PALS [7].

Drug Administration During CPR

Establish IV access as early as possible during PALS. If IV access is challenging, promptly consider intraosseous (IO) access as an alternative [7]. Drug dosing for children is typically based on weight, which can be challenging to determine in emergencies. When the actual weight cannot be obtained, various estimation methods are available [41]

The administration of vasoactive agents during CA aims to improve coronary and cerebral perfusion and increase the likelihood of ROSC. However, optimal timing and overall impact on long-term outcomes are still under investigation [42]

  • Administer epinephrine (10 mcg/kg; max 1 mg; IV or IO ) as soon as possible for non-shockable rhythms. For shockable rhythms, administer epinephrine immediately after the third shock, along with antiarrhythmic drugs. Once given, adrenaline should be repeated every 3–5 minutes until ROSC.

Antiarrhythmic drugs can reduce the risk of recurrent VF or pVT and improve the likelihood of successful defibrillation [43, 44]. Only in shockable rhythms, administer antiarrhythmic drugs immediately after the third shock, along with epinephrine.

  • Amiodarone: 5 mg/kg (max 300 mg); a second dose (max 150 mg) may follow after the fifth shock if the rhythm remains shockable.
  • Lidocaine: 1 mg/kg, as an alternative to amiodarone.

Magnesium sulfate (25–50 mg/kg) should be considered for torsades de pointes. Routine administration of sodium bicarbonate and calcium is not recommended unless specific conditions (e.g., electrolyte imbalances, drug toxicities) are present [45–48].

Flush all IV or IO resuscitation drugs with 5–10 mL of normal saline to ensure delivery to the central circulation.

Defibrillation During PALS

Shockable rhythms in children include pulseless ventricular tachycardia (pVT) and ventricular fibrillation (VF). When identified, defibrillation should be performed immediately, regardless of the ECG amplitude. If there is uncertainty about the rhythm, it should be treated as shockable to avoid delays in care. [7].

The preferred method for defibrillation during pediatric ALS is manual defibrillation, but an automated external defibrillator (AED) can be used if manual defibrillation is unavailable. Currently, self-adhesive defibrillation pads are the standard. When using these pads:

  • Chest compressionsshould continue while the defibrillator charges.
  • The pads should be placed in either the antero-lateral (AL)or antero-posterior (AP) positions:
    • AL position: One pad below the right clavicle and the other in the left axilla.
    • AP position: The front pad in the mid-chest just left of the sternum, and the back pad between the scapulae.

Avoid contact between the pads to prevent electrical arcing.

If self-adhesive pads are unavailable, paddles with gel or pre-shaped gel pads can be used as an alternative. In this case, charging should occur directly on the chest, pausing compressions during the process [7]. Pre-planning each step is critical to minimizing delays during the intervention.

Charge the defibrillator for an initial shock of 4J/kg. Avoid exceeding the maximum doses recommended for adults (typically 120–200J, depending on the defibrillator). Pause chest compressions briefly to deliver the shock, ensuring all rescuers are clear of the patient. Resume CPR immediately after the shock, minimizing the pause to under 5 seconds. Reassess the rhythm every 2 minutes and, if it remains shockable, deliver subsequent shocks at 4J/kg. For refractory VF/pVT (requiring more than 5 shocks), incrementally increase the dose up to 8J/kg (maximum 360J) [7].

CPR should continue until an organized, potentially perfusing rhythm is recognized during a rhythm check and is accompanied by signs of ROSC, identified either clinically (e.g., eye-opening, movement, normal breathing) or through monitoring (e.g., etCO2, SpO2, blood pressure, ultrasound) [7].

A summary of the fundamentals of pediatric ALS can be found in Figure 5.

Figure 5. Pediatric cardiac arrest algorithm [7] CPR: cardiopulmonary resuscitation, EMS: emergency medical services, ALS: advanced life support, VF: ventricular fibrillation, pVT: pulseless ventricular tachycardia, PEA: pulseless electrical activity, IV: intravenous, IO: intraosseous.

Post-cardiac Arrest Management

Achieving ROSC is only the first step in resuscitation. Comprehensive post-CA care is crucial to optimizing outcomes, particularly in pediatric patients. This phase focuses on treating the underlying cause of the event and preventing secondary injuries.

Key Components of Post-Cardiac Arrest Care

Targeted Temperature Management (TTM):

  • For unconscious children after ROSC, TTM helps prevent further brain injury.

Ventilation and Oxygenation:

  • Inspired oxygen should be titrated to maintain oxygen saturation (SpO₂) between 94% and 99%.
  • For intubated patients, confirm endotracheal tube (ETT) placement and monitor ventilation to avoid hyperoxia or hypoxia, as well as hypercapnia or hypocapnia.

Hemodynamic Support:

  • Prevent and treat hypotension using parenteral fluids and vasoactive medications, guided by physiologic endpoints and cardiac function.
  • Monitor for signs of recurrent shock and intervene promptly.

Glucose Management:

  • Maintain blood glucose levels below 180 mg/dL to avoid complications associated with hyperglycemia.

Seizure Management:

  • For unconscious children after ROSC, continuous electroencephalography monitoring is also recommended to detect subclinical seizures. Seizures should be monitored and treated aggressively, as they can exacerbate neurological injury.

Temperature Regulation:

  • Avoid hyperthermia (core temperature >37.5°C) using cooling measures as necessary to reduce metabolic demands and limit neuronal damage.

Summary

Pediatric CA remains a critical event with high mortality and significant morbidity. Unlike adult CA, pediatric cases are often precipitated by respiratory failure and hypoxia, highlighting the need for timely recognition and intervention. Early identification of abnormal vital signs, particularly through tools like PEWS, and a structured approach to initial assessment using the ABCDE framework are paramount in preventing CA. Furthermore, rapid and effective resuscitation, incorporating high-quality CPR, advanced airway management, and appropriate medication use, significantly improves the likelihood of survival and favorable outcomes.

Managing pediatric CA extends beyond achieving ROSC. Comprehensive post-cardiac arrest care, including targeted temperature management, optimized ventilation and oxygenation, hemodynamic support, glucose management, and seizure control, is critical to minimize secondary injuries and improve neurological recovery. Pediatric Advanced Life Support (PALS) algorithms and effective resuscitation team dynamics play essential roles in guiding care.

Ultimately, improving outcomes in pediatric CA requires a systematic approach to prevention, timely recognition, prompt intervention, and evidence-based post-resuscitation care. Continuous education, training, and adherence to updated guidelines are essential for healthcare providers to ensure the best possible outcomes for critically ill or arrested children.

Authors

Picture of Burak Çakar

Burak Çakar

Gaziantep Islahiye State Hospital, Department of Emergency Medicine, Gaziantep, Turkey

Picture of Ayça Koca

Ayça Koca

Ayça Koca is an emergency physician at Ankara University School of Medicine, Department of Emergency Medicine. She completed both her medical degree and residency at Ankara University, where she developed a deep connection to patient care and teaching. With a special interest in medical education and simulation, she is passionate about creating engaging learning experiences to support the growth and confidence of future healthcare providers.

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References

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  37. Andersen LW, Raymond TT, Berg RA, et al. Association Between Tracheal Intubation During Pediatric In-Hospital Cardiac Arrest and Survival. JAMA. 2016;316(17):1786-1797.
  38. Hansen ML, Lin A, Eriksson C, et al. A comparison of pediatric airway management techniques during out-of-hospital cardiac arrest using the CARES database. Resuscitation. 2017;120:51-56.
  39. Ohashi-Fukuda N, Fukuda T, Doi K, Morimura N. Effect of prehospital advanced airway management for pediatric out-of-hospital cardiac arrest. Resuscitation. 2017;114:66-72.
  40. Sutton RM, Reeder RW, Landis WP, et al. Ventilation Rates and Pediatric In-Hospital Cardiac Arrest Survival Outcomes. Crit Care Med. 2019;47(11):1627-1636.
  41. Young KD, Korotzer NC. Weight Estimation Methods in Children: A Systematic Review. Ann Emerg Med. 2016;68(4):441-451.e10.
  42. Campbell ME, Byrne PJ. Cardiopulmonary resuscitation and epinephrine infusion in extremely low birth weight infants in the neonatal intensive care unit. J Perinatol. 2004;24(11):691-695.
  43. Holmberg MJ, Ross CE, Atkins DL, et al. Lidocaine versus amiodarone for pediatric in-hospital cardiac arrest: An observational study. Resuscitation. 2020;149:191-201.
  44. Valdes SO, Donoghue AJ, Hoyme DB, et al. Outcomes associated with amiodarone and lidocaine in the treatment of in-hospital pediatric cardiac arrest with pulseless ventricular tachycardia or ventricular fibrillation [published correction appears in Resuscitation. 2019;142:117-118.]. Resuscitation. 2014;85(3):381-386.
  45. Del Castillo J, López-Herce J, Cañadas S, et al. Cardiac arrest and resuscitation in the pediatric intensive care unit: a prospective multicenter multinational study. Resuscitation. 2014;85(10):1380-1386.
  46. Matamoros M, Rodriguez R, Callejas A, et al. In-hospital pediatric cardiac arrest in Honduras. Pediatr Emerg Care. 2015;31(1):31-35.
  47. Wolfe HA, Sutton RM, Reeder RW, et al. Functional outcomes among survivors of pediatric in-hospital cardiac arrest are associated with baseline neurologic and functional status, but not with diastolic blood pressure during CPR. Resuscitation. 2019;143:57-65.
  48. Lasa JJ, Alali A, Minard CG, et al. Cardiopulmonary Resuscitation in the Pediatric Cardiac Catheterization Laboratory: A Report From the American Heart Association’s Get With the Guidelines-Resuscitation Registry. Pediatr Crit Care Med. 2019;20(11):1040-1047.

Reviewed and Edited By

Picture of Elif Dilek Cakal, MD, MMed

Elif Dilek Cakal, MD, MMed

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

The ABCDE Approach to Undifferentiated Critically Ill and Injured Patient (2024)

~ iEM Education Project Team ~ Leave a comment

by Roxanne R. Maria, Hamid A. Chatha

Authors
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You have a new patient!

A 40-year-old male, a truck driver, is involved in a head-on collision with another vehicle. He has been brought in by ambulance. According to the paramedics, the vehicles were traveling at approximately 85 km/hr, and the patient was restrained by a seatbelt. On arrival at the Emergency Department (ED), the patient is agitated and mildly disoriented. He is tachypneic with a respiratory rate of 30/min, maintaining an O2 saturation of 95% on 12 L/min oxygen via a non-rebreather mask, heart rate of 128 beats/min, blood pressure of 90/52 mmHg, and temperature of 36.1°C. The patient also received 1 L of 0.9% normal saline and 1 unit of O-negative packed red cells in the ambulance. Despite this, his respiratory rate, heart rate, and level of disorientation have worsened.

Emergency Department

In the ED, patients present with a variety of clinical presentations, including both life-threatening and non-life-threatening. Some may have been seen and referred by a clinician before arrival or brought to the department after pre-hospital assessment and care by the emergency medical services (EMS) [1]. Health emergencies affect all age groups and include conditions like acute coronary syndrome, strokes, acute complications of pregnancy, or any chronic illness. Emergency health care providers should respond to these clinically ‘undifferentiated’ patients with symptoms for which the diagnosis may not be known [2].  The root cause of most life-threatening conditions in the ED may be medical or surgical, infection or trauma [2].

In the Emergency Department (ED), there are several potentially life-threatening presentations that demand immediate stabilization. These include trauma, which can result from various forms of accidents or injuries, and shortness of breath, which might indicate critical respiratory distress. An altered mental state also requires prompt attention, as it may signal underlying neurological or systemic issues. Shock, often evidenced by dangerously low blood pressure. Chest pain or discomfort, which could be indicative of a cardiac event, are other urgent concerns. Additionally, cases of poisoning, ingestion of harmful substances, or exposure to toxic materials also necessitate rapid intervention to prevent further harm. Each of these presentations is a medical priority, highlighting the importance of timely and effective response in the ED to ensure patient safety and stability.

These symptoms maybe the only picture that the patients present with, and may constitute the early stage of a critical illness requiring rapid, appropriate intervention and resuscitation, even when the patient seems to appear relatively well [2].

Emergency conditions often require immediate intervention long before a definitive diagnosis is made to stabilize the critically ill patient [3]. Thus, this chapter intends to briefly introduce a basic systematic approach to identifying and managing acute, potentially life-threatening conditions in these patients. This approach will enable all frontline providers, including students, nurses, pre-hospital technicians, and physicians, to manage these patients even in the setting of limited resources [2].

A complete assessment and management of each of the presentations mentioned above is beyond the scope of this chapter. However, the initial approach remains the same, regardless of the patient population or setting [4].

History of the ABCDE approach

The ABC mnemonic’s origins may be traced back to the 1950s. The first two letters of the mnemonic, A and B, resulted from Dr Safar’s description of airway protection techniques and administration of rescue breaths. Kouwenhoven and colleagues later added the letter C to their description of closed-chest cardiac massage [3].

Styner is credited with further developing the Airway, Breathing, Circulation, Disability, and Exposure (ABCDE) approach. After a local aircraft disaster in 1976, Styner and his family were taken to a local healthcare facility, where he saw an insufficiency in the emergency treatment offered. He then founded the Advanced Trauma Life Support course, emphasizing a methodical approach to treating severely injured patients.

The ABCDE approach is universally accepted and utilized by emergency medicine clinicians, technicians, critical care specialists, and traumatologists [3]. Thus, this approach is recommended by international guidelines for suspected serious illness or underlying injury, irrespective of the diagnosis [5]. It is also the first step in post-resuscitation care after the patient achieves return of spontaneous circulation (ROSC) from a cardiac arrest [3]. This systematic approach also aims to improve coordination among the team members and saves time to make critical decisions [3].

The ABCDE approach

Since time is of the essence, the ABCDE method is a systematic approach that can be easily and quickly practiced in the ED. This is incorporated into what is known as ‘Initial patient assessment,’ one of the most crucial steps in evaluation [6]. At each step of this approach, life-threatening problems must be addressed before proceeding to the next assessment step. After the initial assessment, patients must be reassessed regularly to evaluate the treatment response. Anticipate and call for extra help early [7]. Appropriate role allocation and good communication are important for effective team working [7]. Once the patient is stabilized, a secondary survey should be conducted, which includes a thorough history, physical examination, and diagnostic testing [8]. Finally, the tertiary survey is done within 24 hours of presentation to identify any other missed injuries in trauma. Once it is recognized that the patient’s needs exceed the facility’s capabilities, the transfer process must be initiated to an appropriately specialized care center accordingly [8].

Ensure Safe Environment

Before initiating the ABCDE approach, it is essential to ensure both personal safety and a secure environment. This preparation includes addressing any potential risks, such as unexpected or violent behavior, environmental hazards, and the risk of exposure to communicable diseases. Health professionals should consider using appropriate personal protective equipment (PPE) suited to the situation, which may include gloves, gowns, masks, goggles, and thorough hand washing. These precautions are vital to protect both the healthcare provider and the patient, ensuring a safe environment for medical intervention [4].

Initiate First Response

The Resuscitation Council UK (RCUK) (2015) recommends performing a range of initial activities before proceeding with the ABCDE approach [4].

Examine the patient in general (skin color, posture, sensorium, etc.) to determine whether they seem critically ill [4].

After introducing yourself, an initial assessment can be completed in the first 10-15 seconds by asking patients their names and about their active complaints. If they respond normally, it means the airway is patent and brain perfusion is expected [9]. Check for breathing and pulse if the patient appears unconscious or has collapsed. If there is no pulse, call for help and immediately start cardiopulmonary resuscitation (CPR), adhering to local guidelines [9].

Detailed ABCDE Evaluation

Primary Survey

Patients are assessed and prioritized according to their presentations and vital signs. In primary survey, critically ill patients are managed efficiently along with resuscitation. The approach represents the sequence of steps as described below [10]:

A – Airway (with C spine control in Trauma patients)

B – Breathing and Ventilation

C – Circulation (With Hemorrhage control in active bleeding)

D – Disability

E – Exposure / Environment control

A – Airway

Airway obstruction is critical! Gain expert help immediately. If not treated, it can lead to hypoxia, causing damage to the brain, kidneys, and heart, resulting in cardiac arrest and death [4].

Airway management remains the cornerstone of resuscitation and is a specialized skill for the emergency clinician [9].

Assessment of airway patency is the first step. Can the patient talk? If yes, then the airway is patent and not in immediate danger. If not, look for the signs of airway compromise: Noisy breathing, inability to speak, presence of added sounds, stridor or wheezing, choking or gagging, cyanosis, and use of accessory muscles.

The next step is to open the mouth and look for anything obstructing the airway, such as secretions, blood, a foreign body, or mandibular/tracheal/laryngeal fractures [10].

While examining and managing the airway, great care must be taken to restrict excessive movement of the cervical spine and assume the existence of a spinal injury in cases of trauma [11].

Several critical factors can compromise a patient’s airway and must be addressed promptly in emergency settings. A depressed level of consciousness, which may result from conditions such as opioid overdose, head injury, or stroke, can impair airway protection and lead to significant risk [10]. Additionally, an inhaled foreign body, or the presence of blood, vomit, or other secretions, can obstruct the airway and necessitate immediate intervention. Fractures of the facial bones or mandible further complicate airway management due to potential structural damage. Soft tissue swelling, whether caused by anaphylaxis (angioedema) or severe infections like quinsy or necrotizing fasciitis, also seriously threatens the airway. These conditions highlight the importance of vigilant monitoring and rapid response to maintain airway patency and prevent complications.

angioedema - DermNet New Zeeland, CC BY NC ND 3.0
uvula edema - WikiMedia Commons - CC-BY-SA-3.0

Intervention: Several basic maneuvers can help maintain a clear airway. Suctioning should be performed if there are any secretions or blood present. Additionally, using the head-tilt, chin-lift, and jaw-thrust maneuvers can aid in keeping the airway open. For patients with a low Glasgow Coma Scale (GCS) score, placing an oropharyngeal or nasopharyngeal airway can be beneficial in maintaining airway patency. It’s also important to inspect the airway for any obvious obstructions; if a visible object is within reach, it may be removed carefully using a finger sweep or suction. It is crucial to remember that assistance from an anesthetist may be required in some cases. 

Head-Tilt, Chin-Lift maneuver

In trauma patients, to protect the C-spine, perform a jaw-thrust rather than a head-tilt chin-lift maneuver and immobilize the C-spine with a cervical collar [9].

A definitive airway, such as endotracheal intubation, may be necessary in patients with airway obstruction, GCS ≤ 8, severe shock or cardiac arrest, and at risk of inhalation injuries [8].

If intubation has failed or is contraindicated, a definitive airway must be established surgically [11].

B – Breathing and Ventilation

Effective ventilation relies on the proper functioning of the lungs, chest wall, and diaphragm, along with a patent airway and sufficient gas exchange to optimize oxygenation [10]. To assess breathing and ventilation, clinicians should evaluate oxygen saturation, monitor the respiratory rate for any signs of abnormality—such as rapid breathing (tachypnea), slow breathing (bradypnea), or shallow breathing (Kussmaul breathing)—and observe for increased work of breathing, such as accessory muscle use, chest retractions, or nasal flaring. Other critical assessments include checking for neck vein distention, examining the position of the trachea, chest expansion, and any injuries or tenderness, as well as auscultating for bilateral air entry and any additional sounds. Chest percussion should be performed to identify dullness, which may indicate hemothorax or effusion, or hyperresonance, suggestive of pneumothorax. Certain pathologies, like tension pneumothorax, massive hemothorax, open pneumothorax, and tracheal or bronchial injuries, can rapidly disrupt ventilation. Other conditions, including simple pneumothorax, pleural effusion, simple hemothorax, rib fractures, flail chest, and pulmonary contusion, may compromise ventilation to a lesser degree [10].

Interventions:

  • Oxygen – Ensure all patients are adequately oxygenated, with supplemental oxygen delivered to all severely injured trauma patients [11]. Place them on well-fitted oxygen reservoir masks with a flow rate > 10 L/min, which can then be titrated as needed to maintain adequate saturations. Other means of oxygen delivery (nasal catheter, nasal cannula, non-rebreather) can also be used.
  • Bag mask valve ventilation with oxygen – should be given to unconscious patients with abnormal breathing patterns (slow or shallow respiration).
  • Other interventions include salbutamol nebulizers, epinephrine, steroids, needle decompression, chest tube insertion, and the use of noninvasive ventilation and pressure support in different clinical scenarios.

C – Circulation (With Hemorrhage control in active bleeding)

Major circulatory compromise in critically ill patients can result from either blood volume loss or reduced cardiac output. In trauma cases, hypotension is assumed to be due to blood loss until proven otherwise. To assess the hemodynamic status, several key evaluations should be performed. These include checking the level of consciousness, as an altered state may indicate impaired cerebral perfusion, and assessing skin perfusion for signs like pallor, cyanosis, mottling, or flushing. Vital signs such as heart rate and blood pressure should be monitored for abnormalities like tachycardia, bradycardia, hypotension, or hypertension. Auscultation can reveal muffled heart sounds, which may suggest cardiac tamponade or pneumothorax, as well as murmurs or a pericardial friction rub that could indicate pericarditis. Checking the extremities for capillary refill and skin temperature is also essential. Additionally, palpation of the abdomen for tenderness or a pulsatile mass may reveal an abdominal aortic aneurysm, while peripheral edema, such as pedal edema, might indicate heart failure.

Interventions:

  • Two large-bore IV cannulations must be placed. If this attempt fails, intraosseous access is necessary. Hemorrhagic shock—A definitive control of bleeding along with replacement of intravascular volume is essential. Initial resuscitation should start with warm crystalloids, and blood products should be used. Massive Transfusion Protocol (MTP) should be activated according to local guidelines. In hemorrhagic shock, vasopressors and reversal of anticoagulation (if required) can be considered.
  • Hemorrhage control: External hemorrhage can be controlled by direct manual pressure over the site of the wound or tourniquet application.
  • In the case of pelvic or femur fractures, placement of pelvic binders or extremity splints may help to stabilize, although definitive management may be surgical or interventional radiological procedures.
  • Obstructive shock – Immediate pericardiocentesis for cardiac tamponade, chest tube insertion for tension pneumothorax, and thrombolysis for massive pulmonary embolism.
  • Distributive shock – intramuscular epinephrine for anaphylactic shock, empiric antibiotics for sepsis, and hydrocortisone for adrenal crisis.
  • Appropriate antihypertensives in hypertensive emergency.

D – Disability

Evaluate neurological status either with AVPU (Alert, Verbal, Pain and Unresponsive) [5] or GCS (Glasgow Coma Scale).

Evaluate for agitation, head and neck trauma, focal neurological signs (seizure, hemiplegia, etc), lateralizing signs, meningeal signs, signs of raised intracranial pressure, and pupillary examination (size and symmetry). Identify any classic toxidromes (sympathomimetic, cholinergic, anticholinergic, opioid, serotonergic, and sedative-hypnotic toxidromes). 

Choose the best response of patient
EYE OPENING
4: Spontaneously
3: To verbal command
2: To pain
1: No response
BEST VERBAL RESPONSE
5: Oriented and converses
4: Disoriented and converses
3: Inappropriate words; cries
2: Incomprehensible sounds
1: No response
BEST MOTOR RESPONSE
6: Obeys command
5: Localizes pain
4: Flexion withdrawal
3: Flexion abnormal (decorticate)
2: Extension (decerebrate)
1: No response
Glasgow Coma Score (GCS) (Modified from Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness: a practical scale. The Lancet, 304(7872), 81-84.) - Please read this article to get more insight regarding GCS.

The Glasgow Coma Scale (GCS) is a critical tool for assessing the level of consciousness in critically ill patients, providing a score based on eye, verbal, and motor responses. A GCS score ranges from 3 to 15, with lower scores indicating more severe impairment. Scores of 13-15 generally indicate mild impairment, 9-12 suggest moderate impairment, and scores of 8 or below (comatose patient) represent severe impairment and a high risk of poor outcomes. In critically ill patients, a declining GCS score can signal worsening neurological status, potentially due to factors like traumatic brain injury, hypoxia, or systemic deterioration, and often warrants immediate intervention to address underlying causes.

E – Exposure and Environmental control

It is necessary to expose the patient appropriately whilst maintaining dignity and body temperature.

Look at the skin for any signs of trauma (burns, stab wounds, gunshot wounds, etc.), rashes, infected wounds, ulcers, needle track marks, medication patches, implantable devices, tubes, catheters, and stomas; measure core body temperature, and perform logroll (trauma).

Do not forget to check frequently concealed and overlooked areas such as the genital, inguinal, perineal, axilla, back and under dressings [8].

Interventions:

  • Use specialized personal protective equipment (PPE), remove all possible triggers such as wet or contaminated clothing, and maintain core body temperature.
  • Minimize hypothermia (external rewarming, warm IV fluids) and hyperthermia (surface cooling, cold IV fluids, antipyretics for fever).

Adjuncts to primary survey

1. Electrocardiography (ECG)
2. Pulse oximetry
3. Carbon dioxide (CO2) monitoring
4. Arterial blood gas (ABG) analysis
5. Urinary catheterization (to assess for hematuria and urine output)
6. Gastric catheterization (for decompression)
7. Blood lactate level measurement
8. Chest and pelvis X-rays
9. Extended focused assessment with sonography for trauma (eFAST)

These adjuncts help provide a comprehensive evaluation of the patient’s condition [10].

Secondary Survey

After the initial primary survey and stabilization, proceed to the secondary survey. This includes a detailed history (SAMPLE)and a head-to-toe examination, including reassessment of vital signs, as there is a potential for missing an injury or other findings in an unresponsive patient [10].

The SAMPLE mnemonic is a structured approach for gathering essential patient history in emergency settings. It stands for Signs and Symptoms, Allergies, Medications, Past Medical History, Last Oral Intake, and Events leading to the illness or injury [5].

  • “Signs and Symptoms” involves asking the patient, family, or other witnesses about any observable signs or reported symptoms.
    “Allergies” are crucial to identify to prevent harm and may help recognize conditions like anaphylaxis.
  • “Medications” requires a comprehensive list of all current and recent medications, including any changes in dosage.
  • “Past Medical History” provides insights into underlying health conditions that may influence the current illness.
  • “Last Oral Intake” is important for assessing risks of aspiration or complications if the patient requires sedation or surgery.
  • Finally, understanding the “Events” surrounding the illness or injury aids in determining its cause and severity.

Together, these components guide healthcare providers in developing a more accurate and effective treatment plan.

In the secondary survey, a thorough approach is taken to ensure comprehensive care for the patient. This includes performing relevant and appropriate diagnostic tests based on the clinical assessment to confirm diagnoses and guide further treatment. Critical, targeted treatments should be initiated promptly, along with adequate supportive care to stabilize the patient’s condition. If necessary, specialized consults are obtained to address specific medical needs. Additionally, the healthcare team must assess the need for escalation of care or consider an interfacility transfer if the patient requires more specialized resources or advanced care options [8]. This structured approach ensures that all aspects of the patient’s condition are managed effectively. 

Adjuncts to secondary survey

Additional x-rays for the spine and extremities, CT scans of the head, chest, abdomen, and spine, urography and angiography with contrast, transesophageal ultrasound, bronchoscopy, and other diagnostics [10].

If the patient starts to deteriorate, immediately go back to the ABCDE approach and reassess!

Special Patient Groups

In recent ATLS updates, the ABCDE approach has been modified to the xABCDEF approach, where “x” stands for eXsanguinating eXternal hemorrhage control and “F” stands for further factors such as special groups (pediatric, Geriatric, and Pregnancy).  While the xABCDEF approach is universal and applies to all patient groups, specific anatomic and physiological differences in different populations should be considered while evaluating and treating life-threatening conditions. Some special population groups are discussed here:

Pediatrics [10]

Children have smaller body mass but higher body surface area than their body mass and proportionately larger heads than adults. These characteristics cause children to have increased energy transfer, hypothermia, and blunt brain trauma.

A useful adjunct is the Broselow® Pediatric Emergency Tape, which helps to rapidly identify weight-based medication doses, fluid volumes, and equipment sizes.

The ABCDE approach in children should proceed in the same manner as in adults, bearing in mind the anatomical differences.

Airway – Various anatomical features in children, such as large tissues of the oropharynx (tongue, tonsils), funnel-shaped larynx, more cephalad and anteriorly placed larynx and vocal cords, and shorter length of the trachea, make assessment and management of the airway difficult. Additionally, in smaller children, there is disproportionality in size between the cranium and the midface, making the large occiput in passive flexion of the cervical spine, resulting in the posterior pharynx being displaced anteriorly. The neutral alignment of the spine can be achieved by placing a 1-inch pad below the entire torso of the infant or toddler.

The most preferred technique for orotracheal intubation is under direct vision, along with restriction of the cervical spine, to achieve a definitive airway.

Infants are more prone to bradycardia due to laryngeal stimulation during intubation than older children and adults. Hence, when drug-assisted intubation is required, the administration of atropine sulfate pretreatment must be considered. Atropine also helps to dry out oral secretions, further enhancing the view of landmarks for intubation.

When the airway cannot be maintained by bag-mask ventilation or orotracheal intubation, a rescue airway with either a laryngeal mask airway (LMA), an intubating LMA, or a needle cricothyroidotomy is required.

Red flag signs in children include stridor, excessive drooling, airway swelling, and the child’s unwillingness to move the neck. Examine the airway carefully for any foreign bodies, burns, or obstruction.

Breathing and ventilation – Children’s respiratory rates decrease with age. The normal tidal volumes in infants and children vary from 4-6 ml/kg to 6-8 ml/kg while assisting in ventilation. Care must be taken to limit pressure-related barotrauma during ventilation. It is recommended that children weighing less than 30 kg use a pediatric bag valve mask.

Injuries such as pneumothorax, hemothorax, and hemopneumothorax should be treated by pleural decompression, for tension pneumothorax, and needle decompression in the 2nd intercostal space (over the top of the third rib) at the midclavicular line. The site for chest tube insertion remains the same as in adults.

The most common cause of pediatric cardiac arrest is hypoxia, and the most common acid-base abnormality encountered is respiratory acidosis due to hypoventilation.

Circulation – Important factors in assessing and managing circulation and shock are looking for signs of circulatory compromise, ascertaining the patient’s weight and circulatory volume, gaining timely peripheral venous access, delivering an appropriate volume of fluids with or without blood replacement, evaluating the adequacy of resuscitation, and aiming for thermoregulation.

Children have increased physiological reserves. A 30% decrease in the circulating blood volume may be required for a fall in the systolic blood pressure. Hence, it is important to look for other subtle signs of blood loss, such as progressive weakening of peripheral pulses, narrow pulse pressure to less than 20 mm Hg, skin mottling (in infants and young children), cool extremities, and decreased level of consciousness.

The preferred route is peripheral venous access, but if this is unsuccessful after two attempts, intraosseous access should be obtained.

Fluid resuscitation must be commenced at 20 ml/kg boluses of isotonic crystalloids. If the patient has ongoing bleeding, packed red blood cells may be initiated at 10 ml/kg as soon as possible. Given that children have increased metabolic rates, thinner skin, and lack of substantial subcutaneous tissue, they are prone to develop hypothermia quickly, which may impede a child’s response to treatment, increase coagulation times, and affect the central nervous system (CNS) function. Therefore, overhead lamps, thermal blankets, as well as administration of warm IV fluids, blood products, and inhaled gases may be required during the initial phase of evaluation and resuscitation.

Disability – Hypoglycemia is a very common cause of altered mental state in children, and children can present with altered mental state or seizures. Check for blood glucose in children; if low, administer glucose (IV D10 or D25).

Geriatric [10]

In cases of trauma in geriatric patients, physiological events that may have led to it (e.g., cardiac dysrhythmias) must be considered. A detailed review of long-term medical conditions and medications, along with their effect on vital signs, is necessary. Risk factors for falls include physical impairments, long-term medication use, dementia, and visual, cognitive, or neurological impairments.

Elderly patients are more prone to sustaining burn injuries due to decreased reaction times, hearing and visual impairment, and inability to escape the burning structure. Burn injury remains the cause of significant mortality.

Airway – Due to loss of protective airway reflexes, airway management in the elderly can be challenging and requires a timely decision to establish a life-saving definitive airway. Opening of the mouth and cervical spine maneuvering may be challenging with arthritic changes. Loose dentures should be removed, while well-fitted dentures should be better left inside. Some patients may be edentulous, making intubation easier, but bag-mask ventilation is difficult.

While performing rapid sequence intubation, it is recommended to lower the doses of barbiturates, benzodiazepine, and other sedatives to 20% to 40% to avoid the risk of cardiovascular depression.

Breathing – Elderly patients have decreased compliance of the lungs and the chest wall, which leads to increased breathing work, placing them at a higher risk for respiratory failure. Aging also results in suppressed heart rate during hypoxia, and respiratory failure may present alongside.

Circulation – These patients may have increasing systemic vascular resistance in response to hypovolemia, given that they may have a fixed heart rate and cardiac output. Also, an acceptable blood pressure reading may truly indicate a hypotensive state, as most elderly patients have preexisting hypertension.

A systolic blood pressure of 110 mm Hg is used as a threshold for identifying hypotension in adults over 65.

Several variables, namely base deficit, serum lactate, shock index, and tissue-specific lab markers, can be used to assess for hypoperfusion. Consider early use of advanced monitoring of fluid status, such as central venous pressure (CVP), echocardiography, and bedside ultrasonography, to guide resuscitation.

Disability – Traumatic brain injury is one of the significant complications among the elderly. The dura becomes more adherent to the skull with age, which increases the risk of epidural hematoma. Moreover, these patients are commonly prescribed anticoagulant and antiplatelet medications, which puts these individuals at a higher risk of developing intracranial hemorrhage. Therefore, a very low threshold is indicated for further CT scan imaging in ruling out acute intracranial and spinal pathologies.

Exposure – Increased risk of hypothermia due to loss of subcutaneous fat, nutritional deficiencies, chronic medical illnesses, and therapies. Complications of immobility, such as pressure injuries and delirium, may develop.

Rapid evaluation and relieving from spine boards and cervical collars will help to reduce these injuries.

Pregnant [10]

Evaluation and management of pregnant individuals can be challenging due to the physiological and anatomical changes that affect nearly every organ system in the body. Therefore, knowledge of the physiological and anatomical changes during pregnancy regarding the mother and the fetus is important to provide the best and most appropriate resuscitation and care for both.  

The best initial treatment for the fetus is by providing optimal resuscitation of the mother.

Female patients in the reproductive age who present to the ED must be considered pregnant until proven by a definitive pregnancy test or ultrasound exam.

A specialized obstetrician and surgeon should be consulted early in the assessment of pregnant trauma patients; if not available, early transfer to an appropriate facility should be sought.

The uterus is an intrapelvic organ until the 12th week of gestation, around 34 to 36 weeks when it rises to the level of the costal margin. This makes the uterus and its contents more susceptible to blunt abdominal trauma, whereas the bowel remains somewhat preserved. Nevertheless, penetrating upper abdominal trauma in the late gestational period can cause complex intestinal injury due to displacement.

Amniotic fluid embolism and disseminated intravascular coagulation are significant complications of trauma in pregnancy. In the vertex presentation, the fetal head lies in the pelvis, and any fracture of the pelvis can result in fetal skull fracture or intracranial injury.

A sudden decrease in maternal intravascular volume can lead to a profound increase in uterine vascular resistance, thus reducing fetal oxygenation regardless of normal maternal vital signs.

The volume of plasma increases throughout pregnancy and peaks by 34 weeks of gestation. Physiological anemia of pregnancy occurs when there is an increase in red blood cell (RBC) volume, leading to decreased hematocrit levels. In normal, healthy pregnant individuals, blood loss of 1200 to 1500 ml can occur without showing any signs or symptoms of hypovolemia. Nonetheless, this compromise may be seen as fetal distress, indicated by an abnormal fetal heart rate on monitoring.

Leukocytosis is expected during pregnancy, peaking up to 25,000/mm3 during labor. Serum fibrinogen and other clotting factors may be mildly increased, with shorter prothrombin and partial thromboplastin times. However, bleeding and clotting times remain the same.

During late pregnancy, in a supine position, vena cava compression can cause a decrease in cardiac output by 30 % due to lesser venous return from the lower extremities.

In the third trimester of pregnancy, heart rate increases up to 10-15 beats/min than the baseline while assessing for tachycardia in response to hypovolemia. Hypertension, along with proteinuria, indicates the need to manage preeclampsia. Be mindful of eclampsia as a complication during late pregnancy, as its presentation can be similar to a head injury (seizures with hypertension, hyperreflexia, proteinuria, and peripheral edema)

An increase in the tidal volume causes increases in the minute ventilation and hypocapnia (PaCO2 of 30 mm Hg), which is common in the later gestational period. Therefore,

Maintaining adequate arterial oxygenation during resuscitation as oxygen consumption increases during pregnancy is also important.

By the seventh month of gestation, the symphysis pubis widens to about 4 to 8 mm, and sacroiliac joint spaces increase. These alterations must be kept in mind while evaluating pelvic X-ray films during trauma. Additionally, the pelvic vessels that surround the gravid uterus can become engorged, leading to large retroperitoneal hemorrhage after blunt trauma with pelvic fractures.

Every pregnant patient who has sustained major trauma must be admitted with appropriate obstetric and trauma facilities.

Pregnant individuals may present to the ED with non-obstetric causes such as intentional (intimate partner violence, suicide attempt) and unintentional trauma (MVC, fall), and obstetric causes such as ectopic pregnancy, vaginal bleed, contractions, abdominal pain, decreased fetal movement, etc.

“To optimize outcomes for the mother and fetus, assessment and resuscitation of the mother is performed first and then the fetus, before proceeding for secondary survey of the mother.”

Primary Survey - Mother

Airway – Ensure the patient has a patent and maintainable airway with adequate ventilation. In cases where intubation is necessary, maintain appropriate PaCO2 levels according to the patient’s gestational age.  Due to the superior displacement of abdominal organs and delayed gastric emptying, there is an increased risk of aspiration during intubation.

Breathing – These patients may have an increased rate of respiration due to pressure effects or hormonal changes. Pulse oximetry and arterial gas must be monitored as adjuncts. It must be remembered that normal maternal bicarbonate levels will be low to compensate for the respiratory alkalosis.

Circulation – Attempt to manually reposition the uterus towards the left side to relieve the pressure on the inferior vena cava and improve the venous return.

Since pregnant individuals have increased intravascular volumes, they can lose a large amount of blood before the onset of tachycardia, hypotension, or other signs of hypovolemia. Therefore, it is essential to remember that the fetus and the placenta are deprived of perfusion, leading to fetal distress while the maternal conditions appear stable.

Administer crystalloid IV fluids and type-specific blood. Vasopressors must be used only as a last resort to raise maternal blood pressure, as these agents can further cause a reduction of the uterine blood flow, leading to fetal hypoxia.

Primary Survey - Fetus

Leading causes of fetal demise include maternal shock and death, followed by placental abruption.

Assess for signs of abruptio placentae (vaginal bleeding, uterine tenderness, frequent uterine contractions, uterine tetany, and irritability). Another rare injury is the uterine rupture (abdominal tenderness, rigidity, guarding or rebound tenderness, abnormal fetal lie, etc.) accompanying hypovolemia and shock.

By 10 weeks of gestation, fetal heart tones can be assessed by Doppler ultrasound, and beyond 20-24 weeks of gestation, continuous fetal monitoring with a tocodynamometer must be performed. At least 6 hours of continuous monitoring in patients with no risk factors for fetal death is recommended, and 24 hours of monitoring in patients with a high risk of fetal death.

Secondary Survey

Perform the secondary survey for non-pregnant individuals, as mentioned.

An obstetrician should ideally examine the perineum, including the pelvis. The presence of amniotic fluid in the vagina, PH greater than 4.5, indicates chorioamniotic membrane rupture.

All pregnant patients with vaginal bleeding, uterine irritability, abdominal tenderness and pain, signs and symptoms of shock, fetal distress, and leakage of amniotic fluid should be admitted for further care.

All pregnant trauma patients with Rh-negative blood group must receive Rh immunoglobulin therapy unless the injury is remote from the uterus within 72 hours of injury.

Obese Patients [10]

In the setting of trauma, procedures such as intubation can be challenging and dangerous due to their anatomy. Diagnostic investigations such as E-FAST, DPL, and CT scans may also be challenging. Moreover, most of these patients have underlying cardiopulmonary diseases, which hinders their ability to compensate for the stress and injury.

Athletes [10]

Owing to their prime conditioning, they may not exhibit early signs such as tachycardia or tachypnea in shock cases. Additionally, they usually have low systolic and diastolic blood pressure.

Revisiting Your Patient

Let’s get back to the patient we discussed earlier and start assessing him:

Airway – The patient maintains his airway but finds breathing hard. Intervention: Apply 15L Oxygen via a nonrebreather mask.

Breathing—A strap mark contusion is seen with multiple bruises. His chest expansion is asymmetrical, with reduced breath sounds on the right side of his chest. There is a dull percussion note on the right lower half of his chest. He maintains oxygen saturation. Intervention: Prepare for chest tube insertion on the right side.

Circulation – Heart sounds are muffled with marked engorgement of the external jugular veins in the neck, a good pulse still palpable in his left radial, but cold clammy extremities. His pulse is 128/min, and his blood pressure is 92/50 mm Hg. Bedside ultrasound FAST (Focused Assessment Sonography in Trauma) shows a pericardial tamponade. Intervention: IV access was gained with two large-bore IV cannulas, blood was drawn for labs, the massive transfusion protocol for blood products was activated, a Foley catheter was inserted to monitor urinary output, and the surgery team was on board to plan for emergent pericardiocentesis.

Disability – Patient’s GCS remains 15, unremarkable pupillary examination and POC glucose is 7 mmol/dl.

Exposure – you notice the strap mark on his chest secondary to his seatbelt restraint, and the multiple bruises. The remaining evaluation is unremarkable, with no head, spine, abdomen, or limb injury.

Adjunct investigations – A portable chest x-ray shows increased cardiac shadow and multiple bilateral rib fractures. There is opacification in the right lung [12]. 

Discussion

This patient sustained a blunt trauma leading to pericardial tamponade and right-sided hemothorax, leading to hypovolemic shock. The most common cause of shock in a trauma patient is hypovolemic shock due to hemorrhage. However, other types of shock like cardiogenic shock (due to myocardial dysfunction), neurogenic shock (due to sympathetic dysfunction), or obstructive shock (due to tension pneumothorax, obstruction of great vessels) can occur.

Early signs of shock include tachycardia, which is the body’s attempt to preserve cardiac output and cool peripheries, and reduced capillary refill time caused by peripheral vasoconstriction. This is caused by the release of catecholamine and vasoactive hormone, which leads to increased diastolic blood pressure and reduced pulse pressure. For this reason, measuring pulse pressure rather than systolic blood pressure allows earlier detection of hypovolaemic shock, as the body can lose up to 30% of its blood volume before a drop in systolic blood pressure is appreciated.

Initiate fluid resuscitation in these patients and do not wait for them to develop hypotension.
The main aim is to maintain organ perfusion and tissue oxygenation. In children, start with crystalloid fluid boluses of 20 ml/kg, and in adults, an initial 1 L can be given. In patients who have sustained a major blood loss, consider initiating the Massive Transfusion Protocol (MTP) for blood products as soon as possible.

A few current trauma guidelines have recommended ‘permissive hypotension’ or ‘balanced resuscitation,’ where the principle is to stabilize any blood clots that may have been formed, and aggressive blood pressure resuscitation may disrupt this ‘first formed clot’ and may contribute to further hemorrhage.

To evaluate response to fluid resuscitation, assess the level of consciousness, improvement in tachycardia, skin temperature, capillary refill, and urine output (>0.5 ml/kg/hour in adults).
Besides administering packed red blood cells, do not forget to transfuse platelets, fresh frozen plasma, or cryoprecipitate, as large blood loss can develop coagulopathy in 30% of these injured patients. Tranexamic acid (TXA), an antifibrinolytic, can be utilized in addition as a 1 g bolus over 10 minutes followed by 1 g over 8 hours within 3 hours of trauma without an increased risk of thromboembolic events [11].

This systematic approach focuses on identifying and treating this hemorrhagic shock case. Bedside adjuncts such as FAST examination and portable chest X-ray can provide valuable clues to the cause of shock. A trauma CT scan is only performed once the patient is stable enough to go to the scan room.

This patient’s vital signs improve slightly but remain unstable, and blood is kept draining into the chest drain. The patient is taken to the operation theatre for an emergency thoracotomy [12].

Authors

Picture of Roxanne R. Maria

Roxanne R. Maria

Picture of Hamid A. Chatha

Hamid A. Chatha

Listen to the chapter

References

  1. Initial Assessment of Emergency Department patients, The Royal College of Emergency Medicine, Feb 2017
  2. World Health Organization. BASIC EMERGENCY CARE : Approach to the Acutely Ill and Injured.World Health Organization; 2018.
  3. Thim T. Initial assessment and treatment with the airway, breathing, circulation, disability, exposure (ABCDE) approach. International Journal of General Medicine. 2012;5(5):117-121. doi:https://doi.org/10.2147/IJGM.S28478
  4. Peate I, Brent D. Using the ABCDE Approach for All Critically Unwell Patients. British Journal of Healthcare Assistants. 2021;15(2):84-89. doi:https://doi.org/10.12968/bjha.2021.15.2.84
  5. Schoeber NHC, Linders M, Binkhorst M, et al. Healthcare professionals’ knowledge of the systematic ABCDE approach: a cross-sectional study. BMC Emergency Medicine. 2022;22(1). doi:https://doi.org/10.1186/s12873-022-00753-y
  6. Learning Objectives. https://www.moh.gov.bt/wp-content/uploads/moh-files/2017/10/Chapter-2-Emergency-Patient-Assessment.pdf
  7. Resuscitation Council UK. The ABCDE Approach. Resuscitation Council UK. Published 2021. https://www.resus.org.uk/library/abcde-approach#:~:text=Use%20the%20Airway%2C%20Breathing%2C%20Circulation
  8. Management of trauma patients – Knowledge @ AMBOSS. http://www.amboss.com. https://www.amboss.com/us/knowledge/Management_of_trauma_patients/
  9. Oxford Medical Education. ABCDE assessment. Oxford Medical Education. Published 2016. https://oxfordmedicaleducation.com/emergency-medicine/abcde-assessment/
  10. HENRY SM. ATLS Advanced Trauma Life Support 10th Edition Student Course Manual, 10e. 10th ed. AMERICAN COLLEGE OFSURGEO; 2018.
  11. Walls RM, Hockberger RS, Gausche-Hill M, Erickson TB, Wilcox SR. Rosen’s Emergency Medicine : Concepts and Clinical Practice. Elsevier; 2.
  12. Eamon Shamil, Ravi P, Mistry D. 100 Cases in Emergency Medicine and Critical Care. CRC Press; 2018.

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Maxillofacial Trauma (2024)

~ iEM Education Project Team ~ Leave a comment

by Maitha Ahmad Kazim & David O. Alao

Authors
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You have a new patient!

A 48-year-old man was brought to the ED by ambulance shortly after sustaining blunt trauma to the face. The patient was off-loading his quad bike from a truck when it accidentally flipped over and fell directly on his face. He could not recall the incident.

Upon arrival, his vitals were BP: 144/85 mmHg, HR: 104 bpm, T: 36.8°C, RR: 23 bpm, and SPO2: 99% on room air. He was awake on the AVPU score. On examination, the patient was bleeding profusely from his nostrils, breathing from his mouth, and having diffuse facial swelling. You are concerned about the extent of the injuries sustained, and you assemble a team to manage the patient.

Importance

The significance of proficiently managing maxillofacial trauma in the fast-paced emergency medicine setting cannot be overstated. Not only do these traumas cause direct physical harm, but they also impact the patient’s appearance and their ability to perform vital functions like breathing, speaking, and chewing. Given the complex and sensitive nature of the maxillofacial region, emergency physicians must comprehensively understand how to manage such injuries effectively. Proficiency in diagnosing and managing maxillofacial trauma ensures timely and appropriate treatment and prevents potential complications and long-term sequelae. 

Epidemiology

Maxillofacial injuries are a prevalent global health concern. There were an estimated 7.5 million new facial fractures globally in 2017, with 1.8 million individuals living with a disability from a facial fracture [1]. Undoubtedly, the incidence and prevalence vary significantly from one country to another. Singaram et al. reported that the prevalence varied between countries from 17% to 69% [2]. In many regions, inadequate infrastructure, limited access to healthcare, and poor safety regulations contribute to a higher incidence of maxillofacial injuries.

Pathophysiology

Road traffic accidents, interpersonal violence, industrial accidents, and sports-related incidents are the most common etiologies of maxillofacial injuries globally. However, the predominant causes differ in developed and developing countries. Assault is the most common mechanism of injury in developed countries, while motor vehicle accident (MVA) is the most common mechanism in developing countries [3].

Low or high-impact forces can cause maxillofacial injuries. The force needed to cause damage differs from one bone to another. For instance, the zygoma and nasal bones can be damaged by low-impact forces. In contrast, the frontal bone, supraorbital rim, maxilla, and mandible are damaged by high-impact forces [4].

Furthermore, the etiology of maxillofacial trauma can predict the type of facial injuries and fractures sustained. For example, MVAs have been associated with higher instances of mandibular fractures. That is mainly due to its position compared to the rest of the facial bones and its relatively thin structure [5].

Medical History

Maxillofacial injuries often occur in association with other injuries and, thus, can be missed initially. Obtaining a systemic and thorough history can aid the diagnosis. At the initial presentation, the mnemonic “AMPLE” (Allergies, Medications currently used, Past illness/Pregnancy, Last meal, Events/Environment related to the injury) can be used to assess the patient’s pre-injury health status. Then, the following should be probed:

  • What was the mechanism of injury?
    Understanding the cause of the injury (e.g., fall, vehicle collision, assault) provides insights into potential injuries and the extent of trauma. Different mechanisms (blunt vs. penetrating, low vs. high-impact) influence the pattern and severity of injuries and aid in anticipating associated injuries.

    • Environment related to the injury
      Environmental context (e.g., construction site, sports field) can highlight additional risk factors or clues about the nature and potential complications of the injury. It may also help assess the likelihood of secondary injuries or infections.

    • Blunt vs. penetrative
      The type of trauma affects the damage pattern. Blunt trauma may result in fractures or soft tissue injuries, while penetrating trauma may involve more focal injury with a higher risk of infection and internal damage.

    • Low vs. high-impact force
      High-impact injuries are more likely to cause fractures and significant soft tissue damage. Knowing the force helps anticipate the severity and depth of injuries.

    • Direction of force
      The direction can indicate which structures might be compromised (e.g., anterior force could affect the nose, mandible, and dental structures, while lateral force may impact the zygomatic arch or TMJ).

  • Was there a loss of consciousness or an altered level of consciousness?
    Altered consciousness or loss of consciousness may indicate a head injury or neurological involvement, which necessitates further investigation and monitoring for brain injury.

  • Are there any visual disturbances?
    Vision changes can signal orbital fractures or injuries to the optic nerve, potentially affecting ocular function or indicating damage to the orbit and nearby structures.

  • Is there any change in hearing? Is the patient experiencing tinnitus or vertigo? Did they notice any discharge from the ears (clear or bloody)?
    Hearing changes, tinnitus, vertigo, or ear discharge suggest possible basilar skull fractures or damage to the auditory system, which are essential to identify to avoid long-term complications.

  • Any trouble breathing through the nose? Did they notice any discharge (clear or bloody)?
    Difficulty breathing through the nose or nasal discharge may indicate nasal fractures, airway obstruction, or cerebrospinal fluid (CSF) leakage if clear, which is critical to address in traumatic injuries.

  • Any pain while talking? Do the teeth come together normally?
    Pain when speaking or abnormal occlusion may signal fractures in the mandible, maxilla, or TMJ dislocation, impacting facial symmetry, function, and long-term outcomes.

  • Is there difficulty opening or closing the mouth? Is there any pain when biting down the teeth?
    Difficulty or pain in mouth movement often suggests mandibular fractures or TMJ injury. Restricted movement can help identify specific injury locations and aid in planning management.

  • Numbness or tingling sensation in any area of the face?
    Sensory changes suggest possible nerve damage, often related to fractures affecting the infraorbital, mental, or other facial nerves. This information helps predict potential complications and guides treatment planning.

Consider the following symptoms when obtaining a history from maxillofacial trauma patients:

  • Orbital floor fractures commonly present with symptoms such as tingling or numbness around the nose, upper lip, and maxillary gums due to infraorbital nerve damage, along with difficulty looking upward or laterally, double vision (diplopia), and pain during eye movement.
  • Nasal fractures are characterized by swelling, pain, and nosebleeds (epistaxis).
  • Nasoethmoidal fractures can cause cerebrospinal fluid (CSF) rhinorrhea, epistaxis, and tearing (epiphora) due to nasolacrimal duct obstruction.
  • Zygomaticomaxillary complex (ZMC) fractures may lead to numbness around the nose and upper lip, issues with eye movement, double vision, and difficulty opening the mouth (trismus).
  • Maxillary fractures often result in CSF rhinorrhea or epistaxis and may cause mobility in the upper teeth and gingiva.
  • Alveolar fractures are typically associated with gingival bleeding.
  • Mandibular fractures can present as painful jaw movements and tingling or numbness affecting half of the lower lip, chin, teeth, and gingiva.

Red Flags in History

Due to the complex nature of the maxillofacial region, one should be vigilant for red flags when taking history from the patients. Its proximity to the brain and central nervous system makes injuries to these very likely. Thus, identifying them early on can prevent irreversible sequelae and medicolegal implications. Red flags include memory loss, fluctuations in the level of consciousness, nausea/vomiting, and headache that does not improve with analgesia [6].

Neurological involvement can further be assessed by asking about the presence of diplopia or a change in visual acuity. Vision loss usually occurs immediately, but in 10%, symptoms are delayed [7]. Another red flag that is associated with high morbidity and mortality is cervical cord syndrome. Maxillofacial injuries associated with falls are often associated with cervical spinal injury. The patient may complain initially about neck pain or a loss of motor/sensory function in the arms [8].

Physical Examination

Maxillofacial trauma is commonly associated with polytrauma [9]. Thus, it often gets missed in examinations. Physical examination should be done systematically to ensure that all injuries are noted. Like all trauma cases, life-threatening injuries should be addressed first, and the ATLS protocol should be applied accordingly. After that, a physical examination of maxillofacial trauma would involve several key steps. Hard and soft tissue injuries (hematoma, laceration, foreign body, swelling, missing tissue, bleeding, or clear discharge) should be noted upon general inspection of the head and face. Symmetry and alignment of the face should also be noted, bearing in mind that asymmetry may be hidden by edema [10]. Facial elongation and flattening can be seen in midface fractures. Increased intercanthal distance, also known as telecanthus, indicates a nasoethmoidal injury.

Palpation of the whole face should follow, going from top to bottom to avoid missing any injury. Identify step-offs, crepitus, instability or excessive mobility, and malocclusion. Le Fort fractures, complex midface fractures, can be identified during physical examination. 

Next, a complete ocular examination should be done. Assess visual acuity, visual field, pupillary reflex, anterior chamber, and extraocular movements. An ophthalmologic consultation is recommended if any abnormalities are present [10]. The nose and septum should be inspected for any hematoma, bulging mass, or CSF leakage and palpated for any signs of fracture. The oral cavity should be inspected for palatal ecchymoses, lacerations, malocclusion, or missing teeth. Manipulate each tooth individually for movement or pain. Palpate the entire mandible for step-offs or injury. Motor and sensory functions of the face should be evaluated. A thorough cranial nerve examination will help identify sensorimotor injuries. 

Le Fort Classification

Le Fort I Fracture: A Le Fort I fracture, often referred to as a “floating palate,” is a horizontal maxillary fracture that separates the teeth from the upper face. The fracture line passes through the alveolar ridge, lateral nose, and the inferior wall of the maxillary sinus. Patients with this fracture often present with a swollen upper lip, open bite malocclusion, and ecchymosis of the hard palate. When the forehead is stabilized, the maxilla may also have noticeable mobility (including the hard palate and teeth).

Le Fort II Fracture: Known as a “floating maxilla,” the Le Fort II fracture builds upon the characteristics of Le Fort I but extends to involve the bony nasal skeleton, giving it a pyramidal shape. This fracture often leads to a widening of the intercanthal space, bilateral raccoon eyes, epistaxis, and open bite malocclusion. Physical examination may reveal mobility of the maxilla and nose, ecchymosis of the hard palate, and cerebrospinal fluid (CSF) rhinorrhea. Patients may also experience sensory deficits in the infraorbital region extending to the upper lip.

Le Fort III Fracture: Referred to as a “floating face” or “craniofacial disjunction,” the Le Fort III fracture involves a separation of the midfacial skeleton from the base of the skull. The fracture line extends from the frontozygomatic suture across the orbit and through the base of the nose and ethmoid region, running parallel with the skull base. Physical signs include bilateral raccoon eyes, ecchymosis of the hard palate, and a dish-face deformity characterized by elongation and flattening of the face. Additional signs may include enophthalmos (sunken eyes), Battle’s sign (ecchymosis over the mastoid bone), CSF rhinorrhea or otorrhea, and hemotympanum.

Red Flags in Examination

Look for “red flags” during physical examination. These red flags include cervical spine injuries, loss of teeth, Battle’s sign/Raccoon eyes with CSF rhinorrhea, and Le Fort fractures. Facial bones should not be manipulated until cervical spine injuries, which are present in 2.2% of cases, have been ruled out [11]. The oral cavity should be carefully examined for loss of teeth, as it may be aspirated during the injury. For missing teeth, a chest X-ray should be done to rule out or confirm aspiration.

Moreover, facial fractures can extend to the cranium [4]. Depending on the mechanism of injury, the patient may suffer from a concomitant base of the skull fracture, which may present with Battle’s sign and Raccoon eyes as well as CSF rhinorrhea in some cases [11]. LeFort fractures are complex fractures of the midface and are further classified into LeFort I, II, and III. These fractures are considered a red flag as they may cause airway obstruction and life-threatening bleeding [12].

Alternative Diagnoses

Given that the cause is usually known, doctors must identify the injuries sustained and the extent of injuries sustained. While blunt trauma to the face is an apparent cause of maxillofacial injuries, concomitant and alternative diagnoses should not be missed. Patients with maxillofacial trauma can present with a wide range of symptoms that are similar to those from intracranial and cervical spinal injuries.

Acing Diagnostic Testing

The diagnosis of maxillofacial injuries is not based on a single diagnostic test. It is a correlation between history, physical examination, and imaging studies. Given that the etiologies of the injury vary, the differentials are vast, and the clinical presentation differs from one patient to another. Thus, bedside testing and laboratory studies should be tailored to each patient’s clinical presentation and existing symptoms.

Bedside Testing

ECG monitoring is essential for all trauma patients. Dysrhythmias, atrial fibrillation, and ST segment changes can be seen in blunt cardiac injury. Point-of-care (POCT) glucose testing quickly assesses the patient’s glucose level. Hypoglycemia can cause confusion and an altered mental status, which are common findings in patients with maxillofacial trauma. Point-of-care blood gas testing may be beneficial in case of excessive bleeding or airway compromise. In case of tissue hypoperfusion and shock, metabolic acidosis and elevated lactate levels may be noted. Oxygen saturation and carbon dioxide should be monitored in case of midface fractures and suspected airway compromise. A POCT pregnancy test should be done in women of childbearing age, as almost all maxillofacial trauma patients require imaging for diagnosis.

Laboratory Testing

A complete blood count (CBC), particularly hemoglobin and hematocrit, is indicated when the patient is bleeding profusely. LeFort II and III have been associated with an increased risk of life-threatening hemorrhage compared to other facial fractures [12]. Therefore, blood typing and crossmatching are crucial if the patient needs a blood transfusion. A coagulation panel is done to rule out trauma-induced coagulopathy, a preventable factor for progressive brain injury and massive bleeding [13].

A CSF analysis is warranted when there are secretions from the nose or ear. Beta-2 transferrin testing is the current preferred test to confirm the presence of a CSF leak [14]. Other less used methods include beta-trace protein, double-ring sign, and glucose oxidase test. A blood ethanol test and urine toxicology screen can be considered in agitated patients or those with altered levels of consciousness.

Imaging Studies

CT scans are the “gold standard” diagnostic modality for evaluating maxillofacial trauma [15]. Using narrow-cut CT scans without contrast provides detailed cross-sectional images of the facial structures, thus allowing for a comprehensive evaluation of complex fractures. In addition to identifying facial fractures, it can detect head and cervical spinal injuries, air and fluid in the intracranial space and sinuses, periorbital injury, soft tissue injury, and embedded foreign bodies. A non-contrast head CT helps identify intracranial bleeding and distinguish between the types of bleeds if present. This is recommended, especially when the patient experiences loss of consciousness for several minutes. Because maxillofacial trauma is highly associated with cervical spine injury, the physician must have a high index of suspicion for cervical spine fractures. The NEXUS criteria is used to guide imaging in these situations. 

Plain radiographs of the head are used when CT scans are not available. They may be used to screen for fractures and provide some insight into displaced fragments, but they have low sensitivity for detecting and establishing the extent of the injuries. A chest x-ray should be done when a missing tooth is noted on physical examination, as the patient may have aspirated it.

Ultrasound is a helpful bedside diagnostic tool in any trauma patient, and it has been shown to be an accurate diagnostic method when evaluating orbital trauma [16]. It is used when an isolated orbital injury is suspected or a CT scan is not readily available. It can pick up muscle entrapment, soft-tissue herniation, and orbital emphysema.

Risk Stratification

Several risk stratification tools have been developed for maxillofacial trauma. However, these are commonly used in clinical research to assess injury severity and determine the appropriate course of action. Although no specific tool was developed for use in an emergency department, other nonspecific tools like the Glasgow Coma Scale (GCS) and NEXUS criteria come in handy. The GCS score is used to rapidly assess the patient’s level of consciousness, guiding immediate interventions. The NEXUS criteria is used to clear patients from cervical injury clinically without imaging. 

The diagnosis of maxillofacial trauma is based on a combination of clinical assessment and diagnostic imaging. A thorough evaluation of both helps predict the risk. Some common clinical factors that may contribute to poorer outcomes include severe and complex fractures, extensive soft tissue injury, high-energy trauma, open fractures, ocular injuries, and pediatric and geriatric age groups [17,18].

Management

Initial Stabilization

Treating patients with maxillofacial trauma aims to restore function and optimize appearance. However, the primary focus upon presentation is to stabilize the patient. Initial management begins with a primary survey, which constitutes the “ABCDE” approach to identify life-threatening conditions and treat them promptly. 

Airway

Airway patency is a serious concern in maxillofacial trauma, and the nature of the injury often complicates airway management. Airway compromise may be complete, partial, or progressive [9]. Early signs of airway compromise include tachypnea, inability to speak in complete sentences, and abnormal noisy breathing. Agitation and abnormal behavior may indicate hypercapnia.

If the patient has obstruction from soft tissue, perform a jaw thrust maneuver. Cervical spine injury should be presumed in all maxillofacial injury patients until proven otherwise. Therefore, avoid mobilizing the neck until it is cleared. Inspect the oral cavity for any bleeding or secretions and suction accordingly. Consider manual removal with a finger sweep or forceps if a foreign body or debris is identified. Control patients with nasopharynx or oropharynx bleeding with nasal packing or compression with gauze [19].

The need for airway protection increases with severe maxillofacial fractures, expanding neck hematoma, stridor, profuse bleeding or continuous vomiting, and unconsciousness [9]. A nasopharyngeal airway is indicated in a conscious patient without a midface trauma. If the patient was unconscious or had a midface injury, an oropharyngeal airway may help temporarily. However, a definitive airway must be secured in patients who cannot maintain airway integrity. Definitive airway control is done by an endotracheal intubation (nasal or oral). Nasal endotracheal intubation is contraindicated in a base of skull fracture. Given the area’s delicacy and complexity of the injuries sustained, fiberoptic intubation by a skilled physician may provide immediate confirmation of tracheal placement and avoid further complications [10]. If the previous methods cannot be accomplished, a surgical airway (cricothyroidotomy or tracheostomy) should be considered. 

Breathing

The patient’s breathing, ventilation, and oxygenation should be assessed. Check the alignment of the trachea and listen to the patient’s chest bilateral for air entry and added sounds. Deviated trachea and decreased air entry upon auscultation increase the likelihood of tension pneumothorax, and a needle decompression should be performed. Look for soft tissue abnormalities and subcutaneous emphysema.

The patient should be connected to a pulse oximeter to monitor adequate hemoglobin oxygen saturation. If the patient is hypoxic, they should receive oxygen supplementation. Non-invasive ventilation should precede invasive ventilation methods. However, in severe injuries, mask ventilation may be difficult due to the disrupted anatomy of the face [20].

Like all trauma patients, a “full stomach” should be presumed in patients with maxillofacial trauma as digestion stops during trauma. In addition, blood is often swallowed and accumulates in the stomach. Regurgitation and aspiration are a big risk in such patients, and evacuation of stomach content is recommended [20]. A nasogastric tube is contraindicated in a skull base fracture. An orogastric tube is recommended instead to prevent intracranial passage [21].

Circulation

Maxillofacial trauma can cause profuse bleeding that can lead to shock. Monitor blood pressure and heart rate, auscultate, and check capillary refill and hand warmth. Tachycardia precedes low blood pressure in shock. Establish bilateral IV access with two large bore cannulas and draw blood for type and crossmatch. Fluid therapy with crystalloids should be initiated. Identify the source of hemorrhage. If external or intraoral bleeding occurs, apply direct pressure, pack, and suture. Carefully examine the tongue, as persistent bleeding can obscure the airway. In the case of epistaxis, anteroposterior packing will control the bleeding in most cases [10]. Additionally, topical tranexamic acid can be used in anterior epistaxis. In cases of LeFort fractures, intermaxillary fixation might be required when packing fails to stop the bleeding [10]. If the previously mentioned measures fail, consult IR, ENT, or surgery for more advanced interventions like arterial embolization and fracture reduction [22].

Disability

The patient’s mental status and neurologic function should be assessed initially. Glucose is measured at this point if not done upon arrival. The Glasgow Coma Scale helps assess the patient’s level of consciousness. Note any change in the mental status. A brief neurological exam is recommended. 

Exposure

Expose the patient fully while keeping them warm. Look for bruises, bite marks, lacerations, and other injuries, as the etiology of maxillofacial trauma is broad and often presents as polytrauma. Decontamination might be required depending on the nature of the trauma.

Medications

Isotonic crystalloid fluids and blood products are common treatments in trauma patients. Adequate pain management should be provided with NSAIDs, opioids, or local anesthesia. There are no guidelines on the use of prophylactic antibiotics in maxillofacial trauma. Nonetheless, there are specific scenarios where prophylactic antibiotics administration is recommended. Depending on the type of injury sustained, additional medications might be required. Refer to Table to explore the additional medications used in the setting of maxillofacial trauma:

Drug name (Generic)

Potential Use

Dose

Frequency

Cautions / Comments

Acetaminophen

mild-moderate pain (can be given with NSAIDs, with or without Opioids)

325-1,000 mg PO

 

Max Dose: 4 g daily

q4-6h

  • Ask for allergies
  • Ask for if/when they took Acetaminophen at home

Ibuprofen

mild-moderate pain (can be given with Acetaminophen)

600 mg PO

 

Max Dose: 3,200 mg daily

q6h

  • Can cause GI upset and increase risk of GI bleed
  • Renal insufficiency

Hydromorphone

Moderate – severe pain

0.5-4 mg IV/IM/SC

 

Max Dose: n/a

q4-6h

  • Risk of respiratory depression
  • Risk of addiction and abuse

Morphine sulfate

Moderate – severe pain

2.5-10 mg IV/IM/SC

 

Max Dose: n/a

q2-6h

  • Risk of respiratory depression
  • Risk of addiction and abuse
  • Hypotension

Metoclopramide

Nausea and vomiting (to prevent risk of aspiration)

1 to 2 mg/kg/dose IV

 

Max Dose: n/a

Every 2 hours for the first two doses, then every 3 hours for the subsequent doses.

  • Extrapyramidal side effects
  • If acute dystonic reactions occur, 50 mg of diphenhydramine may be injected IM.

Ondansetron

Nausea and vomiting (to prevent risk of aspiration)

0.15 mg/kg IV (not to exceed 16 mg)

 

Max Dose: n/a

q8hr PRN

  • Increased risk of QT prolongation, which increases the risk of cardiac arrhythmia and cardiac arrest.

Amoxicillin-clavulanic acid

Nasal packing (ppx for epistaxis – TSS)

 

Facial fractures communicating with open wounds of the skin

 

Mandibular fractures that extend into the oral cavity

2g PO (extended-release tablets)

 

Max Dose: n/a

q12h (7 days)

  • Ask for allergies
  • Ask if they have taken any antibiotic recently.
  • Hives and skin rash

Procedures

Epistaxis: Epistaxis is a common issue in maxillofacial trauma due to damage to the nasal structures and blood vessels. Managing epistaxis is crucial to prevent blood loss and ensure the airway remains clear. For anterior epistaxis, anterior nasal packing can effectively apply pressure to stop the bleeding. If the bleeding source is posterior, posterior nasal packing using a balloon catheter or Foley’s catheter may be necessary. These techniques help control bleeding and stabilize the patient, especially in cases where blood loss might obstruct the airway or lead to hemodynamic instability.

Inability to Protect Airway: In cases of severe maxillofacial trauma, there may be a risk of airway compromise due to swelling, bleeding, or physical obstruction from broken facial structures. If a patient cannot protect their airway, endotracheal intubation is required to secure it and maintain ventilation. Intubation provides a definitive airway, bypassing obstructions and ensuring adequate oxygenation, which is critical in trauma patients to prevent hypoxia and support life-sustaining measures.

Failed Intubation: Occasionally, intubation may be unsuccessful, particularly in patients with extensive facial injuries or anatomical challenges. In such cases, a cricothyroidotomy is performed. This emergency surgical procedure creates an opening in the cricothyroid membrane, providing an alternative airway route directly into the trachea. Cricothyroidotomy is a life-saving measure when intubation fails, ensuring oxygen can still be delivered to the lungs when other methods are ineffective.

Tension Pneumothorax: Maxillofacial trauma can sometimes be associated with thoracic injuries, leading to complications like tension pneumothorax, where air is trapped in the pleural cavity and compresses the lungs and heart, causing a life-threatening situation. Needle decompression is the first step in relieving the pressure by inserting a needle into the pleural space to allow trapped air to escape. This is followed by a tube thoracostomy (chest tube placement) to maintain the release of air and prevent the recurrence of tension pneumothorax. This procedure is essential to restore normal lung function and stabilize the patient’s respiratory status.

Special Patient Groups

Pediatrics

Pediatric patients’ anatomical and developmental differences should be considered when evaluating them for maxillofacial trauma. An infant’s frontal bone dents, while a child’s frontal bone experiences a depressed fracture under a force that causes facial fractures in adults [4]. Smaller force loads are needed to damage the facial bones than adults [4]. Given pediatric patients’ underdeveloped facial skeletons and sinuses, growth dysplasia is a common outcome of suboptimal treatment. Standard facial radiographs often miss fractures; a CT scan is more reliable in this age group [23]. Assess for orbital fracture thoroughly, as children’s orbital floor is pliable, increasing the risk of entrapment and rectus muscle ischemia [6].

Geriatrics

The impaired physiologic response and frailty of geriatric patients make their treatment more challenging. Although they are subject to the same mechanism of maxillofacial trauma as the other age groups, their response to the injuries differ. They are at a high risk of intracranial hemorrhage, but their basal vital signs often do not reflect signs of hemorrhage or hypoperfusion, making diagnosing shock difficult. Comorbidities and polypharmacy in this age group further mask the normal shock response. In addition, the likelihood of associated injuries in this group is high [24]. Elderly patients were reported to have more frequent cerebral concussions and internal organ injuries [25]. Nonetheless, a GCS of <15 has also been associated with higher mortality rates, especially in those older than 70 years [25]. Putting all of this into perspective when assessing elderly patients, a lower threshold for extensive investigations and referral is necessary.

When to admit this patient

Definitive repair of facial fractures is not a surgical emergency, and patients can be discharged home with a close follow-up in the clinic in most cases. An awake patient with good home care and isolated stable injuries (i.e., mandibular or nasal fracture) may be discharged home. However, admission should be considered in a number of situations. These include severe complex facial fractures, open fractures, the presence of comorbidities, and cases of associated injuries that need close monitoring. Admission is made to the intensive care unit or a surgical ward with a high level of monitoring.

Revisiting Your Patient

A 48-year-old male was brought to the ED by ambulance shortly after sustaining blunt trauma to the face. The patient was loading his quad bike off a truck when it accidentally flipped over and fell directly on his face and upper body. He could not recall what happened thereafter.
Upon arrival, his vitals were BP: 144/85 mmHg, HR: 104 bpm, T: 36.8°C, RR: 23 bpm, and SPO2: 99% on room air. He was awake on the AVPU score. On examination, the patient was bleeding profusely from his nose, breathing from his mouth, and having diffuse facial swelling. You are concerned about the extent of injuries sustained and have assembled your team to manage the patient adequately.

History was taken from his brother, who witnessed the incident. The brother confirmed that the patient had no LOC, dizziness, or vomiting but reported that the patient kept complaining of neck pain. He is known to have L5-S1 disc prolapse, does not take any medication, and has no known allergies.

You worry that the patient might suffer from airway compromise and quickly begin your primary survey. You hear gurgling noises and check the patient’s mouth to find it filled with blood. You suction and look for sources of bleeding in the mouth but find none. The airway becomes patent. You notice that EMS has placed a C-spine collar on the patient already. His lungs are clear bilaterally, and you insert an orogastric tube to suction his stomach contents. He is bleeding profusely from his nostrils, so you pack his nose anteriorly. This does not stop the bleeding, and the patient is spitting out blood. You then apply topical tranexamic acid and more packs, and the bleeding stops. His pulses are present, extremities are warm, and capillary refill time is less than 2 seconds. His GCS is 15/15, and his pupils are reactive to light. Upon exposing him, you notice lacerations on his lips and ears but no other injuries on the rest of his body.

Two large bore IV lines are inserted peripherally, blood is drawn for laboratory investigations, and intravenous normal saline is administered immediately. A 12-lead ECG demonstrated sinus tachycardia. You perform a bedside E-FAST to rule out pneumothorax/hemothorax, pericardial fluid, and peritoneal fluid. You ask for urgent CT scans, including a CT Head and Neck without contrast and a Maxillofacial CT. The CT scan report confirms no C-spine fractures, skull fractures, or brain injury. However, it identifies a Le Fort 1 fracture and fracture involving the right orbital wall. You safely remove the c-spine collar. You consult the Oral and Maxillofacial surgeon and the Ophthalmologist, and both agree to see the patient. You give the patient morphine to alleviate his pain.

You performed a secondary survey to ensure the patient was not deteriorating and to identify any additional injuries. The patient remained stable, and he was admitted to the surgical floor.

Figure: Fracture of the lateral wall left maxilla (long arrow) and a tripod fracture of the right zygoma (short arrows).

Author

Picture of Maitha Ahmad Kazim

Maitha Ahmad Kazim

Dr. Maitha Ahmad Kazim is an Emergency Medicine Resident at Dubai Health, recognized for her dedication in patient care and medical research. She earned her Doctor of Medicine degree from the United Arab Emirates University, where she graduated with distinction. Dr. Kazim is known for her commitment to advancing emergency care, demonstrated by her active engagement in research, mentorship, and medical education.

Picture of David O. Alao

David O. Alao

David is a senior consultant in emergency medicine and associate professor of medicine College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, UAE
He graduated from the University of Ibadan, Nigeria. After initial training in general surgery in Leeds and Newcastle Upon-Tyne, United Kingdom, he had higher specialist training in emergency medicine in the South West of England.
He was a consultant in emergency medicine for 15 years at the University Hospitals Plymouth, United Kingdom where he was a Clinical Tutor, Academic Tutor and, Assistant professor at Plymouth University Peninsular School of Medicine and Dentistry (PUPSMD) UK.
David is a fellow of the Royal College of Surgeons of Edinburgh and the Royal College of Emergency Medicine UK.
His interests are undergraduate and postgraduate medical education, skills training and transfer, trauma systems development and resuscitation science. He has published over 30 papers in peer-reviewed journal.

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References

  1. Lalloo R, Lucchesi LR, Bisignano C, et al. Epidemiology of facial fractures: incidence, prevalence and years lived with disability estimates from the Global Burden of Disease 2017 study. Inj Prev. 2020;26(Supp 1):i27-i35. doi:10.1136/injuryprev-2019-043297
  2. Singaram M, G SV, Udhayakumar RK. Prevalence, pattern, etiology, and management of maxillofacial trauma in a developing country: a retrospective study. J Korean Assoc Oral Maxillofac Surg. 2016;42(4):174. doi:10.5125/jkaoms.2016.42.4.174
  3. Nalliah RP, Allareddy V, Kim MK, Venugopalan SR, Gajendrareddy P, Allareddy V. Economics of facial fracture reductions in the United States over 12 months. Dent Traumatol Off Publ Int Assoc Dent Traumatol. 2013;29(2):115-120. doi:10.1111/j.1600-9657.2012.01137.x
  4. Pappachan B, Alexander M. Biomechanics of Cranio-Maxillofacial Trauma. J Maxillofac Oral Surg. 2012;11(2):224-230. doi:10.1007/s12663-011-0289-7
  5. Sharifi F, Department of Oral & Maxillofacial Surgery, Mashhad University of Medical Sciences, Mashhad, Iran., Samieirad S, et al. The Causes and Prevalence of Maxillofacial Fractures in Iran: A Systematic Review. WORLD J Plast Surg. 2023;12(1):3-11. doi:10.52547/wjps.12.1.3
  6. Van Gijn D. Tips for GP trainees working in oral and maxillofacial surgery. Br J Gen Pract. 2012;62(594):50-51. doi:10.3399/bjgp12X616490
  7. Lynham A, Tuckett J, Warnke P. Maxillofacial trauma. Aust Fam Physician. 2012;41(4):172-180.
  8. Philip MR, Soumithran CS. Prevalence of Neurologic Deficits in Combined Facial and Cervical Spine Injuries: A Retrospective Analysis. Craniomaxillofacial Trauma Reconstr. 2021;14(1):49-55. doi:10.1177/1943387520940182
  9. Saigal S, Khan MM. Primary Assessment and Care in Maxillofacial Trauma. Oral and Maxillofacial Surgery for the Clinician. 2021:983-995. doi:10.1007/978-981-15-1346-6_48
  10. Truong T. Initial Assessment and Evaluation of Traumatic Facial Injuries. Semin Plast Surg. 2017;31(02):069-072. doi:10.1055/s-0037-1601370
  11. Mukherjee S, Abhinav K, Revington P. A review of cervical spine injury associated with maxillofacial trauma at a UK tertiary referral centre. Ann R Coll Surg Engl. 2015;97(1):66-72. doi:10.1308/003588414X14055925059633
  12. Patel BC, Wright T, Waseem M. Le Fort Fractures. In: StatPearls. StatPearls Publishing; 2023. Accessed August 12, 2023. http://www.ncbi.nlm.nih.gov/books/NBK526060/
  13. Peng N, Su L. Progresses in understanding trauma-induced coagulopathy and the underlying mechanism. Chin J Traumatol. 2017;20(3):133-136. doi:10.1016/j.cjtee.2017.03.002
  14. Das D, Salazar L. Maxillofacial Trauma: Managing Potentially Dangerous And Disfiguring Complex Injuries. Emerg Med Pract. 2017;19(4):1-24.
  15. Meara DJ. Diagnostic Imaging of the Maxillofacial Trauma Patient. Atlas Oral Maxillofac Surg Clin North Am. 2019;27(2):119-126. doi:10.1016/j.cxom.2019.05.004
  16. Forrest CR, Lata AC, Marcuzzi DW, Bailey MH. The role of orbital ultrasound in the diagnosis of orbital fractures. Plast Reconstr Surg. 1993;92(1):28-34. doi:10.1097/00006534-199307000-00004
  17. Sharma R, Parashar A. Unfavourable outcomes in maxillofacial injuries: How to avoid and manage. Indian J Plast Surg. 2013;46(2):221. doi:10.4103/0970-0358.118597
  18. Krausz AA, Krausz MM, Picetti E. Maxillofacial and neck trauma: a damage control approach. World J Emerg Surg. 2015;10(1):31. doi:10.1186/s13017-015-0022-9
  19. Hutchison I, Lawlor M, Skinner D. ABC of major trauma. Major maxillofacial injuries. BMJ. 1990;301(6752):595-599. doi:10.1136/bmj.301.6752.595
  20. Barak M, Bahouth H, Leiser Y, Abu El-Naaj I. Airway Management of the Patient with Maxillofacial Trauma: Review of the Literature and Suggested Clinical Approach. BioMed Res Int. 2015;2015:724032. doi:10.1155/2015/724032
  21. Spurrier E, Johnston A. Use of Nasogastric Tubes in Trauma Patients – A Review. J R Army Med Corps. 2008;154(1):10-13. doi:10.1136/jramc-154-01-04
  22. Jose A, Nagori S, Agarwal B, Bhutia O, Roychoudhury A. Management of maxillofacial trauma in emergency: An update of challenges and controversies. J Emerg Trauma Shock. 2016;9(2):73. doi:10.4103/0974-2700.179456
  23. Stewart C, Fiechtl JF, Wolf SJ. Maxillofacial trauma: Challenges in ED diagnosis and management. Emerg Med Pract. 2008;10(2):1-18.
  24. Shumate R, Portnof J, Amundson M, Dierks E, Batdorf R, Hardigan P. Recommendations for Care of Geriatric Maxillofacial Trauma Patients Following a Retrospective 10-Year Multicenter Review. J Oral Maxillofac Surg. 2018;76(9):1931-1936. doi:10.1016/j.joms.2017.10.019
  25. Kokko LL, Puolakkainen T, Suominen A, Snäll J, Thorén H. Are the Elderly With Maxillofacial Injuries at Increased Risk of Associated Injuries?. J Oral Maxillofac Surg. 2022;80(8):1354-1360. doi:10.1016/j.joms.2022.04.018

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Fundamentals of ACLS (2024)

~ iEM Education Project Team ~ Leave a comment

by Mohammad Anzal Rehman

Authors
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You have a new patient!

A 56-year-old man presents to the Emergency Department with complaints of chest pain and dizziness that began an hour ago. Upon assessment by the triage nurse, his vital signs are as follows: his heart rate is 107 beats per minute, and his respiratory rate is 22 breaths per minute. His blood pressure is  96/70 mmHg, and his oxygen saturation is at 90% on room air. His temperature is 36.8°C.

You are the student on shift when this patient arrives, and immediately, your mind begins to jump across differential diagnoses for this patient. As you rush toward the patient’s room to join your senior, you prepare to list out all the potential causes of chest pain proudly. This must be a Myocardial Infarction, or maybe even an Aortic Dissection. Perhaps it is that rare Boerhaave syndrome you read about last night!

You finally catch up to the Emergency Physician, but before you can open your mouth to wax lyrical about esophageal ruptures, the Doctor states “Let’s begin by evaluating the ABCs.”

Initial Assessment

Emergency Medicine is one of the few specialties in medicine where patient evaluation begins in the same way for every patient, regardless of the probable diagnosis. Most clinicians are wired to jump straight to the ‘mystery-solving’ component of clinical presentation, with many undergraduate curriculums based around disease recognition. Emergency Medicine, however, places an emphasis on systematic assessment of the patient, starting with ‘The Primary Survey’.

The Primary Survey – ABCDE Approach

The Primary Survey aims to identify life-threatening conditions rapidly and systematically in critically ill patients, with appropriate stabilizing interventions performed when an abnormality is recognized. Besides streamlining the process in a high-stakes and often chaotic environment, the alphabetical order is designed first to address the most severe causes of mortality [1].

The Primary Survey aims to identify life-threatening conditions rapidly and systematically in critically ill patients, with appropriate stabilizing interventions performed when an abnormality is recognized. Besides streamlining the process in a high-stakes and often chaotic environment, the alphabetical order is designed first to address the most severe causes of mortality [1].

Airway

A patient’s airway connects air, and therefore oxygen, from outside the body to the lungs. Airway management is a term used to evaluate and optimize the passage of oxygen in the upper airway, which may be impaired when there is a blockage or narrowing of this pathway. The most common cause of upper airway obstruction is the tongue, which may ‘close’ the oropharynx posteriorly in patients who are comatose or in cardiopulmonary arrest, for example.

Assessment of the airway typically starts by evaluating any external features that may impact the passage of air through the naso- and oro-pharynx, such as facial or neck trauma, fractures, deformities, and any masses or swelling that may disrupt the airway tract. Allergies, especially anaphylaxis, and significant burns may cause edema of the laryngeal airway and produce obstruction. Excessive secretions may also congest the oropharynx and produce airway obstruction.

A patent or ‘normal’ airway allows a responsive patient to speak in full sentences without difficulty, implying a non-obstructed air passage down the oropharynx and through the vocal cords.

Clinical signs of obstruction may include stridor, gurgling, drooling, choking, gagging, or apnea. A physician may also identify an impending airway obstruction where loss of gag reflex, intractable vomiting, or worsening laryngeal edema may inevitably compromise the passage of air to the lungs and produce a failure to oxygenate or ventilate, prompting a decision to secure the tract through intubation.

Management

In the responsive patient, allow for the patient to be seated or lying in their most comfortable position as you assess the patency of the airway.

‘Opening’ the airway involves positioning the patient’s head in the ‘sniffing position’. In this position, a slight extension of the head with flexion of the neck, keeping the external auditory meatus in line with or above the sternal notch, is used to optimally align the pharyngeal and laryngeal airway segments, preventing obstruction posteriorly by the tongue (Figure 1). This is useful in patients who are unresponsive and cannot consciously protect their airway.

Figure 1 – Use of ‘sniffing position’ to open the airway

Two maneuvers are helpful in opening an unresponsive or sedated patient’s airway, optimizing air entry to the lungs:

1. Head tilt chin lift (Figure 2A) – Using fingertips under the chin, lift the mandible anteriorly while simultaneously tilting the head back using the other hand. Do not use this if cervical spine injury is suspected!

Figure 2A – Head-tilt chin lift

2. Jaw thrust (Figure 2B) – With thenar eminences of both hands anchored over both maxillary regions of the patient’s face, use your fingers at both angles of the mandible to lift it anteriorly. This maneuver is preferable in cases of suspected cervical spine injury as it does not cause hyperextension of the neck.

In unresponsive patients with excessive secretions, use of a rigid suction device can clear fluid and particulate matter such as vomitus.

Intubation may be performed if airway assessment deems it necessary to protect or secure the airway tract in a definitive way. If intubation is required, it should be performed as early as possible to prevent the evolution of a difficult airway, which would lower the chances of a successful intubation. It may also be useful to establish the risk of an inherently difficult airway using the L-E-M-O-N airway assessment method as below:

Look externally – facial trauma, large incisors and/or tongue, hairy beard, or moustache

Evaluate the 3-3-2 rule – where optimal distance between incisors on mouth opening should be 3 finger breadths. Similarly, 3 finger breadths (patient’s fingers) should span the distance from chin to hyoid bone, while the distance from hyoid to thyroid should measure 2 finger breadths.

Mallampati score – grades the view of an open mouth, with class 3 or more predicting a difficult intubation

Obesity/obstruction – Epiglottitis or a tonsillar abscess can inhibit easy passage of an endotracheal tube.

Neck mobility – if limited, positioning is difficult and causes suboptimal views during intubation.

iEM-infographic-pearls-airway - Assessing Airway Difficulty
assessing airway difficulty

Cervical spine immobilization

When the patient arrives in the Emergency Department (ED) following a significant physical trauma, such as head injury or motor vehicle collision, it is crucial to consider the integrity of the cervical spine. If injury is present in this region, further manipulation or movement of the neck may lead to spinal cord damage. Therefore, evaluation and management of airway for these patients should go hand in hand with cervical spine immobilization.

If no specialized equipment is available, or until one is prepared for use, attempts to limit neck movement can be done using manual in-line stabilization, where the provider’s forearms or hands may be positioned at the sides of the patient’s head to prevent indirect movements that could exacerbate underlying injury (see Figure 3).

Cervical spine immobilization is then performed using a rigid cervical collar. It may be augmented with head blocks on lateral sides to limit movement further as the patient is evaluated for injury (see Figure 4). The thoracolumbar region of the spine is immobilized using a spinal backboard, which keeps the patient in a supine position with minimal external force on the spine. Frequently utilized in Emergency Medical Services (EMS) during extrication and transport, all efforts should be made to transition the patient off the spinal board in the ED as it is quite uncomfortable, with prolonged use associated with pressure ulcers and pain.

Breathing

The lungs perform the vital function of delivering oxygen from the airway to the alveoli through ventilation. Perfusion at the alveoli allows for gas exchange; therefore, effective ventilation and perfusion both play a key role in the availability and utilization of oxygen by the human body. Evaluation of the Breathing component assesses factors that would indicate a compromise in ventilation.

The chest inspection should look for respiratory rate, use of accessory muscles, position of trachea (midline versus deviated), symmetry of chest rise, and/or any visible trauma to the thorax. Auscultation evaluates breath sounds for any bilateral inequal air entry or presence of crackles, crepitus, or wheeze. Percussion, though sometimes useful, is often difficult to perform adequately in a resuscitation environment.

Let’s compare the findings in normal lungs, pleural effusion, and pneumothorax based on chest rise, trachea position, percussion, and auscultation.

Normal Lungs: Chest rise is symmetrical with the trachea in the midline position. Percussion reveals a resonant sound. Auscultation presents vesicular breath sounds peripherally and bronchovesicular sounds over the sternum, with no added sounds.

Pleural Effusion: Chest rise remains symmetrical, and the trachea is midline. Percussion is dull over the area of effusion, and auscultation shows decreased breath sounds in the region of the effusion.

Pneumothorax: Chest rise is unequal, and the trachea may be deviated in cases of tension pneumothorax. Percussion reveals a hyper-resonant sound in the area of the pneumothorax, and auscultation shows decreased breath sounds over the pneumothorax region.

Measuring oxygen saturation using pulse oximetry (spO2) provides a percentage of oxygen in circulating blood, with normal levels typically at 95% or above. However, in patients with chronic lung disease, baseline oxygen saturation levels may decrease and can be as low as 88% in many cases. For patients experiencing shortness of breath and showing signs of hypoxia, pulse oximetry readings below 94% suggest that supplemental oxygen may be necessary. This can be administered through various oxygen delivery systems, as outlined in Figure 5 and described below.

Figure 5 – Common equipment used in airway management 1- Nasal cannula, 2- Simple face mask, 3- Nebulizer,* 4- Non-rebreather mask, 5- Venturi mask valves, 6- Rigid suction tip, 7- Bag-valve mask device, 8- Oropharyngeal airway (OPA), 9- Nasopharyngeal airway (NPA), 10- Direct Laryngoscope, 11- Endotracheal tube with stylet, 12- Colorimetric end-tidal CO2 detector, 13- Bougie, 14- Laryngeal Mask Airway (LMA) *NOT an oxygen delivery device, used to administer inhaled medication such as bronchodilators and steroids CO2: Carbon dioxide

General concepts—We typically breathe in room air, which contains 21% oxygen. Each Liter per minute of supplemental oxygen provides an additional 4% inspired oxygen (FiO2) to the patient.

Nasal cannula – Administered through patient nostrils, can provide a maximum flow rate of 4-6 Liters per minute of oxygen, which equals roughly 37 – 45% FiO2

Simple face mask – Applied over the patient’s nose and mouth, can provide a maximum flow rate of 6-10 Liters per minute of oxygen, which equals roughly 40 – 60% FiO2

Venturi mask – Typically used in COPD, where over-oxygenation is avoided. Different colors deliver various flow rates to limit oxygen delivery to the required amount only; Blue (2-4L/min, FiO224%), White (4-6L/min, FiO2 28%), Yellow (8-10L/min, FiO235%), Red (10-12 L/min, FiO2 40%), Green (12-15 L/min, FiO260%)

Non-rebreather mask – Utilizes an attached bag with a reservoir of oxygenated air along with one-way valves on the mask to prevent rebreathing of expired air, optimizing oxygenation. It can provide a maximum flow rate of 15 Liters per minute of oxygen, which equals roughly 85 – 90% FiO2.

Non-invasive ventilation (CPAP/BiPAP) is a tight-fitting mask device that uses high positive pressure to keep the airway open and enhance oxygenation. It is particularly useful in conditions such as COPD exacerbation, acute pulmonary edema/heart failure, and sleep apnea.

Bag-valve mask device: A self–inflating bag attached to a reservoir delivers maximal, high-flow 100% oxygen. This method of manual ventilation is used in rescue breathing and oxygen delivery in nonresponsive or cardiopulmonary arrest patients.

Circulation

The circulation component of the Primary Survey evaluates the adequacy of perfusion by the cardiovascular system. The patient’s general appearance is assessed for signs of pallor, mottling, diaphoresis, or cyanosis, which indicate inadequate or deteriorating perfusion status. Pulses are checked centrally (e.g. carotid pulse, especially if patient with impaired breathing) and peripherally (e.g. radial) alongside hemodynamic assessment, including blood pressure and heart rate checks. Information from this segment also provides valuable insight into potential signs of shock. Extremities are palpated in order to determine any delays in capillary refill time (more than 2 seconds signifies inadequate perfusion, e.g. hypovolemia), peripheral edema in lower extremities (signs of heart failure), and skin temperature (cool or warm to touch).

In cases of trauma, systematic evaluation of circulation also seeks to ascertain areas of potential blood loss or collection, with interventions for any long-bone deformities and/or bleeding from open wounds performed as they are discovered.
Intravenous (IV) line insertion is also performed as part of the management of circulation, as any required fluid or blood products can then be administered through a large-bore IV line (16 gauge or higher). If IV insertion is difficult on multiple attempts, when volume resuscitation is urgently required, Intraosseous (IO) access should be sought to prevent delay in any needed treatment. Insertion of a peripheral venous line often occurs concomitant to blood extraction for any urgent laboratory investigations and/or point-of-care testing. Some common examples of tests performed on critically ill patients include venous blood gas, complete blood count, type and crossmatch, troponin, urea, electrolytes, and creatinine.

Finally, circulation assessment requires an evaluation of cardiac rhythm. Basic auscultation may reveal the rate and regularity of rhythm along with murmurs. However, a critically ill patient will also benefit from the immediate attachment of cardiac pads to the bare chest and connection to a cardiac monitoring device, which provides the physician with the patient’s current cardiac rhythm.

A normal sinus rhythm (Figure 6) consists of a P wave (atrial depolarization), followed by a QRS wave (ventricular depolarization – normally less than 120 ms), with a subsequent T wave (ventricular repolarization). P-R intervals typically have a duration of 120 – 200 ms. A regular rhythm, with a consistent P wave preceding QRS complexes, with a normal heart rate (between 60 – 100 beats per minute (bpm)) is required to consider a rhythm to be normal sinus on the cardiac monitor.

Figure 6 – Normal sinus rhythm

The American Heart Association’s (AHA) Advanced Cardiac Life Support (ACLS) course and guidelines outline a series of internationally recognized cardiac rhythms and their general management when encountered [2]. Some of the most important rhythms, along with the AHA bradycardia and tachycardia algorithms, are summarized below:

Figure 7.1 - Sinus bradycardia (HR < 50 bpm)

Several different conditions, including abnormal heart conduction, damage to the myocardium, metabolic disturbances, or hypoxia, can cause bradycardia. A lower heart rate can result in decreased perfusion to end-organs, such as the brain, with resultant signs and symptoms such as dizziness, confusion, shortness of breath or chest pains. Management (Figure 7.2) aims to treat the underlying cause and increase the heart rate (atropine, dopamine/epinephrine and/or cardiac pacing) if needed to restore the heart’s ability to perfuse organs adequately.

Figure 7.2 – American Heart Association’s Bradycardia Algorithm

Tachycardia (Figure 8.1) is a heart rate of more than 100 bpm that may present as several types of waveforms on the cardiac monitor. Supraventricular tachycardia (SVT) originates in the upper chambers of the heart. The rapid heart rate prevents adequate filling of the heart between contractions, causing signs and symptoms such as dizziness, palpitations, or chest pain.

Figure 8.1 - Supraventricular Tachycardia (SVT)

Management (Figure 8.2) typically involves Valsalva maneuvers, medication (e.g. adenosine), and/or synchronized cardioversion as needed to revert the rhythm back to baseline.

Figure 8.2 – American Heart Association’s Tachycardia Algorithm

SVT produces a narrow-complex tachycardia (QRS segments < 120 ms). In comparison, monomorphic Ventricular Tachycardia (Figure 8.3) originates in the lower chambers of the heart and produces a wide-complex (QRS segments > 120 ms) tachycardia on the cardiac monitor. Similarly, this rhythm may cause dizziness, shortness of breath, or chest pain and is managed with medication or synchronized cardioversion.

Figure 8.3 - Ventricular Tachycardia

ACLS algorithms often divide patients based on “stable” and “unstable” categories. This grouping aims to ascertain which individuals have a pathology severe enough to impair cardiac output to the point of causing serious inadequacies in end-organ perfusion. This ‘instability’ is manifested by altered mental status, ischemic chest pain, drastically low hemodynamic parameters (e.g. systolic BP < 90 mmHg), signs of shock, and signs of acute decompensated heart failure.

Disability

This segment evaluates the level of consciousness and responsiveness of the patient. Level of consciousness may be assessed generally using the AVPU scale (below);

Alert: fully alert patient
Verbal: some form of verbal response is present, though not necessarily coherent.
Pain: response to painful stimulus
Unresponsive: no evidence of motor, verbal or eye-opening response to pain

or more explicitly, using the Glasgow Coma Scale (GCS)

Choose the best response of patient
EYE OPENING
4: Spontaneously
3: To verbal command
2: To pain
1: No response
BEST VERBAL RESPONSE
5: Oriented and converses
4: Disoriented and converses
3: Inappropriate words; cries
2: Incomprehensible sounds
1: No response
BEST MOTOR RESPONSE
6: Obeys command
5: Localizes pain
4: Flexion withdrawal
3: Flexion abnormal (decorticate)
2: Extension (decerebrate)
1: No response
Glasgow Coma Score (GCS) (Modified from Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness: a practical scale. The Lancet, 304(7872), 81-84.) - Please read this article to get more insight regarding GCS.

Exposure

Complete exposure of the patient may be necessary to completely evaluate for any external signs of infection, injury, and rash. This is especially useful in trauma, where log-rolling of the patient is included to ensure the back and spine are also included in a complete assessment for any traumatic injuries. As you expose the patient, obtain consent, be mindful of their dignity, and uncover each segment of the body sequentially, covering it back to prevent any hypothermia for the patient. A core temperature reading also completes vital sign measurements for the patient.

Practical implementation of the Primary Survey

The “cursory” primary survey

It may seem surprising to consider that virtually every patient who enters the Emergency Department, despite the severity of the illness, undergoes some form of a Primary Survey by the treating physician. However, the practicality of this becomes quite obvious when you consider a simple question frequently asked at the beginning of a patient encounter:

“How are you?”

An adequate response of “I am all right” or “Well, I have had this pain in my stomach…” seems fairly standard, but it addresses most of the components detailed in the previous section. A patient who can form words without difficulty or added sounds generally has an intact or patent Airway. Their ability to form words depends on air that has been sufficiently ventilated and moving through the vocal cords, hence the Breathing is adequate. An appropriate response to the question allows us to assume that Circulation adequately perfuses the brain to allow comprehension and formulation of new words oriented to the circumstances of the encounter, hence providing insight into Circulation and, to a degree, Disability.

Synchrony in the Emergency Department

Although systematic assessment during the Primary Survey is laid out in order, it is also important to note that an Emergency Department consists of teams of healthcare professionals who often have the personnel and resources to simultaneously perform tasks to efficiently address all components of the Primary assessment, without delay between segments.
In practice, an example of how synchrony works would involve a patient who, on initial, immediate assessment, is deemed to be in significant distress and/or critically ill. The patient is immediately moved into the ED to a resuscitation area, where team members expose the chest, attach cardiac pads to connect the patient to a cardiac monitor, obtain a fresh set of vital signs, including spO2monitoring, with IV cannula insertion, blood extraction for testing as needed. At the same time, a primary survey is conducted simultaneously by another physician who moves through Airway, Breathing, Circulation, Disability and Exposure. In more advanced systems, a member may be dedicated to each component of the Primary Survey.

Adjuncts

A number of resources are accessible to the Emergency Physician that may aid in diagnosing and investigating the critically ill patient. Utilizing these alongside the initial Primary Survey provides valuable, relevant information that can further guide clinical decision-making and diagnosis during evaluation.

  1. Electrocardiogram – A 12-lead electrocardiogram provides a complete picture of the heart’s electrical activity in various vectors and segments, allowing for a more accurate evaluation for rhythm disturbances, such as in acute myocardial infarction, hyperkalemia, bundle branch blocks, and torsade de pointes. This often ties into the Circulation assessment and allows for a more comprehensive look into the heart’s electrophysiology.
  2. Portable X-rays – Particularly in trauma, urgent chest and pelvic X-ray films can often be obtained without having to transfer the patient to Radiology, hence providing more information on suspected lung pathologies (e.g. pneumothorax, effusion/hemothorax) and pelvic abnormalities (e.g. fracture, displacement).
  3. Urinary/ gastric catheters – Urinary catheters are useful to evaluate fluid status and monitor output for the patient undergoing volume resuscitation. When relevant, gastric tube insertion can assist in gastrointestinal decompression, if needed, as well as minimize the risk of aspiration in certain patients.
  4. Point-of-Care Ultrasonography (PoCUS) – A rapidly evolving and increasingly prevalent modality in the ED is the ultrasound.[3] Various probes, at different frequencies, utilize ultrasound waves to provide the physician with real-time visualization of the body’s internal structures. These images are fast and often very reliable in determining major findings that can guide decision-making in critically ill patients (e.g. presence of post-traumatic intra-abdominal free fluid, pneumothorax, cardiac tamponade). Figure outlines some examples of information that can be extracted using PoCUS.

 

HI-MAP in Shock

Reassessment

Each intervention performed in the Primary Survey should ideally be accompanied by a reassessment of vital signs and patient clinical status and a restarted Primary Survey beginning from Airway. Identifying any improvements, deteriorations, or non-responses that will be pivotal in guiding the initiation or discontinuation of further intervention as per the clinical case is crucial.

Focused History and Secondary Survey

If the patient is appropriately evaluated and stabilized following the Primary Survey, the treating physician may proceed with a focused history and secondary survey appropriate to the clinical circumstances. One example of a focused history incorporates the mnemonic SAMPLE to organize pertinent information as follows:

S – Signs/symptoms of presenting complaint

A – Allergies to any food or drugs

M – Medications (current, recent changes)

P – Pertinent past medical history

L – Last oral intake

E – Events leading to the illness or injury

A secondary survey in the Emergency Department is a more comprehensive physical examination performed systematically in a head-to-toe fashion to investigate any clinically relevant findings. In case of trauma, this also involves careful inspection for any missed injuries, deformities, or signs of underlying blood collection.

As the secondary survey is performed, relevant investigations and/or imaging may be ordered to augment the evaluation of the present clinical condition (e.g. Computerized Tomography (CT) of the brain after signs of basal skull fracture noted on inspection of the face and head). Information gathered from the survey and results of any ordered investigations, coupled with the clinical condition and/or response to therapy in the ED, if any, is used to determine patient disposition at the end of the ED encounter.

Revisiting Your Patient

You assist the Emergency Physician in performing a Primary Survey. The airway is patent, with the patient phonating in full sentences and breathing with mild tachypnea but no added sounds on auscultation. You initiate supplemental oxygen through a non-rebreather mask, with an increase in spO2 to 99%. You reassess and proceed through Airway, Breathing, and Circulation. As you discuss initiating IV fluids with your senior, the patient complains of worsening chest pain, palpitations, and dizziness.You attach the patient to the cardiac monitor and notice the rhythm below:

Cardiac pads have already been attached to the patient. Noting the presence of ischemic chest pain, you correctly identify the patient as having an unstable, narrow-complex tachycardia, most likely an SVT and prepare for synchronized cardioversion. Conscious sedation is conducted after explaining the procedure and obtaining consent from the patient. 50 joules of biphasic energy is then administered for synchronized electrical cardioversion. The rhythm changes on the monitor to the reading below:

You observe an organized rhythm but note that the patient is now unresponsive, with eyes closed and no palpable carotid pulse.

Basic Life Support

Cardiopulmonary arrest occurs when the heart suddenly stops functioning, resulting in lack of blood flow to vital organs in the body, such as the lungs and brain. Therefore, signs of arrest are manifested as a lack of breathing (apnea), lack of pulse and unresponsiveness. The most common cause of cardiac arrest is coronary artery disease.[4] Respiratory arrest refers to a cessation of lung activity, but with a present, palpable pulse and functioning heart.
The International Liaison Committee on Resuscitation (ILCOR) and the American Heart Association (AHA) are some of the key figures who have developed international guidelines on the recognition and management of cardiac arrest patients.[5] Basic Life Support (BLS) and Advanced Cardiac Life Support (ACLS) courses were established to optimize the workflow and, therefore, patient outcomes in Cardiopulmonary Resuscitation (CPR).

CPR forms the cornerstone of BLS to effectively maintain the victim’s circulatory and ventilatory function until circulation either spontaneously returns or is hopefully restored through intervention. The general concepts within BLS are outlined below:

1. A person who has a witnessed collapse, lack of response or who is suspected of being unresponsive due to cardiac arrest should be approached for further assessment and management. However, it is important for the rescuer to first determine whether the scene is safe around the patient before attempting any intervention. An example of this would be a victim drowned in water, who should be removed from the body of water onto a dry surface prior to attempting life-saving chest compressions or defibrillation.

Figure 9 - Witness
Figure 10 - Check for responsiveness

2. Check for responsiveness. Firmly tapping both shoulders with the palms of your hands and a clear, verbal prompt, such as “Hey, are you okay?” should be incorporated to ensure that the victim is, indeed, unresponsive to an otherwise arousable stimulus.

3. You have determined that the patient is unresponsive. If you are alone, shout loudly and clearly for help and assistance. If no help is nearby, call Emergency Medical Services using your mobile phone.

Figure 11 - Call for help
Figure 12 - Open airway, palpate carotid artery, observe the chest

4. Open the patient’s airway (tilt chin upward into sniffing position). Palpate the carotid pulse by placing two fingers (index and middle finger) just lateral to the trachea on the side closest to you while simultaneously observing the chest for any spontaneous chest rise (breathing). The pulse check should take a minimum of five (5) seconds but no more than 10 seconds to avoid delay in life-saving intervention.

5. When help is available, the chain of survival begins by activating the Emergency Response System. In addition to activating the Emergency Response, ask the person who has responded to your call for help getting an Automated External Defibrillator (AED) device. An example of instruction to a bystander (out of hospital) would be to ‘call an ambulance and get an AED!’. Inside a hospital, if another healthcare provider has come to aid, you may ask them to ‘activate the Emergency Response System/’Code Blue’ and get the crash cart/AED.’

6. Begin high-quality chest compressions. Hands are placed with fingers interlaced to exert pressure using the heel of one hand at the center of the chest, over the lower half of the breastbone (sternum), in line with the nipples (in men), with shoulders directly over your hands and arms straight at a perpendicular angle to the victim’s chest. High-quality chest compression is one of the few variables which have been evidenced to improve patient survival in cardiac arrest.

Figure 13 - Chest compression

Keep the following features in mind to maintain high-quality chest compressions:

  • More than 80% of the time in resuscitation or more should be spent on compressions (Chest compression fraction of > 80%)
  • The frequency of compressions should follow a rate of 100–120 compressions per minute.
  • Compression depth in adults is at least 2 inches. In infants and children, depth should be at least one-third of the anterior-posterior diameter of the chest.
  • After each compression, the hands should be withdrawn to allow adequate chest recoil and fill the heart between compressions.
  • Minimize interruptions in chest compression
  • Avoid hyperventilation (see next point).
Figure 14 - Bag-Valve-Mask Ventilation. Two-Hand technique

7. Compressions should follow the ratio 30:2, that is, 30 compressions followed by 2 rescue breaths delivered by a mouth barrier device (pocket mask) in the sniffing position or a Bag-valve mask (BVM) device if another rescuer is present to manage the airway in hospital. The BVM’s mask should be held with a tight seal using the E-C technique over the bridge of the nose and covering the mouth. 

Breaths should be over 1 second, with enough air pushed in to observe a chest rise and no hyperventilation or excessive bagging of the BVM to avoid gastric insufflation. Two attempts at rescue breaths are performed, minimizing time to under 10 seconds and resuming chest compressions immediately after. If a definitive airway (e.g. endotracheal tube) is in place, resume compressions without pause at a rate of 100-120 compressions per minute while breaths are delivered once every 6 seconds.

8. Once an AED or cardiac monitor/defibrillator is available, place the pads on the victim’s bare chest (dry the skin if wet) in either an anterior-lateral or anterior-posterior position.When in doubt, follow the machine’s prompts and the instructions on the pads themselves to guide placement.

Figure 15 - Correct placement of transcutaneous pacing pads.jpg

9. Follow the prompts on the AED. Stop compressions when the device analyzes rhythm and stay clear of the patient (not touching any part of the patient’s body). During an in-hospital resuscitation, as per ACLS workflow, stay clear, as the team leader should analyze the initial rhythm to ascertain the presence of a shockable or non-shockable rhythm. Either way, the device or team leader should prompt whether a shock is advised. Continue compressions as the device charges, but ensure that all rescuers are clear of the patient when the shock is delivered using the AED/defibrillator device.

Figure 16 - Shock delivery.

A victim who is unresponsive but has a palpable pulse has respiratory arrest, which is managed using rescue breathing only. Breaths are delivered once every 6 seconds without chest compressions while transport to a higher level of care and/or management of any underlying cause for the condition is initiated.

Advanced Cardiac Life Support

The Advanced Cardiac Life Support algorithms were designed to deliver a higher level of resuscitative care where providers with increased training and improved resources are available. This type of augmented management is customary to the Emergency Department, where a Rapid Response Team or Code Blue team would respond when activated and initiate a more team-based approach to cardiopulmonary resuscitation.

Instead of an AED, in-hospital settings have a cardiac monitor/defibrillator, usually mounted atop a crash cart consisting of a CPR back-board (to support chest compressions by providing a firm surface to use under the patient’s chest), drawers with medication used during cardiac arrest, and various equipment for airway management and IV/IO access. Once brought to the bedside, the cardiac pads are similarly placed on the patient’s chest while BLS maneuvers (chest compressions and rescue breaths) continue. Once placed, however, compressions should be paused to assess the cardiac monitor’s cardiac rhythm. The type of rhythm should be identified as ‘shockable’ or ‘non-shockable’ (Figure 17s).

Figure 17.1 - NON-SHOCKABLE - Asystol
Figure 17.2 - NON-SHOCKABLE - Pulseless electrical activity – organized rhythm in the absence of palpable pulse
Figure 17.3 - SHOCKABLE - Pulseless Ventricular Tachycardia
Figure 17.4 - SHOCKABLE - Ventricular fibrillation

“Shockable” rhythms (pulseless Ventricular Tachycardia and Ventricular Fibrillation) are a product of aberrant electrical conduction of the heart. Rapid, early correction of this rhythm is the most important step in returning the body to its normal circulatory function. Early defibrillation is one of the few variables that has been evidenced to improve patient survival in cardiac arrest, the other notable one being high-quality chest compressions.[6]

Defibrillation involves using an asynchronous 200J of biphasic (360J if monophasic) energy, delivering an electric current through the cardiac pads attached to the patient’s chest to revert the heart to a rhythm that can sustain spontaneous circulation. Chest compressions should be ongoing while charging, but all persons should stay clear of the patient when shock is being delivered, and this is frequently verified with verbal feedback (‘Clear!’) before pressing the defibrillator button to deliver the shock. Immediately after the shock, chest compressions should resume to minimize interruptions between compressions.

Two minutes of chest compressions and rescue breaths make up each cycle of CPR, at the end of which a rhythm check should be performed for any changes and/or presence of pulse. Figure 18 outlines the ACLS algorithm used to manage shockable and non-shockable rhythms in cardiac arrest. Early shock in shockable rhythms is followed by a cycle of CPR, a second shock if still with a shockable rhythm, after which 1mg of IV epinephrine is given, with subsequent doses every 3 to 5 minutes. During the third cycle of CPR, after 3 shocks have been delivered for a persistent shockable rhythm, a bolus of IV Amiodarone 300mg is typically administered, with a dose of 150mg in a subsequent CPR cycle if still with a shockable rhythm.

“Non-shockable” rhythms (pulseless electrical activity (PEA) and asystole) are not typically a product of disorganized electrical activity in the heart. Instead, an underlying cause has resulted in cardiac arrest for these patients. While the majority of cardiac arrest is caused by coronary artery disease, the consideration of reversible causes by use of the H’s (hypovolemia, hypoxia, hyper-/hypokalemia, hydrogen ions (acidosis), and hypothermia) and T’s (thrombosis/embolism, toxins, tension pneumothorax, and cardiac tamponade) may help recognize and manage other possible etiologies in patients.

The management of non-shockable rhythms focuses on consistent, high-quality CPR, with regular pulse checks every 2 minutes, addressing reversible causes, and administering IV epinephrine 1mg every 3 to 5 minutes.
A palpable pulse with measurable blood pressure signals the Return of Spontaneous Circulation (ROSC).

Figure 18 - ACLS Adult Cardiac Arrest Algorithm

Resuscitation Team Dynamics

The Emergency Department is equipped with the resources and personnel to provide care beyond basic life support. Resuscitation is optimized when multiple providers work together to effectively perform tasks toward management of the patient, thereby multiplying the chances of a successful outcome for the patient. A high-performance team typically consists of members allocated to the following roles and responsibilities:

  • Airway – Opens and maintains the airway. Manages suctioning, oxygenation, and ventilation (Bag-valve mask) and assesses the need for a definitive airway if needed.
  • Medication – Inserts and maintains IV/IO access. Manages medication administration and fluids.
  • Monitor/defibrillator – Ensures attached cardiac pads and AED/cardiac monitor/defibrillator device are working appropriately to display the patient’s cardiac rhythm in clear view of the team leader. Administers shocks using the devices as needed. May alternate with the compressor every 5 cycles or 2 minutes to prevent compression fatigue
  • Compressor – Performance of high-quality chest compressions as part of CPR for the cardiac arrest patient. Focuses on quality and consistency of compressions. You may switch to another standby compressor or monitor/defibrillator every 5 cycles or 2 minutes if compressions are affected by fatigue.
  • Recorder – Documents the timing of medication, intervention (shocks, compression), and communicates these to the Team Leader, with prompts to enable timely dosing of frequent medication (e.g., ensuring epinephrine every 3 to 5 minutes is administered as per the verbalized order)
  • Team leader – A defined leader who coordinates the team’s efforts and organizes them into roles and responsibilities that are clear, well-understood, and within their individual limitations. Provides explicit instructions and direction to the resuscitation effort, focused on patient care and optimized performance from all team members. Promotes understanding and motivates members, identifying any potential deficit or depreciation of quality during resuscitation and facilitating improvement in performance as needed.

All team members are encouraged to conduct themselves with mutual respect and practice closed-loop communication, where each message or order is received with verbal confirmation of understanding, then execution of the order, centralizing all information back to the team leader. Figure 19 provides an example of the possible placement of each member during resuscitation that may optimize their workflow through the resuscitation attempt. Ideally, the team leader remains at the foot of the bed, in clear view of all members, with involvement limited to coordination of the team’s efforts and minimal direct execution of tasks.

Figure 19 - An example of optimized team placement during resuscitation

Post Arrest Care

If the patient is found to have Return of Spontaneous Circulation (ROSC), post-cardiac arrest care should be initiated to enhance the preservation of brain tissue and heart function. This involves a sequential assessment and optimization of Airway, Breathing, and Circulation in the initial stabilization phase. A definitive airway may be placed so ventilation is more appropriately controlled, with parameters set to optimize oxygen administered with ventilatory function. Figure 20 outlines the ACLS algorithm and parameters often used to help guide post-cardiac arrest care. Circulation incorporates fluids, vasopressors, and/or blood products to achieve an adequate systolic blood pressure above 90 mmHg, with Mean Arterial Pressure of at least 65 mmHg typically indicating perfusion within stable parameters.

It is imperative to obtain a 12-lead ECG early to ascertain the presence of an ST-elevation myocardial infarction (STEMI), which will require expedited transfer of the patient to a Cath Lab for definitive reperfusion therapy. The patient’s responsiveness should be reassessed, and the determination for additional investigation should be performed in conjunction with other critical care management as needed.

Of note, unresponsive patients may benefit from Targeted Temperature Management (TTM), which involves the maintenance of core body temperature at a target of 32 – 36 ℃ for 24 hours, or preferably normothermia at 36 °C to 37.5 °C with an emphasis on prevention of hyperthermia, in order to protect and optimize brain recovery post-arrest.[7]

Almost all cardiac arrest survivors will require a period of intensive care observation and management. If no immediate intervention is needed (e.g., reperfusion therapy), patients inside a hospital will need to be transitioned to an Intensive Care Unit (ICU) for further care.

Figure 20 – Post-Cardiac Arrest Care

What do you need to know?

  • Emergency Medicine, especially in critical care, emphasizes a systematic approach to the unwell patient.
  • The Primary Survey is designed to recognize and address life-threatening conditions effectively and timely.
  • The Primary Survey components are Airway (& and C-spine in trauma), Breathing, Circulation, Disability, and Exposure.
  • If an intervention is performed at any level of the survey, you must reassess the patient by commencing the Primary Survey again, starting with Airway.
  • Reassess and review your patient for changes frequently.
  • Many of the actions performed in the initial assessment of the critically ill patient may occur simultaneously when more team members are present in an Emergency Department. Do not let the chaos of the scene distract you from completing each step of the assessment.
  • The AHA has well-established guidelines for assessing and managing patients through the Primary Survey. Use the algorithms and the patient’s status as ‘stable’ or ‘unstable’ to guide the management of recognized pathologies, especially in Circulation.
  • The ED is home to a variety of adjuncts, including portable X-rays, ECG, and point-of-care ultrasound, which can provide the physician with rapid, readily accessible information to guide management.
  • Remember the SAMPLE mnemonic for a focused history in the critically ill patient.
  • An unresponsive patient should be immediately recognized, and Emergency Response Systems should be activated.
  • Performance of Basic and Advanced cardiac life support focuses on preserving blood circulation transiently to maintain the perfusion of organs, such as the brain, until the cause of the condition is reversed or managed.
  • The majority of cardiac arrest is caused due to coronary artery disease.
  • The two most important predictors of patient survival in cardiac arrest are high-quality CPR and early defibrillation (for a shockable rhythm)
  • An effective resuscitation in the ED often relies on the concerted efforts of multiple team members, led by a team leader who coordinates tasks in an organized, effective way to improve patient survival and outcomes.

Author

Picture of Mohammad Anzal Rehman

Mohammad Anzal Rehman

EM Residency Graduate from Zayed Military Hospital in Abu Dhabi, UAE. Founder/President of the Emirates Collaboration of Residents in Emergency Medicine (ECREM). Editor-in-Chief for the Emirates Society of Emergency Medicine (ESEM) Monthly Newsletter. I have a vested interest in sharing updated knowledge and developing teaching tools. As a healthcare professional, I continually strive to incorporate the newest clinical research into practice and am an active advocate for the use of Point of Care Ultrasonography (POCUS) in the ED.

Listen to the chapter

References

  1. Reynolds T. Basic Emergency Care: Approach to the Acutely Ill and Injured. World Health Organization; 2018.
  2. 2020 Advanced Cardiac Life Support (ACLS) Provider Manual. American Heart Association; 2021.
  3. Hashim A, Tahir MJ, Ullah I, Asghar MS, Siddiqi H, Yousaf Z. The utility of point of care ultrasonography (POCUS). Ann Med Surg (Lond). 2021;71:102982. Published 2021 Nov 2. doi:10.1016/j.amsu.2021.102982
  4. Cardiac Arrest Registry to Enhance Survival (CARES) 2022 Annual Report; 2022, https://mycares.net/
  5. Wyckoff MH, Singletary EM, Soar J, et al. 2021 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations: Summary From the Basic Life Support; Advanced Life Support; Neonatal Life Support; Education, Implementation, and Teams; First Aid Task Forces; and the COVID-19 Working Group. Resuscitation. 2021;169:229-311. doi:10.1016/j.resuscitation.2021.10.040
  6. Soar J, Böttiger BW, Carli P, et al. European Resuscitation Council Guidelines 2021: Adult advanced life support [published correction appears in Resuscitation. 2021 Oct;167:105-106]. Resuscitation. 2021;161:115-151. doi:10.1016/j.resuscitation.2021.02.010
  7. Lüsebrink E, Binzenhöfer L, Kellnar A, et al. Targeted Temperature Management in Postresuscitation Care After Incorporating Results of the TTM2 Trial. J Am Heart Assoc. 2022;11(21):e026539. doi:10.1161/JAHA.122.026539

Acknowledgements

  • Marina Margiotta – Illustrator
  • Paddy Kilian – Emergency Physician – Mediclinic City Hospital, Dubai, Director of Academic Affairs – Mohammed Bin Rashid University Of Medicine and Health Sciences
  • Rasha Buhumaid – Consultant Emergency Physician – Mediclinic Parkview Hospital, Dubai, Assistant Professor of Emergency Medicine – Mohammed Bin Rashid University Of Medicine and Health Sciences, President of the Emirates Society of Emergency Medicine (ESEM)
  • Amog Prakash – Medical Student – Mohammed Bin Rashid University Of Medicine and Health Sciences
  • Fatima Al Hammadi- Medical Student – Mohammed Bin Rashid University Of Medicine and Health Sciences

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

The Case of the Perplexing Crepitations

perplexing crepitations
~ Gayatri Lekshmi Madhavan, India ~ 1 Comment

Occam’s Razor – the simplest explanation is most likely to be correct.

In the Emergency Room, we are faced with a multitude of cases, and Occam’s Razor serves best when we need to narrow down on the differential diagnoses.

Sometimes, a few cases may evade this category and continue to baffle us even after a thorough history is obtained or a detailed clinical examination is performed. If we are lucky enough to get the point-of-care (POC) lab tests in time (or the mere availability of POC), they aid in the diagnosis and decision-making. At times, these POC lab tests also may not provide much help.

I have described one such case – a 21-year-old male with fever, dyspnea, desaturation, and multiple petechiae of 3 days duration.

Case Presentation

A 21-year-old male came at 9.30 pm to the ER with fever and breathlessness for three days. Being a healthcare worker himself, he had suspected pneumonia and started oral Amoxiclav, oral Clarithromycin, and Paracetamol. Despite this, there was no improvement in clinical status. He had progressively worsening breathlessness and continuous low-grade fever. On day 3, he developed a few petechial spots over his arms and minimal subconjunctival hemorrhage.

He recalls having myalgia in the lead up to these symptoms, for which he had received several injections of intramuscular Diclofenac. The injection sites now had developed small hematomas. There were no other visible bleeding manifestations. He clearly said that he had had no contact with any infectious patients and had self-isolated after developing these symptoms. His workplace had sent blood and sputum cultures – which came back negative. Their only concern was a continuous rise in the WBC count and sent to our hospital for further management.

Assessment

The patient was very ill-looking and extremely dyspneic with obvious usage of accessory respiratory muscles. He was profusely diaphoretic, had bilateral subconjunctival hemorrhage, multiple petechiae, anasarca, dyspnea, and 99.6⁰F. His Vitals were heart rate – 134/min, blood pressure – 110/70mmHg, respiratory rate – 34/min, SpO2 – 72% in room air; 98% with NIV. There were bilateral crepitations in all lung fields + no obvious abnormalities on CVS, CNS, and abdominal examination. POC ultrasound revealed multiple B-lines in all lung areas. Dilated IVC. The remaining cardiac, abdomen, and limb USGs were normal. ABG revealed Type 1 respiratory failure with elevated lactates. Bedside CXR and chest CT revealed diffuse bilateral lung infiltrates – not typical of pulmonary edema or pneumonia. Probable ARDS was mentioned. Blood samples had been sent for necessary investigations, including cultures and peripheral blood smear.

Management

Meanwhile, opinions were obtained from critical care consultants and pulmonologists regarding further management. Based on the clinical findings, it was decided to start the patient on broad-spectrum antibiotics (BSA), albumin transfusion, diuretics for the fluid overload status, and NIV for respiratory failure [all in suspicion of sepsis with MODS]. The patient was started on BSA before shifting to the ICU. Meanwhile, the blood reports arrived, suggestive of possible Myelodysplastic Syndrome (WBC – 95,000 cu.mm), Hb – 7g/dl. Peripheral Blood Smear report was Acute Myeloid Leukemia – possible M2 or M3.

The patient was immediately started on IV fluids, and oncology consultation was immediately obtained for chemotherapy initiation. Albumin and diuretics were withheld in suspicion of blast crisis and leukostasis / leukemic infiltration of the lungs. The patient was started on Cisplatin and other chemotherapeutic agents; bicarbonate infusion for urine alkalinization; allopurinol to treat hyperuricemia due to cytolysis; aggressive IV fluids for prevention of AKI due to chemotherapy and hyperuricemia [Tumour Lysis Syndrome]. Bone marrow biopsy was done during his hospital stay, which confirmed blast crisis AML-M3. His clinical condition improved considerably, and he was discharged from the hospital on Day 7.

Lessons Learnt

  1. Recognising leukostasis and hyperviscosity in the ED in an undiagnosed AML patient is extremely difficult. https://link.springer.com/chapter/10.1007/978-3-030-22445-5_3
  2. While considering different diagnoses based on clinical findings, always keep an open eye. Rare diseases present to the ED just like all others. https://www.medscape.com/viewarticle/860747_3
  3. Aggressive fluid management is needed in hyperviscosity syndrome. If we had started this patient on diuretics as planned, the blood would have become more viscous and lead to multisystem thrombosis. https://pubmed.ncbi.nlm.nih.gov/22915493/
  4. Increased metabolism in AML can present as pyrexia. With the other features of anemia, leucocytosis, petechiae, and anasarca, we are likely to diagnose this as sepsis. When in doubt, look through other causes of pyrexia (PUO). https://onlinelibrary.wiley.com/doi/full/10.1111/imj.13180
  5. Anasarca in leukemia does not warrant albumin transfusion as this may worsen fluid status. They may actually be in need of steroid therapy. https://www.hindawi.com/journals/crihem/2012/582950/
  6. Point of Care Lab testing is essential to reduce the number of diagnostic errors in the ED. https://acutecaretesting.org/en/articles/
[cite]

Recent Blog Posts By Gayatri L. Madhavan

Physiologically Difficult Airway – Metabolic Acidosis

Physiologically Difficult Airway - Metabolic Acidosis
~ Jule Santos, Brasil ~ Leave a comment

Case Presentation

A 32-year-old male with insulin-dependent diabetes mellitus came to your emergency department for shortness of breath. He was referred to the suspected COVID-19 area. His vitals were as follows: Blood pressure, 100/55 mmHg; pulse rate, 135 bpm; respiratory rate, 40/min; saturation on 10 liters of oxygen per minute, 91%; body temperature, 36.7 C. His finger-prick glucose was 350 mg/dl.

The patient reported that he had started to feel ill and had an episode of diarrhea 1 week ago. He developed a dry cough and fever in time. He started to feel shortness of breath for 2 days. He sought out the ER today because of the difficulty breathing and abdominal pain.

The patient seemed alert but mildly agitated. He was breathing effortfully and sweating excessively. On physical examination of the lungs, you noticed fine crackles on the right. Despite the patient reported abdominal pain, there were no signs of peritonitis on palpation.

An arterial blood gas analysis showed: pH 7.0, PCO2: 24, pO2: 56 HCO3: 8 Lactate: 3.

The point-of-care ultrasound of the lungs showed B lines and small foci of subpleural consolidations on the right.
At this point, what are your diagnostic hypotheses?

Two main diagnostic hypotheses here are:

  • Diabetic ketoacidosis (Hyperglycemia + metabolic acidosis)
  • SARS-CoV2 pneumonia

We avoid intubating patients with pure metabolic decompensation of DKA if possible, as they respond to hydration + insulin therapy + electrolyte replacement well and quickly. 

But in this scenario, the patient is extremely sick and has complicating medical issues, such as an acute lung disease decompensating the diabetic condition, probably COVID19. Considering these extra issues may complicate the recovery time and increase the risk of respiratory failure, you decide to intubate the patient in addition to the treatment of DKA.

You order lab tests and cultures. You start hydration and empirical antibiotics while starting preoxygenation and preparing for intubation.

Will this be a Difficult Airway?

Evaluating the patient for the predictors of a difficult airway is a part of the preparation for intubation. Based on your evaluation, you should create an intubation plan. 

This assessment is usually focused on anatomical changes that would make it difficult to manage the airway (visualization of the vocal cords, tube passage, ventilation, surgical airway), thereby placing the patient at risk.

“Does this patient have any changes that will hinder opening the mouth, mobilizing the cervical region, or cause any obstruction for laryngoscopy? Does this patient have any changes that hinder the use of Balloon-Valve-Mask properly, such as a large beard? What about the use of the supraglottic device? Does this patient have an anatomical alteration that would hinder emergency cricothyroidotomy or make it impossible, like a radiation scar? ”

So the anatomically difficult airway is when the patient is at risk if you are unable to intubate him due to anatomical problems.

The physiologically difficult airway, however, is when the patient has physiological changes that put him at risk of a bad outcome during or shortly after intubation. Despite intubation. Or because of intubation, because of its physiological changes due to positive pressure ventilation.

These changes need to be identified early and must be mitigated. You need to recognize the risks and stabilize the patient before proceeding to intubation or be prepared to deal with the potential complications immediately if they happen.

5 main physiological changes need attention before intubation are: hypoxemia, hypotension, severe metabolic acidosis, right ventricular failure, severe bronchospasm.

Back to our patient: Does he have physiologically difficult airway predictors?

  • SI (Shock Index): 1.35 (Normal <0.8) – signs of shock
  • P / F: 93 (Normal> 300) – Severe hypoxemia
  • pH: 7.0: Severe metabolic acidosis – expected pCO2: 20 (not compensating)
  • qSOFA: 2 + Lactate: 3 (severity predictor)

Physiologically Difficult Airway

"Severely critical patients with severe physiological changes who are at increased risk for cardiopulmonary collapse during or immediately after intubation."

Sakles JC, Pacheco GS, Kovacs G, Mosier JM. The difficult airway refocused.

Severe Metabolic Acidosis

In this post, we will focus only on the compensation of the metabolic part, but do not forget that this is a patient who needs attention on oxygenation and hemodynamics as well. That is, this is intubation with very difficult predictions.

What happens during the rapid sequence of intubation in severe metabolic acidosis?

To perform the procedure, the patient needs to be in apnea. During an apnea, pulmonary ventilation is decreased and the CO2 is not “washed” from the airway. These generate an accumulation of CO2, an acid, decreasing blood pH. In a patient with normal or slightly altered pH, this can be very well-tolerated, but in a patient with a pH of 7.0, an abrupt drop in this value can be ominous.

We know that the respiratory system is one of the most important compensation mechanisms for metabolic acidosis and it starts its action in seconds, increasing the pH by 50 to 75% in 2 to 3 minutes, guaranteeing the organism time to recover. So, even seconds without your proper actions can be risky for critical patients.

In addition, it must be remembered that increased RF is the very defense for the compensation of metabolic acidosis, and most of the time the organism does this very well. So if after the intubation the NORMAL FR and NORMAL minute volume are placed in the mechanical ventilator parameters, again there is an increase in CO2 and a further decrease in pH.

And what’s wrong? After all, a little bit of acidosis even facilitates the release of oxygen in the tissues because it deflects the oxyhemoglobin curve to the right, right?

Severe metabolic acidosis (pH <7.1) can have serious deleterious effects:

  • Arterial vasodilation (worsening shock)
  • Decreased myocardial contractility
  • Risks of arrhythmias
  • Resistance to the action of DVAs
  • Cellular dysfunction

What to do?

Always the primary initial treatment is: treating the underlying cause! In patients with severe metabolic acidosis, it is best to avoid intubation! Especially in metabolic ketoacidosis, which as hydration and insulin intake improves, there is a progressive improvement in blood pH.

Sodium bicarbonate

The use of sodium bicarbonate to treat metabolic acidosis is controversial, especially in non-critical acidosis values ​​(pH> 7.2). If you have acute renal failure associated, its use may be beneficial by postponing the need for renal replacement therapy (pH <7.2).

As for DKA, where sodium bicarbonate is used to the ketoacidosis formed by erratic metabolism due to the lack of insulin and no real deficiency is present, its use becomes limited to situations with pH <6.9.

The dose is empirical, and dilution requires a lot of attention (avoid performing HCO3 without diluting!)

NaHCO3 100mEq + AD 400ml

Run EV in 2h

If K <5.3: Associate KCl 10% 2amp

I would make this solution and leave it running while proceeding with the intubation preparations.

Attention: Remember, according to the formula below, that HCO3 is converted to CO2, and if done in excess, is associated with progressive improvement of the ketoacidosis and recovery of HCO3 from the buffering molecules. In a patient already with limited ventilation, its increase can cause deviation of the curve for the CO2 increase, which is also easily diffused to the cells and paradoxically decrease the intracellular pH, in addition to carrying K into the cell.

H + + HCO3 – = H2CO3 = CO2 + H2O

Mechanical ventilation

I think the most important part of the management of these patients is the respiratory part.

If you choose the Rapid Sequence Intubation: Prepare for the intubation to be performed as quickly as possible: Use your best material, choose the most experienced intubator, put the patient in ideal positioning, decide and apply medications skillfully, to ensure the shortest time possible apnea.

You will need personnel experienced in Mechanical Ventilation and you must remember to leave the ventilatory parameters adjusted to what the patient needs and not to what would be normal!

I found this practice very interesting: First, you calculate what the expected pCO2 should be for the patient, according to HCO3:

Winter’s Equation (Goal C02) = 1.5 X HCO3 + 8 (+/- 2)

And then, according to this table, you try to reach the VM Volume Minute value.
Goal CO2 Minute Ventilation
40 mmHg
6-8 L
30 mmHg
12-14 L
20 mmHg
18-20 L

These are just initial parameters. With each new blood gas analysis repeated in 30 minutes to an hour, you re-make fine adjustments using the formula below:

Minute volume = [PaCO2 x Minute volume (from VM)] / CO2 Desired

With the treatment of ketoacidosis, new parameters should be adjusted, hopefully for the better.

Another safer option for these patients would be to use the Awake Patient Intubation technique so that you would avoid the apnea period. However, Awake Patient Intubation Technique is contraindicated in suspected or confirmed COVID-19 cases due to the risk of contamination.

That’s it, folks, send your feedback, your experiences, and if you have other sources!

Further Reading

  1. Frank Lodeserto MD, “Simplifying Mechanical Ventilation – Part 3: Severe Metabolic Acidosis”, REBEL EM blog, June 18, 2018. Available at: https://rebelem.com/simplifying-mechanical-ventilation-part-3-severe-metabolic-acidosis/.
  2. Justin Morgenstern, “Emergency Airway Management Part 2: Is the patient ready for intubation?”, First10EM blog, November 6, 2017. Available at: https://first10em.com/airway-is-the-patient-ready/.
  3. Salim Rezaie, “How to Intubate the Critically Ill Like a Boss”, REBEL EM blog, May 3, 2019. Available at: https://rebelem.com/how-to-intubate-the-critically-ill-like-a-boss/.
  4. Salim Rezaie, “RSI, Predictors of Cardiac Arrest Post-Intubation, and Critically Ill Adults”, REBEL EM blog, May 10, 2018. Available at: https://rebelem.com/rsi-predictors-of-cardiac-arrest-post-intubation-and-critically-ill-adults/.
  5. Salim Rezaie, “Critical Care Updates: Resuscitation Sequence Intubation – pH Kills (Part 3 of 3)”, REBEL EM blog, October 3, 2016. Available at: https://rebelem.com/critical-care-updates-resuscitation-sequence-intubation-ph-kills-part-3-of-3/.
  6. Lauren Lacroix, “APPROACH TO THE PHYSIOLOGICALLY DIFFICULT AIRWAY”, https://emottawablog.com/2017/09/approach-to-the-physiologically-difficult-airway/
  7. Scott Weingart. The HOP Mnemonic and AirwayWorld.com Next Week. EMCrit Blog. Published on June 21, 2012. Accessed on July 15th 2020. Available at [https://emcrit.org/emcrit/hop-mnemonic/ ].
  8. IG: @pocusjedi: “Pocus e Coronavirus: o que sabemos até agora?”https://www.instagram.com/p/B-NxhrqFPI1/?igshid=14gs224a4pbff

References

  1. Sakles JC, Pacheco GS, Kovacs G, Mosier JM. The difficult airway refocused. Br J Anaesth. 2020;125(1):e18-e21. doi:10.1016/j.bja.2020.04.008
  2. Mosier JM, Joshi R, Hypes C, Pacheco G, Valenzuela T, Sakles JC. The Physiologically Difficult Airway. West J Emerg Med. 2015;16(7):1109-1117. doi:10.5811/westjem.2015.8.27467
  3. Irl B Hirsch, MDMichael Emmett, MD. Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed on July 15, 2020.)
  4. Cabrera JL, Auerbach JS, Merelman AH, Levitan RM. The High-Risk Airway. Emerg Med Clin North Am. 2020;38(2):401-417. doi:10.1016/j.emc.2020.01.008
  5. Guyton AC, HALL JE. Tratado de fisiologia medica. 13a ed. Rio de Janeiro(RJ): Elsevier, 2017. 1176 p.
  6. Kraut JA, Madias NE. Metabolic acidosis: pathophysiology, diagnosis and management. Nat Rev Nephrol. 2010;6(5):274-285. doi:10.1038/nrneph.2010.33
  7. Calvin A. Brown III, John C. Sakles, Nathan W. Mick. Manual de Walls para o Manejo da Via Aérea na Emergência. 5. ed. – Porto Alegre: Artmed, 2019.
  8. Smith MJ, Hayward SA, Innes SM, Miller ASC. Point-of-care lung ultrasound in patients with COVID-19 – a narrative review [published online ahead of print, 2020 Apr 10]. Anaesthesia. 2020;10.1111/anae.15082. doi:10.1111/anae.15082
[cite]

More Posts by Dr. Santos

Oxygenation and Oximetry

Oxygenation and Oximetry
~ Job Guillen, Mexico ~ Leave a comment

Authors: Job Rodríguez Guillén, Chief of Emergency Department. Hospital H+ Querétaro, México. Regina Pineda Leyte Internal Medic, Anahuac Querétaro University, Mexico. 

Introduction

One of the main goals of mechanical ventilation is oxygenation. Both hypoxemia and hyperoxemia must be avoided and the objectives must be individualized according to the clinical situation and comorbidities of each patient. Oxygenation monitoring is possible at the bedside by physical examination (late clinical signs), pulse oximetry (non-invasive continuous monitoring), and arterial blood gas analysis (gold standard for arterial oxygenation analysis).

Determinants of oxygenation

The main determinant of oxygenation is the mean airway pressure (Paw) and the inspired fraction of oxygen (FiO2). Paw is the average pressure to which the lung is exposed during inspiration and expiration mechanical ventilation (Figure 1). Paw improves oxygenation by allowing the redistribution of oxygen from highly compliant alveoli to less compliant alveoli.(1,2)
Oxygenation and Oximetry - figure 1
Figure 1: Mean airway pressure (Paw) is the integral (area under the curve) of pressure and time. PIP: peak inspiratory pressure; PEEP: positive pressure at the end of expiration; Ti: inspiratory time; Te: expiratory time.
According to the determinants of Paw and the relationship between them, there are five different ways to increase it (Figure 2)
Oxygenation and Oximetry - figure 2
Figure 2: Maneuvers to increase the mean airway pressure (Paw). PEEP: positive pressure at the end of expiration. Only maneuvers 3 and 4 are used in clinical practice to increase Paw and improve oxygenation.

The second determinant of oxygenation is Inspired Oxygen Fraction (FiO2). The use of supplemental oxygen at the hospital level is a common practice and a critical element of intensive care in patients with mechanical ventilation for the management of hypoxemia. However, in recent years it has been shown that higher oxygenation is not the goal. (3) In the same way that hypoxemia should be avoided, hyperoxia should be prevented. (4)

Although the FiO2 can be adjusted in ranges of 21% and up to 100% the lowest value required must be set (preferably <60%) to reach the desired oxygen saturation (SO2) target.

Oxygenation monitoring

Pulse oximetry allows non-invasive monitoring of oxygenation (SpO2), it is simple and reliable in many areas of clinical practice. SpO2 has a confidence rate of 95% ± 4%, so readings ranging between 70% and 100% are considered reliable.(5) In patients with mechanical ventilation, the objective is to identify hypoxemia.

It is important to remember that oximeters do not measure arterial oxygen pressure (PaO2), for this reason, they cannot directly diagnose hypoxemia or hyperoxemia (PaO2 <60 mmHg and PaO2> 120 mmHg respectively).(6)  What they do is “estimate” hypoxemia when SpO2 falls <90%, which would correspond to a PaO2 <60 mmHg according to the oxyhemoglobin dissociation curve (Table 1). (7)  However, it must be taken into account that changes in temperature and pH cause changes in this relationship. As the pH increases (alkalosis) or the temperature decreases (hypothermia), the shift of the curve is to the left since hemoglobin binds more strongly with oxygen, delaying its release to the tissues. Acidosis and fever shift the curve to the right as the hemoglobin molecule decreases its affinity for oxygen, facilitating the release of oxygen to the tissues.

Oxygenation and Oximetry - Table 1
Table 1: Estimation of the oxygenation state according to SpO2. SpO2: oxygen saturation by pulse oximetry; PaO2: arterial oxygen pressure.

SpO2 values <70% are not reliable. If necessary, the oxygenation assessment should be supplemented by arterial gas analysis. The arterial oxygen saturation (SaO2) is the oxygen saturation obtained by this test.

Oxygenation Goals

According to the oxyhemoglobin dissociation curve, the goal of oxygen titration is to achieve a PaO2 in the range of 60-65 mmHg or an SpO2 of approximately 90-92%. However, the objectives must be individualized and the current recommendations for oxygen therapy in critically ill patients. (8) are as follows (Table 2).

Table 2: Recommendations for oxygenation by SpO2. O2: oxygen; SpO2: oxygen saturation by pulse oximetry; AMI: Acute myocardial infarction; EVC: Cerebral vascular event; VM: mechanical ventilation; SIRA: Acute respiratory distress syndrome. Some exceptions apply like carbon monoxide poisoning.

It has been suggested that critically ill patients can tolerate lower levels of PaO2 (“permissive hypoxemia”) (9-10), however, studies are limited to make a recommendation to routine clinical practice.

Conclusions

Oxygenation goals should be established once the requirement for mechanical ventilation is indicated according to the clinical condition of each patient and monitoring that these objectives are met. Pulse oximetry allows continuous, non-invasive monitoring at the bedside. It should be remembered that hyperoxemia, as well as hypoxemia, should be avoided.

References

  1. Marini JJ,Ravenscraft SA. Mean airway pressure: physiologic determinants and clinical importance–Part 1: Physiologic determinants and measurements. Crit Care Med. 1992 Oct;20(10):1461-72.
  2. Marini JJ,Ravenscraft SA. Mean airway pressure: physiologic determinants and clinical importance–Part 2: Clinical implications. Crit Care Med. 1992 Nov;20(11):1604-16.
  3. Girardis M, Busani S, Damiani E, et al. Effect of conservative vs conventional oxygen therapy on mortality among patients in an intensive care unit: the Oxygen-ICU Randomized Clinical Trial. JAMA. 2016;316(15):1583-1589.
  4. Bitterman, Haim. “Bench-to-bedside review: oxygen as a drug.” Critical Care1 (2009): 205.
  5. Chan MM,Chan MM, Chan ED. What is the effect of fingernail polish on pulse oximetry?. Chest. 2003 Jun;123(6):2163-4.
  6. Wandrup JH. Quantifying pulmonary oxygen transfer deficits in critically ill patients. Acta Anaesthesiol Scand Suppl 1995;107:37–44
  7. Allen J. Photoplethysmography and its application in clinical physiological measurement. Physiol Meas 2007;28:R1–39
  8. Siemieniuk Reed A C, Chu Derek K, Kim Lisa Ha-Yeon, Güell-Rous Maria-Rosa, Alhazzani Waleed, Soccal Paola M et al. Oxygen therapy for acutely ill medical patients: a clinical practice guideline BMJ 2018;  363 :k4169
  9. Gilbert-Kawai ET, Mitchell K, Martin D, Carlisle J, Grocott MP. Permissive hypoxaemia versus normoxaemia for mechanically ventilated critically ill patients. Cochrane Database Syst Rev 2014;5:CD009931.
  10. Capellier G, Panwar R. Is it time for permissive hypoxaemia in the intensive care unit? Crit Care Resusc 2011;13:139–141.
[cite]

19 Questions and Answers on the COVID-19 Pandemic from a Emergency Medicine-based Perspective

covid 19 - from a Emergency Medicine-based Perspective
~ Francesco Adami, Italy ~ Leave a comment

1) What is COVID-19?

Corona Virus Disease 2019 (COVID-19) is the disease caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).

2) What is SARS-CoV-2?

SARS-CoV-2 is a virus belonging to the Coronaviridae family. Spike proteins (S proteins) on the outer surface of SARS-CoV-2 are arranged in a way that resembles the appearance of a crown when viewed under an electron microscope (see Figure 1). S proteins facilitate viral entry into host cells by binding to the angiotensin-converting enzyme 2 (ACE2) host receptor. Several cell types express the ACE2 receptor, including lung alveoli cells. [1].

Morphology of the SARS-CoV-2
Figure 1 - Morphology of the SARS-CoV-2 viewed under an electron microscope.Note the spikes that adorn the outer surface of the virus, which impart the look of a corona surrounding the virion. (https://phil.cdc.gov/Details.aspx?pid=23312)

3) How is SARS-CoV-2 transmitted?

Viral particles can spread from person-to-person through airborne transmission (e.g., large droplets) or direct contact(e.g., touching, shaking hands). We have to remember that large droplets are particles with a diameter > 5 microns and that they can be spread by coughing, sneezing, talking, etc., so do not forget to wear full PPE in the Emergency Department (ED). Other potential routes of transmission are still being investigated.

4) What is the incubation time?

In humans, the incubation period of the SARS-CoV-2 varies from 4 days to 14 days, with a median of about 4 days [2].

5) Can we say the COVID-19 is like the seasonal flu?

No, we can’t say that. COVID-19 differs from the flu in several ways:

  • First of all, SARS-CoV-2 replicates in the lower respiratory tract at the level of the pulmonary alveoli (terminal alveoli). In contrast, Influenza viruses, the causative agents of the flu, replicate in the mucosa of the upper respiratory tract.
  • Secondly, SARS-CoV-2 is a new virus that has never met our adaptive immune system.
  • Thirdly, we do not currently have an approved vaccine to prevent infection by SARS-CoV-2.
  • Lastly, we do not currently have drugs of proven efficacy for the treatment of disease caused by SARS-CoV-2.

6) Who is at risk of contracting the COVID-19?

We are all susceptible to contracting the COVID-19, so it is essential that everyone respects the biohazard prevention rules developed by national and international health committees. Elderly persons, patients with comorbidities (e.g., diabetics, cancer, COPD, and CVD), and smokers appear to exhibit poor clinical outcome and greater mortality from COVID-19 [3]

7) What are the symptoms of the COVID-19?

There are four primary symptoms of COVID-19: fever; dry cough; fatigue; and shortness of breath (SOB).

Other symptoms are loss of appetite, muscle and joint pain, sore throat, nasal congestion and runny nose, headache, nausea and vomiting, diarrhea, anosmia, and dysgeusia.

8) What is the severity of symptoms from COVID-19?

In most cases, COVID-19 mild or moderate symptoms, so much so it can resolve after two weeks of rest at home. However, onset of severe viral pneumonia requires hospital admission.

9) Which COVID-19 patients we should admit to the hospital?

The onset of severe viral pneumonia requires hospital admission. COVID-19-associated pneumonia can quickly evolve into respiratory failure, resulting in decreased gas exchange and the onset of hypoxia (we can already detect this deterioration in gas exchange with a pulse oximeter at the patient’s home). This clinical picture can rapidly further evolve into ARDS and severe multi-organ failure.

The use of the PSI/PORT score (or even the MuLBSTA score, although this score needs to be validated) can help us in the hospital admission decision-making process.

10) Do patients with COVID-19 exhibit laboratory abnormalities?

Most patients exhibit lymphocytopenia [11], an increase in prothrombin time, procalcitonin (> 0.5 ng/mL), and/or LDH (> 250 U/L).

11) Are there specific tests that allow us to diagnose COVID-19?

RT-PCR is a specific test that currently appears to have high specificity but not very high sensitivity [12]. We can obtain material for this test from nasopharyngeal swabs, tracheal aspirates of intubated patients, sputum, and bronchoalveolar lavages (BAL). However, the latter two procedures increase the risk of contagion.

However, since rapid tests are not yet available, RT-PCR results may take days to obtain, since laboratory activity can quickly saturate during epidemics. Furthermore, poor pharyngeal swabbing technique or sampling that occurs during the early stage of COVID-19 can lead to further decreased testing sensitivity.

Consequently, for the best patient care, we must rely on clinical symptoms, labs, and diagnostic imaging (US, CXR, CT). The use of a diagnostic flowchart can be useful (see Figure 2).

diagnostic flow chart
Figure 2 - A possible diagnostic flow chart for an ill patient admitted to hospital with suspected COVID-19 (from EMCrit Blog)

12) Can lung ultrasound help diagnose COVID-19?

Yes, it can help! The use of POCUS lung ultrasound is a useful method both in diagnosis and in real-time monitoring of the COVID-19 patient.

In addition, we could monitor the patient not only in the emergency department (ED) or intensive care unit (ICU), but also in a pre-hospital setting, such as in the home of a patient who is in quarantine.

In fact, POCUS lung ultrasounds not only allows one to anticipate further complications such as lung consolidation from bacterial superinfection or pneumothorax, but it also allows detection of viral pneumonia at the early stages. Furthermore, the use of a high-frequency ultrasound probe, which is an adoption of the 12-lung areas method [4] and the portable ultrasound (they are easily decontaminated), allow this method to be repeatable, inexpensive, easy to transport, and radiation-free.

There are no known pathognomonic patterns of COVID-19.

The early stages COVID-19 pneumonia results in peripheral alveolar damage including alveolar edema and a proteinaceous exudate [5]. This interstitial syndrome can be observed via ultrasound by the presence of scattered B lines in a single intercostal space (see videos below).

Subsequently, COVID-19 pneumonia progression leads to what’s called “white lung”, which ultrasound represents as converging B lines that cover the entire area of the intercostal space; they start from the pleura to end at the bottom of the screen.

Finally, the later stages of this viral pneumonia lead to “dry lung”, which consists of a pattern of small consolidations (< 1 cm) and subpleural nodules. Unlike bacterial foci of infection, these consolidations do not create a Doppler signal within the lesions. We should consider the development from “white lung” to “dry lung” as an unfavorable evolution of the disease.[6]

(the 5 videos above come from the COVID-19 gallery on the Butterflynetwork website)

13) Can CXR/CT help us in the diagnosis of COVID-19?

Yes, it can help! There are essentially three patterns we observed in COVID-19.

In the early stages, the main pattern is ground-glass opacity (GGO)[7]. Ground glass opacity is represented at the lung bases with a peripheral distribution (see videos below) .

The second pattern is constituted by consolidations, which unlike ground-glass opacity, determine a complete “opacification” of the lung parenchyma. The greater the extent of consolidations, the greater the severity and the possibility of admission in ICU.

The third pattern is called crazy paving[8]. It is caused by the thickening of the pulmonary lobular interstitium.

However, we should consider four things when we do a CXR/CT exam. First, many patients, especially in the elderly, exhibit multiple, simultaneously occurring pathologies, so it is possible to clinically observe nodular effusions, lymph node enlargements, and pleural effusions that are not typical of COVID-19 pneumonia. Secondly, we have to be aware that other types of viral pneumonia can also cause GGO, so they cannot be excluded during the diagnostic process. Thirdly, imaging can help evaluate the extent of the disease and alternative diagnoses, but we cannot use it exclusively for diagnosis. Lastly, we should carefully assess the risk of contagion from transporting these patients to the CT room.

14) What is the treatment for this type of patient?

COVID-19 patients quickly become hypoxic without many symptoms (apparently due to “silent” atelectasis). Therapy for these clinical manifestations is resuscitation and support therapy. In patients with mild respiratory insufficiency, oxygen therapy is adopted. In severe patients in which respiratory mechanics are compromised, non-invasive ventilation (NIV) or invasive ventilation should be adopted.

15) How can we non-invasively manage the airways of patients with COVID-19?

In the presence of a virus epidemic, we should remember that all the procedures that generate aerosolization (e.g., NIV, HFNC, BMV, intubation, nebulizers) are high-risk procedures.

Among the non-invasive oxygenation methods, the best-recommended solution is to have patients wear both a high-flow nasal cannula (HFNC) and a surgical mask[9]. Still, we should also consider using CPAP with a helmet interface. Furthermore, we should avoid the administration of medications through nebulization or utilize metered-dose inhalers with spacer (Figure 3).

Figure 3 – General schema for Respiratory Support in Patients with COVID-19 (from PulmCrit Blog)

16) How can we invasively manage the airways of patients with COVID-19?

We should intubate as soon as possible, even in non-critical conditions (Figure 3). Intubation is a high contagion risk procedure. As a result, we should adopt the highest levels of precaution[10]. To be more precise:

  • As healthcare operator, we should wear full PPE. Only the most skilled person at intubation in the staff should intubate. Furthermore we should consider using a video laryngoscope. Last but not least, we should ensure the correct positioning of the endotracheal tube without a stethoscope (link HERE).
  • The room where intubation occurs should be a negative pressure room. When that is not feasible, the room should have doors closed during the intubation procedure.
  • The suction device  should have a closed-circuit so as not to generate aerosolization outside.
  • Preoxygenation should be done using means that do not generate aerosols. Let us remember that HFNC and BVM both can generate aerosolization. So, it is important to remember to turn off the flow of the HFNC before removing it from the patient face to minimize the risk and to use a two-handed grip when using BVM, interposing an antiviral filter between the BVM and resuscitation bag and ventilating gently.
  • Intubation drugs that do not cause coughing should be used. In addition, we should evaluate the use of Rocuronium in the Rapid Sequence Intubation (RSI) since it has a longer half-life compared to succinylcholine and thus prevents the onset of coughing or vomiting.

In conclusion, let us remember that intubation, extubation, bronchoscopy, NIV, CPR prior to intubation, manual ventilation etc. produce aerosolization of the virus, therefore, it is necessary that we wear full PPE.

17) What is the drug therapy for COVID-19?

Currently, there is no validated drug therapy for COVID-19. Some drugs are currently under study. They include Remdesivir (blocks RNA-dependent RNA polymerase), Chloroquine and Hydroxychloroquine (both block the entry of the virus into the endosome), Tocilizumab and Siltuximab (both block IL-6).

18) Is there a vaccine available for COVID-19?

No, there is still no vaccine currently available to the public.

19) What precautions should we take with COVID-19 infected patients?

As healthcare professionals, we should wear full personal protective equipment (PPE) and know how to wear them (“DONning”) and how to remove them properly (“DOFFing”) (see video below). Furthermore, we should wear full PPE for the entire shift and when in contact with patients with respiratory problems.

Resources on COVID-19

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References

[1] Zheng YY, Ma YT, Zhang JY, Xie X. COVID-19 and the cardiovascular system. NatRev Cardiol. 2020 Mar 5.

[2] del Rio C, Malani PN. COVID-19—New Insights on a Rapidly Changing Epidemic. JAMA. Published online February 28, 2020. doi:10.1001/jama.2020.3072

[3] Yee J et al. Novel coronavirus 2019 (COVID-19): Emergence and Implications for Emergency Care. Infectious Disease 2020. https://doi.org/10.1002/emp2.12034

[4] Belaïd Bouhemad, Silvia Mongodi, Gabriele Via, Isabelle Rouquette; Ultrasound for “Lung Monitoring” of Ventilated Patients. Anesthesiology 2015;122(2):437-447. doi: https://doi.org/10.1097/ALN.0000000000000558.

[5] Qian-Yi Peng, Xiao-Ting Wang, Li-Na Zhang & Chinese Critical Care Ultrasound Study Group (CCUSG). Findings of lung ultrasonography of novel corona virus pneumonia during the 2019–2020 epidemic. 12 March 2020 Intensive Care Medicine.

[6]  Chan JF, Yuan S, Kok KH, et al. A familial cluster of pneumonia associated with the 2019 novel coronavirus indicating person-to-person transmission: a study of a family cluster. Lancet 2020.

[7] Chest CT Findings in Cases from the Cruise Ship “Diamond Princess” with Coronavirus Disease 2019 (COVID-19)

[8] Radiographic and CT Features of Viral Pneumonia Hyun Jung Koo, Soyeoun Lim, Jooae Choe, Sang-Ho Choi, Heungsup Sung, and Kyung-Hyun Do RadioGraphics 2018 38:3, 719-739 doi: https://doi.org/10.1148/rg.2018170048

[9]  WHO – Clinical management of severe acute respiratory infection (SARI) when COVID-19 disease is suspected.

[10] Safe Airway Society. Consensus Statement: Safe Airway Society Principles of Airway management and Tracheal Intubation Specific to the COVID-19 Adult Patient Group. MJA 2020.

[11] GUAN WJ, Ni ZY, Hu Y, Liang WH, et al  Clinical Characteristics of Coronavirus Disease 2019 in China. N Engl J Med. 2020 Feb 28. doi: 10.1056/NEJMoa2002032

[12] Tao Ai et al. Correlation of Chest CT and RT-PCR Testing in Coronavirus Disease 2019 (COVID-19) in China: A Report of 1014 Cases. Radiology, published online February 26, 2020; doi: 10.1148/radiol.2020200642

Clinical examination of the hemodynamically unstable patient

Clinical examination of the hemodynamically unstable patient
~ Job Guillen, Mexico ~ Leave a comment

Authors: Job Rodríguez Guillén. Chief of Emergency Department. Hospital H+ Querétaro. México and Paola Rivero Castañeda. Medical Intern, Anahuac Querétaro University, Mexico. 

Introduction

Clinical examination accounts as a fundamental part in the management of most critical scenarios. Although there are few publications and it remains controversial, its value considered as limited by 50% of medical practicioners (1). None of the well-known semiology books include any section about the physical examination in the critically ill patient (2). Nonetheless, an adequate clinical evaluation at the patient’s bedside may save lives in the context of a serious situation.

Clinical Examination Objectives

The main objectives are identifying and discerning from types of shock, emphasizing in the identification of life-threatening conditions, clinical signs of organic hypoperfusion, as well as to evaluate treatment response regarding therapies employed, and risk stratifying.

Identify hemodynamic instability

  • Life-threatening conditions (Tension pneumothorax, Cardiac tamponade, Pulmonary thromboembolism, Active hemorrhage, etc.)
  • Organ hypoperfusion
    (Altered mental state, decreased uresis, mottled skin, prolonged CFT, etc.)

Evaluate treatment response

  • Vital signs and normalization of the clinical state
    (Mental state improvement, diminished skin mottling, improved uresis, normalization of prolonged capillary filling time, etc.)

Risk stratifying

  • Scale and prognostic scores calculation. Prognostic scores use a combination of clinical and/or laboratoy variables (SOFA: Squential Organ Failure Assessment; APACHE: Acute Physiology and Chronic Health Evaluation; SAPS: Simplified Acute Physiology Score; MPM: Mortality Probability Models, etc.)

Clinical Exam Systematization

The clinician must be able to do a quick and efficient clinical examination to recognize different states of shock as early as possible, or even situations that may compromise organic perfusion. At a given time, it’s suggested to check out the clinical history, re-interrogate the patient and his/her family members, as well as patient’s family/regular physician (or even look for their previous medical notes), in order to help clinical integration, and so for decision making.

Systematization of the evaluating process, based on the previously proposed objectives, can be identified with the following mnemonic: PROA.

PROA - Summary

P - Probabilistic thinking

  • Think about any probability.
  • Look for intentionally.
  • Analyze clinical context and individualize.

R - Risk of dying

Identify life-threatening causes: Cardiac tamponade, Tensionpneumothorax, Pulmonary thromboembolism, Active hemorrhage, etc.

O - Organic hypoperfusion

Cutaneous perfusion signs: examine mottled skin and capillary filling time.

A - Approach of the clinical examination

Clinical exam by regions. Some components may not be relevant for all patients, even requiring other physical maneuvers. Even though laboratory and imaging are not part of the clinical exam, their interpretation must be integrated with the examination findings.

Probabilistic Thinking

Medicine is a science of uncertainty and an art of probability.

— William Osler

Clinical decision making in the emergency department begins with the estimation of the probability of a determined patient to have or do not have specific conditions (Bayesian reasoning or pretest probability).

Example; the probability of septic shock in a young patient after having a car crash is very low compared to the high probability of presenting with hemorrhagic or obstructive shock.

Proposed decisions related to initial probabilistic thinking vary in clinical relevance depending on the patient’s condition. It should always be re-evaluated through available additional data (posttest probability) (Figure 1).

Relationship between probability thresholds and decision‐making zones
Figure 1: Relationship between probability thresholds and decision‐making zones (3).

Risk of Dying

Shock is a momentary pause in the act of death.

— John Collins Warren

Currently, there are four types of shock, all with a common pathophysiological pathway: acute circulatory insufficiency associated with cell oxygen utilization dysfunction (altered-balance between oxygen input and consumption: DO2/VO2 dysfunction), a central situation that takes part in the development of multiorgan dysfunction (4-5).

Initial physical examination should be directed to the identification of immediate life-threating pathologies such as obstructive shock (Tension pneumothorax, cardiac tamponade, pulmonary thromboembolism), hemorrhagic shock etc.

These pathologies require immediate action. Otherwise, early multi-organ dysfunction and death may occur. The Point of Care Ultrasound (PoCUS), is a fundamental tool used for the evaluation of patients with hemodynamic instability of unknown origin.

Organ Hypoperfusion

When assessing the damage an earthquake or fire has caused inside a building, one looks through the windows. Using this analogy, it would be useful to be able to see inside the body to view the damage caused by the shock process.

— Jean-Louis Vincent

The initial approach to clinical examination begins with the skin. It is essential to remember that microcirculation cannot be globally defined through its dependency with macrocirculation, autoregulation mechanisms and organ interactions. Moreover, the availability of devices to evaluate it remains limited. Therefore, the evaluation is done from clinical, biochemical and hemodynamic data integration (6) (Figure 2)

Figure 2: three windows of shock

The correct way of measuring capillary filling time

Approach of The Clinical Examination

Clinical exam is not an art, is an essential ability.

— Leonel Martínez-Ramírez

During the initial evaluation, multiple situations can affect the accomplishment of a detailed physical examination. Therefore, it is recommended to follow a structured exploration method, looking at every main organ system and region. Documenting its results would allow avoiding the inclusion of essential data, and would permit to identify tendencies or any change in the patient’s clinical status.

Clinical examination approach in the critically-ill patient.

7Clinical examination approach emphasized in the critically-ill patient. This examination is realized based on every region in the body. Some components may not be relevant for all patients, or even some other maneuvers shall be executed in the physical examination. The verification list should be modified to be adapted to each patient’s circumstances. Laboratory and other studies analysis does not conform part of the clinical examination, although, their interpretation should be added to exploration findings (7).

  • General appearance

    Introduce yourself to the patient. Evaluate general appearance, physical state, complexity or the presence of particular face patterns, etc.

  • Head

    Inspect pupils' symmetry and reactiveness to light. Look for facial asymmetry and signs of bleeding in nostrils and oropharynx. Inspect lips, mouth and tongue, searching for lesions or signs of ulceration.

  • Neck

    Evaluate neck symmetry, venous distension and tracheal positioning. Palpate searching for adenopathies, subcutaneous emphysema, etc.

  • Thorax

    Expose the thorax, inspect the use of accessory respiratory muscles, diaphragmatic movement, and type of respiration. Also, look for ecchymosis or hematomas. Palpate searching for subcutaneous emphysema or bone crepitations. Auscultate respiratory sounds bilaterally, as well as heart sounds, noting the physiological splitting of the second heart sound, murmurs, friction and gallop rhythm or third heart sound.

  • Upper extremities

    Evaluate upper extremities symmetry. Inspect all arterial and venous line catheters. Evaluate for presence of mottled skin, peripheral pulses and perfusion through capillary filling time.

  • Abdomen

    Take into consideration the diaphragmatic movement during ventilation. Evaluate distension and tympanic sounds during the percussion of the abdomen. Palpate for any rigidity or involuntary guarding. Evaluate abnormal growth of spleen and liver, palpable masses, murmurs or other intestinal sounds.

  • Lower extremities

    Evaluate all sites of vascular accesses and palpate pulses. Evaluate mottled skin, peripheral perfusion and edema.

  • Central Nervous System and Mental State

    Evaluate if the patient is able to follow orders and if his/her four extremities can move equally. Evaluate plantar response as well as withdrawal to pain stimuli. Check pupils and facial symmetry if they were not previously evaluated.

  • Devices and Incisions

    Every possible surgical site should be evaluated, as well as the entrance of every device, including endotracheal tubes, vascular accesses, thoracic tubes, enteral probes and urinary catheters. It should be taken into consideration the characteristics and quantity of urine in the Foley bag.

  • Monitors and waveforms

    The mode, pressures, ventilation per minute and waveforms, hemodynamic monitor (venous pressure, arterial pressure), telemetry and vital signs, as well as any other type of bedside monitor, should be inspected in order to detect any qualitative or quantitative alteration/abnormality.

  • Posterior region

    Exam executed when the patient is in a prone position. Inspect looking for lesions or penetrating wounds. Pressure ulcer appearance should be evaluated.

  • Environment

    Family’s or visitors' moods should be taken into consideration. Light quality, ambient temperature, etc. should be evaluated.

Conclusions

Clinical integration of initial clinical history and the physical examination should be added to the biochemical complementation as well as advanced hemodynamic monitoring parameters, when these are available. Even so, if clinical examination answers raised questions during the initial evaluating process, the clinician must act according to physiological principles. There is no ideal hemodynamic monitoring, meaning that all parameters have to be individualized for each patient and his/her clinical context. Therefore, clinical examination systematization results are an excellent aid for the clinician regarding his/her clinical practice.  

References and Further Reading

  1. Vazquez R, Vazquez Guillamet C, Adeel Rishi M, Florindez J, Dhawan PS, Allen SE, Manthous CA, Lighthall G.  Physical examination in the intensive care unit: opinions of physicians at three teaching hospitals. Southwest J Pulm Crit Care. 2015;10(1):34-43. DOI: http://dx.doi.org/10.13175/swjpcc165-14
  2. Cook CJ, Smith GB. Do textbooks of clinical examination contain information regarding the assessment of critically ill patients?Resuscitation. 2004;60:129–136.
  3. Zehtabchi S, Kline J.A. The Art and Science of Probabilistic Decision‐making in Emergency Medicine. Academic Emergency Medicine, 17:521-523. DOI: http://doi.org/10.1111/j.1553-2712.2010.00739.x
  4. Weil MH, Shubin H. Proposed reclassification of shock states with special reference to distributive defects. Adv Exp Med Biol.1971 Oct;23(0):13-23.
  5. Ince C. The microcirculation is the motor of sepsis. Crit Care. 2005;9 Suppl 4:S13-9. DOI: 1186/cc3753
  6. Vincent JL, Ince C, Bakker J. Clinical review: Circulatory shock–an update: a tribute to Professor Max Harry Weil.Crit Care. 2012 Nov 20;16(6):239. DOI: 10.1186/cc11510.
  7. Metkus TS, Kim BS. Bedside Diagnosis in the Intensive Care Unit. Is Looking Overlooked?. Ann Am Thorac Soc.2015 Oct;12(10):1447-50. DOI: 10.1513/AnnalsATS.201505-271OI.
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Massive Pneumothorax Without A Tension

massive pneumothorax
~ Arif Alper Cevik ~ Leave a comment

Case Presentation

A 24-years-old male with shortness of breath and chest pain presented to the emergency department. He was alert and oriented. Vitals were as follows; BP: 127/65 mmHg, HR: 101 beats per min, RR: 24 breaths per min, T: 37-degree celsius, SatO2: 94%. Physical examination revealed that normal breathing sounds on the left side, but decreased breath sounds on the right side of the chest. No JVD noted. Other examination findings were unremarkable.

Shortness of breath and chest pain started suddenly while he was playing soccer about 30 minutes ago. Since then, shortness of breath and chest pain increased. He has no known medical disease, allergy.

Bedside ultrasound revealed pneumothorax on the right.

Bedside Ultrasound Examination

Above video shows left side B mode ultrasound examination. Investigation was done in lung settings by using Butterfly iQ portable ultrasound. Lung sliding and comet tail artefacts are seen on examination which is normal findings.

Above video shows right side B mode and M-mode ultrasound examination. There is no lung sliding or comet tail artefacts in B mode, and M-mode revealed “barcode sign” which is seen in pneumothorax.

Pneumothorax - US - Lung - M-mode

Image shows “barcode sign” in M-mode examination. 

Bedside Portable Chest X-ray

spontaneous pneumothorax 1 - 18yo male

Bedside portable anteroposterior chest x-ray shows right sided large pneumothorax.

More pneumothorax images

Further reading on pneumothorax

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