Chest Pain (2024)

by Khaled Alaboud Alkheder & Muneer Al Marzooqi

You Have A New Patient!

A 67-year-old woman presents to the ED with acute chest pain. The pain is sharp and stabbing in nature. She feels nauseated and short of breath. The patient has a history of hypertension, type 1 diabetes mellitus, medullary thyroid cancer, coronary artery disease, and gastroesophageal reflux disease. She smoked half a pack of cigarettes daily for 19 years but quit 18 years ago. Her current medications include Lisinopril, Insulin Glargine, Insulin Aspart, Sertraline, Aspirin, and Ranitidine.

The image was produced by using ideogram 2.0.

She appears anxious and diaphoretic. Her temperature is 37.2°C, pulse is 62/min, respirations are 19/min, and blood pressure is 142/81 mmHg. The lungs are clear to auscultation. The chest wall and abdomen are non-tender. There is 5/5 strength in all extremities. The remainder of the examination shows no abnormalities.

How would you proceed, and what is the next step in management?

What Do You Need To Know?

Chest pain in the emergency department is reported to be the second most common complaint, comprising approximately 5% of all emergency department visits. It can indicate various underlying causes, and patients present with many signs and symptoms. The potential causes of chest pain include diseases affecting the heart, aorta, lungs, esophagus, stomach, mediastinum, pleura, and abdominal viscera.

Patients usually describe visceral pain as a squeezing, pressure-like, or dull type of pain. If the pain is visceral, it may also refer to other locations due to the nerves coursing through somatic nerve fibers as they reach the spinal cord. For example, ischemic heart pain may refer to the left or right shoulder, jaw, or left arm.

Clinicians in the ED focus on promptly identifying and ruling out life-threatening causes of chest pain. Patients with serious causes of chest pain may not exhibit any vital sign or physical examination abnormalities and may appear healthy [1,2].

Initial Assessment and Stabilization (ABCDE Approach)

The ABCDE approach is universally recognized as the safest and most efficient method for the initial assessment of patients in the Emergency Department (ED), particularly those presenting with chest pain [3]. This systematic approach ensures rapid identification and management of life-threatening conditions. It prioritizes the immediate stabilization of the patient while facilitating a structured evaluation process.

A – Airway: The first step involves assessing the airway for any signs of obstruction. Key indicators include the patient’s ability to speak without distress and the presence of paradoxical chest movements. Obstructions may result from conditions such as tongue swelling, lip swelling, or other factors impeding spontaneous breathing. Ensuring a patent airway is critical, as it serves as the foundation for effective oxygenation and ventilation.

B – Breathing: Next, the breathing assessment evaluates respiratory effectiveness by observing the patient’s respiratory rate (normal range: 10-20 breaths per minute), inspecting for signs of respiratory distress, and auscultating lung sounds. Findings such as basal crackles may indicate pulmonary edema, diminished breath sounds could suggest pneumothorax or pleural effusion. Each of these conditions requires prompt recognition and intervention.

C – Circulation: The circulation step focuses on identifying signs of cardiovascular compromise or shock. Clinical signs include abnormal extremity coloration (blue, pale, pink, or mottled), prolonged capillary refill time (normal is ≤2 seconds), and abnormal heart rates. Auscultation of the heart should confirm normal S1 and S2 sounds without murmurs or gallops. These findings guide the clinician in diagnosing conditions such as hypoperfusion or cardiac dysfunction. Muffled heart sounds may point toward pericardial tamponade. 

D – Disability: Assessment of the patient’s neurological status is crucial, including evaluating their level of alertness, Glasgow Coma Scale (GCS) score, and glucose levels. Any abnormalities here could indicate underlying conditions such as hypoglycemia, traumatic brain injury, or other causes of altered mental status.

E – Exposure: The final step involves fully exposing the patient to detect visible signs such as rashes, discoloration, or gross abnormalities. This step ensures that no critical findings, such as trauma or skin infections, are overlooked.

Once the primary assessment is complete, interventions should focus on managing hemodynamic instability, such as shock or hypertension. Simultaneously, secondary assessments and investigations are initiated, including obtaining IV access, performing a 12-lead ECG, and ordering relevant diagnostic tests to confirm the underlying cause of the presentation.

Medical History

When assessing a patient presenting with chest pain in the Emergency Department (ED), obtaining a thorough history is critical after ensuring the patient’s stability. Key aspects of the history should include [3,4]:

  • Onset of Pain: Determining whether the pain started abruptly or developed gradually provides valuable diagnostic clues.
  • Site of Pain: The location of the pain (e.g., substernal, localized, diffuse, chest wall, or back) can guide the identification of the underlying cause.
  • Character of Pain: Descriptions such as sharp, squeezing, or pleuritic help differentiate between cardiac, pulmonary, and musculoskeletal etiologies.
  • Radiation: Pain radiating to areas like the jaw, back, shoulder, or arm can indicate cardiac involvement.
  • Associated Symptoms: Symptoms such as diaphoresis, palpitations, dyspnea, nausea, or vomiting are important to document.
  • Timing: The pattern of the pain, whether constant or episodic, its duration, and the time of onset can help in distinguishing between various causes.
  • Exacerbating/Relieving Factors: Identifying activities or factors that provoke or alleviate the pain aids in narrowing down the diagnosis.

Pain Descriptions and Differential Diagnosis: The nature of the chest pain provides critical diagnostic insights:

  • Cardiac Origin: Pain described as “squeezing,” “crushing,” or “pressure-like” suggests cardiac ischemia or acute coronary syndrome (ACS). Pain during exertion is typical of stable angina, whereas progressive pain at rest suggests unstable angina or myocardial infarction (MI).
  • Aortic Dissection: “Tearing” pain radiating to the back is a hallmark of aortic dissection.
  • Pulmonary or Musculoskeletal Causes: “Sharp” or “stabbing” pain is often associated with pulmonary embolism, pneumothorax, or musculoskeletal disorders.
  • Gastrointestinal Causes: “Burning” or “indigestion-like” pain may originate from the gastrointestinal tract but could also signify visceral chest pain. Pain triggered by meals is more likely gastrointestinal in origin.
  • Acute Conditions: Sudden onset pain suggests conditions like aortic dissection, pulmonary embolism, or pneumothorax.

Medical Background and Risk Factors: A comprehensive medical history is essential to assess the risk for specific conditions:

  • Risk Factors for Acute Coronary Syndrome (ACS):
    • Male sex
    • Age over 55 years
    • Family history of coronary artery disease
    • Diabetes mellitus
    • Hypercholesterolemia
    • Hypertension
    • Tobacco use
  • Risk Factors for Pulmonary Embolism: Patients are at an increased risk if they have:
    • Prolonged immobilization (e.g., long-distance travel)
    • Recent surgery, especially orthopedic procedures lasting over 30 minutes
    • Central venous catheterization
    • Trauma
    • Pregnancy
    • Cancer
    • Lung or chronic heart disease
    • A personal or family history of hypercoagulability
    • Use of hormonal contraceptives or chemotherapeutic agents that increase estrogen and progestin levels

This detailed and systematic approach to history-taking allows for accurate and timely diagnosis, ensuring that critical conditions are addressed without delay.

Physical Examination

After obtaining a detailed history, a focused physical examination is crucial to identify any signs that may guide the clinician toward an accurate diagnosis. This examination combines general and systemic assessments, prioritizing findings that can point to life-threatening conditions [5,6].

General Examination and Vital Signs:

The initial step involves assessing vital signs, which often provide significant diagnostic clues:

  • Hypotension may indicate conditions such as tension pneumothorax, pulmonary embolism (PE), or acute myocardial infarction (MI).
  • Tachycardia is a nonspecific finding but is frequently seen in acute MI, PE, aortic dissection, or tension pneumothorax.
  • Hypoxemia suggests pulmonary conditions such as PE, tension pneumothorax, or simple pneumothorax.
  • Fever can be indicative of inflammatory or infectious processes, including PE, pericarditis, myocarditis, or even extrapulmonary causes like cholecystitis.

Cardiovascular Examination:

A detailed cardiovascular assessment should focus on specific findings that may narrow the differential diagnosis:

  • Significant blood pressure differences between upper extremities are a hallmark of aortic dissection.
  • Pericardial rub is a characteristic sign of pericarditis.
  • Jugular venous distension (JVD) may indicate tension pneumothorax, PE, or pericarditis with effusion.
  • Narrow pulse pressure can be associated with pericarditis with effusion, reflecting compromised cardiac output.
  • Pulsus paradoxus, an exaggerated drop in systolic blood pressure during inspiration, is a critical finding in cardiac tamponade and constrictive pericarditis.

Pulmonary Examination:

The pulmonary evaluation should focus on auscultation and observation:

  • Unilateral diminished or absent breath sounds point to tension pneumothorax or simple pneumothorax.
  • Pleural rub, a coarse grating sound, may be heard in PE, indicating pleural irritation.
  • Basal crackles (rales), particularly when bilateral, are often associated with acute MI or pulmonary edema, reflecting fluid overload or cardiac dysfunction.

Integration of Findings:

These physical examination findings must be interpreted in the context of the patient’s history and associated risk factors. For example:

  • A patient presenting with hypoxemia, tachycardia, and JVD warrants an immediate evaluation for PE.
  • Tension pneumothorax should be suspected in cases with hypotension, unilateral absent breath sounds, and JVD.
  • Signs of basal crackles and a pericardial rub may point to a combination of acute MI and pericarditis, necessitating rapid interventions.

By systematically combining history with these focused examination findings, clinicians can efficiently narrow their differential diagnosis and prioritize further investigations and treatments. This structured approach ensures that life-threatening conditions are promptly identified and managed.

When To Ask for Senior Help

Remember that senior residents and attendings supervise you when working in the emergency department. It is important to ask for their help when needed, especially when a patient with chest pain arrives [6]. The following are situations when you need to call for help immediately in a patient with chest pain:

  • Patients clenching their chest with ongoing chest pain and diaphoresis.
  • Chest pain with severe shortness of breath and evidence of pulmonary edema.
  • Chest pain with hypotension.
  • Chest pain with severe bradycardia or tachycardia.
  • Chest pain followed by unresponsiveness.

These examples exhibit life-threatening features of chest pain that can be lethal within minutes. You must call for help, and the team will be assembled to care for the patient and administer lifesaving interventions.

Alternative Diagnoses

Chest pain is a common presentation in the Emergency Department (ED) and requires a systematic and thorough approach to rule out life-threatening conditions. These diagnoses must be prioritized in the differential diagnosis as they carry significant morbidity and mortality if not identified and managed promptly [1,6].

Life-Threatening Diagnoses:

  1. Acute Coronary Syndrome (ACS): ACS encompasses conditions such as unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI). These result from ischemia due to decreased myocardial oxygen supply, often caused by atherosclerotic plaque rupture. Rapid identification through ECG and biomarkers is critical to initiate timely treatment.

  2. Acute Aortic Dissection: This condition arises when a tear in the intimal layer of the aorta allows blood to flow between the layers, creating a false lumen. Patients often present with severe, tearing chest or back pain and may have a significant difference in blood pressure between the upper extremities. Early diagnosis via imaging such as CT angiography is essential to prevent fatal rupture.

  3. Pulmonary Embolism (PE): PE results from the occlusion of pulmonary arteries by thromboemboli, often originating from deep vein thrombosis (DVT). Symptoms include sudden onset dyspnea, chest pain, and hypoxemia. Clinical suspicion should be high in patients with risk factors like prolonged immobilization, recent surgery, or hypercoagulable states.

  4. Tension Pneumothorax: This is a critical condition where air accumulates in the pleural space under pressure, compressing the lungs and mediastinum. Patients may present with hypotension, respiratory distress, and absent breath sounds on the affected side. Immediate needle decompression is lifesaving.

  5. Pericardial Tamponade: This occurs when fluid accumulates in the pericardial sac, impairing cardiac filling and output. Classic findings include hypotension, jugular venous distension, and muffled heart sounds (Beck’s triad). Pulsus paradoxus is another critical clue. Echocardiography confirms the diagnosis, and pericardiocentesis is the treatment.

  6. Esophageal Rupture with Mediastinitis: Esophageal rupture, also known as Boerhaave syndrome, can lead to mediastinitis due to leakage of gastric contents into the mediastinum. Patients typically present with severe chest pain following vomiting, subcutaneous emphysema, and signs of sepsis. Prompt surgical intervention is required.

Other Diagnoses to Consider:

  1. Simple Pneumothorax: Unlike tension pneumothorax, simple pneumothorax lacks hemodynamic compromise but still requires prompt recognition. Patients may present with pleuritic chest pain and diminished breath sounds on the affected side. Treatment typically involves observation or chest tube placement, depending on severity.

  2. Pericarditis: This inflammatory condition of the pericardium often presents with sharp, pleuritic chest pain that is relieved by sitting up and leaning forward. A pericardial rub is the hallmark auscultatory finding. ECG changes, including diffuse ST elevation, aid in the diagnosis. Most cases are viral and self-limiting, though complications like effusion and tamponade must be monitored.

Acing Diagnostic Testing

To accurately diagnose the cause of chest pain, a combination of bedside tests and advanced investigations are essential. These tests provide critical information that can guide immediate management, particularly in identifying life-threatening conditions [1,2].

Bedside Tests

Electrocardiogram (ECG):

The 12-lead ECG is a cornerstone of chest pain evaluation and must be performed within 10 minutes of the patient’s presentation or EMS arrival. It aids in identifying acute coronary syndromes (ACS), including ST-elevation myocardial infarction (STEMI).

STEMI Criteria:
  • General Criteria: At least 1 mm of ST elevation in two contiguous leads, excluding V2 and V3.
  • Specific Criteria for V2 and V3 ST Elevation:
    • Women: ≥1.5 mm elevation.
    • Men <40 years: ≥2.5 mm elevation.
    • Men ≥40 years: ≥2 mm elevation.
Source: Hernandez JM, Glembocki MM, McCoy MA. Increasing Nursing Knowledge of ST-Elevated Myocardial Infarction Recognition on 12-Lead Electrocardiograms to Improve Patient Outcomes. The Journal of Continuing Education in Nursing. 2019;50(10):475-480. doi:10.3928/00220124-20190917-10
Inferior ST segment elevations with anterior and lateral reciprocal changes. Inferior MI, so the right side of the heart should be evaluated with right side chest leads. V2 ST depression is very prominent, therefore, posterior leads should be applied form V7 to V12 for the left side.
43 years-old patients with left sided chest pain. Courtesy of Khaled Alaboud Alkheder and Muneer Al Marzooqi
Clinical Interpretation of the ECG above:
  • For instance, an ECG from a 43-year-old male presenting with severe left-sided chest pain showed ST elevation in anteroseptal leads (V1-V4) with J point elevation >2 mm and reciprocal ST depression in inferior leads, indicative of an acute anterior STEMI. This finding underscores the importance of identifying patterns such as J point elevation, which marks the transition between the QRS complex and the ST segment.

ECG Limitations and Additional Considerations:

  • While some patients exhibit a classic STEMI pattern, many may present with a normal or non-diagnostic ECG. A normal ECG at admission cannot rule out ACS or other conditions, necessitating further testing if clinical suspicion remains high.
  • If the initial ECG is inconclusive, it should be repeated after a 10-minute interval, especially if chest pain recurs.
  • Additional leads should be utilized when clinical suspicion exists for specific myocardial infarctions:
    • Posterior leads (V7-V9): For suspected posterior MI.
    • Right-sided leads (V3R and V4R): For patients with acute inferior MI, to assess for right ventricular involvement.
  • In suspected pulmonary embolism (PE), the S1Q3T3 pattern (prominent S wave in lead I, Q wave in lead III, and inverted T wave in lead III) may suggest right heart strain, though it is neither sensitive nor specific for PE [5].
S1Q3T3 - Courtesy of Khaled Alaboud Alkheder and Muneer Al Marzooqi
ECG 54-yo male chest pain for the last 3 days. S1 Q3 T3, Tachycardia, minor ST depressions on lateral leads (V5-6)

The ECG is a highly valuable tool for ruling in STEMI or other acute conditions. However, its limitations in ruling out conditions underscore the necessity of adjunct investigations and clinical correlation. For example, repeated ECGs, additional lead placements, and further imaging or lab tests (such as cardiac biomarkers or D-dimer for PE suspicion) ensure comprehensive evaluation and timely intervention.

By systematically incorporating these investigative steps into the diagnostic process, clinicians can optimize patient outcomes and address the underlying etiology of chest pain effectively.

Laboratory Tests

In the assessment of patients presenting with chest pain, laboratory investigations play a crucial role in diagnosing life-threatening conditions such as acute myocardial infarction (AMI) and pulmonary embolism (PE). Among the most valuable tests are cardiac troponins and D-dimer levels, each serving distinct purposes based on clinical suspicion and patient presentation.

Cardiac Troponins:

  • Utility in AMI Diagnosis:
    Cardiac troponins, specifically high-sensitivity troponin I and T, are the preferred laboratory markers for diagnosing AMI. These biomarkers can reliably detect myocardial injury within 3 hours of symptom onset. Their high sensitivity and specificity make them the gold standard in confirming myocardial infarction (MI).

  • Role in Ruling Out MI:
    While cardiac troponins are essential for diagnosing AMI, a single set of negative cardiac enzyme results is insufficient to rule out MI, especially in early presentations. However, in patients presenting with chest pain lasting over 2 hours, a single undetectable troponin T level can help exclude MI in certain cases [1].

  • Detection of Unstable Angina:
    High-sensitivity troponin assays can also detect subtle elevations associated with unstable angina, aiding in the identification of patients at risk for adverse cardiac events. However, serial testing may be required to observe trends and confirm the diagnosis.

D-Dimer:

  • Screening for Pulmonary Embolism (PE):
    D-dimer testing is particularly valuable in patients with suspected PE. In low-risk patients, a negative D-dimer test effectively rules out PE, eliminating the need for further imaging.

  • High-Risk Patients:
    Patients identified as high-risk based on clinical assessment or pretest probability should proceed directly to diagnostic imaging, such as computed tomography pulmonary angiography (CTPA). Similarly, patients with an intermediate or high pretest probability should not rely solely on D-dimer results but instead undergo confirmatory imaging [5].

These laboratory investigations provide critical insights when integrated with clinical findings and other diagnostic tools. For example:

  • In patients presenting with prolonged chest pain and an elevated troponin level, AMI is highly likely, warranting immediate intervention.
  • Conversely, in patients with a low-risk Wells score for PE and a negative D-dimer, further imaging can be safely avoided, reducing unnecessary radiation exposure and costs.

Imaging

In the assessment of chest pain, imaging plays a pivotal role in identifying life-threatening conditions and narrowing the differential diagnosis. A combination of imaging techniques can provide vital insights into both cardiac and non-cardiac causes of chest pain.

Chest X-Ray
  • Role in Emergency Evaluations:
    Chest X-rays are widely used in emergency departments as an initial imaging modality. They are particularly useful for identifying acute and life-threatening conditions, including pericardial effusion, acute aortic dissection, pulmonary embolism (PE), pneumothorax, and pneumonia.

    • Timeliness: In cases of high clinical suspicion, a chest X-ray should be performed and interpreted within 30 minutes to avoid delays in diagnosis and treatment.

  • Limitations:
    While chest X-rays are a valuable starting point, their sensitivity and specificity may be limited for certain conditions, necessitating further imaging in many cases.

Significant dilation and tortuosity of the aortic arch and descending aorta, exerting a mass effect on the trachea, causing rightward displacement and mild narrowing. Despite the patient's rightward rotation, a degree of mediastinal shift toward the left is observed. There are increased interstitial markings throughout both lungs, along with left apical pleural capping. - Source: Hacking C Large thoracic aortic aneurysm. Case study, Radiopaedia.org (Accessed on 31 Dec 2024) https://doi.org/10.53347/rID-73356
Pneumothorax on the left side (courtesy of Mohd Mokhtar and Raja Ahmad)
Ultrasonography
  • Advantages of POCUS:
    Point-of-care ultrasound has become an indispensable tool in emergency settings due to its rapid and dynamic assessment capabilities. It can evaluate both cardiac and non-cardiac causes of chest pain with high accuracy.

  • Cardiac Applications:

    • Detection of pericardial effusion and cardiac tamponade is a primary use of POCUS.

    • Example: A significant pericardial effusion may appear as a fluid collection around the heart, as visualized in Figure 5.

  • Pulmonary Applications:

    • POCUS has a higher sensitivity and specificity than chest X-rays for detecting pleural effusion and pneumothorax.

    • Pneumothorax Findings: The absence of the seashore sign (lung sliding) and the presence of the barcode sign on M-mode ultrasound strongly suggest pneumothorax.

    • Acute Heart Failure Findings: In cases of acute ischemic chest pain, lung B-lines detected on ultrasound indicate pulmonary edema due to heart failure.

Subxiphoid 4 Chambers View. PE = Pericardial Effusion, RV = Right Ventricle, LV = Left Ventricle
CT Pulmonary Angiography (CTPA)
  • Gold Standard for PE Diagnosis:
    CT pulmonary angiography (CTPA) is the imaging modality of choice for diagnosing acute pulmonary embolism (PE). Its high sensitivity and specificity make it invaluable for confirming or excluding PE in patients with high clinical suspicion.

  • Additional Findings:
    Beyond diagnosing PE, CTPA can reveal other significant pathologies, including [3,5]:

    • Pneumonia
    • Pericardial abnormalities
    • Musculoskeletal injuries
Pulmonary Embolism - Bilateral thrombus in main pulmonary arteries

Management

Patients presenting with typical chest pain are at a high risk of having Acute Coronary Syndrome. Empiric and symptomatic treatment is paramount in the ED to help control the situation and alleviate the patient’s pain. A common mnemonic used is (MONA), where patients can be given Morphine, which is an opiate, to help relieve the pain. Oxygen supplementation is recommended, but studies have shown that hyperoxygenation and hyperoxia are harmful and can lead to oxygen radicals; therefore, patients are maintained with oxygen saturation between 94–96% [2,6].

As a sublingual administration, Nitroglycerin is used to overcome coronary vasospasm and helps with vasodilation of the coronary vessels to improve blood flow to the myocardium and relieve ischemic chest pain. Finally, Aspirin, as an antiplatelet agent, is used empirically to prevent further clot formation and is one of the mainstay treatments when Acute Coronary Syndrome is suspected.

Aspirin

Dose: 162 to 325 mg in cases of acute coronary syndrome (ACS).
Frequency: Single dose.
Maximum Dose: 4 grams in 24 hours.
Category in Pregnancy: Category C.
Cautions/Comments: Prior to administration, check for allergies, bleeding disorders, or a history of bleeding gastrointestinal (GI) ulcers, as these conditions contraindicate the use of aspirin.

Nitroglycerin (Sublingual or Puffs)

Dose: For sublingual tablets, 0.4 mg per dose. For metered spray, 400 mcg of nitroglycerin per puff.
Frequency: For sublingual administration, up to 3 doses; for puffs, administer every 5 minutes with no more than 3 sprays in a 15-minute period.
Maximum Dose: Up to 3 doses (sublingual) or sprays (puffs) within a 15-minute period.
Category in Pregnancy: Category C.
Cautions/Comments: Nitroglycerin may cause hypotension, particularly with an upright posture. It is contraindicated in patients using phosphodiesterase inhibitors (e.g., for erectile dysfunction).

Morphine

Dose: 4 to 10 mg.
Frequency: Administer 2.5 to 5 mg every 3-4 hours as needed (PRN) or infused over 4-5 minutes.
Maximum Dose: 0.1 to 0.2 mg/kg.
Category in Pregnancy: Classified as Category CFR (consult further resources for more information).
Cautions/Comments: Monitor patients for respiratory depression. Co-ingestion with alcohol increases the risk of a fatal overdose and should be avoided.

Special Patient Groups

Pediatrics

Chest pain in children presenting to the emergency department can be a challenging clinical scenario, as it often raises concerns about serious underlying conditions, including cardiac issues, although they are relatively rare in this population. The differential diagnosis for pediatric chest pain includes musculoskeletal pain, respiratory conditions, gastrointestinal issues, and, less commonly, cardiac abnormalities such as myocarditis or pericarditis [7]. A thorough history and physical examination are essential to differentiate between these causes, considering factors such as the nature of the pain, associated symptoms, and the child’s medical history [8]. While most cases of chest pain in children are benign, it is crucial for healthcare providers to maintain a high index of suspicion and to utilize appropriate diagnostic tools, such as electrocardiograms and imaging studies, when indicated [9].

Pregnant Patients

Aortic dissection in pregnant patients is a rare but critical condition that necessitates swift recognition and management in the emergency department. Pregnancy itself can act as an independent risk factor for aortic dissection, particularly in women with preexisting connective tissue disorders, Turner’s syndrome, or a bicuspid aortic valve [35]. The physiological changes during pregnancy, such as increased blood volume and hormonal influences, may exacerbate underlying vascular conditions, leading to dissection [36]. Upon diagnosis, immediate treatment is crucial; intravenous nitroprusside and a β-blocker should be initiated to control blood pressure and reduce shear stress on the aorta [37]. Surgical intervention is mandatory for type A dissections, which pose a higher risk of mortality [38]. Furthermore, obstetric management must be tailored to the patient’s condition, with specific recommendations for cesarean delivery and gestational age based on the size of the aortic root [39]. Close collaboration with an obstetrician/gynecologist is essential for ongoing care and monitoring throughout the pregnancy [40,41].

Geriatrics

Older adults often experience less classic symptoms of myocardial infarction, such as chest pressure or pain, and may instead report vague symptoms like fatigue, shortness of breath, or confusion, which can complicate diagnosis [14]. Additionally, the presence of multiple chronic conditions may lead to an increased risk of complications and poorer outcomes [15]. Timely and accurate assessment is critical, as delays in diagnosis can significantly impact morbidity and mortality rates in this population [16]. Therefore, a high index of suspicion and thorough evaluation, including appropriate imaging and laboratory tests, are essential in managing chest pain in geriatric patients effectively [17].

When To Admit This Patient

Disposition decisions for patients presenting with chest pain in the emergency department (ED) are critical for ensuring appropriate care and minimizing the risk of adverse cardiovascular events. According to guidelines established by the American College of Cardiology and the American Heart Association (ACC/AHA), patients exhibiting high-risk features, such as ST-segment elevation on an electrocardiogram (ECG), hemodynamic instability, or signs of heart failure, should generally be admitted to the hospital for further evaluation and management [18]. Additionally, those presenting with intermediate-risk features—such as abnormal ECG readings, elevated cardiac biomarkers like troponin, or a history of coronary artery disease—also warrant hospitalization [19]. Conversely, low-risk patients, characterized by a normal ECG and negative cardiac biomarkers, may be safely discharged based on clinical judgment and validated risk stratification tools [19]. Ultimately, the decision to admit a patient with chest pain hinges on a comprehensive assessment of their symptoms, medical history, and individual risk factors for serious cardiovascular events, ensuring that high-risk patients receive the necessary care while minimizing unnecessary hospitalizations for those at lower risk [20].

Risk Stratification

The HEART Score is a clinical tool used to evaluate the risk of major adverse cardiac events (MACE) in patients presenting with chest pain. It assesses five key components: history, ECG findings, age, risk factors, and troponin levels, with each category assigned a score ranging from 0 to 2 points. The total score determines the level of risk and guides subsequent management.

History is assessed based on clinical suspicion. A highly suspicious history earns 2 points, a moderately suspicious history scores 1 point, and a slightly or non-suspicious history scores 0 points. This subjective component emphasizes the importance of a thorough clinical evaluation.

ECG findings are evaluated next. Significant ST-depression earns 2 points, nonspecific repolarization changes score 1 point, and a normal ECG scores 0 points. This category highlights the significance of electrocardiographic abnormalities in cardiac risk stratification.

Age is another important factor. Patients aged 65 years or older receive 2 points, those aged between 45 and 65 years earn 1 point, and patients 45 years or younger score 0 points, reflecting the age-related risk of cardiac events.

Risk factors are categorized based on their number and severity. Patients with three or more risk factors or a history of coronary artery disease (CAD) receive 2 points. Those with one or two risk factors score 1 point, while individuals with no risk factors score 0 points. Risk factors include diabetes mellitus (DM), hypertension (HTN), hyperlipidemia (HLP), smoking (current or recent), obesity, and a family history of CAD.

Troponin levels are also considered. Levels three or more times the normal limit score 2 points, levels one to three times the normal limit earn 1 point, and normal troponin levels score 0 points. This biomarker is critical in identifying myocardial injury.

The total HEART Score helps categorize patients into low, moderate, or high risk for MACE over the next six weeks. A score of 0-3 corresponds to a 2.5% risk and suggests discharge home. A score of 4-6 indicates a 20.3% risk, warranting clinical observation. Scores of 7-10 reflect a 72.7% risk, prompting early invasive strategies. This systematic approach helps clinicians make evidence-based decisions for managing patients with chest pain.

Each variable is scored from 0 to 2, allowing for a comprehensive assessment of the patient’s risk profile. For instance, the patient’s history is examined for indicators of coronary artery disease (CAD), while the ECG is scrutinized for signs of ischemia, such as ST-segment depression [21]. Age is considered a significant risk factor, as older patients are at higher risk for CAD, and the presence of additional risk factors like hypertension, hyperlipidemia, smoking, and diabetes further elevates this risk [22]. Elevated troponin levels serve as a critical marker for myocardial ischemia or infarction. The total HEART score, ranging from 0 to 10, categorizes patients into different risk levels, guiding management decisions regarding further testing, hospitalization, or early discharge [23]. However, it is essential to use the HEART score in conjunction with clinical judgment, as it should not be the sole determinant in decision-making processes [24].

Revisiting Your Patient

The patient had presented with complaints of chest pain, shortness of breath, diaphoresis, and nausea, raising the suspicion of Acute Coronary Syndrome and possible Myocardial Infarction. This suspicion had been supported by her significant risk factors, which included insulin-dependent diabetes mellitus, hypertension, a 12-pack-year smoking history, and a history of ischemic heart disease.

Initial stabilization measures had been promptly undertaken. The patient had been placed in a monitored bed and connected to a cardiac monitor. The ABCDE approach had been followed, and it had been noted that she was vitally stable. A quick history had been obtained, which revealed a sudden onset of central chest pain, described as sharp and stabbing, accompanied by diaphoresis and nausea. On physical examination, equal air entry had been observed with no wheeze or crackles on chest auscultation. A cardiovascular examination had also been planned.

Based on the initial presentation and clinical findings, a cardiac workup had been deemed necessary. This included ordering Troponin T and I tests, performing a 12-lead ECG, and obtaining a portable chest X-ray to rule out potential complications such as congestive heart failure, pneumonia, or pneumothorax.

Therapeutic interventions had been initiated promptly. The patient had been started on supplemental oxygen via a nasal cannula or face mask. Analgesics had been administered while ensuring no contraindications or allergies were present. These included IV paracetamol, IV opioids such as morphine or fentanyl, and sublingual nitroglycerin, either as a puff or tablet. These measures had been aimed at relieving the patient’s symptoms and stabilizing her condition.

Authors

Picture of Khaled Alaboud Alkheder

Khaled Alaboud Alkheder

Tawam Hospital Emergency Medicine Residency Program, United Arab Emirates

Picture of Muneer Abdulla Al Marzooqi

Muneer Abdulla Al Marzooqi

Dr. Muneer is a Consultant Emergency Medicine Physician from the UAE. He completed his EM residency at Tawam Hospital in 2017 and has served as an attending physician and educator there since. He is the Program Director of the Emergency Medicine Residency Program at Tawam Hospital, focusing on medical education, peer development, EM Resuscitation, Simulation, and POCUS. Dr. Muneer has organized and lectured at various seminars and workshops in the MENA region for medical students, residents, and healthcare professionals, including Basic Ultrasound, POCUS, Airway, Suturing, ENT Emergencies Workshops, and the Chief Resident Leadership Program.

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References

  1. Stepinska J, Lettino M, Ahrens I, et al. Diagnosis and risk stratification of chest pain patients in the emergency department: focus on acute coronary syndromes. Eur Heart J Acute Cardiovasc Care. 2020;9(1):76-89. doi:10.1177/2048872619885346.
  2. Hollander JE, Chase M. Evaluation of the adult with chest pain in the emergency department. In: Post TW, ed. UpToDate. UpToDate; 2022. Accessed April 26, 2023. www.uptodate.com.
  3. Malik MB, Gopal S. Cardiac Exam. In: StatPearls. StatPearls Publishing; 2021. Accessed April 26, 2023. https://www.ncbi.nlm.nih.gov/books/NBK553078/
  4. Resuscitation Council UK. The ABCDE approach. Resuscitation Council UK. Published 2021. Accessed April 26, 2023. https://www.resus.org.uk/library/abcde-approach
  5. Thompson BT, Kabrhel C, Pena C. Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism. In: Post TW, ed. UpToDate. UpToDate; 2022. Accessed April 26, 2023. www.uptodate.com.
  6. Brown JE. Chest Pain. In: Walls R, Hockberger R, Gausche-Hill M, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 10th ed. Elsevier; 2022:202-210.
  7. Ravindranath S, et al. Chest Pain in Children: A Review. Pediatrics. 2017;140(3):e20173032.
  8. Baker R, et al. Pediatric Chest Pain: A Review of the Literature. J Emerg Med. 2020;58(5):738-746.
  9. Glickstein JS, et al. Evaluating Chest Pain in the Pediatric Emergency Department. Pediatr Emerg Care. 2019;35(4):233-238.
  10. Hoffman MK, et al. Chest Pain in Pregnancy: A Review. Am J Obstet Gynecol. 2020;222(5):453-460.
  11. Hernandez AF, et al. Acute Coronary Syndrome in Pregnancy: A Comprehensive Review. Circulation. 2021;143(6):545-558.
  12. Miller JM, et al. Noninvasive Cardiac Imaging in Pregnancy: Safety and Efficacy. J Am Coll Cardiol. 2019;73(2):234-243.
  13. Bennett KJ, et al. Collaborative Care Models in Managing Cardiovascular Disease in Pregnant Women. Obstet Gynecol. 2022;139(4):678-689.
  14. Hernandez AF, et al. Atypical Presentations of Myocardial Infarction in Older Adults. J Geriatr Cardiol. 2022.
  15. McCarthy MJ, et al. Comorbidities and Outcomes in Elderly Patients with Chest Pain. Emerg Med J. 2023.
  16. Huang WC, et al. Impact of Delayed Diagnosis on Outcomes of Chest Pain in Older Adults. Am J Emerg Med. 2021.
  17. Lee JH, et al. Evaluation and Management of Chest Pain in Geriatric Patients. Clin Geriatr. 2023.
  18. Amsterdam EA, et al. 2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes. Circulation. 2014;130(25):e344-e426.
  19. Morrow DA, et al. Acute Coronary Syndromes: A Review of Current Guidelines. J Am Coll Cardiol. 2013;62(12):1103-1110.
  20. Fihn SD, et al. 2014 ACC/AHA/ACP/PCNA/SCAI/STS Focused Update of the Guideline for the Management of Patients with Stable Ischemic Heart Disease. J Am Coll Cardiol. 2014;64(18):1929-1949.
  21. Backus BE, Six AJ, Kelder JC, et al. A prospective validation of the HEART score for chest pain patients at the emergency department. Int J Cardiol. 2013;168(3):2153-2158.
  22. Kahwati LC, Weber RP, Pan H, et al. Screening for Coronary Artery Disease: A Systematic Review for the U.S. Preventive Services Task Force. Ann Intern Med. 2016;165(7):485-495.
  23. Six AJ, Backus BE, Kelder JC. Chest pain in the emergency room: a multicenter validation of the HEART Score. Crit Pathw Cardiol. 2013;12(3):121-126.
  24. Böhm M, Reil JC, Tschöpe C. The HEART score: a new tool for risk stratification in acute chest pain. Clin Res Cardiol. 2018;107(9):746-754.

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.

Spontaneous Pneumothorax (2024)

by Mohd Fazrul Mokhtar & 
Raja Amir Fikri Raja Sulong Ahmad

You have a new patient!

A 24-year-old male with no significant medical history presents to the emergency department for shortness of breath for two days duration. The symptom is associated with left-sided pleuritic chest pain. He denies fever, cough, constitutional symptoms, or trauma. He is an active smoker.

a-photo-of-a-24-year-old-male (the image was produced by using ideogram 2.0)

On assessment, the patient was mildly tachypneic and well-perfused. Auscultation reveals reduced breath sounds over the left lung. There is hyperresonance on percussion over the left lung as well. There is no tracheal deviation. Vital signs are as follows:

Blood pressure – 108/75 mmHg
Pulse rate – 74/minute
Respiratory rate – 24/minute
Oxygen saturation – 98% under room air
Temperature – 36.8o Celcius
Pain score – 4/10

What do you need to know?

Importance

Pneumothorax is defined as the presence of air in the pleural space. Pneumothoraces can be further divided into primary spontaneous pneumothorax (PSP), which occurs in patients spontaneously without any apparent underlying pleural disease, or secondary pneumothorax in patients with underlying diseases such as tuberculosis and lung malignancy [1,2]. Iatrogenic pneumothorax can also occur due to procedures such as thoracocentesis and central venous line insertion [2].

Identifying a pneumothorax is important, as a delay in management can lead to hemodynamic instability. In unstable patients with respiratory and circulatory compromise, the differential diagnosis of tension pneumothorax must be excluded.

Epidemiology

The incidence of primary spontaneous pneumothorax varies significantly between genders. Among the male population, it is reported to occur at a rate of 7.4 to 18 cases per 100,000 individuals annually. In contrast, the incidence in the female population is comparatively lower, ranging from 1.2 to 6 cases per 100,000 individuals per year [1].

Pathophysiology

Under normal circumstances, the pressure in the pleural space is negative compared to atmospheric pressure. This negative pressure is generated due to the opposing forces between the lung’s tendency to collapse because of elastic recoil and the outward expansion of the chest wall [2]. When there is communication between the alveoli and pleural space, the introduction of air alters the gradient until pressure equilibrium is reached, resulting in partial or total lung collapse. Tension pneumothorax occurs when inhaled air accumulates in the pleural space but cannot exit due to a one-way valve mechanism [2].

This condition leads to the clinical presentation of dyspnoea and chest pain. In tension pneumothorax, the increased intrathoracic pressure can decrease venous return and restrict lung function, ultimately leading to shock and hypoxia [2].

Medical History

In patients with a primary spontaneous pneumothorax, mild symptoms may be reported as they often tolerate the consequences of a pneumothorax better compared to those with underlying respiratory problems. The most common symptoms are chest pain and shortness of breath [3].

When inquiring about pain, the SOCRATES mnemonic may be helpful:

  • Site: Pain on the affected side
  • Onset: Usually, sudden onset of pain
  • Character: Typically described as sharp
  • Radiation: Radiation to the ipsilateral shoulder
  • Associated symptoms: Breathlessness
  • Time: Although the onset of pain may be acute, patients may present late if they can tolerate symptoms
  • Exacerbating/relieving factors: Pleurisy (pain worsening on inspiration) is common
  • Severity: Quantify the pain score when possible

Asking about risk factors may also help in strengthening the diagnosis of pneumothorax, including cigarette smoking, male gender, mitral valve prolapse, Marfan’s syndrome, and changes in ambient pressure. It is also important to ask about the history of trauma and recent medical procedures. Family history may be relevant as there may be a genetic predisposition to the condition.

Finally, enquire about the presence of a chronic cough and constitutional symptoms such as weight loss, loss of appetite, and fatigue to help ascertain whether the pneumothorax may be due to an underlying pleural disease.

Physical Examination

When assessing a patient with a potential pneumothorax, examine systematically using the ABC approach to avoid missing potential signs, especially those of a tension pneumothorax, as this condition requires immediate intervention [4].

  • Airway: Tracheal deviation is a late sign of tension pneumothorax, though it is not always indicative.
  • Breathing: Signs include tachypnoea, hypoxia, unequal chest rise, subcutaneous emphysema, hyperresonance, and absent or reduced breath sounds.
  • Circulation: Hypotension (a key sign of tension pneumothorax), tachycardia, and cold peripheries may be present.

Differential Diagnoses

The patients present mostly with shortness of breath (SOB). Therefore, pulmonary, cardiac and other causes of SOB should be considered first.

  • Pulmonary
    • Airway obstruction
    • PE
    • Pulmonary edema
    • Anaphylaxis
    • Asthma
    • Cor pulmonale
    • Aspiration
  • Cardiac
    • MI
    • Tamponade
    • Pericarditis
  • Others
    • Esophageal rupture
    • Toxin ingestion
    • Epiglottitis
    • Anemia

Acing Diagnostic Testing

The diagnosis of spontaneous pneumothorax is confirmed by imaging. After the diagnosis is confirmed, the clinical evaluation, including the history obtained and the patient’s clinical condition, should determine the management strategy.

Chest X-ray

The standard view is the erect PA chest x-ray. However, in a polytrauma patient, when the patient must be kept in the supine position, supine and lateral decubitus views can be performed.

Chest X-ray has been the mainstay diagnostic modality for pneumothorax. Typically, it demonstrates the visceral pleural edge, which appears as a thin, sharp white line. The peripheral space is more radiolucent compared to the adjacent lung (Image 1). A deep sulcus sign can be observed on a supine X-ray (Image 2).

More x-ray images can be found in iEM’s Flickr account – https://www.flickr.com/search/?user_id=158045134%40N08&view_all=1&text=pneumothorax

Image 1: Left pneumothorax. (Image courtesy of Ian Bickle, Radiopaedia.org, rID: 86926)
Image 2: Right pneumothorax with a deep sulcus sign. (Image courtesy of Mohammad Osama Hussein Yonso, Radiopaedia.org, rID: 18975)

A chest x-ray provides information about the size of the pneumothorax and assists in determining the next steps in management.

In a patient with suspected pneumothorax, a chest x-ray should be performed [5]. However, if clinical assessment suggests features of tension pneumothorax (e.g., hypotension, tracheal deviation, distended neck vein), a needle thoracocentesis must be performed first, as a chest x-ray may delay this life-saving intervention.

CT scan

The presence of bullous lung disease can lead to a misdiagnosis of pneumothorax on a chest x-ray. In patients with chronic lung disease who develop bullae, a chest x-ray may show features similar to pneumothorax. Therefore, if uncertainty exists, a CT scan of the thorax is strongly recommended.

More CT images can be found in iEM’s Flickr account – https://www.flickr.com/search/?user_id=158045134%40N08&view_all=1&text=pneumothorax

Image 3: CT scan showing right pneumothorax in a diseased lung. (Image courtesy of David Cuete, Radiopaedia.org, rID: 26570)

CT scan is considered the “gold standard” for detecting small pneumothoraces and is the most accurate method to determine the size of a pneumothorax [6]. However, practical drawbacks, such as limited availability, make it unsuitable as the first imaging modality for diagnosing pneumothorax.

Lung Ultrasound

In the emergency department, a lung ultrasound can be performed at the bedside immediately after a physical examination to evaluate undifferentiated respiratory failure. It is part of the point-of-care ultrasound protocol in emergency settings.

In a lung ultrasound, the normal lung interface with pleura shows lung sliding with Z-lines, which appear as vertical comet tails descending from the pleural surface. In pneumothorax, this sliding and the comet tail artifacts from the pleura are absent. Visualizing the intersection between the sliding lung sign and the absence of sliding is referred to as the lung point, which is nearly 100% specific for pneumothorax [7].

Additional ultrasound findings:

  • Absence of B-lines
  • Cessation of lung pulse (lung oscillation in tandem with cardiac contraction)

On M-mode, the following signs are observed:

  • Seashore sign: Indicates normal lung sliding.
  • Barcode/stratosphere sign: Indicates pneumothorax.

More US images can be found in iEM’s Flickr account – https://www.flickr.com/search/?user_id=158045134%40N08&view_all=1&text=pneumothorax

Image 4- Lung ultrasound showing the seashore sign. (Image courtesy of Srikar Adikhari et al. [2014], ResearchGate)
Image 5- Lung ultrasound showing the Barcode:stratosphere sign. (Image courtesy of Maulik S Patel, Radiopaedia.org, rID- 61141)

Laboratory Tests

ABG is indicated when oxygen saturation is below 90% on room air. It is performed to assess the patient’s oxygenation level, as some patients with pneumothorax may present with hypoxemia [8].

Risk Stratification

Pneumothorax is classified into primary spontaneous pneumothorax (PSP) and secondary pneumothorax (SSP). PSP occurs in healthy patients; hence, it is termed “spontaneous,” while SSP is associated with underlying lung diseases such as chronic obstructive pulmonary disease and pulmonary tuberculosis. PSP patients are typically taller than healthy controls [9-11]. Within the first four years, the risk of recurrence of PSP is as high as 54%, with isolated risk factors including smoking, height, and age above 60 years [10, 12,13]. Age, pulmonary fibrosis, and emphysema are risk factors for the recurrence of SSP [11,13].

Since patients with pre-existing lung diseases tolerate a pneumothorax less well, distinguishing between PSP and SSP at the time of diagnosis is critical for determining the next steps in care. Many patients, particularly those with PSP, do not seek medical attention until several days after their symptoms first appear. Meanwhile, the majority of patients with SSP present with more severe clinical symptoms.

Management

General Principle

Airway

The majority of patients with pneumothorax experience breathing issues rather than airway compromise. However, it is essential to assess the airway and breathing simultaneously.

Breathing

Provide supplemental oxygen with a high-flow mask. Oxygen treatment accelerates the resolution of pneumothorax by lowering the partial pressure of nitrogen in the alveoli relative to the pleural cavity. This creates a diffusion gradient for nitrogen, which hastens recovery.

The diagram from the British Thoracic Society guideline summarizes the management of pneumothorax [14].

[8] MacDuff A, Arnold A, Harvey J Management of spontaneous pneumothorax: British Thoracic Society pleural disease guideline 2010 Thorax 2010;65:ii18-ii31.
Image 6: Measurement of the apex-to-cupola distance and interpleural distance. (Images courtesy of the British Thoracic Society)

When To Admit This Patient

Patients requiring chest tube thoracostomy insertion must be admitted for monitoring and removal prior to discharge home. Those utilizing a pigtail catheter experience fewer complications, shorter hospital stays, and faster time-to-device removal. While many patients will require hospitalization, some can be discharged after a period of observation, aspiration, or with a Heimlich valve in pigtail catheters [14,15].

Revisiting Your Patient

The patient presented to the Emergency Department in a stable condition, showing no signs of respiratory distress, and was initially seen in the non-critical zone. After a chest X-ray confirmed the diagnosis of pneumothorax, the patient was transferred to the resuscitation zone for management and close monitoring.

Image 7 - Left Pneumothorax (image courtesy of Mohd Mokhtar and Raja Ahmad

A systematic assessment and management plan for patients with pneumothorax should prioritize the identification and stabilization of hemodynamically unstable patients.

Airway
There was no airway compromise in this patient, so no intervention was needed. The examination also revealed no tracheal deviation, which decreases the suspicion of a tension pneumothorax.

Breathing
Although the patient did not appear to be in respiratory distress, high-flow oxygen was administered through a non-rebreather mask to expedite the resorption of the pneumothorax.

Circulation
The patient was not in a tension pneumothorax state, as he remained hemodynamically stable. Therefore, he did not require immediate needle decompression or chest drain insertion.

The next step was to decide on the treatment approach. Following the algorithm set out by the British Thoracic Society, needle aspiration is recommended for this patient with a spontaneous pneumothorax, especially since he was experiencing breathlessness.

Needle aspiration is preferred in cases of spontaneous primary pneumothorax, as it is associated with a higher rate of successful discharges and fewer complications. However, if needle aspiration fails, chest drain insertion and admission will be necessary. The failure rate of needle aspiration in cases of secondary pneumothorax is high, which is why chest drains are typically favored in those instances.

Authors

Picture of Mohd Fazrul Mokhtar

Mohd Fazrul Mokhtar

Dr Mohd Fazrul Mokhtar is a Consultant Emergency Physician at Faculty of Medicine Universiti Teknologi MARA, Malaysia. He obtained his postgraduate training in emergency medicine at Universiti Kebangsaan Malaysia. He has special interest in sepsis, medical simulation; and emergency critical care. He is currently the Coordinator of the Clinical Simulation Centre. His research niche includes CPR educational technologies, cardiac arrest and sepsis. He is the council member of Malaysian Sepsis Association and Malaysian Resuscitation Association.

Picture of Raja Amir Fikri Raja Sulong Ahmad

Raja Amir Fikri Raja Sulong Ahmad

I am currently a second year postgraduate trainee in Emergency Medicine in Malaysia. My interests are point of care ultrasound and critical care.

Listen to the chapter

References

  1. Noppen M. Spontaneous pneumothorax: epidemiology, pathophysiology, and cause. European Respiratory Review. 2010;19(117):217-219. doi:https://doi.org/10.1183/09059180.00005310
  2. McKnight CL, Burns B. Pneumothorax. Nih.gov. Published 2019. https://www.ncbi.nlm.nih.gov/books/NBK441885
  3. Aljehani YM, Almajid FM, Niaz RC, Elghoneimy YF. Management of Primary Spontaneous Pneumothorax: A Single-center Experience. Saudi J Med Med Sci. 2018 May-Aug;6(2):100-103. doi: 10.4103/sjmms.sjmms_163_16. Epub 2018 Apr 16. PMID: 30787829; PMCID: PMC6196700.
  4. Newman MJ. A mistaken case of tension pneumothorax. BMJ Case Rep. 2014 May 16;2014:bcr2013203435. doi: 10.1136/bcr-2013-203435. PMID: 24835806; PMCID: PMC4024963.
  5. Matsumoto, S., Kishikawa, M., Hayakawa, K., Narumi, A., Matsunami, K., & Kitano, M. (2011). A method to detect occult pneumothorax with chest radiography. Annals of emergency medicine57(4), 378–381. https://doi.org/10.1016/j.annemergmed.2010.08.012
  6. Do, S., Salvaggio, K., Gupta, S., Kalra, M., Ali, N. U., & Pien, H. (2012). Automated quantification of pneumothorax in CT. Computational and mathematical methods in medicine2012, 736320. https://doi.org/10.1155/2012/736320
  7. Volpicelli G. (2011). Sonographic diagnosis of pneumothorax. Intensive care medicine37(2), 224–232. https://doi.org/10.1007/s00134-010-2079-y
  8. Inoue S, Egi M, Kotani J, Morita K. Accuracy of blood-glucose measurements using glucose meters and arterial blood gas analyzers in critically ill adult patients: systematic review. Crit Care. 2013 Mar 18;17(2):R48. doi: 10.1186/cc12567. PMID: 23506841; PMCID: PMC3672636.
  9. Withers JN, Fishback ME, Kiehl PV, et al. Spontaneous pneumothorax. Am J Surg 1964;108:772–6.
  10. Sadikot RT, Greene T, Meadows K, et al. Recurrence of primary pneumothorax. Thorax 1997;52:805–9.
  11. Videm V, Pillgram-Larsen J, Ellingsen O, et al. Spontaneous pneumothorax in chronic obstructive pulmonary disease: complications, treatment and recurrences. Eur J Respir Dis 1987;71:365–71.
  12. West JB. Distribution of mechanical stress in the lung, a possible factor in the localisation of pulmonary disease. Lancet 1971;1:839–41.
  13. Lippert HL, Lund O, Blegrad S, et al. Independent risk factors for cumulative recurrence rate after first spontaneous pneumothorax. Eur Respir J 1991;4:324–31.
  14. MacDuff A, Arnold A, Harvey J; BTS Pleural Disease Guideline Group. Management of spontaneous pneumothorax: British Thoracic Society Pleural Disease Guideline 2010. Thorax. 2010 Aug;65 Suppl 2:ii18-31. doi: 10.1136/thx.2010.136986. PMID: 20696690.
  15. Thelle A, Gjerdevik M, SueChu M, Hagen OM, Bakke P. Randomised comparison of needle aspiration and chest tube drainage in spontaneous pneumothorax. European Respiratory Journal. 2017;49(4). doi:https://doi.org/10.1183/13993003.01296-2016

FOAm and Further Reading

  • CDEM curriculum – https://cdemcurriculum.com/pneumothorax/ – link
  • FLIPPED EM Classroom – https://flippedemclassroom.wordpress.com/2013/05/26/pneumothorax/ – link

Reviewed and Edited By

Picture of Erin Simon, DO

Erin Simon, DO

Dr. Erin L. Simon is a Professor of Emergency Medicine at Northeast Ohio Medical University. She is Vice Chair of Research for Cleveland Clinic Emergency Services and Medical Director for the Cleveland Clinic Bath emergency department. Dr. Simon serves as a reviewer for multiple academic emergency medicine journals.

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.

Question Of The Day #23

question of the day
qod23
3. PEA

Which of the following is the most appropriate next step in management for this patient’s condition?

This patient presented to the emergency department with acute pleuritic chest pain, dyspnea, and experienced a cardiac arrest prior to a detailed physical examination. The cardiac monitor shows a narrow complex sinus rhythm morphology. In the setting of a cardiac arrest and pulselessness, this cardiac rhythm is known as pulseless electric activity (PEA). PEA includes any cardiac rhythm that is not asystole, ventricular fibrillation, or pulseless ventricular tachycardia. The ACLS algorithm divides the management of patients with pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF) and patients with pulseless electric activity (PEA) or asystole. Assuming adequate staff and medical resources are present, patients with all of these rhythms receive high-quality CPR, IV epinephrine, and airway management. Patients with pVT or VF receive electrical cardioversion, while patients with PEA or asystole do not receive electrical cardioversion. Patients with PEA or asystole generally have a poorer prognosis than those with pVT or VF. Out of hospital cardiac arrests that present to the emergency department with PEA or asystole on initial rhythm have a survival rate of under 3%. The etiology of PEA in cardiac arrest includes a wide variety of causes. A traditional approach to remembering the reversible causes of PEA are the “Hs & Ts”. The list of the “Hs & Ts” along with their individual treatments are listed in the table below.

PEA treatments

Sodium bicarbonate (Choice A) would be the correct choice for a patient whose PEA arrest was caused by severe acidosis. This can occur in severe lactic acidosis (i.e. sepsis), diabetic ketoacidosis, certain toxic ingestions (i.e. iron, salicylates, tricyclic antidepressants), as well as other causes. Calcium gluconate (Choice B) would be the correct choice for a patient whose PEA arrest was caused by hyperkalemia. This can occur in renal failure, in the setting of certain medications, rhabdomyolysis (muscle tissue breakdown), and other causes. Blood products (Choice D) would be the correct choice for a patient whose PEA arrest was due to severe hemorrhage, such as gastrointestinal bleeding or in the setting of traumatic injuries. This patient has symptoms and risk factors for pulmonary embolism, including pleuritic chest pain, dyspnea, and a cancer history. These details make pulmonary embolism the most likely cause of PEA arrest in this scenario. The best treatment for this diagnosis would be thrombolysis (Choice C).

References

[cite]

Question Of The Day #22

question of the day
qod22
1. VFib

Which of the following is the most appropriate next step in management for this patient’s condition?

This patient presents to the Emergency Department after a cardiac arrest with an unknown medical history. Important components of Basic Life Support (BLS) include early initiation of high-quality CPR at a rate of 100-120 compressions/minute, compressing the chest to a depth of 5 cm (5 inches), providing 2 rescue breaths after every 30 compressions (30:2 ratio), avoiding interruptions to CPR, and allowing for adequate chest recoil after each compression. In the Advanced Cardiovascular Life Support (ACLS) algorithm, intravenous epinephrine is administered every 3-5 minutes and a “pulse check” is performed after every 2 minutes of CPR. The patient’s cardiac rhythm, along with the clinical history, helps decide if the patient should receive additional medications or receive unsynchronized cardioversion (defibrillation, or “electrical shock. The ACLS algorithm divides management in patients with pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF) and patients with pulseless electric activity (PEA) or asystole.

The cardiac rhythm seen during the pulse check for this patient is ventricular fibrillation. The ACLS algorithm advises unsynchronized cardioversion at 150-200 Joules for patients with pVT or VF. Continuing chest compressions (Choice A) with minimal interruptions is a crucial component of BLS, however, this patient’s cardiac rhythm is shockable. Defibrillation (Choice B) takes precedence over CPR in this scenario. Amiodarone (Choice C) is an antiarrhythmic agent that is recommended in patients with pVT, in addition to unsynchronized cardioversion. This patient has VF, not pVT. Sodium bicarbonate (Choice D) is an alkaline medication that is helpful in cardiac arrests caused by severe acidosis or certain toxins (i.e. salicylates or tricyclic antidepressants). The next best step in this patient scenario would be defibrillation for the patient’s VF (Choice B).

References

[cite]

Question Of The Day #21

question of the day
qod21

Which of the following is the most appropriate next step in management for this patient’s condition?

This patient experienced a witnessed cardiac arrest at home, after which pre-hospital providers initiated cardiopulmonary resuscitation (CPR, or “chest compressions”) and Advanced Cardiovascular Life Support (ACLS). ACLS includes the tenets of Basic Life Support (BLS), such as early initiation of high-quality CPR at a rate of 100-120 compressions/minute, compressing the chest to a depth of 5 cm (2 inches), providing 2 rescue breaths after every 30 compressions (30:2 ratio), avoiding interruptions to CPR, and allowing for adequate chest recoil after each compression. In the ACLS algorithm, intravenous epinephrine is administered every 3-5 minutes and a “pulse check” is performed after every 2 minutes of CPR. The patient’s cardiac rhythm, along with the clinical history, helps decide if the patient should receive defibrillation (“electrical shock”) or additional medications. The ACLS algorithm divides management into patients with pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF) and patients with pulseless electric activity (PEA) or asystole.

The cardiac rhythm seen during the pulse check for this patient is a wide complex tachycardia with a regular rhythm. In the setting of cardiac arrest, chest pain prior to collapse, and a history of acute coronary syndrome, ventricular tachycardia is the most likely cause. The ACLS algorithm advises unsynchronized cardioversion at 150-200 Joules for patients with pVT or VF. Watching the cardiac monitor for a rhythm change (Choice A) or checking for a pulse (Choice D) are not recommended after defibrillation. A major priority of both BLS and ACLS is to avoid interruptions to CPR, so the best next step in management is to continue CPR (Choice B) after defibrillation. Administration of intravenous adrenaline (Choice C) is helpful for cardiac arrests to initiate shockable rhythm and should be repeated every 3-5 minute or every 2 cycle of CPR, particularly valuable in asystole patients. Calcium gluconate is another drug that can be used in patients with hyperkalemia and indicated in a patient with known kidney disease, missed hemodialysis sessions, or a history of usage of medications that can cause hyperkalemia. Magnesium can be used for patients who show polymorphic VT, particularly Torsades de Pointes. The next best step in this scenario is to continue CPR, regardless of the etiology of the cardiac arrest. Correct Answer: B.

References

[cite]

Question Of The Day #20

question of the day
cod20
608 - Figure3 - pericardial effusion - ECG

Which of the following is the most appropriate next investigation for this patient’s condition?

This patient’s EKG demonstrates alternating amplitudes of QRS complexes, a phenomenon known as electrical alternans. This is caused by the heart swinging back and forth within a large pericardial effusion. The patient is tachycardic and borderline hypotensive, which should raise concern over impending cardiac tamponade. The next best investigation to definitively diagnose a large pericardial effusion with possible tamponade would be a cardiac sonogram (Choice B). This investigation could also guide treatment with pericardiocentesis in the event of hemodynamic decompensation and the development of obstructive shock. Other EKG signs of a large pericardial effusion are diffusely low QRS voltages and sinus tachycardia. Chest radiography (Choice C) may show an enlarged cardiac silhouette in this case and evaluate for alternative diagnoses (i.e. pneumothorax, pleural effusions, pneumonia, atelectasis), however, cardiac echocardiography is the best next investigation. CT pulmonary angiography (Choice D) would demonstrate the presence of a pericardial effusion along with differences in cardiac chamber size indicative of tamponade. Still, bedside cardiac sonogram is a faster test that prevents a delay in diagnosis. Sending a potentially unstable patient for a CT scan may also be dangerous. Arterial blood gas testing (Choice A) has no role in diagnosing pericardial effusion or cardiac tamponade. Correct Answer: B

References

[cite]

Question Of The Day #19

question of the day
qod19
52 - Perforated Viscus

Which of the following is the most likely cause of the patient’s condition?

All patients who present to the emergency department with chest pain should be evaluated for the top life-threatening conditions causing chest pain. Some of these include myocardial infarction, pulmonary embolism, esophageal rupture, tension pneumothorax, cardiac tamponade, and aortic dissection. Many of these diagnoses can be ruled-out or deemed less likely with a detailed history, physical exam, EKG, and sometimes imaging and blood testing. This patient presents with vague, burning chest pain, nausea, and tachycardia on exam. Pulmonary embolism (Choice A) is hinted by the patient’s tachycardia, but the patient has no tachypnea or risk factors mentioned for PE. Additionally, the chest X-ray findings demonstrate an abnormality that can explain the patient’s symptoms. Pancreatitis (Choice B) and Gastroesophageal reflux disorder (Choice D) are also possible diagnoses, especially with the location and description of the patient’s pain. However, Chest X-ray imaging offers an explanation for the patient’s symptoms. The patient’s Chest X-ray demonstrates the presence of pneumoperitoneum. In the presence of NSAID use, this radiological finding raises concern over a perforated viscus from advanced peptic ulcer disease (Choice C). Peptic ulcer disease (PUD) is most commonly caused by Helicobacter pylori infection, but NSAIDs, iron supplements, alcohol, cocaine, corrosive substance ingestions, and local infections can cause PUD. PUD is a clinical diagnosis which can be confirmed visually via endoscopy. The treatment for PUD includes initiation of a proton pump inhibitor (H2-receptor blockers are 2nd line), avoiding the inciting agent, and H.pylori antibiotic regimens in confirmed H.pylori cases. The treatment for a perforated peptic ulcer with pneumoperitoneum is IV fluids, IV antibiotics, Nasogastric tube placement, and surgical consultation for repair.

References

[cite]

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Question Of The Day #18

question of the day
qod18
839 - diffuse ST elevation - pericarditis?

Which of the following is the most appropriate next step in management for the patient’s condition?

This patient presents to the emergency department with signs and symptoms consistent with acute pericarditis from a likely viral etiology. Common causes of acute pericarditis include idiopathic, infectious (viral, bacterial, or fungal), malignancy, drug-induced, rheumatic disease-associated (lupus, rheumatoid arthritis, etc.), radiation, post-MI (Dressler’s Syndrome), uremia, and severe hypothyroidism. The chest pain associated with this diagnosis is typically worse with supine positioning, improved with sitting forward, worse with inspiration, and may radiate to the back. A pericardial friction rub may be heard on auscultation of the chest, and there may be a low-grade fever on the exam. The hallmark EKG demonstrates diffuse ST-segment elevation with PR segment depression, although normal ST segments or T wave inversions can be seen on EKG later in the disease process. The treatment of acute pericarditis depends on the underlying cause of the disease. This patient has likely viral pericarditis with no clinical signs of myocarditis (i.e. fluid overload, cardiogenic shock, etc.) or cardiac tamponade (i.e. obstructive shock, distended neck veins, muffled heart sounds, low voltage QRS complexes or electrical alternans on EKG). A cardiac sonogram would be prudent to evaluate for a pericardial effusion. This patient’s disease course likely will resolve with NSAIDs in 1-2 weeks. Ibuprofen (Choice C) is the preferred treatment over aspirin (Choice A) or steroids (Choice B). Colchicine (Choice D) can be useful in recurrent episodes of pericarditis to reduce recurrence and in acute pericarditis not responding to NSAIDs. Correct Answer: C 

References

[cite]

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Troponin and nothing more

troponin and nothin more

It’s almost impossible to have an ER shift without encountering a chest pain patient!

The first thing that always comes to mind is to rule out STEMI; well, unless the patient is having chest pain, and you see a knife stabbed in his chest!

It’s a no brainer situation; investigations wise, you will start with an EKG, and a set of labs, including cardiac markers.

Acute coronary syndrome (ACS) with its subcategories, ST-elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina, is responsible for one third of total mortality in individuals more than 35 years of age.(1)

The role of cardiac markers in diagnosis and management of ACS and cardiovascular problems is vital. In the United States cardiac biomarkers testing occurs in nearly 30 million emergency department visits nationwide each year.(2)

What is a biomarker?

The National Institutes of Health defined a biomarker as “a characteristic that is objectively measured and evaluated as an indicator of normal biological processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention.” (3)

Biomarkers utilization in cardiovascular medicine is a wide domain; it’s used in screening, diagnosis, prognosis and monitoring. (4)

What’s available?

Numerous cardiac markers are available today and can be classified as:

  1. Biomarkers of myocardial injury, which is further divided into:
    1. Biomarkers of myocardial necrosis: CK-MB fraction, myoglobin, cardiac troponins
    2. Biomarkers of myocardial ischemia: Ischemia-modified albumin (IMA), heart-type fatty acid-binding protein (H-FABP)
  2. Biomarkers of hemodynamic stress: Natriuretic peptides (NPs): atrial natriuretic peptide (ANP), N-terminal proBNP (NT-proBNP), B-type natriuretic peptide (BNP)
  3. Inflammatory and prognostic markers: hs C-reactive protein (CRP), sCD40L, homocysteine. (4)

What’s best?

Cardiac Troponin and the B type cardiac natriuretic peptides are the two markers recommended by ACEP and AHA in diagnosis of ACS and heart failure respectively.(5)

The ACS biomarker of choice

ACS is subcategorized based on ECG and cardiac troponin. The fourth universal consensus definition of Myocardial Infarction (MI); by the European Society of Cardiology (ESC) and American College of Cardiology (ACC), takes Troponin as a detrimental parameter in case definition, because of its high sensitivity and specificity.(6)

ACEP and AHA guidelines recommend the use of Troponin as level A class 1 in diagnosis of ACS. (7) It was practiced before to consider multiple markers dealing with ACS, more precisely in NSTEMI ruling out recommendation. However, this practice is now outdated with the use of hs cT solely.(7-9)

What’s troponin and why do we like it?

It’s a protein that regulates the interaction between actin and myosin filaments, found in skeletal and cardiac myocytes. Cardiac troponin (cTn) has three subunits troponin T, troponin C and troponin I. Troponin T and I are highly specific and sensitive.(10) The half-life of troponin T and troponin I in the blood is about 2 hours and last in serum for 4 to 10 days10

For ACS, the sensitivity of troponin is about 95%, and the specificity is about 80%, higher than any other marker available.(12)

However, many causes can elevate serum troponin which includes pericarditis, myocarditis, heart failure and chest trauma; non-cardiac conditions are sepsis, renal disease, pulmonary embolism, COPD, strenuous exercise and hypertension.(14)

High-sensitivity cardiac troponin (hs-cTn T and I) can detect troponin at concentrations much lower than the old cTn tests, and has replaced it.7 For ACS, hs cT substituted and limited the roles of other markers; it’s proven to be safe, cost effective, and a valuable prognostic factor. (7-9, 14)

For all of the above and the heart score… In ACS, use Troponin and nothing more!

References and Further Reading

  1. Anumeha Singh; Abdulrahman S. Museedi; Shamai A. Grossman. Acute Coronary Syndrome. StatPearls[Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan.
  2. Alvin MD, Jaffe AS, Ziegelstein RC, Trost JC. Eliminating Creatine Kinase–Myocardial Band Testing in Suspected Acute Coronary Syndrome: A Value-Based Quality Improvement. JAMA Intern Med. 2017;177(10):1508-1512. doi:10.1001/jamainternmed.2017.3597.
  3. Biomarkers and surrogate endpoints: preferred definitions and conceptual framework. Biomarkers Definitions Working Group. Clin Pharmacol Ther. 2001 Mar; 69(3):89-95. doi.org/10.1067/mcp.2001.113989.
  4. Jacob R, Khan M. Cardiac Biomarkers: What Is and What Can Be. Indian J Cardiovasc Dis Women WINCARS. 2018 Dec; 3(4): 240–244. doi: 10.1055/s-0039-1679104.
  5. Richards AM. Future biomarkers in cardiology: My favourites. European Heart Journal Supplements, Volume 20, Issue suppl_ G, 1 August 2018, Pages G37-G44. doi.org/10.1093/eurheartj/suy023.
  6. Thygesen K, Alpert JS, Jaffe AS, et al., on behalf of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction. Fourth Universal Definition of Myocardial Infarction (2018). J Am Coll Cardiol. 2018. Volume 72 DOI: 10.1016/j.jacc.2018.08.1038. 
  7. Ezra A. Amsterdam, Nanette K Wenger, Ralph G. Brindis, Donald E. CaseyJr, Theodore G. Ganiats, David. HolmesJr, Allan S. Jaffe, Hani Jneid, Rosemary F. Kelly, Michael C. Kontos, Glenn N. Levine, Philip R. Liebson,Debabrata Mukherjee, Eric D. Peterson, Marc S. Sabatine, Richard W. Smalling, Susan J. Zieman. 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014; 130:e344–e426. 2014. doi.org/10.1161/CIR.0000000000000134.
  8. Edward W Carlton, Louise Cullen, Martin Than, James Gamble, Ahmed Khattab, Kim Greaves. A novel diagnostic protocol to identify patients suitable for discharge after a single high-sensitivity troponin. Heart. 2015 Jul 1; 101(13): 1041–1046. doi: 10.1136/heartjnl-2014-307288.
  9. Ron M. Walls, Robert S. Hockberger, Marianne Gausche-Hill, Katherine Bakes, Jill Marjorie Baren, Timothy B. Erickson, Andy S. Jagoda, Amy H. Kaji, Michael VanRooyen, Richard D. Zane. Rosen’s Emergency Medicine: Concepts and clinical practice. 9th edition. Elseivier; 2018.
  10. Ooi DS1, Isotalo PA, Veinot JP. Correlation of antemortem serum creatine kinase, creatine kinase-MB, troponin I, and troponin T with cardiac pathology. Clin Chem. 2000 Mar; 46(3):338-44.
  11. Harvey D. White, DSC. Pathobiology of Troponin Elevations: Do Elevations Occur With Myocardial Ischemia as Well as Necrosis?. Journal of the American College of Cardiology. Vol. 57, No. 24, ISSN 0735-1097/$36.00 Published by Elsevier Inc. doi:10.1016/j.jacc.2011.01.029.
  12. John E. Brush, Jr., Harlan M. Krumholz. A Brief Review of Troponin Testing for Clinicians. American College of Cardiology. 2017 Aug 7th. acc.org/latest-in-cardiology/articles/2017/08/07/07/46/a-brief-review-of-troponin-testing-for-clinicians.
  13. Asli Tanindi, Mustafa Cemri. Troponin elevation in conditions other than acute coronary syndromes. Vasc Health Risk Manag. 2011; 7: 597–603. PMID: 22102783. doi: 10.2147/VHRM.S24509.
  14. Donald Schreiber, Barry E Brenner. Cardiac Markers. emedicine.medscape.com/article/811905-overview [Accessed 2020 March 23rd].
[cite]

Question Of The Day #1

question of the day

Which of the following is the most appropriate next step in management for this patient‘s condition?

The patient in this scenario has an aortic dissection until proven otherwise. Administering anticoagulation (Choice A: Unfractionated Heparin Drip) would be the correct treatment for a pulmonary embolism. Although the patient has mild tachycardia and tachypnea on the exam, characteristics of the history and exam point closer to a diagnosis of aortic dissection. Features of the history that support a diagnosis of aortic dissection include pain described as “tearing”, “ripping”, or sharp pain radiating to the back. Other characteristics include unequal blood pressures in the extremities or neurological symptoms. Aortic dissections that migrate proximally may cause cardiac tamponade or a STEMI if they involve the coronary arteries. Choice C (Aspirin) would be the treatment for Acute Coronary Syndrome. Choice D (Call a Cardiology consultation) would not be appropriate for a patient with aortic dissection. A cardiothoracic surgical consultation would be appropriate in a patient with an aortic dissection involving the ascending aorta (Type A aortic dissection). Aortic dissections distal to the left subclavian artery that involve the descending aorta (Type B aortic dissection) are typically managed medically with blood pressure control. Choice B (IV Labetalol) is the correct answer as Aortic Dissections require aggressive blood pressure control with a goal of less than 120/80 mmHg. Beta-blockers, like Labetalol, are considered first-line therapy as they provide both alpha and beta-adrenergic receptor blockade. This allows the reduction of blood pressure without a reflex tachycardia response. Esmolol is an alternative therapy. Beta-blockers decrease vessel shearing forces that could worsen intimal vessel tearing. If beta-blockers alone cannot control blood pressure sufficiently, other medications can be included in the treatment regimen, like nicardipine, nitroglycerin, nitroprusside.

Reference

Johnson GA, Prince LA. “Chapter 59: Aortic Dissection and Related Aortic Syndromes”. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9th ed. McGraw-Hill.

[cite]

Triads in Medicine – Rapid Review for Medical Students

triads in medicine

One of the most convenient ways of learning and remembering the main components of disease and identifying a medical condition on an exam are Triads, and medical students/interns/residents swear by them.

Be it a question during rounds, a multiple-choice exam question to be solved, or even in medical practice, the famous triads help physicians recall important characteristics and clinical features of a disease or treatment in an instant.

Since exam season is here, this could serve as a rapid review to recall the most common medical conditions.

While there are a vast number of triads/pentads available online, I have listed the most important (high-yy) ones that every student would be asked about at least once in the duration of their course.

1) Lethal Triad also known as The Trauma Triad of Death
Hypothermia + Coagulopathy + Metabolic Acidosis

2) Beck’s Triad of Cardiac Tamponade
Muffled heart sounds + Distended neck veins + Hypotension

3) Virchow’s Triad – Venous Thrombosis
Hypercoagulability + stasis + endothelial damage

4) Charcot’s Triad – Ascending Cholangitis
Fever with rigors + Right upper quadrant pain + Jaundice

5) Cushing’s Triad – Raised Intracranial Pressure
Bradycardia + Irregular respiration + Hypertension

6) Triad of Ruptured Abdominal Aortic Aneurysm
Severe Abdominal/Back Pain + Hypotension + Pulsatile Abdominal mass

7) Reactive Arthritis
Can’t See (Conjunctivitis) + Can’t Pee (Urethritis) + Can’t Climb a Tree (Arthritis)

8) Triad of Opioid Overdose
Pinpoint pupils + Respiratory Depression + CNS Depression

9) Hakims Triad – Normal Pressure Hydrocephalus
Gait Disturbance + Dementia + Urinary Incontinence

10) Horner’s Syndrome Triad
Ptosis + Miosis + Anydrosis

11) Mackler’s Triad – Oesophageal Perforation (Boerhaave Syndrome)
Vomiting + Lower Thoracic Pain + Subcutaneous Emphysema

12) Pheochromocytoma
Palpitations + Headache + Perspiration (Diaphoresis)

13) Leriche Syndrome
Buttock claudication + Impotence + Symmetrical Atrophy of bilateral lower extremities

14) Rigler’s Triad – Gallstone ileus
Gallstones + Pneumobilia + Small bowel obstruction

15) Whipple’s Triad – Insulinoma
Hypoglycemic attack + Low glucose + Resolving of the attack on glucose administration

16) Meniere’s Disease
Tinnitus + Vertigo + Hearing loss

17) Wernicke’s Encephalopathy- Thiamine Deficiency
Confusion + Ophthalmoplegia + Ataxia

18) Unhappy Triad – Knee Injury
Injury to Anterior Cruciate Ligament + Medial collateral ligament + Medial or Lateral Meniscus

19) Henoch Schonlein Purpura
Purpura + Abdominal pain + Joint pain

20) Meigs Syndrome
Benign ovarian tumor + pleural effusion + ascites

21) Felty’s Syndrome
Rheumatoid Arthritis + Splenomegaly + Neutropenia

22) Cauda Equina Syndrome
Low back pain + Bowel/Bladder Dysfunction + Saddle Anesthesia

23) Meningitis
Fever + Headache + Neck Stiffness

24) Wolf Parkinson White Syndrome
Delta Waves + Short PR Interval + Wide QRS Complex

25) Neurogenic Shock
Bradycardia + Hypotension + Hypothermia

Further Reading

[cite]

A case of decreasing resistance in ER

a case decreasing resistance in er

I keep games on the 4th home screen of my cell phone. The third screen is blank. A minuscule of energy required to swipe my thumb has prevented me one too many times from mindlessly launching an RPG. Only to realize 2 hours later I had other plans for those 2 hours. An American comedian, the late Mitch Hedberg famously joked once,

Mitch Hedberg (1968-2005)
Mitch Hedberg (1968-2005)

I have always believed that the subtle truths kneaded so artfully in seemingly light, small-talk-worthy jokes are what makes a comedian a genius. How many times have you thought that you need to pick up that particular grocery or fill up that one conference form only to instead get consumed by what was easily available?

Our mind is built so that it follows the path of least resistance no matter how insignificant the resistance is. Although smudged all over the canvas of self-help, non-fiction genre, medicine somehow isn’t used frequently to exemplify the path of least resistance.

Today, I present to you a case that inspired us at Beltar, to remove one such small resistance from our workflow. The implications as you will see were no less than life-saving.

Rural Health System : Oversimplified

Before I present to you the case, a small preamble: Health care in rural Nepal is still run mostly by paramedics. No matter what spectrum you fall in terms of appreciating their work, the fact remains that they are the major workforce we have at the rural. It suffices to say that they are the portal of entry to the health system of our country for many. All emergency cases, once screened and declared complicated, the medical officer (usually a MBBS doctor) at the PHC sees the patient. Majority of cases are seen only by paramedics – considering 3 to 5 paramedics, usually and barely one medical officer in most PHCs.

A mobile game I wouldn't play

Now that the characters are in place, let’s dive right into the no less than a fairy tale land of the rural health system. Lamenting about the obvious lack of resources has been so old school that I don’t even make a typo while typing about it these days. We had one ECG machine at Beltar. The old ECG machine with its squeaky sound and myriad varieties of artifacts stood with all its mighty bulk inside a locked door of a room. The key protected from no one in particular by the office assistant who would open the door, drag the machine out, bring it to the bedside. The paramedic who decided to do the ECG would then untangle the wire glazed with what little of gel we had applied to the previous patient. He would then connect the limb leads and the pre-cordial leads with the trusty suction knobs which hopefully has some gel left from the previous use and then comes the biggest connection to be made: connecting the machine to the power grid. “Don’t you keep your machine charged!?”, you ask. We do. But the Li-ion battery probably has undergone autophagy, or whatever fancy name the process is given. That is a lot of steps and by extension, a lot of resistance. If this were a mobile game, I don’t think I would be addicted to it.

A Race Against Time

A patient with diabetes who had visited our ER a couple of times before was being monitored for chest pain at around 7 AM on a Saturday morning. I was washing my clothes on the first floor unaware that my Saturday is not going to be about laundry and daily chores. When I was called to check the patient, she was already deteriorating at a rate far greater than our PHC could ever catch up. We tried to borrow the speed of an ambulance and refer the patient to a higher center. An ST elevation in any two contiguous lead is an MI. Our paramedics knew that. To everybody’s surprise, ECG was not done! Given the fact that we did not have cardiac enzymes available at the PHC and Aspirin was all we could have prescribed before discharge anyway: we gave the patient 2 Aspirin tablets to chew and referred her as fast as we could. My paramedic colleagues have demonstrated utmost clinical competence and professionalism too many times to doubt any of that. The work environment was still error-prone and the circumstance demanded a change. Could we have changed the outcome given the same resources and clinical scenario? Maybe we need to decrease the resistance I thought. Changing how we store ECG (shown in the picture below), making it more accessible not only increased the frequency with which it was being used but also served as a reminder. A physical question hanging down the IV stand asking anyone who is attending a case, “Do you need to use me?”

ECG machine in plain sight with IV stand holding the limb and pre-cordial leads for accessibility

Workarounds: Because Solutions are Late to the Party.

If you have been following my writings, you’d have noticed this as another small tweak, a workaround, a nudge to the existing system so to speak that isn’t the substitute for the actual sustainable solution. Robust training that helps hard-working paramedics conceptualize and understand the protocols related to the use of basic yet life-saving diagnostics like ECG can be a start. We tried printing and pasting some protocols on the walls; another workaround we hope would help make patient care better until it actually sustainably improves. Another workaround that a friend suggested was: everyone who aches above the waist, gets an ECG. Such simplification works well to decrease the resistance in learning complex protocols. I am sure there are plenty of workarounds used worldwide, a necessity, after all, is the mother of invention. I leave you with a thought: What effect do you think will a systematic sharing of such workarounds among the rural healthcare workers will produce?

Guides to ECG electrode placement and protocols
[cite]

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