Back Pain (2024)

December 3, 2024December 3, 2024 ~ iEM Education Project Team ~ Leave a comment

by Paila Naveen & Manjith Reddy

You have new patients!

A 30-year-old male patient presents to the ED with an abnormal gait and no history of comorbidities. He complains of low back pain that started three days ago after performing a deadlift during a gym competition. The patient reports experiencing a snapping sensation during the lift, followed by a shooting pain radiating down the left leg, which subsided after a short time. However, the low back pain gradually worsened over the past three days and became unbearable upon arrival. He also reports weakness in the left foot since this morning, making it difficult for him to walk properly. This concern prompted him to seek medical attention in the ED.

What do you need to know?

Importance

Back pain is a term that, while commonly used, oversimplifies a condition affecting a much larger area of the body. It is often not taken seriously, possibly due to the time-consuming nature of evaluation, a lack of proper clinical skills, inadequate anatomical knowledge, or the pressures of a busy emergency department. This oversight can result in difficulty accurately identifying the cause of the pain, ultimately leading to increased morbidity and mortality.

This approach must change, as underestimating back pain can have fatal consequences. The condition encompasses a wide spectrum of causes, ranging from a minor muscle strain to severe conditions such as cauda equina syndrome, aortic dissection, or even worse.

Epidemiology

Up to 84% of adults experience low back pain at some point in their lives [1]. It is one of the top five most common complaints in emergency departments (ED) [2]. Low back pain accounts for 3.15% of all ED visits, with 65% of these cases resulting from injuries sustained at home [3]. Despite its prevalence, an estimated 85% of patients presenting with low back pain cannot be accurately diagnosed; however, nearly all of these patients recover within 4–6 weeks [4]. In contrast, 5–10% of patients with acute back pain suffer from more serious underlying conditions. While most visits for back pain are benign, they can be time-consuming and frustrating for both physicians and patients. Emergency physicians must remain vigilant in identifying and managing potentially dangerous conditions [5].

Pathophysiology

Acute back pain is a multifaceted condition characterized by various underlying mechanisms that contribute to its pathophysiology. It typically arises from damage to somatic structures, leading to nociceptive pain, which is transmitted through the peripheral and central nervous systems [6]. The pathophysiology of back pain involves multiple structures, including peripheral nerves, the central spinal cord, skeletal muscles, and blood vessels spread across the back. These structures can be affected by various underlying causes, broadly categorized as vascular, structural, referred pain, inflammation, infection, metabolic disorders, neoplasms, or trauma.

Acute back pain primarily involves nociceptive pathways, which transmit pain signals from damaged tissues such as the lumbar spine, ligaments, and muscles. In many acute cases, muscle spasms significantly contribute to pain; however, there is ongoing debate regarding whether these spasms are a primary cause or a secondary response to the injury. The progression from acute to chronic pain often involves central sensitization, a process where the nervous system becomes increasingly sensitive and responsive to pain stimuli [6].

When assessing a patient, it is crucial to first evaluate the nature of the pain. Determine whether the pain is localized, which may indicate an underlying fracture, or diffuse, as seen in conditions like an epidural abscess. Consider the possibility of referred pain originating from retroperitoneal structures. Additionally, assess for systemic symptoms or signs of inflammation, such as weight loss, which could point to a neoplasm or other serious pathology.

A thorough history-taking process is essential, including both positive and negative findings, to narrow down the differential diagnosis. Employ a structured approach to guide your assessment; once you refine the differential through history and clinical examination, investigations can confirm the diagnosis and facilitate effective management.

Initial Assessment and Stabilization

As emergency physicians, our approach to back pain differs from that of other specialties, as we must remain highly alert and responsive. While stable cases allow for a thorough history to be taken, unstable patients require a critical and focused approach to quickly identify the underlying cause. The following outlines this critical approach:

Airway/Breathing

When assessing a critical patient, prioritize airway and breathing management, and prepare for intubation. Key considerations include proper positioning, adequate suctioning, aspiration prevention, and effective visualization while securing the airway. Use videolaryngoscopy for improved visualization unless visualization is expected to be poor. To minimize aspiration risk, avoid over-ventilation and ensure the availability of two high-volume suction devices. Refrain from placing the patient in a supine or prone position to further reduce aspiration risk. Enhance first-pass success by using a bougie, and place a nasogastric tube once the airway has been secured.

Circulation

In patients with undifferentiated back pain presenting in shock, apply standard shock management measures. Begin with the insertion of two large-bore IVs to establish access for fluid and blood administration. If conditions such as abdominal aortic aneurysm (AAA), retroperitoneal hemorrhage, or ruptured ectopic pregnancy are suspected, cross-match for six units of blood. For suspected spinal epidural abscess, obtain blood cultures, administer appropriate antibiotics, and consider vasopressors if the patient remains unresponsive to a fluid bolus of 30 mL/kg. Use point-of-care ultrasound to assess the aorta for AAA and evaluate the bladder for urinary retention, particularly if cauda equina syndrome is a concern. Residual urine volumes greater than 100–150 mL are abnormal. Ultrasound is the preferred method for screening urinary retention due to its accuracy, non-invasiveness, and patient comfort, though a Foley catheter can also be used to measure residual urine volume [7].

The assessment of neurological status and additional exposure findings should be completed during the initial evaluation of the undifferentiated unstable back pain patient.

Medical History

A comprehensive history is essential when evaluating patients with back pain. The acronym SOCRATES provides a structured approach to effectively assess the nature of the pain:

SITE: Determine the exact location of the pain.
ONSET: Enquire about when and where the pain initially started.
CHARACTER: Ask about the quality of the pain, such as pricking, stabbing, burning, or squeezing. Pain at rest, accompanied by sweating or sleep disturbance, is often associated with conditions like rheumatoid arthritis, ankylosing spondylitis, or malignancies. Burning pain usually indicates neuropathy, while tearing pain may suggest aortic dissection. Sharp, shooting pain with localized tenderness may indicate spinal fractures, muscle spasms, or pulmonary embolism.
RADIATION: Explore whether the pain radiates to specific regions. For instance, cervico-genic headaches can radiate to the head, chest pain may suggest myocardial infarction or aortic dissection, and radiculopathy often involves the upper or lower limbs due to nerve root compression. Loin-to-groin radiation is characteristic of renal colic, while pain extending to the buttocks or legs may point to sciatic nerve compression. Abdominal radiation is commonly associated with constipation, mesenteric ischemia, or an abdominal aortic aneurysm (AAA).
ASSOCIATED SYMPTOMS: Enquire about symptoms accompanying back pain. Important symptoms to explore include sensory or motor deficits (indicating nerve root or spinal cord compression, such as in radiculopathy or cauda equina syndrome), urinary retention or incontinence (specific to cauda equina syndrome), hematuria (suggestive of kidney injury or malignancy), fever (associated with epidural or spinal abscesses), weight loss (indicative of malignancy), and morning stiffness (linked to rheumatoid arthritis or ankylosing spondylitis) [7].
TIME COURSE: Assess how the pain has evolved over time and use a pain severity scale (1–10) to gauge its intensity.
EXACERBATING OR RELIEVING FACTORS: Ask about factors that worsen or alleviate the pain, such as coughing, sneezing, walking, lying down, compression, medications, or physical support.
SEVERITY: Beyond numerical scales, explore how the pain impacts the patient’s daily activities and ability to perform routine tasks.

A thorough patient history should include surgical, family, medication, and social factors that may contribute to back pain.

Surgical history should document any previous back procedures, as they may influence the current presentation.

Family history is essential to identify any hereditary predisposition to vascular or inflammatory diseases.

Medication history should include the use of immunosuppressive therapies, anticoagulants, or glucocorticoids, as these can increase the risk of infections, bleeding, or osteoporosis-related complications.

Finally, social history should explore lifestyle factors such as intravenous drug use, alcohol consumption, smoking, and pregnancy status, all of which can significantly impact the diagnosis and management of back pain.

Special attention should be given to traditional “red flag” symptoms for back pain during the patient history, as these symptoms often warrant immediate imaging in the emergency department.

These red flags can be remembered using the mnemonic TUNA FISH [8]:

T for trauma,
U for unexplained weight loss,
N for neurological symptoms,
A for age over 50 years,
F for fever,
I for IV drug use or immunocompromised status,
S for steroid use or syncope, and
H for a history of cancer.

Physical Examination

A thorough physical examination is essential for patients presenting with undifferentiated back pain, especially when red flags are not evident in the history. It is critical to carefully evaluate for red flags during the examination and document all findings meticulously. The red flags on examination include abnormal vital signs (e.g., hypotension, fever, tachycardia, hypoxemia, or pulse deficits), motor weakness, saddle anesthesia, urinary retention, loss of rectal tone, abnormal reflexes (such as a positive Babinski sign), and pain on percussion of the spinous processes. In addition to identifying red flags, the physical examination should also cover other key areas to narrow the differential diagnosis.

Key Components of the Physical Examination:

Red Flags for Back Pain:

Abnormal vital signs: Hypotension, fever, tachycardia, hypoxemia, pulse deficits.
Motor weakness.
Saddle anesthesia.
Urinary retention.
Loss of rectal tone.
Abnormal reflexes: Positive Babinski sign.
Pain on percussion of spinous processes.

Other Important Aspects:

Inspection:
- Examine the back for signs of trauma, infection, asymmetry, scoliosis, kyphosis, or herpes zoster.
- Assess hip, pelvis, and spine anatomy and function.
Percussion/Palpation:
- Check for vertebral or soft tissue tenderness.
- Palpate for pulsatile abdominal masses.
Neurologic Examination:
- Assess reflexes (e.g., diminished or abnormal knee and plantar reflexes).
- Evaluate strength (weakness in the upper or lower extremities).
- Observe gait, ataxia, limp, or inability to ambulate.
- Check for signs of cauda equina syndrome, including loss of rectal tone or sensation.
Testing for Sciatic Nerve Root Irritation:
- Perform straight leg raising tests.
- Look for bilateral weakness, paresthesia, sensory level abnormalities, saddle anesthesia, muscle atrophy, and decreased rectal sphincter tone.
Vascular Assessment:
- Measure upper extremity blood pressures for discrepancies (e.g., aortic dissection).
- Listen for murmurs (aortic insufficiency) or signs of peripheral vascular disease [9].
Genitourinary Examination:
- Assess for urinary retention or incontinence.
- Measure post-void residual (abnormal if >100 mL).
- Perform a prostate exam if appropriate, considering prostatic hypertrophy as a possible cause of retention.
Rectal Examination:
- Conduct a rectal exam in all high-risk patients to assess for abnormalities in tone or sensation.

Additional Considerations:

Repeat the neurological exam throughout the encounter to detect any changes or progression in symptoms.
Remember that the spinal cord ends at L1; herniation above this level results in upper motor neuron findings (e.g., weakness, hyperreflexia, increased tone), while herniation below L1 leads to lower motor neuron findings (e.g., weakness, hyporeflexia, atrophy).
Consider the psychosocial context of lower back pain. Inconsistencies in physical findings due to patient distraction should not be dismissed as malingering. Instead, view these inconsistencies as the patient’s way of seeking help, just as with any other presentation.

Special examinations for back pain, often referred to as provocative tests, are used to assess specific conditions or structures causing discomfort. These include the Straight Leg Test, which evaluates nerve root irritation, commonly associated with lumbar disc herniation [10]. A variant of this test may be performed to refine diagnostic accuracy. The Tripod Sign Test assesses hamstring tightness and its relation to nerve irritation or musculoskeletal dysfunction [11]. Lastly, the Femoral Stretch Test is used to identify pathology in the femoral nerve or upper lumbar nerve roots [12]. Together, these tests provide targeted insights into the underlying causes of back pain.

Primary Goal

The primary goal when evaluating back pain is to rule out life-threatening, non-spinal causes. These include acute aortic aneurysm (AAA), thoracic aneurysm, aortic dissection, ectopic pregnancy, and epidural compression from abscess or hemorrhage. Once these critical conditions are excluded, attention should shift to nonspecific low back pain, which may originate from nerves, nerve roots, musculoskeletal structures, or even nonorganic causes. During the rapid physical examination, the presence of red flag signs should prompt immediate concern. These warning signs include abnormal vital signs, motor weakness, saddle anesthesia, urinary retention, loss of rectal tone, abnormal reflexes, and pain on percussion of the spinous processes.

Not-to-Miss Diagnoses and Red Flags

DIAGNOSIS	RED FLAG`S
Acute aortic pathology	Pain abdomen Blood in urine Pulse deficit in extremities Abdominal bruit/thrill Palpable abdominal mass
Infection (Spinal epidural abscess, Discitis, Osteomyelitis)	Fever Intra venous drug use Immunodeficiency/HIV Diabetes Steroid use
Fracture (Traumatic, Pathologic)	Recent fall/trauma, Age > 60yrs Previous traumatic fracture Spinal tenderness
Malignancy (Primary / metastasis)	Unusual Weight Loss Night sweats Fatigue Chronic pain H/O cancer Pain unresponsive to analgesia
Cauda Equina Syndrome/Disc Herniation	Weakness Loss of sensation Decreased reflexes Inability to walk Bowel & Bladder incontinence Bladder distension

Alternative / Differential Diagnoses

When evaluating patients with back pain, it is crucial to consider a broad differential diagnosis encompassing various systemic and localized causes. Back pain may arise from vascular, infectious, mechanical, immunologic, rheumatologic, inflammatory, non-organic, or pharmacologic origins. Each category includes potentially life-threatening and benign conditions that require careful assessment. By systematically approaching the possible causes, clinicians can better identify the underlying pathology and prioritize interventions based on the severity and acuity of the patient’s presentation. The following is a categorized list of potential diagnoses to guide clinical evaluation and management.

Vascular Causes

Abdominal aortic aneurysm
Acute coronary syndromes
Acute vaso-occlusive crisis
Cardiac tamponade
Severe aortic insufficiency/regurgitation
Thoracic aortic dissection
Pulmonary embolism
Renal artery dissection or thrombosis
Retroperitoneal hematoma
Spinal/epidural hematoma

Infectious Causes

Discitis
Epidural abscess
Meningitis
Osteomyelitis
Pelvic inflammatory disease
Pericarditis
Pneumonia
Prostatitis
Pyelonephritis
Tuberculosis (Pott’s disease)

Mechanical Causes

Cauda equina syndrome (from disc herniation or fracture)
Disc herniation
Ectopic pregnancy
Lumbar radiculopathy
Metastatic cancer
Pneumothorax
Pneumomediastinum
Scoliosis
Spinal stenosis
Syringomyelia
Traumatic or pathologic vertebral fracture
Ureteral calculus

Immunologic Causes

Transverse myelitis

Rheumatologic Causes

Gout and pseudo-gout
Osteoarthritis
Rheumatoid arthritis

Inflammatory Causes

Cholecystitis
Herpes zoster
Myocarditis/pericarditis
Musculoskeletal strain
Pancreatitis
Perforated viscus

Non-organic Causes

Factitious disorder
Depression

Pharmacologic Causes

Tolerance, dependence, addiction

Acing Diagnostic Testing

When life-threatening, non-spinal causes of low back pain have been ruled out through history and physical examination, laboratory tests are generally unnecessary for most patients. However, there are specific situations where laboratory investigations may provide valuable diagnostic insight [13,14]. These include cases where infection, malignancy, immune suppression, or other red flags are suspected. Below is a list of relevant laboratory tests and their clinical significance:

Laboratory Tests for Low Back Pain:

Complete Blood Count (CBC):

Helps identify infection, malignancy, or immune suppression.
Elevated white blood cell counts are present in only 66% of patients with spinal epidural abscesses [15].

C-Reactive Protein (CRP) and Erythrocyte Sedimentation Rate (ESR):

These markers may aid in diagnosing inflammatory or malignant conditions [16].
Elevated levels are associated with osteomyelitis and discitis [17].
Due to poor sensitivity, CRP and ESR are not recommended for patients without red flags and are not typically used when disc herniation or epidural hematoma is the primary diagnosis [18].

Pregnancy Testing:

Should be performed on all women of childbearing age to rule out pregnancy-related causes and guide management.

Radiographic Examination for Back Pain

Radiographic examination is crucial for evaluating, interpreting, and reviewing patients experiencing back pain due to spinal issues. This section discusses the use of various imaging modalities and diagnostic tools to assess potential life-threatening and spinal-related conditions.

Point-of-Care Ultrasound

Point-of-care ultrasound (POCUS) is a rapid bedside diagnostic tool that allows for quick and accurate detection of various emergency conditions. It aids in deciding whether further imaging is necessary.

Cardiac Ultrasound: Perform a cardiac ultrasound to detect ascending aortic dissection and pericardial effusion. Use the sub-xiphoid view and evaluate:
1. Pericardial effusion
2. Right atrial (RA) and diastolic right ventricular (RV) collapse
Additionally, the physical examination should include checking for pulsus paradoxus.
Parasternal – long axis view provide information about ascenting aorta and possible aortic dissection.
Abdominal Aortic Ultrasound: Perform this ultrasound to rule out abdominal aortic aneurysm (AAA).
Targeted Ultrasound for Trauma: Examine for free fluid in the pelvis and, if a ruptured ectopic pregnancy is suspected, include the uterus and adnexa in the evaluation.
Suspected Cauda Equina Syndrome: Conduct a residual urine test, as urinary retention (>100-150 mL) is abnormal. Ultrasonography of the bladder is preferred to calculate residual urine volume because it is accurate, noninvasive, and more comfortable for the patient. Alternatively, a Foley catheter can be used to measure residual urine after urination. [19]

Chest Radiograph

A chest radiograph is a valuable tool for identifying emergency causes of back pain, including:

Dilated mediastinum (indicative of thoracic aortic dissection)
Pneumothorax
Pneumomediastinum
Free air under the diaphragm (suggestive of a perforated viscus)

Once life-threatening non-spinal causes of back pain have been excluded, imaging can be ordered based on prominent symptoms and findings from the patient’s history and physical examination. The primary imaging modalities include plain radiographs, computed tomography (CT), and magnetic resonance imaging (MRI). [20]

Plain Radiographs

Plain radiographs have limited diagnostic utility but can be helpful in specific situations:

Fracture Detection: Anterior-posterior and lateral radiographs may identify vertebral fractures, although they are less sensitive than CT scans.
Infection or Malignancy: When combined with erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) tests, plain radiographs can reduce the likelihood of infection or malignancy.
Incidental Fractures: Plain radiographs may also reveal incidental fractures.

Computed Tomography (CT)

CT provides better resolution and higher sensitivity/specificity than plain radiographs. It is especially useful for suspected spinal fractures. However, CT has limitations:

It does not adequately image the spinal cord, making it less effective for diagnosing epidural abscesses and disc herniations.
Consider CT only when MRI is contraindicated. [21]

Magnetic Resonance Imaging (MRI)

MRI is the imaging modality of choice for urgent spinal conditions, including:

Spinal/epidural hematomas
Epidural abscesses
Cauda equina syndrome
Transverse myelitis
MRI Without Contrast: This provides detailed imaging of intervertebral discs, canal anatomy, nerves, ligaments, and epidural fat. Clinical guidelines recommend early MRI for uncomplicated occupational low back pain only if red flags are absent [21].
MRI With Gadolinium Contrast: Adding gadolinium improves diagnostic accuracy by differentiating surgical scarring from disc disease and evaluating vascular function in real-time.

Myelography

Myelography may be used in patients unable to undergo MRI. It evaluates the spinal cord, nerve roots, and meninges, offering a valuable alternative in specific cases.

Management

Approach To the Non-Critical Patient

Providing care to non-critical patients with back pain involves early pain management, targeted therapy, and continuous evaluation for red flags. This approach enhances patient satisfaction and ensures effective management.

Early Pain Management

Early analgesia is a critical aspect of care. Non-narcotic analgesics are preferred, combined with an empathic attitude from healthcare providers. These measures significantly improve patient comfort and satisfaction. [22]

Targeted Therapy

Treatment should be aimed at addressing the specific underlying cause of the back pain. Common conditions to consider include:

Lumbar Radiculopathy
Sciatica with Nerve Root Compression
Spinal Stenosis
Musculoskeletal Strain
Scoliosis

However, it is important to note that the majority of patients (approximately 85%) experience nonspecific back pain without a readily identifiable underlying condition. [23]

Reevaluation and Multidisciplinary Approach

Patients with persistent back pain should be reevaluated for red flags that may indicate serious underlying conditions. In the absence of red flags:

Initiate appropriate treatment tailored to the patient’s symptoms.
Consider referral to a physician for further evaluation and management as needed.
A multidisciplinary approach, involving physical therapy, pain management specialists, and other healthcare providers, may provide additional benefits for long-term management.

Non-Pharmacologic Management

Non-pharmacologic interventions play an essential role in managing back pain, particularly in acute, subacute, and chronic stages. These methods are effective, safe, and recommended by guidelines to complement or substitute pharmacologic treatment.

Heat Therapy

According to the 2017 American College of Physicians guidelines, superficial heat therapy is recommended as a form of nonpharmacologic analgesia for back pain. It provides relief by improving blood flow and relaxing muscles, making it an effective first-line treatment for many patients.

Activity Recommendations

Acute Phase: Patients should remain as active as possible. While engaging in structured exercise is not advised during the acute phase, maintaining light activity is beneficial. [24]
Bed Rest: Patients who remain on bed rest tend to recover more slowly and report more pain compared to those who stay ambulatory. Encouraging mobility helps expedite recovery. [25]

Exercise for Subacute and Chronic Pain

For patients with subacute or chronic low back pain, engaging in regular physical activity is crucial for long-term management. No specific type of exercise has proven superior; instead, various forms can be beneficial, including:

Aerobic exercise
Stretching
Pilates
Walking
Yoga
Tai Chi

The choice of activity should be tailored to the patient’s preferences and physical capacity to ensure adherence and maximize benefits. [26]

Trigger Point Injection Therapy

Trigger point injection therapy is a valuable but often underappreciated treatment for managing regional musculoskeletal pain. This therapy targets specific areas of muscle tightness, commonly associated with myofascial pain syndrome.

Characteristics of Trigger Points

A trigger point is a localized area of muscle pain that typically worsens with movement. These points are often identified during physical examination by the presence of a “twitch” response or the radiation of pain upon palpation. [27]

Pathogenesis of Trigger Points

The exact scientific mechanism behind the formation of trigger points remains unclear. However, many researchers suggest that acute trauma or repetitive microtrauma plays a significant role. Several contributing factors have been identified, including:

Suboptimal physical conditioning
Surgical scars
Insomnia
Joint dysfunction
Vitamin deficiencies
Poor posture [28]

Application of Trigger Point Injections

Although trigger point injections are not commonly utilized in emergency department (ED) settings, they represent a safe and effective alternative to narcotic pain management. By targeting the localized source of pain, this therapy can provide significant relief, especially in patients with myofascial pain syndrome. Increased awareness of this technique may help expand its use in broader clinical practice.

Some recommended anesthetic agents and their dosage are below;

Lidocaine 1%

Dosage: The recommended dosage of lidocaine 1% is 3 mg, with a maximum allowable dose of 5 mg.
Pregnancy Considerations: Lidocaine may induce premature labor; therefore, it is essential to seek expert advice before administering it to pregnant patients.
Precautions: Ensure accurate dosing to avoid complications. Monitor for signs of local anesthetic toxicity during and after administration.

Bupivacaine 0.25%

Dosage: The standard dosage for bupivacaine 0.25% is 0.75 mg, with a maximum limit of 1.25 mg.
Pregnancy Considerations: Like lidocaine, bupivacaine may also induce premature labor, necessitating expert consultation before use in pregnant patients.
Precautions: Accurate dosing is critical. Watch for potential symptoms of local anesthetic toxicity to ensure patient safety.

Injection Procedure

When administering injections, limit the procedure to a maximum of three sites while strictly adhering to sterile technique. Inject 0.3-0.5 mL into each site, carefully infiltrating the subcutaneous and muscle tissue. It is unnecessary to approach the spine or deeper muscle layers during this process. [29]

Use of Lidocaine 5% Topical Patches

Lidocaine 5% transdermal patches may also be utilized for pain management. Patients should be advised to remove the patch every 12 hours to prevent potential skin irritation. Proper application and timing are essential to maximize effectiveness while minimizing side effects.

Non-opioid analgesics (acetaminophen and non-steroidal anti-inflammatory drugs [NSAIDs], topical analgesics)

Non-opioid analgesics are considered the first-line treatment for pain management. Among these, non-steroidal anti-inflammatory drugs (NSAIDs) are widely used for their efficacy. However, their application must be tailored to individual patient needs and conditions.

Common NSAIDs and Their Guidelines

Ibuprofen:

- Dose: 400 mg, with a maximum of 800 mg
- Frequency: Every 6 hours
- Use in Pregnancy: Category C in the first and second trimesters
- Caution: Avoid in patients with acute kidney injury (AKI), congestive heart failure (CHF), or liver disease.

Naproxen:

Dose: 250 mg, with a maximum of 500 mg
Frequency: Every 12 hours
Use in Pregnancy: Not recommended
Caution: Use cautiously in patients with a history of stomach ulcers.

Diclofenac:

Dose: 50 mg, with a maximum of 75 mg
Frequency: Every 12 hours
Use in Pregnancy: Category C in the first and second trimesters
Caution: Avoid in patients with NSAID allergies.

Meloxicam:

Dose: 7.5 mg, with a maximum of 15 mg
Frequency: Once every 24 hours
Use in Pregnancy: Category C in the second and third trimesters
Caution: Contraindicated in patients with chronic kidney disease (CKD), chronic liver disease (CLD), or post-coronary artery bypass graft (CABG) surgery.

In clinical practice, the management of pain, particularly low back pain, often varies due to limited high-quality data. Low back pain remains one of the most common reasons patients are prescribed opioids, despite the availability of non-opioid alternatives [31,32].

Emerging data suggest that topical therapies can provide safe and effective treatment options for patients experiencing chronic, localized musculoskeletal and neuropathic pain. These therapies serve as an alternative for individuals who may not tolerate oral NSAIDs or opioids. [33]

Opioid Analgesics

Opioids are commonly used for pain relief in patients with low back pain, particularly in emergency department (ED) settings. However, their use should be carefully considered due to limited evidence of long-term benefits.

Prevalence of Opioid Use

A national study authored by Friedman revealed that opioids are administered to two out of three patients presenting to the ED with low back pain. This high prevalence highlights the reliance on opioids in acute care settings. [34]

Patient Population and Data Interpretation

Patients presenting to the ED often have more acute illnesses or severe pain compared to those seen in primary care settings. This distinction may skew the data and influence treatment patterns, as ED physicians are tasked with managing severe pain in a short timeframe.

Limitations of Opioid Therapy

Opioids provide temporary pain relief but lack evidence of improving functional outcomes or reducing long-term disability in patients with acute low back pain. For this reason, they are not recommended as first-line therapy for managing such conditions.

Appropriate Use of Opioids

Opioids should be reserved for specific scenarios:

When all other alternatives have been exhausted
When low-dose treatment can facilitate a return to mobility in the emergency setting

By reserving opioid use for carefully selected cases, clinicians can minimize the risk of dependency and prioritize treatments that improve long-term outcomes.

Muscle Relaxants

Muscle relaxants are often considered for managing muscle spasms and associated pain, but their effectiveness and appropriate use require careful evaluation.

Evidence suggests that muscle relaxants are not more effective than nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, or aspirin for managing pain. These alternatives are often preferred due to their similar efficacy and more favorable safety profiles. [35, 36]

A single dose of a benzodiazepine may be considered in the emergency department (ED) for acute muscle spasms. However, benzodiazepines are categorized as second-line agents for this purpose and are not recommended for routine prescription at discharge. Limiting their use helps reduce the risk of dependency and other potential side effects.

Steroids

The role of steroids in managing low back pain remains a topic of confusion and debate. While oral steroids can provide initial symptom relief, their long-term outcomes are less favorable. Studies have shown that patients who use oral steroids may experience complicated outcomes after one year, raising questions about their routine use in this context.

Surgery

Although it is not a primary focus of emergency medicine, providing appropriate recommendations for patients based on institutional resources regarding surgical options can be valuable for their management. For patients who do not respond to pharmacologic therapy, surgical interventions may be considered. These options are typically reserved for individuals with persistent symptoms or structural abnormalities requiring correction [37].

Special Patient Groups

Pediatrics

Unlike adults, children presenting with back pain are more likely to have an underlying serious medical condition. This is especially true for children aged four years or younger, or for any child whose back pain is accompanied by concerning symptoms.

Warning Signs Associated with Back Pain in Children

Parents and caregivers should be alert to the following red flags:

Fever or Weight Loss: These symptoms may indicate an infection or systemic illness.
Weakness or Numbness: Neurological deficits can suggest nerve involvement or spinal cord compression.
Difficulty Walking: Impaired mobility may point to musculoskeletal or neurological issues.
Radiating Pain: Pain that spreads to one or both legs could signal spinal conditions.
Bowel or Bladder Problems: Issues with bowel movements or urination may indicate spinal cord dysfunction.
Sleep Disruption: Pain severe enough to prevent the child from sleeping requires urgent evaluation.

Importance of Early Diagnosis and Treatment

Serious causes of back pain in children must be identified and addressed promptly. Delayed diagnosis and treatment can lead to worsening symptoms and potentially long-term complications. Careful clinical evaluation and appropriate imaging or laboratory tests are essential to rule out conditions such as infections, tumors, or structural abnormalities. Emergency physicians should always think about possibility of child abuse and traumatic injuries in this age group.

Geriatrics

In elderly individuals, back pain requires careful evaluation due to the increased risk of fractures and other serious conditions. Vertebral fractures can occur even with minimal force, making it critical to consider the possibility of compound vertebral fractures in older patients, even in the absence of trauma.

Life-Threatening Diagnoses to Rule Out

When evaluating back pain in elderly patients, it is important to rule out life-threatening conditions that are more common in this age group, including:

Aortic Dissection: A tear in the inner layer of the aorta that can cause severe back pain.
Abdominal Aortic Aneurysm: A potentially fatal condition involving the enlargement and potential rupture of the abdominal aorta.

Common Causes of Back Pain in the Elderly

In addition to ruling out life-threatening diagnoses, healthcare providers should consider the following common causes of back pain in older adults:

Osteoarthritis: A degenerative joint condition leading to stiffness and pain in the spine.
Degenerative Disc Disease: The wear-and-tear breakdown of intervertebral discs, which can result in chronic back pain.
Facet Joint Osteoarthritis: Degeneration of the small joints in the spine, contributing to localized pain and reduced mobility.

Pregnant Patients

Back pain is one of the most common issues experienced during pregnancy, particularly in the later months. While this discomfort often subsides after childbirth, many women continue to experience back pain for months postpartum.

Common Causes of Low Back Pain and Pelvic Girdle Pain in Pregnancy

Several factors contribute to low back pain and pelvic girdle pain during pregnancy, including:

Hormonal Changes: Hormonal fluctuations can loosen ligaments and joints, leading to instability and pain in the pelvic region.
Increased Weight: The growing weight of the baby places added stress on the lumbar vertebrae, causing discomfort and strain.
Compression of the Inferior Vena Cava (IVC): As the uterus enlarges, it may compress the IVC, leading to venous congestion and associated back pain.
Poor Nutrition: Inadequate nutrition during pregnancy can weaken muscles and bones, exacerbating pain.

Serious Causes Requiring Aggressive Management

In some cases, back pain during pregnancy may indicate more serious underlying conditions that require prompt attention and treatment. These include:

Lumbar Disc Herniation
Trauma
Infections
Masses

Identifying and addressing these causes is critical to ensuring the safety and well-being of both the mother and the baby.

IV Drug Users

Patients in this category may present with isolated back pain or more severe manifestations such as full-blown sepsis, meningitis, or septic shock. Prompt recognition and thorough examination of these patients are crucial. Immediate administration of antibiotics is essential to prevent further complications and reduce the risk of long-term morbidity. Timely intervention can significantly improve outcomes in these critical cases.

When To Admit This Patient

Patients presenting with back pain may be safely discharged if all the following criteria are met:

The patient has no neurological deficits or red flag findings on physical examination.
The patient is able to ambulate without difficulty.
Pain is under control, and no emergency cause has been identified.

For patients with uncontrolled pain or inability to care for themselves, an overnight stay in a hospital observation unit or nursing facility may be required for further management [38].

Admission is warranted in patients who exhibit significant abnormalities or require specialist intervention. The following scenarios outline the need for admission and further consultation:

Abnormal Physical Examination Findings:
- Patients with abnormal signs on physical examination should be referred for emergency consultation with the appropriate inpatient service.
Vascular and Mechanical Syndromes:
- Conditions such as abdominal aortic aneurysm (AAA), vascular spinal cord syndromes (e.g., spinal or epidural hematoma), and mechanical spinal cord syndromes (e.g., cauda equina syndrome or syringomyelia) necessitate immediate consultation with vascular or spine specialists for intervention and potential admission.
Spinal Fractures:
- Patients with spinal fractures require evaluation by an orthopedic surgeon and/or neurosurgeon. Admission is determined based on the fracture’s stability and the patient’s level of pain control.
Infectious Spinal Syndromes:
- Conditions such as epidural abscesses, osteomyelitis, or discitis require admission and consultation with specialists in Infectious Diseases and Spine.
Immunologic Spinal Cord Syndromes:
- Patients with conditions like transverse myelitis should be referred to neurology for consultation and further management.

Revisiting Your Patient

Firstly, as the patient is stable, which means A, B, and C are clear, the patient should be managed for pain (pain scale 8/10). On an emergent basis, Opioid was given for rapid relief. Further examination revealed the patient had foot drop, neurological deficits, motor weakness (S1 myotome), and a decrease in left foot reflexes causing him to have a high steppage gait on arrival to ED. At this juncture, it is clear the patient is having a nerve compression as there are focal neurological deficits. Here, you can call for senior help, as neurological deficits need to be reassessed for proper documentation. MRI of the whole spine showed prolapse of the L4/L5 intervertebral disc with compression on the thecal sac and bilateral neural foramina with osseous spinal canal stenosis at the L4 L5 vertebrae. The patient was admitted according to the admission criteria described earlier in the chapter, was made to wear a lumbar belt, and received epidural analgesia with corticosteroid injection. The patient was monitored for further neurological deterioration, which did not develop. Hence, he was discharged with supportive management, including physiotherapy and follow-up.

Authors

Paila Naveen

Dr. Paila Naveen, MBBS, CCT-EM, MRCEM, SEMI (Society of Emergency Medicine India) member, Consultant in Emergency Medicine, India, has fallen in love with this specialty, which he describes as his adrenaline pump for the rest of his medical service. He has a vision to spread the word about the importance of this specialty and the full potential of an emergency physician that can be achieved with the right skills and techniques in hand to save lives and bring smiles to the world. He is a strong supporter of FOAMed and runs a site exclusively for Emergency Medicine where he teaches, discovers new things, and tries to make a difference in every step he takes forward. He spreads awareness about this branch, as it is still in its infancy in India, through every possible medium where students and other doctors are connected in a collaborative way to further enhance the beauty of EMERGENCY MEDICINE.

Manjith Reddy

Dr. Manjith K S is an emergency physician with over 4 years of experience. He completed his medical school in 2012 and his residency in emergency medicine in 2019. Passionate about providing high-quality care, Dr. Manjith is dedicated to ensuring the best possible outcomes for his patients. He stays up-to-date with the latest medical research and practices and is a strong advocate for patient safety and quality improvement. Dr. Manjith is highly skilled in quickly assessing and diagnosing patients with a wide range of conditions and is an expert in the use of emergency medical equipment and procedures. His professional interests include trauma and cardiac emergencies. In addition to his clinical expertise, he serves as a mentor to junior physicians and residents, fostering the next generation of emergency medicine professionals. As a lifetime member of the Society of Emergency Medicine India (SEMI), Dr. Manjith is committed to advancing the field of emergency medicine. He currently works as a full-time consultant for a private healthcare organization. Proud to be part of the emergency medicine community, Dr. Manjith believes that emergency physicians are the frontline of healthcare.

Listen to the chapter

References

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Reviewed and Edited By

Jonathan Liow

Jonathan conducts healthcare research in the Emergency Department at Tan Tock Seng Hospital. A graduate of the University at Buffalo with a BA in Psychology and Communication, he initially worked on breast cancer research studies at GIS A*STAR. His research interests focus on integrating AI into healthcare and adopting a multifaceted approach to patient care. In his free time, Jonathan enjoys photography, astronomy, and exploring nature as he seeks to understand our place in the universe. He is also passionate about sports, particularly badminton and football.

James Kwan

James Kwan is the Vice Chair of the Finance Committee for IFEM and a Senior Consultant in the Department of Emergency Medicine at Tan Tock Seng Hospital in Singapore. He holds academic appointments at the Lee Kong Chian School of Medicine, Nanyang Technological University, and the Yong Loo Lin School of Medicine, National University of Singapore. Before relocating to Singapore in 2016, James served as the Academic Head of Emergency Medicine and Lead in Assessment at Western Sydney University's School of Medicine in Australia. Passionate about medical education, he has spearheaded curriculum development for undergraduate and postgraduate programs at both national and international levels. His educational interests focus on assessment and entrustable professional activities, while his clinical expertise includes disaster medicine and trauma management.

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.

Acute Ischemic Stroke (2024)

December 2, 2024December 3, 2024 ~ iEM Education Project Team ~ Leave a comment

by Hassan Khuram, Parker Maddox, & Scott Goldstein

You have a new patient!

Mrs. A, a 63-year-old female, was brought to the emergency department by her daughter after she noticed that her mother was unable to speak normally, and her face was droopy on the right side. Upon arrival, Mrs. A was lying on a stretcher in no acute distress. The daughter reported that her symptoms started suddenly about 30 minutes ago.

Vital signs showed a blood pressure of 170/90 mmHg, heart rate of 90 beats per minute, respiratory rate of 18 breaths per minute, Temperature is 36.6 C (98 F), and oxygen saturation of 98% on room air. The patient had a history of hypertension, hyperlipidemia, and type 2 diabetes mellitus. On neurological examination, Ms. A was found to have right-sided facial droop, right arm pronator drift, and slurred speech. The NIH Stroke Scale (NIHSS) score was 8.

What do you need to know?

Importance

Acute ischemic stroke (AIS) is a major public health concern that affects millions of people worldwide. Stroke, ischemic or hemorrhagic, is the third most common cause of disability and the second most common cause of death worldwide [1]. It is estimated that 12.2 million strokes occur around the world annually, with the vast majority being ischemic [1,2]. Early recognition and management of acute ischemic stroke are vital as outcomes are directly tied to the time between the onset of symptoms and initiation of treatment. For every hour treatment is delayed, the brain loses as many neurons as it does in approximately 3.6 years of normal aging, which has led to the adage “time is brain” [3]. Therefore, emergency department physicians must be well-versed in diagnosing and managing acute ischemic stroke to maximize patient outcomes. The main goals in the acute management of ischemic stroke are to minimize ischemic damage to the penumbra, treat any complications because of the infarction, and diagnose the etiology to prevent a recurrence. The primary objectives of this chapter are to present a thorough overview of the major ideas and practices involved in the early evaluation and treatment of acute ischemic stroke in the emergency room.

Epidemiology

Understanding epidemiology can help elucidate risk factors that can result in faster recognition of stroke and its acute management. The vast majority of strokes occur beyond the 5th decade, with the age of onset being lower in low to middle-income countries [4]. In an acute setting, it is critical to identify if a stroke is ischemic or hemorrhagic, as treatment varies significantly [4,11]. This risk increases significantly with age, along with other lifestyle factors. These factors are listed in the table below (with the highest risk factors listed in descending order.)

Table 1. Modifiable and Non-modifiable risk factors for stroke [1,4–6]

Modifiable Risk Factors	Non-Modifiable Risk factors
Hypertension	Prior history of stroke or TIA
Cigarette smoking	Age ≥ 65 years
Diabetes mellitus	Sex ♂ > ♀
Atrial Fibrillation	Family History
Carotid artery stenosis	Genetic disorders (e.g., sickle cell)
Dyslipidaemia	Migraine with aura
Obesity and Metabolic syndrome
Diet/Nutrition
Sedentary Behavior
Alcohol/Recreational drug use (e.g. cocaine)
Coagulopathy
Hormone Replacement Therapy/OCP

Pathophysiology

Acute ischemic strokes can occur due to thrombotic or embolic causes. One common link behind all the risk factors discussed above is that, in one form or another, they cause damage or dysfunction to blood vessels in the brain, reducing blood flow to the brain. Consequently, the parenchyma of the brain is unable to carry out its metabolic functions, which eventually leads to necrosis [7]. The exact mechanisms of how different risk factors contribute to stroke vary, but they ultimately all result in the damage of blood vessels in the brain. While there are many causes behind the damage of blood vessel walls, atherosclerosis and Virchow’s triad- blood stasis, endothelial injury, and hypercoagulability- remain the primary pathological process behind the vast majority of strokes [6,7]. For example, in Hypertension, the high pressures in the vessels cause shearing of the endothelial lining of blood vessel walls, which can result in rupture or thrombus formation. As the atherosclerotic plaques grow and become more advanced, they can lead to blood flow obstruction and turbulence, which can promote blood stasis. Blood stasis, in turn, can increase the risk of thrombosis within the affected blood vessel. The formation of a thrombus can obstruct blood flow to the brain and cause a stroke [7].

Similarly, smoking can cause inflammation and oxidative stress on blood vessels, causing an inflammatory response that ultimately results in the narrowing of the vessels and thrombus formation [8]. This framework also explains why older individuals are at higher risk since they have an increased prevalence of the modifiable risk factors listed in Table 1. [9]. Etiologies arising from circulatory system issues outside the brain require additional urgent management [5].

Medical History

A good history remains a key cornerstone in evaluating and managing stroke patients. Most typical presentations of strokes will be older adults presenting with acute onset focal neurological deficits. Patients might present with complaints of sudden onset speech difficulties, vision, sensation, strength, or coordination [10]. The acuity of neurologic dysfunction should clue physicians that stroke is an important differential. Another vital component when suspecting stroke is determining the time since the onset of symptoms. If this is unknown, then the last time the patient was seen well or at their neurological baseline can be used as a surrogate [11]. This step is critical as it helps determine whether the patient is within the window for reperfusion therapy and endovascular thrombectomy [5]. The 6S mnemonic list in Table 2. can be utilized to help clue clinicians that the patient might be having a stroke [12]:

Table 2. 6S mnemonic detailing core signs of stroke

S	Sudden onset
S	Slurred speech
S	Side weakness (unilateral deficits in face, arm, or leg)
S	Spinning (Vertigo)
S	Severe headache
S	Seconds (time since symptoms started)

The presence of this constellation should cue physicians to the immediate need for further evaluation of a serious process requiring labs and neuroimaging. The collection of symptoms can also give clues as to which vascular territory might be affected and can prompt the clinician to evaluate for further signs in that territory to help confirm the location. A general gestalt listed in Table 3. below can be used to help clinicians orient themselves as to which general vascular territory in the brain might be affected and what questions/exam findings to further probe for. The table is not exhaustive or mutually exclusive, and a more detailed discussion of the lesion site and associated neurologic findings is presented in the physical exam section.

Table 3. List of deficits and their associated territories [13]

Vascular territory	Associated deficits
Anterior Cerebral Artery (ACA)	Feet and legs
Middle Cerebral Artery (MCA)	Hands, Arms, Face, and Speech
Posterior Cerebral Artery (PCA)	Visual
Vertebrobasilar Artery (Brainstem)	Crossed signs (Contralateral hemiplegia & ipsilateral cranial nerve abnormalities)
Cerebellar Arteries	Coordination

The pace and course of symptoms can clue clinicians into the different subtypes of stroke that may be affecting the patient. Acute ischemic strokes due to embolic sources tend to occur suddenly, and the maximal deficit is perceived during this time. However, etiologies due to thrombosis tend to fluctuate and progress stepwise [14].

Other crucial components of medical history to assess are the risk factors mentioned in Table 1. They can help determine the precipitating factor for the stroke and can help guide management. For example, if the patient has a history of atrial fibrillation or carotid artery stenosis, then that could explain an embolic cause for the stroke and would require a more extensive workup along with additional management measures. Hypertension should also be sought out as it is the number one modifiable risk factor for stroke [2,6]. A review of current medications is also important because it can affect management. If a patient has been on anti-coagulation medications, then that is a strict contraindication for thrombolytics in stroke as it may lead to a hemorrhagic conversion [15]. In patients with acute ischemic stroke, a detailed medical history is crucial in directing the diagnostic and therapeutic decision-making process.

Physical Examination

Based on history, a focused physical and neurological exam can aid in localizing the lesion and provide clues as to the cause. Time is brain, and therefore, clinical suspicion of acute ischemic stroke should be rapidly confirmed with physical exam findings to minimize the time between the door to neuroimaging and recognize candidates for reperfusion therapy or endovascular thrombectomy [5,11,15]. As in all emergent cases, airway, breathing, circulation, disability, and exposure (ABCDE) should be prioritized in that order before attending to other steps in management. The physical exam should be tailored based on history to save time.

For example, if there is a history of atrial fibrillation, then a cardiac exam should be conducted to look for murmurs that might indicate an embolic cause. Patients with a history of atherosclerosis risk factors should also be examined for bruits in the neck that may reveal an embolic source. Papilledema on ocular exam may signify possible hemorrhagic stroke or cerebral edema as a complication of stroke that requires immediate intervention [16]. A neurologic exam is vital to confirm clinical suspicion of stroke and rule out other stroke mimics such as hypoglycemia or Bell’s palsy. Deficits on the exam can help point the clinician to the location of the lesion and the severity of the prognosis [13]. Table 4 below can be used to help localize the lesion based on clinical symptoms.

Table 4. A non-exhaustive list of common brain lesions and associated symptoms [13]

Vascular Territory	Common Neurologic Findings
Anterior Cerebral Artery (ACA)	Contralateral somatosensory & motor deficit mostly in lower extremity Abulia Urinary incontinence Emotional disturbance
Middle Cerebral Artery (MCA)	Aphasia (dominant hemisphere) Hemineglect (non-dominant hemisphere) Contralateral somatosensory & motor deficit mostly in upper limbs and lower half of face than lower limbs Conjugate eye deviation towards side of infract Contralateral homonymous hemianopia without macular sparing
Posterior Cerebral Artery (PCA)	Agnosia and alexia without agraphia (Dominant hemisphere) Prosopagnosia (Non-dominant hemisphere) Contralateral homonymous hemianopia with macular sparing
Anterior inferior cerebellar artery (AICA)	Ipsilateral deafness, facial motor/sensory loss, limb ataxia Decreased pain/temperature in contralateral body
Posterior inferior cerebellar artery (PICA)	Ipsilateral palatal weakness, limb ataxia Wallenberg syndrome Decreased pain/temperature in contralateral body
Vertebrobasilar system lesion (brainstem)	Contralateral hemiplegia & ipsilateral cranial nerve abnormalities (Crossed signs) Possible ataxia

The National Institutes of Health Stroke Scale (NIHSS) is one of the most studied and validated scales in clinical practice that should be used to provide a structured and quantifiable neurologic examination [5,11,12,16]. It includes 11 items (Table 5) and can be done in less than 10 minutes. The scale can quantify neurologic deficits and provide information about patient outcomes [17]. Facial paresis, arm weakness, and abnormal speech on the NIHSS are the most predictive findings for acute ischemic stroke [18].

Table 5. Snapshot of the National Institute of Health Stroke Scale (NIHSS) [5,19]

Instructions

Scale Definition

1a. Level of consciousness (LOC)

0 = Alert

1 = Drowsy- arousable by minor stimulation to obey, answer, or respond

2 = Obtunded; requires repeated stimulation to attend or is obtunded and requires strong or painful stimulation to make movements (not stereotyped).

3 = Unresponsive; Responds only with reflex motor or autonomic effects or unresponsive, flaccid, and areflexic.

1b. Orientation Questions (2)

0 = Answers both questions correctly.

1 = Answers one question correctly.

2 = Answers neither question correctly.

1c. Response to commands (2)

0 = Performs both tasks correctly

1 = Performs 1 task correctly

2 = Performs neither

2. Gaze

0 = Normal horizontal movements

1 = Partial gaze palsy

2 = Complete gaze palsy

3. Visual fields

0 = No visual field defect

1 = Partial hemianopia

2 = Complete hemianopia

3= Bilateral hemianopia

4. Facial movement

0 = Normal

1 = Minor facial weakness

2 = Partial facial weakness

3= Complete unilateral palsy

5. Motor function (Arm)

5a. Left arm

5b. Right arm

0 = No drift

1 = Drift before 10 s

2 = Falls before 10 s

3= No effort against gravity

4=No movement

6. Motor function (Leg)

6a. Left leg

6b. Right leg

0 = No drift

1 = Drift before 10 s

2 = Falls before 10 s

3= No effort against gravity

4=No movement

7. Limb ataxia

0 = No ataxia

1 = Ataxia in 1 limb

2 = Ataxia in 2 limbs

3= No effort against gravity

4=No movement

8. Sensory

0 = No sensory loss

1 = Mild sensory loss

2 = Severe sensory loss

9. Language

0 = Normal

1 = Mild aphasia

2 = Severe aphasia

3= Mute or global aphasia

10. Articulation

0 = Normal

1 = Mild dysarthria

2 = Severe dysarthria

11. Extinction or inattention

0 = Absent

1 = Mild loss (1 sensory modality lost)

2 = Severe loss (2 modalities lost)

Vital signs play a critical role in the evaluation and management of acute ischemic stroke and conditions that may mimic stroke. Temperature, in particular, is a key parameter, as abnormalities can influence neurological function and mimic or exacerbate stroke symptoms. Hyperthermia (elevated body temperature) is associated with worsened outcomes in stroke patients due to increased metabolic demand and potential exacerbation of ischemic injury. On the other hand, hypothermia (lowered body temperature) can also cause altered mental status, which may resemble stroke-like presentations. Monitoring and correcting these temperature abnormalities is essential to optimize neurological recovery and rule out underlying infections or systemic conditions. Additionally, blood pressure, heart rate, respiratory rate, and oxygen saturation must be carefully assessed, as significant deviations can indicate complications such as increased intracranial pressure, arrhythmias, or hypoxia, which can impact stroke presentation and management.

Alternative Diagnoses

The differential diagnosis for acute-onset focal neurologic deficits, such as those found in acute ischemic stroke, is broad, and it is important to have a framework to rule out other causes. The VIINDICATES mnemonic (Table 6) can be useful in grouping the most frequent and important causes of acute neurologic dysfunction [20].

Table 6. Non-exhaustive differential diagnosis of acute ischemic stroke [21]

Vascular	Hemorrhagic stroke, cerebral venous thrombosis, arteriovenous fistulas, aneurysms
Infectious	Meningitis, Encephalitis, Progressive multifocal leukoencephalopathy
Immune system dysfunction/autoimmune	Multiple Sclerosis, Bell palsy, Guillain-Barré syndrome, Anti-NMDA encephalitis
Neoplasm	Brain tumors, paraneoplastic syndromes, lung cancer
Drugs	Alcohol withdrawal, drug intoxication (opioids, barbiturates, etc.)
Cerebral/Neurologic	Transient ischemic attack (TIA), syncope, seizure, postictal paralysis, migraine aura
Trauma	Traumatic brain injury, Subdural hematoma, epidural hematoma, Brown-Séquard syndrome
Endocrine/Metabolic	Diabetic Ketoacidosis, hyponatremia, hypoglycemia
Social/Psychiatric	Conversion disorder, malingering

The clinician must pay close attention to the physical exam and medical history results that may favor one of these diagnoses over another to distinguish between them. Timing is critical and it is important to understand if the symptoms appeared suddenly or have been slowly brewing over time [12,16,21].

Acing Diagnostic Testing

When suspicion of acute ischemic stroke is high, time is of the essence due to the time limitations of thrombolytics or mechanical thrombectomy. Therefore, oxygen saturation, finger stick blood glucose, non-contrast head CT and angiography should be prioritized over all other tests as they are the only requirements before the administration of thrombolytics [5,11]. Oxygen saturation can help rule out hypoxia as a cause of neurological dysfunction [12,21]. Blood glucose is important as it can rule out hypoglycemia, DKA, or hyperosmolar hyperglycaemic state, which can all present like symptoms of stroke and can worsen outcomes with the administration of thrombolytics [22]. Neuroimaging is essential because it can help differentiate acute ischemic stroke from a hemorrhagic stroke, which has very different management. Neuroimaging can also rule out most other differential diagnoses discussed earlier when combined with physical history and exam. Loss of grey-white differentiation is an early CT finding in ischemic stroke, while increased density within the occluded vessel can represent a thrombus (Figure 1) [5,13,15,16,23].

Figure 1 - Non-contrast computed tomography (CT) with multiple planar reconstructions (MPR) revealed a hyperdense middle cerebral artery (MCA) sign in the left MCA (Picture A and B, arrow). Repeat CT after completion of the alteplase administration revealed resolution of the hyperdense MCA sign but the appearance of an M2 dot sign (Picture C and D, arrowhead). Angiography showed the occlusion of the left MCA M2 segment, corresponding to the M2 dot sign (Picture E, arrowhead) [23].jpg

Complete blood counts and coagulation studies should not delay the administration of thrombolytic therapy unless there is a high suspicion of coagulopathy or a history of the patient being on anticoagulating agents [5,12,16].

Electrocardiogram and cardiac markers such as troponin are also important to rule out cardiac causes. They may illuminate a source for emboli, such as atrial fibrillation, but this should not delay neuroimaging [5].

Other non-urgent lab tests that may be indicated depending on patient presentation include [5,10]:

Complete Metabolic Panel (CMP): Assesses electrolyte imbalances, renal function, and glucose levels, which are critical in stroke patients to rule out mimicking conditions (e.g., hypoglycemia) and to ensure safe administration of interventions like thrombolysis.

Blood Alcohol Level and Toxicology Screen: Helps identify substances that might contribute to altered mental status or stroke-like symptoms, such as intoxication or drug use, which can influence treatment decisions and prognosis.

Pregnancy Test in Women of Childbearing Age: Mandatory before imaging procedures involving radiation (e.g., CT) or medications (e.g., thrombolytics), as these might pose risks to a fetus.

Arterial Blood Gas (ABG): Assesses oxygenation, ventilation, and acid-base status. Useful in patients with suspected respiratory compromise or to evaluate hypoxia, which may exacerbate neurological deficits.

Chest Radiograph (CXR): Evaluates for underlying or concurrent conditions such as pneumonia, aspiration, or cardiac issues (e.g., heart failure) that could complicate stroke management.

Lumbar Puncture (LP): Performed if a hemorrhage is strongly suspected but not visible on a CT scan. Helps detect xanthochromia or elevated red blood cell count, which are indicative of subarachnoid hemorrhage.

Electroencephalogram (EEG): Recommended if seizures are suspected, as post-stroke seizures or seizure-like activity can mimic stroke symptoms or complicate recovery.

Urinalysis and Blood Cultures: Indicated in febrile patients to identify infections, such as urinary tract infections or sepsis, which might cause or exacerbate stroke-like presentations and impact recovery.

Blood Type and Cross-Match: Necessary if there is coagulopathy requiring reversal with fresh frozen plasma or if massive blood transfusion is anticipated in cases of hemorrhagic transformation.

MRI: Provides superior imaging of the brain compared to CT, identifying small or early infarcts and areas of ischemia. MRI is particularly valuable for stroke patients with ambiguous CT findings.

Risk Stratification

The presence of certain red flags, such as severe headache, papilledema, neck stiffness, loss of consciousness, or rapidly worsening neurological deficits, may indicate a worse outcome and the need for more aggressive management. These symptoms may indicate that the lesion has affected certain vital regions in the brain or there has been a conversion to hemorrhagic stroke [5,11]. Severe hypo/hyperglycemia (glucose < 50 mg/dL or > 400 mg/dL) or hypertension (> 185/110 mm Hg) also indicate a poor outcome as these need to be managed before reperfusion therapy can be utilized, which results in further neurologic insult [5]. The NIHSS score can be utilized to predict outcomes such as disability, recurrent stroke, or death. The higher the NIHSS score, the more severe the stroke and the worse the prognosis. In general, patients with an NIHSS score of 0-4 have a good prognosis, while those with a score of 20 or higher have a higher risk of death or severe disability [5,17,24].

Management

Stroke patients are treated as critically ill patients and require urgent management. This includes assessing and stabilizing the patient’s airway, breathing, and circulation (ABCs), conducting a thorough evaluation to determine whether thrombolytic therapy is appropriate, and addressing any underlying medical conditions, such as hypertension, that may complicate treatment [5,12,16].

Airway and breathing can be compromised due to damage to areas central to consciousness, breathing, or swallowing as listed in Table 7.

Table 7. Possible locations of lesions compromising the airway [25]

Levels of Consciousness	Breathing	Swallowing
Thalami	respiratory centers in the cortex, pons, and medulla	Medulla & brainstem connections
Limbic system	Pons
Reticular formation in the brainstem	Medulla

Damage to any of these areas requires securing the airway and maintaining breathing by positing the head of the bed to 30° to prevent aspiration. The specific approach will depend on the severity of the patient’s presentation [25]. Assessing the level of consciousness can provide valuable information to guide judgment. If a patient is awake, alert, and responsive, then they may be able to secure their airway and provide adequate ventilation on their own. Respiratory rate and effort should be assessed by looking for the rate of breathing, use of accessory muscles, or increased work of breathing. Airway patency can be determined by looking for signs of obstruction, such as snoring or stridor [16]. If oxygen saturation is below 94%, supplemental oxygen should be provided. Oxygen support is not beneficial if saturation is above 94% [5]. It is important to note that the neurologic exam can be severely limited if the patient requires intubation. Therefore, the clinician should pick up on subtle signs since the interaction with the patient began that can clue the physician on the baseline status, such as language function or any asymmetric motor activity, before the patient is pharmacologically paralyzed to be intubated [10].

Once breathing is secured, the next step is to ensure circulation is not compromised. Patients presenting with acute ischemic stroke frequently will be hypertensive as this is the body’s natural response to reperfuse the ischemic regions [16]. However, it is also not uncommon for patients to present with hypotension and hypovolemia. Due to the time-sensitive nature of acute ischemic stroke, correcting blood pressure takes priority [5]. When a patient with acute ischemic stroke has severe hypertension (systolic blood pressure >220 mmHg or diastolic blood pressure >120 mmHg), it may be necessary to lower their blood pressure to a safe level as administration of thrombolytics at this level can lead to hemorrhage [15]. Medications such as intravenous labetalol, nicardipine, or clevidipine can be used for cautious reduction (Table 8).

Table 8. Drug dosing for treatment of arterial hypertension in acute ischemic stroke [5]

Labetalol	10–20 mg IV over 1–2 min, may repeat 1 time
Nicardipine	5 mg/h IV, titrate up by 2.5 mg/h every 5–15 min, maximum 15 mg/h; when desired BP reached, adjust to maintain proper BP limits
Clevidipine	1–2 mg/h IV, titrate by doubling the dose every 2–5 min until desired BP reached; maximum 21 mg/h

In randomized controlled trials (RCTs) of intravenous (IV) thrombolytics, patients were required to have a systolic blood pressure <185 mm Hg and a diastolic blood pressure <110 mm Hg before treatment and <180/105 mm Hg for the first 24 hours after treatment [5]. Therefore, it is reasonable to aim for the blood pressure targets used in the RCTs of IV alteplase. In contrast, for patients with mild to moderate hypertension, it is generally advised to withhold blood pressure-lowering medications in the first few hours after the onset of stroke. This is because the rapid reduction in blood pressure can decrease cerebral perfusion and worsen ischemic injury [7].

Following stabilization, neuroimaging and lab tests discussed in the diagnostic test are prioritized to further aid in management. Figure 2 summarizes the steps discussed so far.

Once the diagnosis of acute ischemic stroke has been established, the next step is to figure out if the patient is eligible for thrombolysis (Table 9).

Table 9. Inclusion and exclusion criteria for rtTPA [5,15]

Inclusion Criteria	patients ≥ 18 years old symptom onset within 4.5 hours meets clinical criteria e.g. ischemic stroke
Strict Exclusion Criteria	History of ischemic stroke, severe head trauma, intracranial surgery, and intracanal hemorrhage within the last 3 months Blood pressure > 185/110 mm Hg Platelets <100,000/mm³ or glucose <50 mg/dL Anticoagulant use with INR > 1.7, PT >15 sec, or increase in active PTT Active intracranial bleeding Intracranial neoplasm

Intravenous recombinant tissue plasminogen activator (tPA) agents such as Alteplase or Tenecteplase should be used (Table 10) [5,15,26]. Mechanical thrombectomy may be indicated if a large artery occlusion (LVO) is causing a stroke, and it has been less than 24 hours since symptom onset. The eligibility for mechanical thrombectomy and thrombolysis in individuals with ischemic stroke is assessed separately. Patients may be qualified for one, both, or neither of these treatments depending on the timing of their appearance (4.5 hours for thrombolysis, 24 hours for mechanical thrombectomy) [5,27]. However, if the patient is not eligible for either chemical thrombolysis or mechanical thrombectomy, immediate dual antiplatelet therapy (DAPT) with agents such as aspirin and clopidogrel should begin [5,28]. In the acute management of ischemic stroke (even if caused by atrial fibrillation [AF]), parenteral anticoagulation (e.g., intravenous heparin) should not be used because it increases the chance of hemorrhagic conversion [5,11].

Table 10. Dosing for rtTPA in the management of acute ischemic stroke [5]

Alteplase	IV 0.9 mg/kg over 60 minutes (max. dose 90 mg), with an initial 10% of dose given as a bolus over 1 minute
Tenecteplase	IV 0.25 mg/kg as a bolus, max. dose 25 mg
Aspirin	160 to 325 mg loading dose, followed by 50 to 100 mg daily (for 21 days)
Clopidogrel	300 to 600 mg loading dose, followed by 75 mg daily (for 21 days)

Special Patient Groups

When a patient presents with symptoms of acute ischemic stroke, clinical considerations differ based on age and special patient groups. Pediatric patients may experience stroke due to congenital heart disease, sickle cell disease, or infections. Symptoms may be less obvious and include seizures, vomiting, and headaches [29]. Diagnosis of stroke in pregnant patients is challenging, and thrombolytic agents may increase the risk of hemorrhage in both the mother and fetus [30]. Special patient groups, including those with sickle cell anemia or undergoing surgery, may also be at increased risk of stroke and require careful management. Treatment options should be carefully considered in these patient groups with an understanding of the potential risks and benefits [31].

When To Admit This Patient

Patients with acute ischemic stroke are generally admitted to the hospital for further investigations and treatment [5]. Early discharge may be considered for patients with mild symptoms, no significant comorbidities, and a low risk of complications, provided they have a reliable caregiver and access to appropriate follow-up care. Severe or progressive symptoms, significant comorbidities, or high risk of complications require admission to a stroke unit or critical care unit [5,16]. Discharge decisions should be based on a careful assessment of clinical status, risk of complications, and social circumstances. Clear instructions on medication, follow-up care, and stroke prevention strategies should be provided, along with safety-netting arrangements for timely and appropriate care if complications or worsening symptoms occur after discharge [5,32].

Revisiting Your Patient

Based on the initial assessment, Mrs. A is presenting with symptoms that are consistent with a stroke. The patient’s daughter reported that the symptoms started suddenly, and upon examination, Mrs. A has right-sided facial droop, right arm drift, and slurred speech. Her past medical history is significant for hypertension, hyperlipidemia, and type 2 diabetes mellitus. The NIHSS score of 8 indicates a moderate to severe stroke. Immediate management includes stabilizing the patient’s vital signs and providing supportive care, including oxygen and intravenous access. Given the suspicion of a stroke, a non-contrast head CT scan should be obtained to rule out a hemorrhagic stroke. Mrs. A should be considered for thrombolytic therapy with alteplase as she is within the appropriate time window, and there are no contraindications.

Authors

Hassan KHURAM BS, MS

Hassan Khuram is a 4th year medical student at Drexel University College of Medicine, with a background in psychology, biotechnology, and business of healthcare. He graduated Magna Cum Laude with a Bachelor of Science in Psychology from Virginia Commonwealth University and a Master of Science in Biotechnology from Georgetown University. He is passionate about neurocritical care, medical education, and bioethics. He has an extensive background in research, having conducted studies on various subjects, including substance misuse, Parkinson's disease, mindfulness meditation and more. He has published articles on neurological emergencies and ethical issues in neurological care.

Parker MADDOX BA, MS

Parker Maddox is a fourth-year medical student at Sidney Kimmel Medical College at Thomas Jefferson University in Philadelphia. He graduated from the University of Virginia with a double major in Biology and Chemistry and went on to obtain a master’s degree in Biophysics and Physiology at Georgetown University. Since arriving to medical school, Parker has developed a passion for Emergency Medicine and has performed research on a wide range of topics including early sepsis recognition, pandemic viruses including Coronavirus 2019 and Monkeypox, ischemic stroke, Bell’s palsy, and international ECMO critical care protocol. This work has yielded multiple publications and a presentation at the Society for Academic Emergency Medicine (SAEM) 2022 Conference.

Scott GOLDSTEIN, DO, FACEP, FAEMS, FAAEM, EMT-PHP

Dr. Scott Goldstein started his medical career at New York College of Osteopathic Medicine in New York where he received his Doctorate of Osteopathy and continued his training at Einstein Healthcare Network in the field of Emergency Medicine, Philadelphia. Dr. Goldstein is dual-boarded through the American Board of Emergency Medicine in Emergency Medicine and Emergency Medicine Services (EMS). He currently works at a Level 1 academic trauma center, Temple University Hospital, in Philadelphia where he is the Chief of EMS and Disaster Medicine. He has continued to be an active member of the education community and EMS community where he holds the title of Fellow of American College of Emergency Medicine through ACEP, Fellow of the Academy of Emergency Medical Services through NAEMSP and Fellow of the American Academy of Emergency Medicine through AAEM. His current academic title is one of Clinical Associate Professor of Emergency Medicine at Lewis Katz School of Medicine at Temple University.

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References

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Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Epilepsy and Status Epilepticus (2024)

December 2, 2024December 9, 2024 ~ iEM Education Project Team ~ Leave a comment

by Rand Redwan Al Sari & Imad Khojah

You have a new patient!

A 22-year-old woman is brought to the ER because of violent, jerky movements of her limbs that started 30 minutes ago. Her husband reports that the patient has a history of epilepsy. She is unresponsive. Her examination reveals tonic-clonic episodes and blood in her mouth. How would you manage this case? What are the initial steps you would take? What actions are needed to stop the seizure?

What do you need to know?

Epidemiology and Importance

Epilepsy is one of the most common neurological diseases that can present to the emergency department [1]. It affects about 50 million people around the world, with an incidence of approximately 50.4 to 81.7 per 100,000 per year [1]. Epilepsy refers to having a lower seizure threshold than normal due to genetic, pathological, or unknown causes [2]. It is characterized by recurrent unprovoked seizures that present with motor, sensory, autonomic, or cognitive function alterations [2]. Previously diagnosed patients can present to the ED with breakthrough seizures due to factors like changes in the anti-seizure regimen or noncompliance with medication [2]. Other factors like sleep deprivation, stress, and flashing lights can also precipitate breakthrough seizures [2].

Prolonged or repetitive uncontrollable seizures are termed status epilepticus [2,3]. This emergency requires prompt treatment to prevent neuronal injury, severe disability, coma, or death [3]. The overall case fatality rates can reach up to 15% [2].

Pathophysiology

Neurons are normally stabilized by a balance between excitatory and inhibitory neurotransmitters [2]. A disruption of this balance leads to abnormal electrical discharge [2]. This discharge can propagate to nearby areas in the brain, which is evident clinically by the stepwise spread of the seizure (known as Jacksonian March) [2, 4]. Loss of consciousness in some cases is explained by the widespread involvement of large areas of the brain [2]. Many drugs used to restore this balance work by enhancing inhibitory activity through targeting GABAA subtype receptors [2]. Prolongation of the seizure leads to sequestration of GABAA receptors and upregulation of excitatory receptors; therefore, patients become unresponsive to medication [2, 5]. This explains the importance of timely treatment through early seizure control to prevent morbidity and mortality in patients with status epilepticus [2,3].

Medical History

A common scenario presenting to the ER is a patient complaining of a seizure-like episode with a sudden loss of consciousness and motor activity involvement [6]. However, various other presentations of seizures and other differential diagnoses with similar complaints should not be neglected. If the patient presents with status epilepticus, timely management, depending on the seizure type, is urgently needed (see management) [2].

Through history and examination, distinguishing a seizure from other acute medical conditions is important. An accurate diagnosis has crucial, direct consequences for activity restriction and therapy planning. Paying attention to features, especially at the onset, can help in identifying the seizure type for therapeutic implications and facilitate communication between physicians. Semiology at onset is important to classify seizures as focal, focal with impaired awareness (complex seizures), generalized, or unknown [7]. Further classification divides motor and non-motor seizures based on the descriptive assessment of the first symptom, which can vary widely according to the area of the brain affected [2].

The main aim of history-taking is to identify seizures from other similar conditions, classify them, identify triggers of new seizures, and detect a cause for a decreased seizure threshold in a patient previously diagnosed with epilepsy [8].

It is important for any patient with seizures to consider critical causes such as eclampsia, toxic ingestion, hypoglycemia, electrolyte imbalance, and increased intracranial pressure [9]. Emergent diagnoses, such as infection, acute brain injury, and serious mimics of seizure activity, must be identified and treated as soon as possible [2].

Initial history approach to a patient with suspected seizure [2] is a systematic evaluation, starting with the assessment of whether the event is likely to be a seizure, followed by differentiation of first-time versus recurrent seizures, and identifying factors that may trigger or reduce seizure thresholds [10].

Algorithmic Approach in Seizure History [2]

Determining Likelihood of a Seizure

The process begins by evaluating whether the event could be a seizure. Key indicators include:

Aura: A subjective sensation preceding the seizure.
Abrupt onset: Sudden occurrence of the event.
Non-suppressible limb shaking: Movements that are not voluntary or suppressible.
Postictal state: A transient neurological state after the event, characterized by confusion or fatigue.
History of epilepsy: Previous diagnosis or known history can strongly support the likelihood.

If these features are absent, the clinician is prompted to consider alternative diagnoses, such as:

Syncope (fainting),
Stroke,
Complex migraine, or
Non-epileptic spells, which may mimic seizures but lack neurological underpinnings.

Differentiating First-Time Seizures

If the event is determined to likely be a seizure, the next step is assessing whether it is the patient’s first seizure. For first-time events, the focus shifts to identifying potential triggers, including:

Medications: Use of or withdrawal from drugs that may lower the seizure threshold.
Exposures: Environmental or toxicological factors.
Immunosuppression: Conditions that may predispose to infections affecting the brain.
History of head trauma: A common precipitant for seizures.
Pregnancy: Associated risks like eclampsia.

Characterization of the Seizure

If it is not a first-time seizure, further characterization of the event is essential. Key aspects include:

Onset: Understanding preceding events to identify immediate triggers and auras.
Duration: Length of the seizure episode.
Awareness: Assessing the patient’s level of consciousness during the seizure.
Automatisms: Involuntary, purposeless movements that occur during the seizure and can be observed by others.
Postictal state: The presence of transient neurological deficits following the seizure (absent in some types, such as absence seizures).

The clinician also verifies whether the current event is consistent with the patient’s previous seizure patterns.

Exploring Factors Reducing the Seizure Threshold

For patients with recurrent seizures, it is crucial to evaluate factors that might decrease the seizure threshold, including:

Non-compliance or changes to anti-seizure drug (ASD) regimens.
Illness or trauma: Physical or psychological stressors.
Drug or alcohol use: Acute intoxication or withdrawal.
Catamenial exacerbations: Hormonal influences in menstruating individuals.
Pregnancy: Increased risk of seizures due to physiological changes or complications.
Sleep deprivation: A well-documented precipitant of seizures.

This step ensures that modifiable triggers or exacerbating factors are identified and addressed.

Physical Examination

Physical examination is crucial for identifying etiologies and directing the management plan. During an active seizure, pay close attention to posture, motor activity, eye deviation, and nystagmus, observing asymmetries and focal findings [11]. Check if the clonic activity is suppressible by applying gentle pressure. Unlike insuppressible seizures, suppression suggests a different diagnosis, such as nonepileptic spells or movement disorders. Check for mydriasis in the eyes, which is commonly found during seizures, but its persistence afterward can indicate toxic exposure [2].

Vital signs should be measured after seizure activity has ceased. They are of high importance and may direct the physician to possible causes (e.g., fever suggests meningoencephalitis, tachycardia and hypertension suggest toxic sympathomimetic exposure, while hypertension and bradycardia can indicate herniation syndromes) [2].

Moreover, a general examination should aim to search for both findings and sequelae of the seizures. Physical findings such as nuchal rigidity, stigmata of substance abuse, and lymphadenopathy may be present. Potential sequelae of seizures should also be assessed [12]. Evaluation of soft tissue and skeletal trauma is important, as injuries are common. Check for head trauma, tongue injury, shoulder dislocation, bone fractures, or aspiration [2].

Finally, a complete neurological examination should be performed. Immediately following the seizure, hyperreflexia, focal motor deficit (Todd’s paralysis), and extensor plantar response (positive Babinski) can occur and are expected to generally resolve within an hour [13]. If Todd’s paralysis does not resolve quickly, it raises the suspicion of a focal structural deficit that caused the seizure (e.g., stroke). The persistence of altered consciousness or signs of ongoing subtle seizures, such as automatisms, abnormal eye movements, and facial myoclonus, suggests the persistence of the seizure and must not be missed (nonconvulsive seizures and status epilepticus) [2].

Alternative Diagnoses

Although no single clinical finding or diagnostic modality is 100% confirmatory of the diagnosis of seizures [14, 15], understanding the circumstances of the event and the factors surrounding it can help rule out or confirm diagnoses with similar presentations [2].

Findings that make the diagnosis of seizures more probable include postictal disorientation and amnesia, cyanosis during the event, lateral tongue biting, non-suppressible limb shaking, and dystonic posturing [2, 15].

If the patient experienced diaphoresis, palpitations, nausea, and vomiting before the seizure, it may suggest transient cerebral ischemia due to arrhythmias [2].

The presence of motor activity, commonly including a tonic extension of the trunk or myoclonic jerks of the extremities associated with bradycardia, raises the suspicion of convulsive syncope [16]. Once cerebral perfusion is restored, convulsions stop without any postictal period [2].

The diagnosis of migraine can sometimes be misleading due to the presence of a preceding aura that might be confused with nonconvulsive seizures (e.g., the positive visual phenomenon in occipital seizures) [17]. Unlike occipital seizures, migraines have a peak preceded by gradual evolution and followed by gradual resolution. Moreover, patients typically have a positive history of migraines with a similar presentation [2].

Nonepileptic spells or psychogenic seizures mimic status epilepticus in their presentation [18]. Due to the prolonged duration of the spells (five minutes or more, and sometimes exceeding 20 minutes), patients commonly receive high doses of benzodiazepines and need to be monitored for any respiratory compromise. Findings consistent with this diagnosis include a stop-and-go pattern of the convulsions, horizontal head shaking, forward pelvic thrusting, asynchronous bilateral convulsions with eyes closed, a short postictal period despite the long duration of spells, avoidance of noxious stimuli, and preserved recollection of events. Furthermore, laboratory testing lacks reactive leukocytosis and lactic acidosis, which are present in nearly all cases of prolonged generalized convulsive seizures or status epilepticus [2, 19].

Acing Diagnostic Testing

Due to the challenges of diagnosing a seizure, seeking diagnostic testing is of high value. Laboratory studies, radiology, and other special procedures frequently provide important elements in patient assessment [20]. Although some cases require extensive metabolic testing, it is not indicated for cases with an unremarkable history and normal examination findings. Serum glucose levels should be measured in all cases, as hypoglycemia is a common cause of provoked seizures [21]. It is also important to note that hypoglycemia could result from prolonged seizures. If correcting the glucose level does not stop a seizure, an alternate diagnosis should be evaluated. Lactic acid and creatinine kinase should also be measured in cases of prolonged seizures to assess for acute metabolic acidosis and rhabdomyolysis, respectively [22]. A low level of lactic acid during a prolonged convulsive episode makes a seizure less likely (nonepileptic convulsions) [2].

On the other hand, the presence of advanced age, comorbidities, abnormal examination findings, or an ill appearance demands comprehensive metabolic testing. Such testing includes serum glucose, creatinine kinase, lactic acid, electrolytes, complete blood count, urea nitrogen, creatinine, AST, ALT, anti-seizure drug levels, pregnancy tests, and drug-of-abuse screening. Checking for electrolyte derangements is important, as these can trigger seizures (e.g., hyponatremia, hypocalcemia, and hypomagnesemia) [23]. Patients with a low bicarbonate level should undergo blood gas analysis. An anion gap metabolic acidosis resulting from lactic acidosis is expected to decline within the first hour after the convulsive seizure stops unless another cause is present. Liver enzymes are tested to check for liver-mediated metabolic abnormalities that can impact therapeutic decisions [2].

Furthermore, patients on antiseizure medication should have their levels checked to confirm compliance. Some drugs are known to be epileptogenic, and it may be necessary to test their levels as well. Drug-of-abuse screening can also be considered in patients presenting with first-time seizures, despite the fact that such testing cannot prove causation or change outcomes [2, 24].

Urgent neuroimaging is indicated for most cases of a first-time seizure, whereas patients with epilepsy who have returned to baseline do not require one. Prompt neuroimaging and CT consideration in the ER is indicated for patients with coma, focal neurological deficits, immunocompromised states, advanced age, anticoagulation use, malignancy, previous intracranial hemorrhage, severe thunderclap headache, status epilepticus, neurocutaneous syndromes, or suspected trauma [25]. Computed tomography (CT) is widely available, but MRI and CT perfusion can provide additional information. If an infection is suspected, lumbar puncture is indicated [2].

Electroencephalography (EEG) is useful for diagnosing nonconvulsive seizures, epilepsy, nonepileptic spells, and status epilepticus [26]. EEG can guide therapy and monitor the treatment of refractory cases. Although it is not cost-effective, it is a high-yield modality for cases with an unclear diagnosis [2].

Lastly, ECG monitoring might benefit patients with preceding or ongoing cardiac symptoms. It can provide early clues in cases of drug toxicity and help understand the etiology of the seizure [2, 27].

Risk Stratification

The presentation and findings of a seizure case can provide clues as to whether this case has any red flags that demand urgent care. History and examination findings such as immunocompromisation, the presence of a thunderclap headache, sudden neurological deficit, status epilepticus presentation, head trauma, persistent altered consciousness, and concurrent infection can indicate a worse outcome [10]. Such patients require extensive investigations and prompt treatment to minimize morbidity and mortality due to the cause of the seizure or as a consequence of the seizures themselves [28]. Critical care for these patient groups is essential to reduce complications such as infection-related issues, irreversible intracranial structural disease, refractory status epilepticus, hemodynamic compromise, and death [2].

The risks of experiencing a secondary seizure following the current presentation may change the management plan to include secondary seizure prophylaxis. Risk stratification, weighing the chances of recurrence (higher in patients with previous brain insult, abnormal EEG, brain imaging abnormalities, and the presence of nocturnal seizures) against the risks of adverse effects from antiseizure medication, should be conducted in collaboration with a consulting neurologist [2].

Management

The initial priorities in managing unstable patients are to recognize and treat hypoxia, hypotension, and hypoglycemia, and to initiate pharmacologic treatment when needed [2, 28, 29].

Initial stabilization of patients with active seizures presenting to the ER includes the following [2, 28, 29]:

Assess airway, breathing, and circulation: Do not use nasopharyngeal airway devices during the seizure, as they can cause injury and increase the risk of aspiration.
Pulse oximetry.
Electrocardiogram (ECG).
Finger stick: If the glucose level is less than 60 mg/dL, administer IV dextrose.
Aspiration precaution: Place the patient in the lateral decubitus position.
Abortive treatment: Administer if the seizure lasts more than 5 minutes or in the case of hemodynamic compromise.

First-line therapy [2, 28, 29]

The first-line pharmacological therapies for managing epilepsy, include three benzodiazepine agents: diazepam, lorazepam, and midazolam. These agents are commonly used for their rapid onset and efficacy in controlling seizures, especially status epilepticus. The table includes critical details on dosing, frequency, maximum permissible dose, pregnancy category, and specific cautions.

Diazepam

Dose per kilogram: 0.15-0.2 mg/kg intravenously (IV).
Frequency: Administered every 5 minutes as needed.
Maximum Dose: Limited to 10 mg per individual dose and a cumulative total of 30 mg across all doses.
Pregnancy Category: D (indicating a potential risk to the fetus, but benefits may outweigh risks in life-threatening situations).
Cautions/Comments:
- Continuous monitoring of respiration is essential due to the risk of respiratory depression, a common side effect of benzodiazepines.

Lorazepam

Dose per kilogram: 0.1 mg/kg intravenously (IV).
Frequency: Administered every 5 minutes as necessary.
Maximum Dose: 4 mg per dose, with a cumulative maximum of 12 mg across all doses.
Pregnancy Category: D.
Cautions/Comments:
- Similar to diazepam, respiratory monitoring is mandatory.
- Intramuscular (IM) administration is contraindicated for lorazepam, likely due to inconsistent absorption or slower onset compared to IV administration.

Midazolam

Dose per kilogram: 0.2 mg/kg, administered via multiple routes including IV, intramuscular (IM), or intranasal (IN).
Frequency: Doses can be repeated every 5 minutes as needed.
Maximum Dose: 10 mg per individual dose.
Pregnancy Category: D.
Cautions/Comments:
- Respiratory monitoring is critical due to the sedative effects of midazolam.
- The half-life of midazolam is approximately 7 hours, making it a relatively short-acting agent compared to others, which can influence its clinical use depending on seizure recurrence risk.

All three agents are effective for rapid seizure control but share common risks, including respiratory depression, necessitating vigilant monitoring, particularly in critical care or emergency settings. Their classification in pregnancy category D highlights the need for careful consideration of maternal and fetal risks versus benefits. Midazolam offers more flexibility in administration routes, making it a practical choice in situations where IV access is not readily available.

If the seizure stops, coordinate a disposition plan and consider non-convulsive status epilepticus in patients who do not return to baseline. However, if the seizure does not stop, ensure adequate dosing of first-line therapy, then proceed to second-line therapy, and finally to third-line therapy, one step at a time [2, 28, 29].

Second-line therapy [2, 28, 29]

The second-line treatment options for epilepsy, include on a variety of antiepileptic drugs. These agents are typically used when first-line benzodiazepines are insufficient to control seizures. The table details dosing, frequency, maximum permissible doses, pregnancy categories, and relevant cautions for clinical use.

Levetiracetam

Dose per kilogram: 40-60 mg/kg administered intravenously (IV).
Frequency: Administered once over a 10-minute period.
Maximum Dose: 4500 mg.
Pregnancy Category: C (indicating that risks cannot be ruled out, but the drug may be used if benefits outweigh potential risks).
Cautions/Comments:
- Requires renal clearance, so dose adjustments may be necessary in patients with renal impairment.

Fosphenytoin

Dose per kilogram: 10-20 mg PE/kg (phenytoin equivalents) given IV or intramuscularly (IM).
Frequency: Additional 5 mg PE/kg can be administered after 10 minutes if needed.
Maximum Dose: 150 mg PE/kg.
Pregnancy Category: D (associated with risk but can be used in life-threatening situations).
Cautions/Comments:
- Can cause hypotension and dysrhythmias, requiring cardiac monitoring during administration.

Lacosamide

Dose per kilogram: 200-400 mg IV.
Frequency: An additional 5 mg/kg can be administered if necessary.
Maximum Dose: 250 mg.
Pregnancy Category: C.
Cautions/Comments:
- Can cause arrhythmias.
- Renal clearance is required, so adjustments are needed for patients with renal insufficiency.

Phenobarbital

Dose per kilogram: 15-20 mg/kg IV.
Frequency: Additional 5-10 mg/kg can be given as needed.
Maximum Dose: Not explicitly mentioned but calculated based on repeated doses.
Pregnancy Category: D.
Cautions/Comments:
- Monitor respiration closely due to the sedative and respiratory depressant effects.
- A strong P450 enzyme inducer, which can affect the metabolism of other drugs.

Phenytoin

Dose per kilogram: 15-20 mg/kg IV.
Frequency: Additional 5-10 mg/kg can be administered if necessary.
Maximum Dose: 30 mg/kg.
Pregnancy Category: D.
Cautions/Comments:
- Risk of hypotension and dysrhythmias during administration, necessitating monitoring.
- A strong P450 enzyme inducer, which impacts the metabolism of other medications.

Valproic Acid

Dose per kilogram: 20-40 mg/kg IV.
Frequency: Additional doses of 20 mg/kg can be administered if necessary.
Maximum Dose: 3000 mg.
Pregnancy Category: D.
Cautions/Comments:
- Strong P450 enzyme inducer.
- May cause hepatotoxicity and platelet dysfunction, warranting caution in patients with liver disease or coagulopathy.

The second-line agents are reserved for scenarios where first-line therapy fails to achieve seizure control. Each agent has specific risks and monitoring requirements. For example:

Levetiracetam and lacosamide are generally well-tolerated but require dose adjustments in renal impairment.
Phenobarbital, phenytoin, and valproic acid necessitate respiratory and hepatic monitoring due to their systemic side effects.
Fosphenytoin and phenytoin require cardiac monitoring due to their potential to induce arrhythmias.

The choice of agent depends on the patient’s clinical status, underlying conditions, and the safety profile of the drug.

Third-line therapy [2, 28, 29]

The third-line therapy agents for managing refractory epilepsy, particularly in patients requiring intubation, mechanical ventilation, and hemodynamic support are administered in critical care settings to control seizures when first- and second-line therapies fail. Each drug is described with its dosing regimen, frequency, maximum dose, pregnancy category, and significant precautions.

Ketamine

Dose per kilogram:
- Loading dose: 1.5 mg/kg intravenously (IV).
- Maintenance dose: 0.5 mg/kg every 3-5 minutes as needed.
Maximum Dose: Not explicitly stated, but administered as required to control seizures.
Pregnancy Category: N (Not classified).
Cautions/Comments:
- Ketamine acts as an NMDA antagonist, a unique mechanism among anticonvulsants.
- Hypotension is a potential side effect, necessitating blood pressure monitoring.

Midazolam

Dose per kilogram:
- Loading dose: 0.2 mg/kg IV.
- Maintenance dose: 0.2-0.4 mg/kg every 3-5 minutes.
Maximum Dose: 2 mg/kg for the loading dose.
Pregnancy Category: D (Risk to the fetus exists, but use may be justified in emergencies).
Cautions/Comments:
- Midazolam may cause hypotension and requires continuous hemodynamic monitoring.

Pentobarbital

Dose per kilogram:
- Loading dose: 5-15 mg/kg IV.
- Additional doses of 5-10 mg/kg may be given if required.
Maximum Dose: 25 mg/kg for the loading dose.
Pregnancy Category: D.
Cautions/Comments:
- Pentobarbital has a long half-life (22 hours), which makes it effective for sustained seizure control but may prolong sedation.
- It carries significant risks, including hypotension, ileus, myocardial suppression, immunosuppression, and thrombocytopenia, requiring vigilant monitoring in an intensive care setting.

Propofol Infusion

Dose per kilogram:
- Loading dose: 1-2 mg/kg IV.
- Maintenance dose: 0.5-2 mg/kg every 3-5 minutes as needed.
Maximum Dose: 10 mg/kg for the loading dose.
Pregnancy Category: B (Lower risk, but use must be cautious).
Cautions/Comments:
- Propofol has a short half-life (0.6 hours), allowing for rapid onset and recovery.
- Side effects include hypotension, respiratory depression, hypertriglyceridemia, pancreatitis, and the rare but potentially fatal propofol infusion syndrome. Close monitoring of triglycerides and cardiac function is necessary.

Third-line therapies are used in severe, refractory cases of epilepsy where intubation, ventilation, and hemodynamic support are required. These drugs induce deep sedation or anesthesia to suppress seizure activity effectively. Key considerations for their use include:

Ketamine: Offers a unique mechanism (NMDA antagonism), useful in resistant cases.
Midazolam and pentobarbital: Provide effective sedation but require careful respiratory and cardiovascular monitoring due to risks of hypotension and prolonged sedation.
Propofol: Its short duration of action allows for precise titration, but metabolic side effects and infusion syndrome necessitate caution.

The choice of agent depends on the clinical scenario, patient stability, and institutional protocols. These medications are used alongside comprehensive critical care support to manage complications and optimize outcomes.

Special Patient Groups

Certain notes are important to remember regarding special patient groups. In cases of seizures during pregnancy, considering the diagnosis of eclampsia is a high priority. Magnesium is the drug of choice for acute eclamptic seizures [30]. If a pregnant patient was previously diagnosed with epilepsy, a lower seizure threshold may result due to noncompliance, adjusted regimens, sleep deprivation, nausea and vomiting, or increased drug clearance. When managing status epilepticus, the risks to the fetus from the seizure are higher than the risks from the medication; therefore, manage the patient as you would a nonpregnant individual [31]. In the case of a new, non-eclamptic seizure, a workup is indicated as previously mentioned [2].

When To Admit This Patient

The decision to admit or discharge should be individualized based on the underlying illness, recurrence risk, and need for maintenance pharmacotherapy [32]. Admission for observation alongside neurological consultation should be considered for patients with an uncertain diagnosis, a history of neurological disease or other comorbidities, or in situations where follow-up is unlikely. In contrast, patients can be discharged home with early referral to a neurologist if they have normal examination findings, no significant comorbidities, no known structural brain disease, did not require more than a single dose of benzodiazepines, and are expected to comply with follow-up instructions [2].

Discharge instructions should include guidance on car driving, potentially dangerous activities (e.g., swimming, cycling, climbing ladders), and information regarding any needed follow-up [2, 33].

Revisiting Your Patient

A 22-year-old woman with a previous history of epilepsy was brought to the ER due to generalized tonic-clonic insuppressible movements of her limbs that started 15 minutes ago.

You immediately assessed the airway, breathing, and circulation and placed the patient in the lateral decubitus position to prevent aspiration, as she had a tongue injury. Blood sugar was measured using a finger stick, ruling out hypoglycemia. Lorazepam was then administered as abortive treatment.

You began taking a history from her husband. They were having lunch together when his wife suddenly started seizing, and he was unable to stop it. She had not regained consciousness since then. He mentioned that she had been inconsistent with her antiepileptic medication because she wanted to get pregnant and had read online about potential harms of the medications on a growing baby.

Her lactic acid level was high, her pregnancy test was negative, and the rest of her laboratory findings were within normal limits.

The patient was diagnosed with status epilepticus, a medical emergency requiring urgent management. The ABC approach was performed to ensure the patient’s safety, followed by the administration of benzodiazepines. If first-line therapy fails, second- and third-line therapies should be administered sequentially. Inconsistency with antiepileptic medication highlights the need for patient education and further discussion regarding her concerns and available treatment options.

Authors

Rand Redwan Al Sari

Dr Rand Al Sari is a dedicated General Physician practicing in Saudi Arabia. With a strong commitment to patient care, she is also actively engaged in medical research, staying at the forefront of healthcare advancements and integrating this knowledge into her clinical practice. Passionate about medical writing and journaling, Dr Al Sari reflects on her experiences to contribute meaningfully to the medical community, with a focus on evidence-based healthcare and improving patient outcomes.

Imad Khojah

Listen to the chapter

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Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Fundamentals of Pediatric Advanced Life Support (2024)

December 2, 2024December 4, 2024 ~ iEM Education Project Team ~ Leave a comment

by Burak Çakar & Ayça Koca

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:

Airway: Signs include stridor, drooling, and retractions, which indicate significant airway obstruction or distress.
Breathing: Irregular respiration, bradypnea, gasping respirations, and cyanosis are warning signs of severe respiratory compromise.
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.
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].

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

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

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.

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

Burak Çakar

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

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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Reviewed and Edited By

Elif Dilek Cakal, MD, MMed

Arif Alper Cevik, MD, FEMAT, FIFEM

Emergency Department Triage (2024)

December 1, 2024December 1, 2024 ~ iEM Education Project Team ~ Leave a comment

by Priya Arumuganathan and Scott Findley

Introduction

Triage is the process of sorting patients by severity of illness to ensure care is administered in a timely fashion according to each patient’s need. When specifically applied to the emergency department, “Emergency Department (ED) Triage” is used to quickly assess, risk-stratify, and manage incoming patients before their complete evaluation. A triage process allows systems to safely operate an influx of multiple patients with varying acuity levels in situations when clinical demand exceeds capacity. Formal triage systems have been employed since as early as the 19th century in warfare settings to effectively handle the growing amounts of field casualties [1].

Today, emergency triage can be generally separated into three distinct phases: prehospital triage, triage at the scene, and emergency department triage. Many different types of triage systems have been developed and implemented worldwide [2]. In this section, we will focus on emergency department triage and some of the most well-known triage systems globally.

Performing a Rapid Triage Assessment

The “rapid triage assessment” is essential to any triage system. Those performing the rapid triage assessment should have some clinical experience and a keen eye to quickly identify patients who need to be seen urgently. The goal of triage is to determine which patients need immediate attention, which patients can wait to be seen, and to manage large patient volumes safely. To accomplish this, one must gather pertinent history and physical exam findings quickly and efficiently.

Performing a Focused History

Obtaining a quick and focused history is of utmost importance during the rapid triage assessment. To summarize, providers must be able to get symptoms pertinent to the patient’s presentation, any relevant events leading to their presentation, and pertinent past medical history and allergies. One mnemonic that is useful and used by many for history-gathering is SAMPLE (as below) [3]:

The SAMPLE mnemonic is a structured method for gathering key clinical information during an emergency assessment. It serves as a framework for emergency medical personnel to obtain essential details quickly and efficiently, allowing them to prioritize care and decide on the best course of action. Each component of the mnemonic corresponds to a specific area of focus in history-gathering, which is vital for rapid triage in the emergency department or pre-hospital setting. Below is a more detailed breakdown of each element:

S – Signs & Symptoms
The first and most immediate part of the assessment focuses on the patient’s presenting signs and symptoms. These may include both subjective (what the patient describes) and objective (what the healthcare provider observes) data. For example, a patient may report chest pain, difficulty breathing, or nausea, while a provider might note abnormal vital signs or physical findings. It’s crucial to obtain a clear description of the symptoms, including onset, duration, intensity, and any factors that may have worsened or alleviated them. Understanding the signs and symptoms will help determine the severity of the condition and direct the urgency of intervention.

A – Allergies
Gathering information about any known allergies is vital in guiding treatment decisions, especially in emergencies where medications or interventions are required quickly. For example, if a patient has a known allergy to penicillin, it is essential to avoid using antibiotics in that class. Allergies to food, medications, environmental triggers, and latex should all be considered. In addition, healthcare providers should be mindful of potential allergic reactions that could complicate the management of the patient’s condition.

M – Medications
A comprehensive medication history helps identify substances that may impact the patient’s current clinical situation. This includes prescribed medications, over-the-counter drugs, supplements, and any recent changes to a medication regimen. For example, a patient taking blood thinners such as warfarin may require careful monitoring for signs of bleeding, while those on insulin may need their blood sugar levels closely monitored. Knowledge of recent changes, doses, and the possibility of drug interactions is crucial in the emergency setting.

P – Past Pertinent History
Past medical history (PMH) can provide essential context for understanding the patient’s current presentation. This includes chronic conditions such as diabetes, hypertension, or asthma, as well as previous hospitalizations, surgeries, or significant illnesses. Understanding a patient’s medical history helps healthcare providers anticipate complications and tailor their approach. For instance, if a patient with a history of seizures presents with altered mental status, healthcare providers will prioritize ruling out or treating seizure activity or postictal states.

L – Last Oral Intake
Knowing the last oral intake—what the patient has eaten or drunk—can provide valuable information about the patient’s condition, especially in cases of poisoning, drug overdoses, or gastrointestinal distress. For example, the timing of food or drink ingestion could suggest an issue with digestion or absorption, which may influence the choice of interventions. In cases of poisoning, knowing whether the patient ingested a toxic substance recently can impact the decision to administer activated charcoal or other antidotes. Additionally, the last oral intake can be crucial if the patient is scheduled for surgery or other procedures, as it helps assess the risk of aspiration or anesthesia complications.

E – Events Leading to the Incident
Understanding the sequence of events that led to the current emergency is essential for diagnosing the cause and assessing the patient’s clinical needs. For example, was the patient involved in a motor vehicle accident, or did they experience a sudden onset of chest pain while exercising? Gathering this information helps to identify the mechanism of injury or the type of acute event, which could significantly alter the emergency management plan. It also provides insight into potential causes of the symptoms and any necessary preventive or therapeutic actions.

Purpose and Application of the SAMPLE Mnemonic in Rapid Triage

The SAMPLE mnemonic is a concise tool designed to quickly gather relevant historical information that can significantly impact clinical decision-making in the emergency department. This structured approach is particularly helpful in high-pressure environments where time is critical, such as during triage or when managing patients with complex or time-sensitive conditions.

The goal during history-gathering in an emergency is to obtain just enough, but not too much detail. Too much detail may delay treatment, while too little may result in missing critical information. For example, a lengthy review of a patient’s family history may be less pertinent in an acute situation compared to knowing their current medication list or the events leading to the emergency. The SAMPLE framework ensures that the provider gathers relevant information to make informed decisions about the next steps in care, whether that be immediate intervention, further diagnostics, or a more detailed secondary assessment.

The SAMPLE mnemonic is an effective tool for emergency practitioners to rapidly gather crucial information during triage and initial assessment. By focusing on the most important elements—signs and symptoms, allergies, medications, past medical history, last oral intake, and events leading up to the incident—providers can prioritize interventions, anticipate potential complications, and provide optimal care in emergency settings.

Performing a Focused Physical Exam

After performing a focused history, it is important to use the information gathered to guide your focused physical exam. For example, a patient presenting with the chief complaint of sore throat should receive an expedited examination of the head, ears, mouth, and neck. The rest of the physical exam should be deferred unless the patient has another complaint that is not covered by these sections. The purpose of the focused physical exam is to look for “red flag” exam findings that would warrant more immediate attention and intervention, such as the peritonitic abdomen in the patient presenting with abdominal pain, oropharyngeal swelling in the patient presenting with shortness of breath and rash, left-sided flaccidity in the patient presenting with sudden onset weakness and tingling, and other concerning findings [4].

Vital Signs and Objective Data

There are clues to key providers about how sick their patients are. One of the most important clues is a patient’s set of vitals; therefore, it is exceedingly important to obtain a full set of vitals for all patients arriving at the emergency department. Vitals at either extreme of the spectrum are equally important, and grossly abnormal vitals should prompt a more expedited triage and shorter waiting times. Other clues that help identify sick patients include the level of pain, duration of symptoms, level of consciousness, and mechanism of injury. Suppose someone is determined to be in distress at any point during the triage process. In that case, they must be brought to a designated patient care area for immediate ED provider attention. In the paragraphs below, we will discuss this further regarding adult populations.

Heart Rate

Bradycardia is a heart rate of less than 60 bpm, while tachycardia is a heart rate of more than 100 bpm [5]. If a patient is experiencing associated hypotension with an abnormal heart rate, then it is obvious that they are sick. However, there are other key questions that you may ask in the physical exam to elucidate further a patient’s severity of illness regarding an abnormal heart rate. For example, experiencing associated chest pain, palpitations, extreme fatigue or weakness, altered mental status, shortness of breath, or nausea can be signs that the abnormal heart rate is due to a concerning underlying pathology in the patient. Tachycardia can be indicative of infection, dysrhythmia, acute blood loss, and toxin exposure amongst other etiologies. It is also important to ask about medication use in these patients as this can be your first sign of an accidental (or intentional) chronotropic medication overdose – such as with beta-blockers, calcium channel blockers, and other medications that need to be seen by a medical provider quickly.

Blood Pressure

Hypotension is defined as a blood pressure less than 90/60 mmHg, while hypertension is defined as more than 140/90 mmHg [5]. With hypotension, it is important to first quickly assess if a patient is experiencing a decreased mental status and level of alertness in order to determine if any immediate interventions are needed – if so, this patient is definitely sick and cannot wait for care. Next, it is important to assess for possible causes of hypotension and severe illness, such as septic, hemorrhagic, neurogenic, and anaphylactic shock. For hypertension, it is important to assess for signs that could indicate end-organ failure, such as chest pain, shortness of breath, and focal neurologic deficits. Patients exhibiting the above symptoms should be evaluated sooner rather than later.

Respiratory Rate

Tachypnea is defined as a respiratory rate above 20 bpm, while bradypnea is defined as a respiratory rate below 12 bpm [5]. Apnea is the total absence of breathing. Bradypnea and apnea can be seen in many conditions, including traumatic brain injury and heroin overdose. Tachypnea is seen in many conditions, including asthma exacerbation and conditions causing metabolic derangement, such as diabetic ketoacidosis. If a patient is not breathing or experiencing decreased oxygen saturation along with abnormal respirations, then it is obvious they are sick. However, for those cases that are less obvious, it is important to observe the patient’s work of breathing with their respirations. Those who appear to have a significantly increased respiratory effort, are becoming tired, or are experiencing shallow respirations will need medical evaluation and care sooner rather than later. Their fatiguing respiratory effort will eventually lead to respiratory failure and hypoxia. Those with stories concerning an underlying process that could quickly compromise respiratory function should also be prioritized. For example, a patient who presents with a story suspicious of intracranial hemorrhage who appears sleepy and only moans in response to questions is at high risk for respiratory decompensation.

Oxygen Saturation

Hypoxia is defined as an oxygen saturation below 92% [5]. While different patients can tolerate various oxygen saturation levels depending on their smoking status, history of lung disease, and other past medical history, it is important to assess the work of breathing and level of alertness in patients with low readings. Patients who appear to have increased work of breathing, decreased respirations, or decreased level of alertness are at risk for respiratory decompensation. These patients should be evaluated and treated sooner rather than later.

Temperature

Hypothermia is defined as a temperature below 35 C. In contrast, hyperthermia is defined as a temperature above 38 C [5]. Hypothermic patients must be rewarmed depending on the degree of hypothermia (this will be discussed in later chapters). It is important to determine the reason for their hypothermia – such as sepsis, submersion injury, and prolonged cold exposure. There are many reasons for hyperthermia, including but not limited to infection, prolonged heat exposure, and certain types of medication overdose. The hyperthermic patient must be physically cooled and given antipyretics or other medications depending on the cause of their hyperthermia. These are all causes for concern and immediate interventions.

Pain

The severity and location of pain can also help identify patients who need prompt attention. Patients in severe pain will need immediate attention and medications to alleviate their pain. The location of pain can also be a clue to a patient’s severity of illness. For example, chest pain radiating to the back could represent an aortic dissection, right lower quadrant abdominal pain could represent appendicitis, and headache with neck stiffness could represent bacterial meningitis. Patients with concerning pain severity and location should be prioritized [6].

Duration and Mechanism

The duration of symptoms can also be a clue to a patient’s severity of illness. In general, acute complaints, or complaints that occur with a sudden or recent onset, should raise higher suspicion for serious etiologies than a chronic complaint that has been occurring without change for weeks to months [6]. A patient’s mechanism of injury is also important to consider; for example, a person who has fallen from a significant height or has been involved in a high-speed accident should be evaluated quickly as well.

Level of Consciousness

Level of consciousness exists on a spectrum, from those who are unresponsive to those who are completely awake and alert. Unresponsive patients should receive immediate attention and interventions, including chest compressions if they are without a pulse and intubation. Lethargic patients and those experiencing quickly decreasing levels of alertness should also be prioritized. Those sleepy or confused should be seen urgently, while those fully awake and alert may wait to be seen if they are without other concerning signs/symptoms [6].

Triage is a complex process involving several components, and it can be challenging. Triage providers play a crucial role in ensuring the efficiency and safety of the ED. They must quickly and accurately assess a patient’s severity of illness to determine how long different patients can safely wait for care. It is essential that they do not focus on diagnosing the patient’s condition during triage, as this can delay the process. Such delays can compromise care for all patients, allowing seriously ill individuals to go unnoticed for extended periods while their condition worsens. Remember that a comprehensive history, examination, diagnostic work-up, and treatment will occur once the patient is admitted to a care area.

Triage Systems

Triage is a complex process that needs to be done expediently, especially when facing large patient volumes. Fortunately, many triage systems have been developed to help guide providers in quickly and accurately risk-stratifying patients during the rapid triage assessment. We will discuss some of the most popular and widely used triage systems, such as the Manchester Triage System and the Emergency Severity Index.

Manchester Triage System

One of the most well-known and globally used triage systems is the Manchester Triage System (MTS). It was developed in the UK and is widely used worldwide. This triage system helps ensure patient safety by defining the maximum time each patient can wait before being seen and treated. The MTS contains flowcharts for various presenting complaints that help to distinguish the severity of illness based on key “discriminators” (signs and symptoms) [7]. Each level of severity is assigned a different color. Red indicates immediate evaluation, while blue indicates non-urgent evaluation (can wait up to 240 minutes). Flowcharts are available for various chief complaints in adult and pediatric patients. The MTS (Figure) for the adult chief complaint of “chest pain” is discussed below [8].

RED: Immediate/Life-Threatening

The red category signifies the highest level of urgency, where the situation is life-threatening and requires immediate medical intervention. The maximum waiting time is 0 minutes, indicating that the patient must receive attention without delay. Correlating examples for chest pain in this category include airway compromise, inadequate breathing, or shock. These conditions are critical as they can lead to rapid deterioration or death if not addressed promptly. Immediate treatment might involve airway management, advanced resuscitation, or stabilization of vital signs.

ORANGE: Emergent/Could Become Life-Threatening

The orange category represents conditions that are not immediately life-threatening but could escalate to critical levels if left untreated. The maximum waiting time in this category is 10 minutes, emphasizing the need for swift medical evaluation and intervention. Examples of chest pain scenarios in this category include severe pain, cardiac pain, acute shortness of breath, or abnormal pulse. These symptoms often indicate serious underlying issues such as myocardial infarction, severe arrhythmias, or pulmonary embolism, all of which require urgent diagnostic and therapeutic measures to prevent deterioration.

YELLOW: Urgent/Not Life-Threatening

In the yellow category, conditions are urgent but not immediately life-threatening. The maximum waiting time is 60 minutes, providing a moderate window for assessment and treatment. Correlating examples for chest pain include pleuritic pain, persistent vomiting, history of cardiac disease, or moderate pain. These symptoms may point to less severe causes, such as musculoskeletal issues, gastroesophageal reflux, or pleurisy. However, the history of cardiac disease suggests a need for careful evaluation to rule out more serious conditions.

GREEN: Semi-Urgent/Not Life-Threatening

The green category involves semi-urgent conditions where the likelihood of life-threatening complications is low. Patients in this category can wait up to 120 minutes for treatment. Examples include vomiting, mild pain, or recent problems. Chest pain in this category is typically associated with benign causes, such as anxiety, mild gastrointestinal issues, or a musculoskeletal strain. While these cases are not critical, timely assessment ensures patient comfort and prevents unnecessary progression of symptoms.

BLUE: Non-Urgent/Needs Treatment When Time Permits

The blue category is for non-urgent conditions that require treatment only when time permits. The maximum waiting time is 240 minutes, as these cases are unlikely to escalate to a critical level. Examples include other complaints that may not even directly relate to chest pain or are minor in nature. These could involve mild discomfort or non-specific symptoms that do not pose any immediate threat to the patient’s health. Such cases can be safely managed without priority over more urgent categories.

Emergency Severity Index

Much like the Manchester Triage System, the Emergency Severity Index triage system (developed in the USA) is also globally known and used. It stratifies patients into five levels: level 1, the most urgent, and level 5, the least urgent. It also helps to determine what resources are necessary to move a patient toward disposition. It is based on four key decision points: does the patient require life-saving interventions (Step A), are they in a high-risk situation (Step B), how many resources do they need (Step C), and what are their vitals (Step D)? The ESI Triage Algorithm, types of resources, and level of urgency, along with examples, are discussed below [9].

Step-by-Step ESI Triage Algorithm

Step A: The first question asks whether the patient requires immediate, life-saving interventions. If the answer is “Yes,” the patient is classified as Level 1, indicating the highest level of urgency. If “No,” the triage proceeds to Step B.
Step B: This step evaluates whether the patient is in a high-risk situation, is lethargic, confused, or in severe pain. A “Yes” response classifies the patient as Level 2, while a “No” response advances the process to Step C.
Step C: At this stage, the need for medical resources is assessed. If the patient requires only one resource, they are categorized as Level 4. If multiple resources are needed, they may qualify for a higher urgency level, prompting a review in Step D.
Step D: This step determines whether the patient exhibits “danger zone” vital signs, such as abnormal heart rate, respiratory rate, or oxygen saturation. A “Yes” response results in a Level 2 classification, while “No” leads to a Level 3 classification.

Types of Resources Defined by ESI

Resources play a critical role in the ESI system, as they help determine patient levels during Step C. Common resource types include:

Diagnostic Tools: Labs, EKG/ECG, X-rays, CT scans, MRI, or ultrasounds.
Treatment: IV fluids, IV/IM/nebulized medications, and specialist consultations.
Procedures: Simple procedures, such as laceration repair or Foley catheter insertion, are counted as one resource. Complex procedures, including conscious sedation, fracture reduction, and intubation, may require additional considerations.

Points according to required resources;

1 point for Labs (e.g., blood tests), EKG/ECG or X-rays, or Advanced Imaging (e.g., CT, MRI, or ultrasound).
1 point for IV fluids.
1 point for IV, IM, or nebulized medications.
1 point for a Specialist consultation.
1 point for a Simple procedure, such as laceration repair or Foley catheter placement.
2 points for a Complex procedure, such as conscious sedation, fracture reduction, or intubation.

These resource definitions allow triage staff to assess patient needs objectively. A higher number of resources often correlates with a more urgent ESI level.

ESI Levels and Their Corresponding Urgency

The ESI system categorizes patients into five levels of urgency based on their condition and resource needs:

Level 1 (Immediate): Patients need immediate attention due to life-threatening conditions like cardiac arrest.
Level 2 (Emergent): These patients are at high risk of rapid deterioration, such as those experiencing an asthma attack.
Level 3 (Urgent, Multiple Resources): Patients with conditions requiring multiple resources, like abdominal pain, fall into this category.
Level 4 (Stable, One Resource): These patients need only one resource, such as laceration repair.
Level 5 (Stable, No Resources): Patients with stable conditions requiring no resources, such as a prescription refill, are classified here.

Advanced Triage

Once you are comfortable with the above basic triage concepts, you can familiarize yourself with advanced triage considerations, such as ordering an initial diagnostic work-up and treatments.

Ordering an Initial Diagnostic Work-Up and Other Orders

As soon as a patient is determined to be sick or unstable, your priority should be to place them in a patient care area as quickly as possible for medical attention. You can then place initial orders, which should be directed toward stabilizing them. Placing IVs early and facilitating early medication/fluid administration can be life-saving measures. Be sure to ask these patients (or their loved ones) early in their evaluation regarding their wishes for cardiopulmonary resuscitation (CPR) and intubation. Once a patient is stable, or if they’re already stable, you can use their pertinent history and physical exam findings to guide your initial diagnostic imaging and labs. Consider your most likely diagnoses and “can’t miss diagnoses” when placing these initial orders [10].

Author

Priya Arumuganathan

Priya Arumuganathan, MD is a third year Emergency Medicine resident at West Virginia University. After residency, she will be completing a Global Emergency Medicine Fellowship at the University of Pennsylvania. During residency, Priya served as a Chief Resident and was very active in teaching core EM content, ultrasound skills, and procedural basics to medical students and new residents. Her rural background and training at several critical access hospitals have helped her build a foundation for working in low-resource environments, and she has been able to translate these skills to her global work. Her academic interests include EM education & training in low-resource environments, telemedicine, and rural health.

Scott Walker Findley

Dr. Findley is an associate professor with the WVU Department of Emergency Medicine. He splits time between the larger WVU academic centers and outlying rural emergency departments, spending most of his clinical time in single coverage facilities. After recognizing the challenges inherent in rural emergency medicine (EM), he designed and developed the WVU Division of Rural EM. Dr. Findley secured a federal telemedicine grant to expand telemedicine services in WV critical access hospitals, an institutional HOPE grant to assess per-birth needs in rural emergency departments, assisted with a rural specific response to COVID – 19, secured a position as medical director and advisor for Adventure WV, successfully launched a multisite rural EM rotation for residents, facilitated rural rotations for medical students, and oversaw the integration of rural EM lectures and simulated cases into the resident curriculum. In addition to remaining academically connected, Dr. Findley works closely with the WVU Emergency Department Divisions of ultrasound, EMS and Education to bring resources into the community sites and rural areas. Dr. Findley also sits on the national American College of Emergency Physicians (ACEP) Rural Emergency Medicine’s Task Force. He has taken an active role in research with local and national presentations as well as publishing in academic journals. Although these opportunities have been rewarding, Dr. Findley believes nothing teaches you more, maintains drive and sharpens focus better than pulling shifts and seeing patients and he plans to continue working the majority of his clinical hours in smaller departments.

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References

Robertson-Steel I. Evolution of triage systems. Emerg Med J. 2006;23(2):154-155. doi:10.1136/emj.2005.030270
Yancey CC, O’Rourke MC. Emergency Department Triage. In: StatPearls. Treasure Island (FL): StatPearls Publishing; August 31, 2022.
West Virginia Office of Emergency Medical Services. (2016, January 1). Assessment Mnemonics. Appendix D. Retrieved April 23, 2023, from https://www.wvoems.org/files/protocols/appendix/appendix-d-assessment-mnemonics
Society for Academic Emergency Medicine. (2008). Performing a complaint-directed history and Physical Examination. Clerkship Directors in Emergency Medicine. Retrieved April 23, 2023, from https://www.saem.org/about-saem/academies-interest-groups-affiliates2/cdem/for-students/online-education/m3-curriculum/group-focused-chief-complaint-history-physical-examination-and-differential-diagnosis/performing-a-complaint-directed-history-and-physical-examination
Balakumaran, J. (2020, June 30). Interpreting critical vital signs. Medical Concepts. Retrieved April 23, 2023, from https://canadiem.org/interpreting-critical-vital-signs/
Mackway-Jones, K., Marsden, J., & Windle, J. (2014). The Triage Method. In Emergency Triage (2nd ed., pp. 10–21). John Wiley & Sons.
Cicolo, E. A., Ayache Nishi, F., Ciqueto Peres, H. H., & Cruz, D. A. (2017). Effectiveness of the Manchester Triage System on time to treatment in the emergency department: a systematic review protocol. JBI database of systematic reviews and implementation reports, 15(4), 889–898. https://doi.org/10.11124/JBISRIR-2016-003119
Ganley, L., & Gloster, A. S. (2011). An overview of triage in the emergency department. Nursing standard (Royal College of Nursing (Great Britain) : 1987, 26(12), 49–58. https://doi.org/10.7748/ns2011.11.26.12.49.c8829
Gilboy N, Tanabe T, Travers D, Rosenau AM. (2011). Emergency Severity Index (ESI): A Triage Tool for Emergency Department Care, Version 4. Implementation Handbook 2012 Edition. AHRQ Publication No. 12-0014. Rockville, MD. Agency for Healthcare Research and Quality.
International Emergency Medicine Education Project. (2019, March 4). Core Senior EM Clerkship Topics. Emergency Medicine Clerkship – Approach to Chief Complaints. Retrieved April 23, 2023, from https://iem-student.org/em-clerkship-topics/

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Antidotes (2024)

December 1, 2024December 1, 2024 ~ iEM Education Project Team ~ Leave a comment

by Sarah Alzaabi

Introduction

An antidote is a specific agent designed to counteract the toxic effects caused by drugs or poisons [1]. These substances play a crucial role in toxicology, as they can effectively mitigate or reverse the harmful consequences of various toxic exposures. In clinical practice, the availability of antidotes is somewhat limited, with only a select number approved for use depending on the type of toxin involved [2].

It’s important to note that antidotes are not administered indiscriminately; instead, they are used based on clearly defined clinical guidelines. Each antidote has specific indications that dictate when it should be given, ensuring that patients receive the appropriate treatment in situations of toxicity. Proper identification of the toxin and the clinical scenario is essential to determine the need for an antidote and to maximize its therapeutic efficacy.

Many poisons have no true antidote, and the poison(s) involved may initially be unknown [3, 4]. Furthermore, limiting the differential diagnosis to poisoning can deter the identification of other pathologies that may exist in these patients [3, 4]. Therefore, the initial approach should be to assess and stabilize [4, 5] thoroughly. Similar to any compromised patient, the attention is directed toward securing the airway, breathing, circulation, and decontamination [4, 5]. There are only a few indications where antidotes are prioritized over cardiopulmonary stabilization, i.e., naloxone for opioid toxicity, cyanide antidotes for cyanide toxicity, and atropine for organophosphate poisoning [5]. Otherwise, most patients will have good outcomes with supportive management and a period of observation [1, 3, 4, 5].

Administration of pharmacologic antagonists may worsen the outcome in some situations and is not recommended [2, 3]. Therefore, the physician should know the indications and contraindications of each antidote [2, 3]. When in doubt, consult a poison control center or a medical or clinical toxicologist [2, 4].
In summary, it’s important to understand that antidotes should be utilized as complementary treatments rather than the sole focus in managing poisoning cases [1]. The primary objective should always be to address the patient’s overall condition, taking into account their symptoms and needs, rather than concentrating exclusively on the specific toxin involved [4]. This approach ensures a more comprehensive and effective care strategy for individuals affected by poisoning.

Pregnant Patients and Antidotes

Limited data is available on the use of antidotes in pregnancy [4]. Hence, the teratogenic potential of antidotes is not fully understood [7]. The general initial management principles are the same, and stabilization of the mother is the priority [6].

The risks and benefits of using or withholding antidotes must be assessed. In general, antidotes are not used for uncertain indications, but proven effective treatments should not be withheld from the mother based on theoretical danger to the fetus [4].

There is no known indication for fetal antidote therapy [7]. However, if an antidote is to be given for fetal benefit, it should be done rapidly in the acute setting [7]. This specifically applies to chelators such as dimercaprol, calcium EDTA, and deferoxamine, which will prevent the toxin from passing into fetal circulation [7].

The following section presents information about various antidotes, organized in alphabetical order.

Antidotes

Atropine

General Information

Anticholinergic agent, competitive muscarinic antagonist [3, 4, 5, 8].

Indications

Organophosphate poisoning, carbamates, nerve agents [3, 4, 5, 8].

Precautions

Excessive doses may cause anticholinergic symptoms [5].

Dose/Administration

Adults: Start with 1-2 mg IV, double the dose every 2-3 minutes to reach the goal [3, 4, 5, 8].
Children: 0.02 mg/kg IV (minimum of 0.1 mg) [3].

Other Notes

Large doses may be required.
Goal: Drying of respiratory secretions/improved work of breathing [3, 8].
Tachycardia is not the endpoint (atropine helps with muscarinic effects; pralidoxime is used for nicotinic effects) [3, 8].

Calcium

General Information

Calcium chloride 10% (1 g/10 mL, 27.2 mg/mL elemental Ca).
Calcium gluconate 10% (9 mg/mL elemental Ca), one-third strength of calcium chloride [5].

Indications

Calcium channel blocker toxicity, hydrofluoric acid exposure, hyperkalemia, hypermagnesemia [4, 5, 9].

Precautions

Calcium chloride extravasation can cause soft tissue necrosis; prefer central line administration [9].
Continuous monitoring is recommended [9].

Dose/Administration

Adults:
- Calcium chloride: 0.5-1 g IV (5-10 mL) [5, 9].
- Calcium gluconate: 1-3 g IV (10-30 mL) [5].
Children: 0.15 mL/kg calcium chloride IV [5].
IV bolus over 5-10 minutes; repeated doses every 10-20 minutes as needed, guided by serum Ca+ or QT interval [9].
Infusion available [9].

Other Notes

For HF acid skin burns: Topical 2.5% calcium gel or local injection of calcium gluconate [9].
Regional block with intra-arterial or IV calcium gluconate for extremity exposure [9].
Nebulized calcium gluconate for HF acid inhalation injury [9].

Cyproheptadine

General Information

Antihistaminic and antiserotonergic agent; also has anticholinergic activity [10].

Indications

Serotonin syndrome [4, 10].

Dose/Administration

Adults: 8 mg every 8 hours for 24 hours (if response observed) [10].
Children: 4 mg (not well established) [10].

Deferoxamine

General Information

Iron-chelating agent that converts iron to a water-soluble complex for renal clearance [3, 11].

Indications

Systemic iron toxicity (e.g., severe gastroenteritis, shock, metabolic acidosis, altered mental status) [3, 4, 11].
Iron levels >500 µg/dL or multiple pills on radiography [3, 4, 11].
Chronic iron overload [3, 4, 11].

Precautions

Hypotension may occur at rapid infusion rates; ensure adequate hydration [3].
Cardiac monitoring is needed [11].

Dose/Administration

Start with IV infusion: 15 mg/kg/h (maximum 1 g/h) over 6 hours; re-evaluate [3, 11].
Infusion rate can be increased in critical patients if blood pressure allows [11].

Other Notes

Urine may become rusty-red as iron is excreted [3, 11].

Digoxin Immune Fab

General Information

Fab fragments of antibodies to digoxin, reversing cardiotoxic effects [1, 3].

Indications

Digoxin overdose with potassium >5 mEq/L after acute ingestion, hemodynamic instability, or life-threatening dysrhythmias [3].
Poisoning by other cardiac glycosides (e.g., Oleander) [1, 3, 5, 12].

Precautions

Close monitoring of digoxin serum levels, vital signs, and ECG. Resuscitation equipment should be ready [12].

Dose/Administration

Acute overdose:
- Stable patients: 5 vials.
- Unstable patients: 10-20 vials [3, 5].
Chronic overdose: Start with 1-2 vials, repeat after 60 minutes if needed [12].
Calculate dose if the ingested dose is known (40 mg Fab binds 0.6 mg digoxin) [3, 5].
Bolus in life-threatening conditions (e.g., cardiac arrest) or infusion over 30 minutes, monitoring clinical response [3, 12].

Other Notes

For other cardiac glycoside poisoning: Start with 5 vials [3, 12].

Dimercaprol (BAL)

General Information

Heavy metal chelator [1, 14].

Indications

Severe lead, inorganic arsenic, and mercury poisoning [1, 4, 13].

Precautions

Severe adverse effects include nephrotoxicity; consider using EDTA or succimer instead if possible [13].

Dose/Administration

3 mg/kg IM every 4 hours for 48 hours, then every 12 hours for 7-10 days based on clinical response [13].

Ethanol

General Information

Blocks formation of toxic metabolites of alcohols [14].

Indications

Methanol and ethylene glycol poisoning (second-line to fomepizole) [5, 14].

Precautions

Maintain blood ethanol concentration between 100-150 mg/dL [14].

Dose/Administration

IV:
- Loading: 10 mL/kg of 10% ethanol.
- Maintenance: 1-2 mL/kg/h of 10% ethanol [14].
Oral:
- Loading: 1.8 mL/kg of 43% ethanol.
- Maintenance: 0.2-0.4 mL/kg/hour of 43% ethanol [14].

Flumazenil

General Information

Competitive antagonist of GABA-benzodiazepine receptors [1, 2, 3, 15].

Indications

Benzodiazepine overdose (limited role), reversal of procedural sedation, accidental pediatric ingestion [1, 3, 5, 15].

Precautions

May cause withdrawal or seizures, especially in benzodiazepine dependence or mixed overdoses [2, 3, 15].

Dose/Administration

Adults: 0.2 mg IV over 30 seconds, repeat every minute until reversal (maximum 3 mg) [1, 3, 5, 15].
Children: 0.01-0.02 mg/kg, repeat every minute [1, 5, 15].

Other Notes

Limited role due to risk of seizures [1, 3, 15].

Fomepizole

General Information

Alcohol dehydrogenase inhibitor [1, 3, 16].

Indications

Methanol and ethylene glycol toxicity (first-line due to better side effect profile) [1, 3, 5, 16].

Dose/Administration

Loading dose: 15 mg/kg IV infusion in 100 mL normal saline or 5% dextrose over 30 minutes [1, 3, 16].
Maintenance dose: 10 mg/kg every 12 hours for 48 hours, then 15 mg/kg every 12 hours until alcohol concentrations <20 mg/dL [1, 16].
In dialyzed patients: Give every 4 hours or continuous infusion of 1 mg/kg/h [16].

Other Notes

Continue therapy until alcohol concentrations are <20 mg/dL and the patient is asymptomatic [3].

Glucagon

General Information

Increases cyclic AMP (cAMP).
Positive inotropic and chronotropic properties, similar to beta-agonists [18].

Indications

β-blocker toxicity (adjunct).
Calcium channel blocker toxicity [5, 17, 18].

Precautions

Induces vomiting; consider anti-emetics and airway management [18, 19].

Dose/Administration

Adults: 5-10 mg IV bolus over 1-2 minutes [5, 18, 19].
Children: 0.05-0.1 mg/kg IV [19].

Other Notes

If there is a clinical response, start an infusion [18].
Intravenous fluids, vasopressors, and high-dose insulin with dextrose are first-line treatments for β-blocker toxicity [19].

Hydroxocobalamin

General Information

Precursor of Vitamin B12 [20].

Indications

Cyanide toxicity (forms cyanocobalamin by displacing hydroxyl group) [3, 5, 20].

Precautions

Safe drug with low side effects.

Dose/Administration

Adults: 5 g in 100 mL normal saline IV infusion over 15 minutes; repeat if needed [3, 5, 20].
Children: 70 mg/kg IV over 15 minutes (maximum 5 g) [3, 5].

Other Notes

Causes orange-red discoloration of skin and urine, resolving within 24-48 hours [3].

Insulin (High Dose)

General Information

Strong inotropic effects [21].

Indications

Calcium channel blocker and β-blocker toxicity [5, 21].

Precautions

Monitor for hypoglycemia, hypokalemia, hypomagnesemia, and hypophosphatemia [21].

Dose/Administration

Adults:
- Glucose 25 g (50 mL of dextrose 50%) IV bolus → 1 IU/kg IV bolus of short-acting insulin → 25 g/h glucose and 0.5-1 IU/kg/h short-acting insulin infusion [21].
Titrate glucose to maintain levels between 6-8 mmol/L [21].

Intravenous Lipid Emulsion

General Information

20% lipid emulsion as a parenteral nutrient.
Expands the lipid compartment within the intravascular space, sequestering lipid-soluble drugs from tissues [1, 5].

Indications

Overdose by drugs with high protein binding and large volume of distribution, e.g., local anesthetics (bupivacaine), β-blockers, and calcium channel blockers [1, 5].

Dose/Administration

Adults: 100 mL IV bolus over 1 minute (repeat every 5 minutes, maximum 2 doses) → 18 mL/min IV infusion for 20 minutes [5].
Children: 1.5 mL/kg IV bolus over 1 minute (repeat every 5 minutes, maximum 2 doses) → 0.25 mL/kg/min IV infusion for 20 minutes [5].

Methylene Blue

General Information

Reduces methemoglobin (MetHb) to hemoglobin [5, 22].

Indications

Symptomatic methemoglobinemia.
MetHb levels >20% in asymptomatic patients.
Oxidizing toxins (e.g., nitrites, benzocaine, sulfonamides) [5, 22].

Precautions

Pulse oximetry is unreliable in methemoglobinemia.
May cause hemolysis in G6PD deficiency [3, 22].

Dose/Administration

1-2 mg/kg slow IV injection over 5 minutes; may repeat after 30-60 minutes [5, 22].

Other Notes

Monitor MetHb levels frequently until a consistent decrease is observed [22].

N-acetylcysteine (NAC)

General Information

Prevents hepatocellular injury by restoring glutathione stores, which conjugate the toxic metabolite NAPQI [1, 3, 23].

Indications

Serum acetaminophen levels above toxic threshold (>4 hours after ingestion).
Single ingestion >150 mg/kg.
Evidence of liver injury [1, 3, 4, 23].

Dose/Administration

Oral: 140 mg/kg loading dose → 70 mg/kg every 4 hours for 17 doses [1, 3, 23].
IV: 150 mg/kg in 200 mL of 5% dextrose over 60 minutes → 50 mg/kg diluted in 500 mL of 5% dextrose over 4 hours → 100 mg/kg diluted in 1000 mL of 5% dextrose over 16 hours [1, 3, 23].

Other Notes

Oral therapy may not be well tolerated due to taste and odor [23].

Naloxone

General Information

Opioid antagonist, diagnostic, and therapeutic agent [1, 2, 3].

Indications

Opioid toxicity with respiratory and CNS depression [1, 2, 3, 5].

Precautions

Re-sedation may occur due to naloxone’s short half-life; monitor for at least 4 hours.
Withdrawal in chronic/opioid-dependent users [1, 2, 3].

Dose/Administration

Adults: 0.4-2 mg IV; repeat every 2-3 minutes up to a maximum of 10 mg [1, 2, 3].
Children: 0.01 mg/kg IV [1, 3].

Other Notes

Goal: Adequate respiratory rate, normal oxygen saturation on room air, improved level of consciousness [3, 5].
Miosis is an unreliable indicator [5].

Octreotide

General Information

Synthetic analogue of somatostatin [24].

Indications

Hypoglycemia secondary to sulfonylurea [24].

Precautions

Breakthrough hypoglycemia may occur [24].

Dose/Administration

Adults:
- 50 µg IV bolus → 25 µg/h infusion.
- Alternatively, 100 µg IM or SC every 6 hours [24].
Children: 1 µg/kg IV bolus or SC → 1 µg/kg/h IV infusion [24].

Other Notes

Euglycemia needs to be maintained for 12 hours off the infusion before the patient is medically cleared [24].

Physostigmine

General Information

Reversible acetylcholinesterase inhibitor [25].

Indications

Neurological anticholinergic symptoms, e.g., delirium and seizures (crosses the blood-brain barrier) [5, 25].

Precautions

Contraindicated in bradycardia, AV block, and bronchospasm [25].

Dose/Administration

Adults: 0.5-1 mg slow IV push over 5 minutes; repeat in 10-30 minutes if needed [25].
Children: 0.02 mg/kg IV (maximum dose of 0.5 mg) [25].

Other Notes

Confirm absence of conduction defects on a 12-lead ECG before administration.
Rapid administration may cause a cholinergic crisis; treat with atropine if this occurs [25].

Pralidoxime

General Information

Reactivates acetylcholinesterase inhibition [1, 3, 26].

Indications

Early organophosphate poisoning (<2 hours).
Nerve agents [1, 3, 5, 26].

Precautions

Rapid administration can cause laryngospasm, muscle rigidity, and transient respiratory impairment [3].

Dose/Administration

Adults: 1-2 g IV in 100 mL of 0.9% saline over 15-30 minutes → 500 mg/h IV infusion [3, 26].
Children: 25-50 mg/kg → 10-20 mg/kg/h infusion [3, 26].

Other Notes

Administer in the early phase before irreversible acetylcholinesterase binding occurs.
Adequate atropine doses should be given concurrently [1, 3, 26].

Pyridoxine (Vitamin B6)

General Information

Vitamin B6, essential for GABA production [3, 27].

Indications

Isoniazid, hydrazine, and Gyromitra poisoning.
Ethylene glycol poisoning (adjunct therapy) [3, 5, 27].

Dose/Administration

Adults:
- For isoniazid poisoning: 1 g per gram of ingested isoniazid, given as 0.5 g/min infusion until seizures stop. If unknown, give 5 g IV empirically [3, 5, 27].
Children: 70 mg/kg IV, maximum 5 g [5, 27].

Other Notes

For ethylene glycol toxicity: 50 mg IV every 6 hours [27].

Sodium Bicarbonate

General Information

Hyperosmolar sodium bicarbonate injection [28].

Indications

Cardiotoxicity due to fast sodium channel blockade presenting as QRS widening and ventricular dysrhythmias (e.g., TCA poisoning).
Urine alkalinization [2, 5, 28].

Precautions

Monitor for hypokalemia and hypernatremia.
Maintain serum pH between 7.50-7.55 [28].

Dose/Administration

Start with 1-2 mEq/kg IV over 1-2 minutes → 0.3 mEq/kg per hour IV infusion if needed [5].
Repeated doses may require intubation and hyperventilation to maintain pH >7.5-7.55 [28].

Sodium Calcium Edetate (EDTA)

General Information

IV heavy metal chelator [29].

Indications

Severe lead toxicity with lead levels >70 µg/dL [29].

Precautions

Risk of nephrotoxicity, ECG changes, and transaminitis.
Hospital admission required [29].

Dose/Administration

Dilute 25-50 mg/kg in 500 mL of 0.9% saline or 5% dextrose; infuse over 24 hours, starting 4 hours after the first dose of dimercaprol [29].
In encephalopathy, continuous infusion for 5 days until stabilization [29].

Other Notes

Once clinically improved, switch to oral succimer if tolerated [29].

Sodium Thiosulfate

General Information

Assists the body in detoxifying cyanide [1, 30].

Indications

Cyanide poisoning [1, 5, 30].

Precautions

In severe cases, use with other antidotes (e.g., hydroxocobalamin) [30].

Dose/Administration

Adults: 50 mL of 25% solution (12.5 g; 1 ampoule) IV over 10 minutes [1, 5, 30].
Children: 1.65 mL/kg IV; repeat after 30 minutes if clinically indicated [30].

Succimer (DMSA)

General Information

Oral heavy metal chelator [31].

Indications

Symptomatic lead poisoning.
Asymptomatic lead poisoning with lead levels >60 µg/dL in adults or >45 µg/dL in children [5, 31].

Precautions

Reversible neutropenia, gastrointestinal upset, and liver function abnormalities [31].

Dose/Administration

10 mg/kg three times a day for 1 week → two times a day for 2 weeks [31].

Other Notes

Monitor serum lead levels during treatment [31].

Antidotes play a crucial role in managing toxicological emergencies in the emergency department. While their use is often specific and limited, they provide life-saving interventions in cases of confirmed poisonings such as opioid overdoses, cyanide poisoning, or organophosphate exposure. However, their administration requires careful assessment of indications, contraindications, and potential adverse effects. Emergency clinicians must prioritize stabilizing airway, breathing, and circulation before considering antidote administration, except in scenarios where antidotes are critical to immediate survival. The decision to use an antidote should be guided by clinical judgment, toxicology consultation, and evidence-based guidelines. Ultimately, antidotes should be viewed as adjunctive therapies, emphasizing the principle of treating the patient comprehensively rather than focusing solely on the poison.

Author

Sarah Alzaabi

Sarah Alzaabi, MD is a graduate from the United Arab Emirates University. She is currently a medical intern at Sheikh Shakhbout Medical City, Abu Dhabi, with a longstanding interest in Emergency Medicine. She is a big advocate for the FOAMed movement; and is proud to be a part of the fantastic team at iEM. She is excited to develop innovative ways to provide accessible education for anyone in need. Sarah has a particular interest in lifestyle and nutrition and spends time learning about how to educate others about succeeding in medicine while maintaining a healthy lifestyle.

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References

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Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Seizure (2024)

December 1, 2024December 1, 2024 ~ iEM Education Project Team ~ Leave a comment

by Ardi Knobel Mendoza, Danielle Charles-Chauvet, Erik J. Blutinger

Introduction

Seizures are caused by abnormal cortical neuronal activity that manifests as changes in alertness or neurological symptoms. While seizures account for only 1% of all emergency department (ED) visits and 3% of prehospital transports, their potential for significant morbidity undermines the importance of rapid assessment and treatment in emergency settings [1]. The etiology of seizures varies by age group, with the most common causes being fever in infants and metabolic derangements or structural abnormalities in adults over 75. This chapter will explore various seizure presentations, diagnostic assessment tools, and considerations for treatment and disposition decisions in the ED.

You have a new patient!

A 24-year-old female presents to the emergency room after being found on the street. She is minimally responsive, alert, and oriented only to herself. Her heart rate is 87 bpm, blood pressure is 141/94 mmHg, respiratory rate is 14 bpm, and she is afebrile, with oxygen saturation of 99% on room air. She has a gravid uterus with a fundal height of approximately 29 cm (11.4 inches) but is otherwise atraumatic.

What do you need to know?

Seizure Presentation and Classification

It is essential to investigate the cause and categorize the type of seizure after an acute episode to inform the diagnostic and treatment plan. Seizures are often classified as provoked, which occur within 7 days of a neurologic, metabolic, or infectious precipitator, or unprovoked, which has no association with an inciting factor. A history of seizures, febrile illness, malignancy, new medications, recreational drug use, or pregnancy can help to elucidate this. A complete neurological examination, which includes an assessment of mental status, should be performed as an altered postictal state follows most primary seizures. In addition to a change in mental status, the postictal state can present as motor deficits or paresis. Postictal paresis suggests a structural lesion as the cause of the seizure and should prompt cranial imaging [2]. Given that seizures are a manifestation of cortical neuronal activity, the extent of cortical involvement can lead to various symptoms at presentation [3].

Partial seizures involve only some of the cortex. They are classified as either simple, in which the patient is alert throughout, or complex, in which the patient has decreased alertness. Seizures can also begin as partial seizures, involving only some of the cortex, and spread to involve the entire cortex. Seizures involving the entire cortex are termed “generalized” seizures, resulting in decreased alertness. Generalized seizures are further classified based on their physical manifestations:

Absence Seizure: no collapse, automatisms (blinking, staring, lip smacking)

Tonic-clonic Seizure: collapse with stiff non-rhythmic convulsive movements.

Atonic Seizure: collapse without convulsions (similar to syncope) [4].

Febrile seizures typically occur in children 6 months-6 years of age with fevers greater than 38℃ and no neurological infection. 80% of febrile seizures are tonic-clonic in presentation, self-limiting, and do not recur after resolution of the inciting fever [5].

Eclamptic seizures are typically tonic-clonic in presentation and are considered unstable, as they carry significant mortality risk to the mother and fetus. Therefore, any pregnant patient with altered mental status and hypertension, identified as systolic >140 or diastolic >90, should be assessed for eclampsia. In cases with high suspicion of preeclampsia or eclamptic seizures, patients should be treated with magnesium for seizure prophylaxis [6].

Psychogenic seizures present similarly to generalized tonic-clonic seizures but are not associated with cortical neuronal derangements. In the ED, it is difficult to differentiate these seizures from neurogenic seizures, as there is limited access to EEG. However, psychogenic seizures present with more rhythmic and symmetric movements, patients are typically completely aware and conversant throughout, and there is no postictal state.

It is important to consider the duration of a seizure episode in all patients. Most seizures last from 30 seconds to 2 minutes. Seizures lasting longer than 5 minutes meet the criteria for status epilepticus. These patients are considered unstable, as prolonged seizure activity is associated with an increased risk of permanent brain damage. Not all patients with status epilepticus have convulsive seizures, so it is important to assess for subtle symptoms of seizure activity in the unresponsive patient, as they may have non-convulsive status epilepticus—a medical emergency.

Medical History

Thorough history taking in patients with seizure disorders is crucial for accurate diagnosis and effective management. This process involves a structured yet flexible approach to gathering relevant information, ensuring that all aspects of the patient’s condition are considered. Key components of this history include the patient’s medical background, seizure characteristics, and psychosocial factors.

Key Components of History Taking

Presenting Complaints: Document the chief complaints, including the nature, frequency, and duration of seizures [7].
Seizure Onset and Triggers: Investigate the age of onset, potential triggers (e.g., photosensitivity), and environmental factors that may provoke seizures [8].
Medical and Family History: Collect information on past medical history, family history of seizures or neurological disorders, and any relevant social history [7,9].
Psychosocial Aspects: Assess the impact of seizures on the patient’s daily life, including emotional and social challenges [8].

A comprehensive history-taking process in seizure patients is crucial for accurate diagnosis and effective management of various seizure types. By gathering essential information regarding seizure semiology, triggers, and patient-specific factors, clinicians can develop tailored treatment strategies to improve outcomes. Seizure semiology, for example, provides valuable insights into the nature of seizures, helping to classify them as either focal or generalized [10]. Detailed accounts of auras and observable signs can further indicate the anatomical origins of seizures, guiding appropriate diagnostic testing [10]. Additionally, identifying seizure triggers, such as environmental factors or specific stimuli, plays a vital role in both diagnosis and management. For instance, patients with photosensitivity may require targeted questions to uncover visual triggers that provoke seizures [8]. Together, these aspects of thorough history-taking form the foundation for effective and personalized seizure management.

When conducting history-taking in patients with seizure disorders, clinicians must be mindful of several common pitfalls that can lead to misdiagnosis or ineffective treatment. These issues often arise from inadequate questioning, overemphasizing certain symptoms, and neglecting the broader context of the patient’s experiences.

Inadequate history-taking, such as missing or incomplete accounts from witnesses, can result in misinterpreting seizure types [11]. Failing to gather detailed descriptions of seizure events, including pre-ictal and post-ictal states, may further obscure the diagnosis [12].

Additionally, an overemphasis on specific symptoms, such as those associated with focal seizures, may mislead clinicians, as these symptoms do not always correlate with the seizure type [13].

Another critical factor is the neglect of contextual elements, such as environmental triggers, which may result in missed diagnoses of reflex seizures, especially in photosensitive patients [8]. Furthermore, ignoring psychosocial aspects and the patient’s overall health can complicate the understanding of seizure disorders [14]. While advancements in technology and neuroimaging provide valuable objective data, the art of listening and thorough history-taking remains an irreplaceable cornerstone in the diagnostic process.

While a comprehensive history is essential, it is also important to recognize that some patients may present atypically, necessitating a tailored approach to history taking that considers individual circumstances and variations in symptom presentation.

Physical Examination

A comprehensive physical examination for patients presenting with seizures in the emergency department is essential for accurate diagnosis and effective management. Key components include a thorough neurological assessment, which involves evaluating consciousness, motor function, and sensory responses to identify any neurological deficits [15]. Monitoring vital signs is equally critical, as instability such as hypotension or tachycardia may indicate underlying issues requiring immediate attention [16]. Additionally, a systematic head-to-toe physical examination can help identify signs of trauma or systemic illness that may contribute to seizure activity [15].

In the emergency department, recognizing physical examination findings indicative of a severe or prolonged seizure episode is critical for timely diagnosis and management, particularly in cases of status epilepticus or non-convulsive seizures. Altered mental status, characterized by confusion, disorientation, or a prolonged postictal state, is a key finding that can suggest non-convulsive status epilepticus (NCSE) [17]. Neurological signs, such as subtle twitching, blinking, or fluctuating sensorium, may also indicate ongoing seizure activity [17]. In cases of generalized tonic-clonic seizures (GTCS), convulsive activity manifests with muscle rigidity and jerking movements, making it a more apparent diagnosis [18]. Additionally, focal seizures can result in specific neurological deficits, which may be misinterpreted as other neurological conditions. While these findings are crucial for identifying severe seizure episodes, it is important to acknowledge that some patients may present with atypical symptoms or lack overt signs of seizure activity, complicating the diagnostic process [17].

While the value of a comprehensive examination cannot be overstated, it is also important to recognize that some patients may present with atypical symptoms or underlying conditions that complicate the diagnosis. This highlights the need for a tailored approach to each case, ensuring that individual factors are carefully considered [16].

Alternative Diagnoses

The diagnosis of seizures primarily relies on the patient’s clinical history, with particular emphasis on accounts provided by witnesses. This is especially important because many seizure types involve impaired consciousness, leaving patients unaware of their episodes. Clinical findings can be supported by interictal electroencephalogram (EEG) abnormalities, although it is essential to note that such abnormalities may also occur in healthy individuals and their absence does not rule out epilepsy. It is equally critical to differentiate seizures from other conditions that may present similarly. These include syncope, such as cardiac arrhythmias or vasovagal episodes; metabolic disturbances like hypoglycemia or hyponatremia; and vascular events such as transient ischemic attacks. Additionally, migraine auras, sleep disorders like narcolepsy or night terrors, movement disorders such as paroxysmal dyskinesia, and gastrointestinal conditions like esophageal reflux in neonates and infants can mimic seizures. Psychiatric conditions, including conversion disorders, panic attacks, malingering, or episodes driven by secondary gain, must also be considered [19].

Acing Diagnostic Testing

When considering diagnostic testing such as labs and imaging, there is a lack of consensus on a set of tests required for all seizing patients. Rather, the diagnostic workup for a patient presenting with a seizure depends on a variety of factors, such as the suspected etiology of the seizure and whether the patient has a known seizure disorder or is presenting with a first-time seizure [20]. In patients with known seizure disorders, it is generally accepted test for levels of the anti-epileptic drug (AED) the patient takes, such as levetiracetam, phenytoin, carbamazepine, phenobarbital, or valproic acid. However, levels can often take hours to days to result or may not be available at a certain facility. In patients without a known seizure disorder, or if there is concern for an etiology for a seizure besides breakthrough from AED treatment, a more extensive workup is warranted. Basic testing should include a finger stick glucose, a urine or serum pregnancy test, and serum chemistry, including calcium and magnesium. Urine/serum toxicologies can also be obtained if there is concern for potential toxic ingestion as a cause. A lactic acid can be obtained, which should be markedly elevated immediately after the seizure and normalize after an hour of seizure onset [21].

A Computed Tomography (CT) Head should be obtained in all first-time seizure patients to assess for a structural lesion such as a mass, a bleed either as the etiology or sequelae of the seizure, or signs of an infection. Seizure sequelae such as significant head trauma can also be assessed with CT imaging to look for a large hematoma or skull fracture in patients who fail to return to baseline mental status after a seizure [22]. Magnetic Resonance Imaging (MRI) can be considered to reveal other diagnoses such as a brain abscess or central vascular event such as infarction; however, this imaging modality is often less available in the emergency setting and may require admission vs. outpatient referral to obtain an image [23]. Electroencephalography (EEG)is when diagnostic testing such as labs and imaging is considered, but there is a lack of consensus on a set of tests required for all seizing patients. Rather, the diagnostic workup for a patient presenting with a seizure depends on a variety of factors, such as the suspected etiology of the seizure and whether the patient has a known seizure disorder or is presenting with a first-time seizure [20]. In patients with known seizure disorders, it is generally accepted test for levels of the anti-epileptic drug (AED) the patient takes, such as levetiracetam, phenytoin, carbamazepine, phenobarbital, or valproic acid. However, levels can often take hours to days to result or may not be available at a certain facility. In patients without a known seizure disorder, or if there is concern for an etiology for a seizure besides breakthrough from AED treatment, a more extensive workup is warranted. Basic testing should include a finger stick glucose, a urine or serum pregnancy test, and a serum chemistry, including calcium and magnesium. Urine/serum toxicologies can also be obtained if there is concern for potential toxic ingestion as a cause. A lactic acid can be obtained, which should be markedly elevated immediately after the seizure and normalize after an hour of seizure onset [21].

Risk Stratification

The presence of comorbidities plays a critical role in the risk stratification, prognosis, and management of epilepsy, highlighting the need for a holistic approach to patient care. In the emergency department, recognizing these comorbidities is crucial for tailoring immediate interventions and ensuring acute and comprehensive follow-up care. Studies reveal that 60-70% of adults and 80% of children with epilepsy experience multimorbidity [25]. Among patients with senile epilepsy, 81% have at least one comorbidity, with neurological (61%) and cardiovascular (45%) conditions being the most prevalent [26]. Emergency clinicians must remain vigilant for these conditions, as they may exacerbate seizure episodes or complicate acute management. These comorbidities significantly impact seizure outcomes, as patients with neurological and psychiatric disorders face a higher risk of recurrent seizures and reduced likelihood of achieving seizure freedom [26]. Conditions like depression and anxiety are particularly associated with a more severe course of epilepsy [27], and their identification in the emergency setting can guide referrals for further psychiatric evaluation. Additionally, multimorbidity is linked to lower health-related quality of life and increased healthcare costs due to frequent hospitalizations [25]. Cognitive and psychiatric comorbidities often impair daily functioning more than the seizures themselves [28], necessitating a multidisciplinary approach starting from the emergency department. Addressing these comorbidities, however, has been shown to improve overall health outcomes and enhance the quality of life for patients, emphasizing the importance of comprehensive, patient-centered care [28].

Management

The most important intervention in a patient actively seizing is ensuring adequate brain oxygenation. The airway should be protected via maneuvers that include rolling the patient on their side, jaw thrusts, applying a nasopharyngeal airway, applying supplemental oxygen, and preventing aspiration with suction as needed. Oxygenation status should be monitored with continuous pulse oximetry and capnography when possible.

Providers should also anticipate the impending decompensation of the clinical course and the need for intubation by preparing airway equipment, medications, and IV access, which will be discussed later in the chapter. Along with oxygenation, patients must be protected from injury, e.g., from falling out of bed and preventing trauma.

Most seizures stop on their own within one to two minutes of onset, but the longer the seizure lasts, the less likely it is to stop on its own and can become self-sustaining.

Seizures that are continuous or intermittent, lasting more than 5 minutes without recovery of consciousness, are known as status epilepticus. Medical therapies to terminate a seizure are divided into three stages based on escalation of need and inability to terminate the seizure.

Benzodiazepines are considered first-line agents in terminating seizures, followed by second-line agents such as Levetiracetam, Valproate, Phenytoin, and Fosphenytoin [29]. The third-line medications are infusions of benzodiazepines, propofol, or barbiturates, prepared for likely intubation with paralytics and continued infusions [30].

The following lists these medications by stage, dose, and considerations [31, 32]:

Midazolam (1st Line Agent – Benzodiazepine)

Loading Dose:
- 10 mg IM or 0.1-0.2 mg/kg IV.
Maintenance Dose: 0.001 mg/kg/min.
Pediatric Dose:
- IV or IN: 0.2 mg/kg (max 5 mg).
- IM:
  - <13 kg: 0.2 mg/kg.
  - 13-39 kg: 5 mg.
  - 39 kg: 10 mg.
Considerations:
- IM dosing can be used if no IV is established.
- Acts faster than Lorazepam but has a shorter duration.
- May cause respiratory depression and hypotension.

Diazepam (1st Line Agent – Benzodiazepine)

Loading Dose: 10 mg over 2 minutes. Repeat every 5-10 minutes to a max of 30 mg.
Maintenance Dose: N/A.
Pediatric Dose: 0.15 mg/kg IV.
Considerations:
- May cause respiratory depression and hypotension.

Levetiracetam (2nd Line Agent)

Loading Dose: 60 mg/kg (up to a max of 4,500 mg), infused over 10 minutes.
Maintenance Dose: Same as the loading dose.
Pediatric Dose: Same as loading dose.
Considerations:
- If the patient weighs >75 kg, the dose is 4.5 g.
- If seizures stop, continue to give Levetiracetam to prevent recurrence.

Phenytoin (2nd Line Agent)

Loading Dose: 18-20 mg/kg with a max rate of 50 mg/min.
Maintenance Dose: N/A.
Pediatric Dose: N/A.
Considerations:
- Cardiac monitoring is necessary for QRS complex widening.

Fosphenytoin (2nd Line Agent)

Loading Dose: 15-20 mg/kg with a max rate of 150 mg/min.
Maintenance Dose: Same as loading dose.
Pediatric Dose: N/A.
Considerations:
- Cardiac monitoring is necessary for QRS complex widening.

Valproate (2nd Line Agent)

Loading Dose: 20-40 mg/kg over 10 minutes. Repeat if needed.
Maintenance Dose: Same as loading dose.
Pediatric Dose: Same as loading dose.
Considerations: N/A.

Propofol (3rd Line Agent)

Loading Dose: 1-2 mg/kg IV over 5 minutes (max load 10 mg/kg).
Maintenance Dose: 50-80 mcg/kg/min (3-5 mg/kg/hr) as an infusion.
Pediatric Dose: N/A.
Considerations:
- May cause respiratory depression and hypotension.

Phenobarbital (3rd Line Agent)

Loading Dose: 10-15 mg/kg bolus up to 60 mg/min.
Maintenance Dose: 120-240 mg every 20 minutes.
Pediatric Dose: N/A.
Considerations: N/A.

Midazolam (for 3rd Line use) (3rd Line Agent)

Loading Dose: 0.2 mg/kg IV.
Maintenance Dose: 0.1-2 mg/kg/hr.
Pediatric Dose: N/A.
Considerations:
- Can be used in patients with hypotension.

Once the provider considers 3rd line medications and starting infusions, they should prepare for intubation as the patient is likely in status epilepticus, requiring continued medication and airway protection. Induction medications for intubation are often the same medications listed above in the 3rd stage of treatment, such as propofol or midazolam, and can be on board before paralytics. Paralytics are used to stop the seizure-like activity and aid in intubation, but it is important to remember that they are not meant to terminate the seizure. Patients can still have seizures despite the lack of tonic-clonic seizure activity such as NCSE. Rocuronium is the preferred paralytic agent as it is not associated with the hyperkalemia seen in succinylcholine, which is a risk for patients seizing for an extended period who could develop rhabdomyolysis. Rocuronium paralysis lasts much longer, which should be a consideration when monitoring for further seizures with EEG.

Finally, other conditions can cause seizures or seizure-like activity that require their own treatment strategies, which are discussed below:

Eclampsia, a life-threatening condition often associated with pregnancy, is treated with magnesium to control seizures, benzodiazepines for acute management, and blood pressure control to address underlying hypertension. For seizures due to isoniazid toxicity, the recommended treatment is pyridoxine (vitamin B6), which counteracts the drug’s neurotoxic effects. In cases of hypoglycemia, seizures can be managed by administering Dextrose 50% in Water (D50W) to restore blood glucose levels rapidly. Hypocalcemia, another potential seizure trigger, requires the administration of calcium gluconate or calcium chloride to normalize calcium levels. For seizures induced by hyponatremia, 3% hypertonic saline is used to increase serum sodium levels safely.

In cases of toxicity from aspirin, tricyclic antidepressants (TCAs), or lithium, hemodialysis is indicated to effectively remove the offending agents from the bloodstream. For seizures caused by meningitis, prompt initiation of appropriate antibiotics is critical to address the underlying infection and prevent further complications.

Special Patient Groups

Pediatrics

Seizures in pediatric patients can present with diverse etiologies ranging from febrile seizures to more serious underlying conditions such as intracranial infections, metabolic disturbances, or congenital disorders. In children under 5, febrile seizures are the most common cause of convulsions and are generally self-limited, though they require careful differentiation from more serious causes like meningitis or encephalitis. Clinical reasoning should prioritize a detailed history, including the onset of the seizure, vaccination status, and any family history of epilepsy or neurodevelopmental disorders. Laboratory tests and imaging may be indicated if there is a high suspicion of an underlying structural or metabolic issue, such as in children with a prolonged postictal state or a first-time seizure without a clear precipitant. In the emergency department (ED), rapid assessment of the child’s airway, breathing, and circulation (ABCs) is paramount, along with ensuring the seizure is appropriately controlled, often with medications like lorazepam or diazepam. Close follow-up is necessary to assess for recurrent seizures or potential neurological sequelae.

Geriatrics

Seizures in elderly patients often present a diagnostic challenge due to the overlap with other common age-related conditions, such as syncope, transient ischemic attacks (TIA), or dementia-related behavioral changes. In this population, new-onset seizures should prompt an urgent evaluation for reversible causes, including cerebrovascular events, metabolic disturbances (such as hyponatremia or hypoglycemia), brain tumors, or infections like meningitis or encephalitis. Seizures in older adults may also be a manifestation of progressive neurodegenerative diseases, including Alzheimer’s or Parkinson’s disease. Emergency management in the ED should focus on stabilizing the patient while considering potential drug interactions, as elderly patients are more likely to be on multiple medications that may lower the seizure threshold (e.g., antipsychotics, antidepressants, or antihypertensives). Antiepileptic drug (AED) therapy initiation, while necessary in recurrent or long-duration seizures, must be approached cautiously due to age-related pharmacokinetic changes and the increased risk of side effects. A thorough evaluation for underlying causes, including neuroimaging and laboratory tests, is critical.

Pregnant Patients

Seizures during pregnancy present unique challenges in both diagnosis and treatment. The differential diagnosis includes pregnancy-specific conditions like eclampsia, in addition to the possibility of preexisting epilepsy or new-onset seizures due to metabolic derangements or intracranial pathology. In a pregnant patient with a seizure, the clinical priority is to ensure both maternal and fetal well-being. Eclampsia, a severe complication of preeclampsia, must be ruled out, as it presents with generalized tonic-clonic seizures and may lead to maternal and fetal morbidity if not promptly treated. Once eclampsia is excluded, consideration should be given to other causes such as hypoglycemia, cerebrovascular accidents, or drug toxicity (e.g., withdrawal from anticonvulsant medications). Emergency management in the ED should prioritize seizure control, typically with benzodiazepines, while avoiding teratogenic medications. Magnesium sulfate is the treatment of choice for eclampsia. Fetal monitoring should be initiated, and careful planning for delivery may be required depending on the severity of the condition and gestational age. The clinical approach should balance the need for immediate seizure control while minimizing risks to both the mother and fetus.

When To Admit This Patient

Few definitive practice guidelines are available to emergency physicians making disposition decisions for seizure episodes. However, all critically ill patients must be admitted to the inpatient setting since overall risk assessment is important for deciding whether to safely discharge patients home. For alternative clinical presentations, the physician should reliably assess whether the patient’s overall presentation warrants further medical interventions in a clinical setting.

For emergency physicians, seizure recurrence, morbidity, and mortality are useful measures to consider for safe discharge. Studies suggest that seizure recurrence most often depends upon EEG findings and the underlying cause—normal EEG and undetectable cause are associated with lower recurrence rates [33]. With positive neuroimaging findings (e.g., structural findings), initiating AED therapy for first-time seizures is recommended given a high 1-year recurrence risk of up to 65% [34].

Any patients with abnormal neurologic signs or symptoms who have not fully recovered from their seizure should not be discharged. Other important clinical benchmarks are the presence of normal vital signs, CT head imaging, EKG, basic lab results (especially renal function and blood counts), and follow-up. As part of the physician’s risk assessment of the patient’s overall condition, social factors must also be taken into account: lack of follow-up care, history of being lost to follow-up, and insufficient assistance available at home should all weigh towards admitting the patient for further monitoring (and possible seizure workup).

Generally, stable patients are those who return to their baseline mental status, do not exhibit any new neurological deficits, have no significant lab result abnormalities, and remain at low risk for recurrent seizure activity in the short term. Coordinating reliable follow-up is important, and all patients should be educated about the “red flag” signs and symptoms that warrant urgent evaluation and treatment.

Revisiting Your Patient

Altered mental status in the gravid, hypertensive patient is concerning for eclampsia. This patient should be started on 2mg of Mg as seizure prophylaxis. Obstetrics should be consulted as urgent delivery via cesarean section is the definitive treatment for this patient’s seizures. After delivery, the patient should be monitored closely for postpartum eclamptic seizures, which can occur up to 6 weeks postpartum.

Authors

Ardi Knobel Mendoza

Ardi Mendoza, MD is a resident at the Mount Sinai Hospital Emergency Medicine Program. He is interested in Health System and Emergency System Strengthening and local partner/local government-led collaborations. He has prior experiences in the field of Global Surgery while at Rutgers Robert Wood Johnson Medical School, assessing financial risk protection from impoverishing and catastrophic expenditure due to surgical care in the Colombian Healthcare System. He lived in Lima, Peru for a year working with Peruvian researchers at the University Cayetano Heredia as a research coordinator helping to develop a point-of-care diagnostic screening tool for Autism using eye-tracking technology.

Danielle Charles-Chauvet

Danielle Charles-Chauvet, MD is an Emergency Medicine resident at the Mount Sinai Hospital in New York. She is deeply invested in medical education and health disparities and, in affiliation with Harlem Children's Zone, has led several community-based educational initiatives to address these disparities. She designed and taught a course entitled Health and Structures of Oppression at Brown University's medical school. Her dedication to education earned her the 2022 National Outstanding Medical Student Award from the Academic College of Emergency Physicians and the 2021 Medical Education Award from the Society of Academic Emergency Medicine. She is currently working to expand her impact internationally by building Haiti's medical education infrastructure.

Erik J. Blutinger

Erik J. Blutinger, MD, MSc, FACEP is a full-time emergency physician at Mount Sinai Queens Hospital in New York City and Medical Director to the Community Paramedicine program at Mount Sinai Health Partners. He completed his residency training at the University of Pennsylvania, Master's at the London School of Hygiene & Tropical Medicine, and has worked on a variety of health initiatives in quality and patient experience with formal leadership training in Quality Improvement (QI). Erik has worked in multiple national healthcare systems and underserved communities, including townships in South Africa and Guatemala, Bhutan, India, and Austria.

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References

Jagoda, (2010). Seizures: An issue of Emergency Medicine Clinics. Elsevier Saunders.
Werhahn, J. (2010). Weakness and focal sensory deficits in the postictal state. Epilepsy & Behavior, 19(2), 138–139. https://doi.org/10.1016/j.yebeh.2010.06.029
Kim, , Cho, J.-W., Lee, J., Joo, E. Y., Hong, S. C., Hong, S. B., & Seo, D.-W. (2011). Seizure duration determined by subdural electrode recordings in adult patients with intractable focal epilepsy. Journal of Epilepsy Research, 1(2), 57–64. https://doi.org/10.14581/jer.11011
Kumar, , Sharma Maini, K., & Arya, K. (n.d.). Simple partial seizure. National Center for Biotechnology Information. Retrieved April 10, 2023, from https://pubmed.ncbi.nlm.nih.gov/29763181/
Heon, (n.d.). Febrile seizures. Core EM. Retrieved April 10, 2023, from https://coreem.net/core/febrile-seizures/
Wagner, K. (2004, December 15). Diagnosis and management of preeclampsia. American Family Physician. Retrieved April 10, 2023, from https://www.aafp.org/pubs/afp/issues/2004/1215/p2317.html
Hiroshi, S., Hallett, M., ‘History taking’, The Neurologic Examination: Scientific Basis for Clinical Diagnosis, 2 edn (2022; online edn, Oxford Academic, 1 Aug. 2022), https://doi.org/10.1093/med/9780197556306.003.0002, accessed 1 Dec. 2024.
Brinciotti, M., Bouilleret, V, Masnou, P. (2021). Optimizing the Patient’s History: A Modern Approach. 10.1007/978-3-319-05080-5_26.
Dulak SB. A practical guide to a thorough history. RN. 2004;Suppl:14-21.
Wolf P, Benbadis S, Dimova PS, et al. The importance of semiological information based on epileptic seizure history. Epileptic Disord. 2020;22(1):15-31. doi:10.1684/epd.2020.1137
Smith PE. If it’s not epilepsy… J Neurol Neurosurg Psychiatry. 2001;70 Suppl 2(Suppl 2):II9-II14. doi:10.1136/jnnp.70.suppl_2.ii9
Trevathan E. Patient page. The diagnosis of epilepsy and the art of listening. Neurology. 2003;61(12):E13-E14. doi:10.1212/wnl.61.12.e13
Henry JC. Comment: Be careful what you ask when interviewing patients with epilepsy. Neurology. 2015;85(7):594. doi:10.1212/WNL.0000000000001843
Kanner, A. (2008). Common Errors Made in the Diagnosis and Treatment of Epilepsy. Seminars in neurology. 28. 364-78. 10.1055/s-2008-1079341.
Wan, XH & Zeng, R. (2020). Handbook of Clinical Diagnostics. 10.1007/978-981-13-7677-1.
Bank, A & Bazil, C. (2019). Emergency Management of Epilepsy and Seizures. Seminars in Neurology. 39. 073-081. 10.1055/s-0038-1677008.
Hasan, Ahmed. (2016). Non-Convulsive Status Epilepticus in Emergency Department: A Diagnostic Challenge. Journal of Medical Science And clinical Research. 10.18535/jmscr/v4i8.103.
Virani, D., Sangani, S., Patel, C, Patel, V., Saha, J., Kalsariya, R. (2024). 5. Study of Clinical Profile, Management and Outcome of Patients Presented with Seizures in Emergency Medicine Department. BJ Kines: National Journal of Basic & Applied Sciences, doi: 10.56018/bjkines2024065
Ko DY. Epilepsy and Seizures Differential Diagnoses (updated Jul 26, 2002). From https://emedicine.medscape.com/article/1184846-differential?&icd=login_success_email_match_fpf Accessed: Nov 1,
Burgess M, Mitchell R, Mitra B. Diagnostic testing in nontrauma patients presenting to the emergency department with recurrent seizures: A systematic review. Acad Emerg Med. 2022 May;29(5):649-657. doi: 10.1111/acem.14391. Epub 2021 Oct 1. PMID: 34534387.
Teran F, Harper-Kirksey K, Jagoda A. Clinical decision making in seizures and status epilepticus. Emerg Med Pract. 2015 Jan;17(1):1-24.
Harden CL, Huff JS, Schwartz TH, Dubinsky RM, Zimmerman RD, Weinstein S, Foltin JC, Theodore WH; Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Reassessment: neuroimaging in the emergency patient presenting with seizure (an evidence-based review): report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2007 Oct 30;69(18):1772-80. doi: 10.1212/01.wnl.0000285083.25882.0e. PMID: 17967993.
Gelisse P, Crespel A, Genton P, Jallon P, Kaplan PW. Lateralized Periodic Discharges: Which patterns are interictal, ictal, or peri-ictal? Clin Neurophysiol. 2021 Jul;132(7):1593-1603. doi: 10.1016/j.clinph.2021.04.003. Epub 2021 Apr 27. PMID: 34034086.
Rosenthal Seizures, Status Epilepticus, and Continuous EEG in the Intensive Care Unit. Continuum (Minneap Minn). 2021 Oct 1;27(5):1321-1343. doi: 10.1212/CON.0000000000001012. PMID: 34618762.
Gaitatzis A, Majeed A. Multimorbidity in people with epilepsy. Seizure. 2023;107:136-145. doi:10.1016/j.seizure.2023.03.021
Cao, Z., Li, Y., Liu, S. et al.Clinical characteristics and impact of comorbidities on the prognosis of senile epilepsy in Southwest China: a retrospective cohort study. Acta Epileptologica 6, 11 (2024). https://doi.org/10.1186/s42494-024-00153-8
Kanner, A.M., Ribot, R. and Mazarati, A. (2018), Bidirectional relations among common psychiatric and neurologic comorbidities and epilepsy: Do they have an impact on the course of the seizure disorder?. Epilepsia Open, 3: 210-219. https://doi.org/10.1002/epi4.12278
Mula M, Coleman H, Wilson SJ. Neuropsychiatric and Cognitive Comorbidities in Epilepsy. Continuum (Minneap Minn). 2022;28(2):457-482. doi:10.1212/CON.0000000000001123
Silbergleit R, Durkalski V, Lowenstein D, Conwit R, Pancioli A, Palesch Y, Barsan W; NETT Intramuscular versus intravenous therapy for prehospital status epilepticus. N Engl J Med. 2012 Feb 16;366(7):591-600. doi: 10.1056/NEJMoa1107494. PMID: 22335736; PMCID: PMC3307101.
Falco-Walter JJ, Bleck Treatment of Established Status Epilepticus. J Clin Med. 2016 Apr 25;5(5):49. doi: 10.3390/jcm5050049. PMID: 27120626; PMCID: PMC4882478.
Brophy GM, et : Guidelines for the evaluation and management of status epilepticus. Neurocrit Care 17:3-23, 2012.
Seizure: Emergency Medicine, Second Editor; Adams, James G., MD, 2013, 2008 by Saunders, an imprint of Elsevier Inc. Book Chapter 99
Berg AT, Shinnar The risk of seizure recurrence following a first unprovoked seizure: a quantitative review. Neurology 1991;41:965–72.
Jagoda A; Gupta, K. “The Emergency Department Evaluation of the Adult Patient Who Presents with a First-Time ” Emergency Medicine Clinics of North America, U.S. National Library of Medicine, https://pubmed.ncbi.nlm.nih.gov/21109101/.

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Peripheral Intravenous Line Access and Blood Sampling (2024)

November 30, 2024December 1, 2024 ~ iEM Education Project Team ~ Leave a comment

by Omar F. Al- Nahhas, Mansoor M. Husain

Introduction

Peripheral IV Cannulation is a critical skill for healthcare providers in the Emergency Department, clinics, and the field. Knowing that it is one of the most essential procedures in the United States, where it is estimated that more than 25 million patients have peripheral intravenous (IV) catheters placed each year for vascular access for the administration of medications and fluids and the sampling of blood for analysis [1], makes it essential to master the technique, understand the subtleties of anatomy, and perform the procedure frequently to maintain this skill.

IV access plays a critical role in the emergency department as it permits the administration of medicines and fluids directly into the patient’s bloodstream, allowing prompt treatment of severe conditions such as dehydration, shock, and severe infections. The speed of treatment delivery is crucial in emergency scenarios, and peripheral IV access provides an efficient and effective way to deliver life-saving therapies. Additionally, it enables the frequent and easy sampling of blood, which is crucial for diagnosing and monitoring the patient’s condition. Therefore, healthcare providers in the emergency department must develop quick and reliable peripheral IV access skills to guarantee the best possible patient outcomes.

Indications

Administration of fluids: Patients who are dehydrated or unable to tolerate oral fluids may require IV fluids to maintain hydration and electrolyte balance [2].
Medication administration: Certain medications, such as antibiotics, chemotherapy drugs, and pain relievers, may need to be administered intravenously to achieve the desired effect.
Blood transfusions: Patients who have lost a significant amount of blood due to trauma or surgery may require a blood transfusion via an IV cannula.
Monitoring: IV access may be necessary for frequent blood draws or to monitor certain parameters, such as blood glucose levels.
Contrast material administration: Some imaging studies, such as CT scans, require the administration of contrast material via IV cannulas to help visualize certain structures.

Contraindications

There are no absolute contraindications. Relative contraindications include

Coagulopathy
The presence of local infection
Burns, or compromised skin at the intended site of insertion
Previous lymphatic nodal clearance, arteriovenous fistula formation, or deep venous thrombosis on the affected limb.

In such cases, clinical judgment must be used to balance the benefits and risks of proceeding with line placement at that site [2].

Equipment and Patient Preparation

Equipment

Gloves
Skin disinfectant (Povidine and Alcohol Swabs),
16-18 gauge IV catheter (smaller catheters are better used in the pediatric population)
Tape
Syringe
3-way stopcock
Tourniquet

Optional

Topical anesthetic, e.g., EMLA ( 2.5% lidocaine and prilocaine),
Transilluminator light
Ultrasound with a vascular probe.

Patient Preperation

To perform the procedure, obtaining consent from the patient after discussing the procedure and its associated risks and benefits is important. The preferred site for cannulation is the Cephalic vein in the forearm, followed by the Medial Brachial Vein in the Antecubital Sulcus. The dorsum of the hand is also a common site, but this can be more painful for the patient, and often, smaller gauge cannulas are used. Always use universal precautions, such as wearing gloves, during the procedure. The selected vein should be visualized and palpated, as it will have a slight “give” compared to surrounding tissue.

The overlying skin should be disinfected, and a topical anesthetic may be applied as desired. While transillumination or ultrasound may provide additional guidance, care should be taken to avoid contamination of the clean, prepped site to be accessed.

Procedure Steps

The procedure for peripheral IV cannulation involves several steps [3]:

Apply a tourniquet or blood pressure cuff inflated above the diastolic reading proximal to the intravenous site.
Prepare the site with an antiseptic solution.
Insert the IV catheter using a no-touch technique distal to and along the line of the vein at a 10 to 15-degree angle to the skin.
Slowly advance the needle and catheter into the vein, waiting for a flash of blood to enter the catheter, which may not always occur.
Slowly advance the needle an additional 1 to 2 millimeters and slide the cannula into the vein while securing the needle in place.
Remove the needle while pressing on the overlying skin over the cannula proximal to the insertion site to stem the blood flow.
Attach a 3-way stopcock and flush the stopcock and cannula with 5 ml of saline to prevent clotting. Assess the fluid flow through the catheter and watch for skin bulge, which may suggest fluid extravasation.
Secure the catheter with tape or dressing and release the tourniquet or blood pressure cuff.
Attach intravenous tubing to the 3-way stopcock, attach it to the fluid of choice, and initiate flow. Watch again for fluid extravasation. Medications may be administered through another port of the stopcock or added to the IV solution as desired.
Ensure that the tourniquet is removed before administering drug or fluid infusion.
If fluid extravasation occurs, remove the catheter and repeat the procedure at a more proximal site, avoiding distal attempts.
These steps should be performed carefully and with appropriate attention to detail to ensure successful IV cannulation.

Blood Sampling

Blood sampling is a fundamental procedure in clinical practice for diagnostic and monitoring purposes. Various tubes are available for collecting blood samples, each designed for specific laboratory tests. For instance, the Vacutainer system offers a range of tubes with different additives to facilitate accurate test results. The choice of the tube depends on the required analyses, such as complete blood count (CBC), basic chemistry panels, coagulation studies, blood cultures, or specialized tests. Adhering to the appropriate tube selection based on the intended tests is crucial for obtaining reliable laboratory results. The amount of blood required for each tube varies depending on the specific test being conducted.

Generally, a CBC requires 2-4 mL of blood to obtain sufficient quantities of plasma or serum for cell counting and differential analysis [4]. Basic chemistry panels often necessitate larger volumes, ranging from 5-10 mL, to provide enough serum or plasma for multiple analytes, such as electrolytes, liver function tests, and renal function tests [4].On the other hand, blood culture bottles usually require 10 mL of blood to optimize the sensitivity of microbial detection [5]. Understanding the recommended blood volumes for each tube is crucial for ensuring adequate sample collection and accurate test results.

In summary, proper tube selection is essential for blood sampling to ensure accurate laboratory results. Various tubes with specific additives are available and tailored for different tests. The amount of blood needed for each tube varies depending on the type of analysis being conducted. Familiarity with the recommended blood volumes for each tube is crucial to obtaining sufficient sample quantities and optimizing diagnostic accuracy.

Complications

Despite the widespread use, IV cannulation is not without complications.

Phlebitis: This refers to vein inflammation, which can cause redness, warmth, and pain at the catheter site. The incidence of phlebitis ranges from 2% to 50% in adult patients and is related to various factors, including catheter gauge, insertion site, and duration of catheterization. [6]

Catheter-related bloodstream infections (CRBSIs): These are serious infections that can result from the colonization of the catheter by microorganisms. The incidence of CRBSIs is estimated to be 1-10% and is associated with prolonged catheterization, immunocompromised patients, and inadequate catheter site care.[7]

Infiltration and extravasation: Infiltration occurs when the fluid administered leaks into the surrounding tissue, while extravasation occurs when the medication or solution irritates the surrounding tissue, leading to tissue damage. The incidence of infiltration ranges from 4% to 38%, while extravasation occurs in less than 6% of patients. [8]

Hematoma: This is a collection of blood at the site of the catheter, which can occur due to trauma during catheter insertion or catheter displacement. Hematoma is reported in 0.5-8% of cases. [9]

Nerve injury: Nerve injury can occur due to direct trauma during catheter insertion, leading to motor and sensory deficits. The incidence of nerve injury is low, reported in less than 1% of cases. [10]

In conclusion, peripheral IV catheterization is a commonly performed procedure but not without complications. Careful attention to technique and site care can help minimize the risks of complications.

Hints and Pitfalls

To successfully perform peripheral IV cannulation, it’s important to use the correct technique and select an appropriate site with a visible vein.

Start by applying heat and a tourniquet to enhance blood flow, making the vein more prominent.
Once you have identified the vein, stabilize it and insert the cannula at an angle of 10 to 30 degrees, advancing it slowly while monitoring for proper placement.
Finally, secure the cannula using a transparent dressing or tape, ensuring it is not too tight.

Proper care and maintenance of peripheral intravenous (IV) lines are crucial to prevent complications and ensure patient safety. According to evidence-based guidelines, dressing care plays a vital role in IV line maintenance. Transparent semipermeable dressings are recommended by the Infusion Nurses Society (INS) as they provide a barrier against contamination and allow easy visualization of the insertion site [11]. Regular inspection of the dressing is important to identify any issues such as loosening, soiling, or moisture accumulation, and compromised dressings should be promptly replaced using sterile technique to reduce the risk of infection.

Flushing and locking peripheral IV lines are essential for maintaining patency. The INS recommends flushing with 0.9% sodium chloride (normal saline) solution before and after medication administration and at least every 8-12 hours for continuous infusions [11]. This practice helps prevent blood clot formation and ensures proper line functioning. When intermittent infusion is not expected for an extended period, the INS suggests using a saline or heparin lock to maintain line patency [11].

Vigilant monitoring and assessment of the peripheral IV site are critical to detect any signs of infection or complications. According to the Centers for Disease Control and Prevention (CDC), routine site inspection should be performed at least daily, paying close attention to redness, swelling, warmth, tenderness, or drainage [12]. Timely reporting and appropriate intervention in case of any abnormalities are crucial to prevent complications like phlebitis or infiltration.

Patient education is an essential aspect of peripheral IV line care. Educating patients and their caregivers about proper hand hygiene, signs of infection or complications, and when to seek medical assistance is vital. Patients should receive clear instructions to promptly report any pain, tenderness, or changes at the IV site.

It is important to note that specific institutional protocols may vary, and adherence to local guidelines is essential. These recommendations are based on current evidence and best practices in peripheral IV line care, aiming to promote patient safety and achieve optimal outcomes.

There are some pitfalls to avoid. Failure to use proper technique or choosing an inappropriate site can increase the risk of infection and complications such as infiltration, extravasation, or phlebitis. Applying too much heat or pressure with the tourniquet can cause burns or damage to the veins. Failure to stabilize the vein or inserting the cannula at the wrong angle can make cannulation more difficult or cause complications. Advancing the cannula too quickly or over-tightening the dressing can cause pain or discomfort, restrict blood flow, or damage the vein.

In time-critical cases with known difficult peripheral access or where multiple attempts at peripheral line placement have already failed, an ultrasound-guided technique may be necessary, or the clinician may consider using alternative routes of drug administration (such as oral, intramuscular, intraosseous, or central venous access).

Special Patient Groups

Certain populations, including pediatric, geriatric, and pregnant patients, require special considerations during peripheral IV catheterization.

Pediatrics

Pediatric patients have unique anatomical and physiological differences that affect the success of IV catheterization. The smaller size of their veins and thinner skin can make it challenging to locate and access suitable sites for catheter insertion [13].

Additionally, children have a higher risk of experiencing pain, discomfort, and anxiety during the procedure, which can lead to complications such as vasovagal syncope and catheter dislodgement. Therefore, healthcare providers need to use appropriate-sized catheters and consider non-pharmacological interventions, such as distraction techniques and topical anesthetics, to minimize the pain and discomfort associated with the procedure [13].

Geriatrics

Geriatric patients also require special consideration during peripheral IV catheterization. As individuals age, their veins become less elastic and more fragile, making it challenging to cannulate veins and increasing the risk of complications such as hematoma, infiltration, and extravasation. Furthermore, geriatric patients often have multiple comorbidities and take multiple medications, which can increase the risk of adverse reactions and interactions with IV medications. Therefore, healthcare providers must assess the patient’s venous status and consider alternative routes of medication administration when appropriate [14].

Pregnant Patients

Pregnant patients pose unique challenges during peripheral IV catheterization due to the physiological changes that occur during pregnancy. Increased blood volume, decreased venous compliance, and increased peripheral resistance make locating and accessing suitable veins for catheter insertion difficult. Additionally, certain medications and fluids can affect the mother and fetus, requiring careful consideration of the medication’s safety and potential risks. Therefore, healthcare providers can use ultrasound guidance and consider the patient’s gestational age, medical history, and current medications when selecting the site and medication for IV catheterization [15].

In summary, peripheral IV catheterization requires special considerations in pediatric, geriatric, and pregnant patients. Healthcare providers should assess the patient’s anatomical and physiological status and select appropriate-sized catheters. They should also consider non-pharmacological interventions to reduce pain and discomfort and carefully select the site and medication for IV catheterization to minimize the risk of complications.

Authors

Omar F. Al- Nahhas

Dr. Omar Al-Nahhas is a Senior Emergency Medicine Resident at STMC, Al-Ain, UAE, and an MSc Candidate in Medical Education at the University of Warwick. He is an Adjunct Clinical and Simulation Tutor at Ajman University and a certified BLS and ACLS Instructor. With publications in emergency medicine, his interests include Trauma, Sports Medicine, Critical care and Advanced Emergency Medicine, emphasizing education, research, and resuscitation practices.

Mansoor M. Husain

Consultant Emergency Medicine, Tawam Hospital – Alain

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References

Chopra V, Anand S, Hickner A, Buist M, Rogers MA, Saint S, Flanders SA. “Risk of venous thromboembolism associated with peripherally inserted central catheters: a systematic review and meta-analysis.” Lancet. 2013 Jul 27;382(9889):311-25. doi: 10.1016/S0140-6736(13)60592-9. Epub 2013 May 30. PMID: 23726390.
Beecham GB, Tackling G. Peripheral Line Placement. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK539795/
Keith A. “Intravenous (IV) Line Access” (n.d.). International Emergency Medicine Education Project, Available athttps://iem-student.org/intravenous-iv-line-access/.
Clinical and Laboratory Standards Institute (CLSI). (2017). Procedures for the Collection of Diagnostic Blood Specimens by Venipuncture; Approved Standard—Eighth Edition. CLSI Document GP41-A8. CLSI.
Clinical and Laboratory Standards Institute (CLSI). (2020). Principles and Procedures for Blood Cultures; Approved Guideline—Third Edition. CLSI Document M47-A3. CLSI.
Helm RE, Klausner JD, Klemperer JD, et al. Accepted but unacceptable: peripheral IV catheter failure. J Infus Nurs. 2015;38(3):189-203.
Blot SI, Depuydt P, Annemans L, et al. Clinical and economic outcomes in critically ill patients with nosocomial catheter-related bloodstream infections. Clin Infect Dis. 2005;41(11):1591-1598.
Dougherty L, Lister S. Infusion Nursing: An Evidence-Based Approach. Elsevier Health Sciences; 2014.
Feleke Y, Mekonnen N, Assefa A. Magnitude and associated factors of intravenous catheter-related hematoma in the adult emergency department of Tikur Anbessa Specialized Hospital, Addis Ababa, Ethiopia. BMC Emerg Med. 2018;18(1):10.
Wallis MC, McGrail M, Webster J, et al. Risk factors for peripheral intravenous catheter failure: a multivariate analysis of data from a randomized controlled trial. Infect Control Hosp Epidemiol. 2014;35(1):63-68.
Infusion Nurses Society. (2021). Infusion therapy standards of practice. Journal of Infusion Nursing, 44(1S), S1-S224.
Centers for Disease Control and Prevention. (2021). Guidelines for the Prevention of Intravascular Catheter-Related Infections. Retrieved from https://www.cdc.gov/infectioncontrol/guidelines/bsi/index.html
Naik VM, Mantha SSP, Rayani BK. Vascular access in children. Indian J Anaesth. 2019 Sep;63(9):737-745. doi: 10.4103/ija.IJA_489_19. PMID: 31571687; PMCID: PMC6761776.
Gabriel, J. (2017). Understanding the challenges to vascular access in an ageing population. British Journal of Nursing, 26(14), S15–S23. doi:10.12968/bjon.2017.26.14.s
Tan PC, Mackeen A, Khong SY, Omar SZ, Noor Azmi MA. Peripheral Intravenous Catheterisation in Obstetric Patients in the Hand or Forearm Vein: A Randomised Trial. Sci Rep. 2016 Mar 18;6:23223. doi: 10.1038/srep23223. PMID: 26987593; PMCID: PMC4796788.

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Basics of Bleeding Control (2024)

November 30, 2024December 2, 2024 ~ iEM Education Project Team ~ Leave a comment

by Tasnim Ahmed & Abdulla Alhmoudi

Introduction

The primary objective in the resuscitation of traumatic hemorrhage is to achieve effective hemostasis and maintain hemodynamic stability. The severity of bleeding depends on the depth of the wound and the type of injured vessel. The approach to bleeding control should be tailored to the type and size of the bleeding vessel and the specific anatomical regions involved. Delayed or ineffective haemorrhage management can complicate the healing process and, in severe cases, lead to fatality. Extremity haemorrhage has historically contributed significantly to high mortality rates from casualties during wars [1]. Therefore, the prompt implementation of appropriate haemostatic techniques is a crucial aspect of efficient trauma management. This critical task is typically initiated by the prehospital team and followed by more advanced, invasive techniques provided by the trauma team in a controlled hospital setting

Types of Wounds

Wound is an impairment to the structural integrity of biological tissues, including the skin, mucous membranes, and organ tissues. This disruption in tissue integrity may arise from a diverse range of causes, including traumatic injuries, pathological processes, or surgical interventions. Metric parameters such as size (length), depth, shape, and whether they are open or closed are used to describe wounds.

The subsequent descriptors represent the terminology utilized for the classification of wounds:

Contusions

Contusions result from perpendicular blunt force to the skin, usually through a layer of clothes. Rupture of subcutaneous capillaries can occur, resulting in the formation of a hematoma (Figure 1). The recommended management for this type of wound consists of analgesics and following the “RICE” protocol (Rest, Ice, Compression, and Elevation) [2].

Abrasion

Abrasion is the scraping or scratching of the surface layers of skin (epidermis) when subjected to oblique forces (Figure 2). Proper wound care involves cleansing the wound, applying a sterile bandage, administering analgesics, ensuring tetanus protection, and implementing the RICE protocol [2].

Incision

Incision is defined as a cut that features straight edges along the margins of the wound. It can be caused by sharp objects like scalpels, knives, sharp metal pieces, or glass (Figure 3). Tissue loss is uncommon, and the wound margins can be easily aligned for closure with medical glue or sutures [1,2,3].

Lacerations

Characterized irregular or jagged edges, appearing torn rather than neat incisions [1,3]. They can have an irregular or linear direction and may branch out (Figure 4). Objects with broken or serrated edges or blunt impact on tissue overlying bone typically cause lacerations. Treatment approaches for lacerations are similar to those for incision wounds. However, the appropriate subspecialty should manage deep, complex lacerations or those involving sensitive areas like the face, joints, or tendons.

Avulsion

Avulsion involves a full-thickness laceration-type wound, which usually creates a flap of tissue (Figure 5) [1,3]. Mechanical accidents involving fingers (degloving injuries) can cause avulsions. More severe cases may include exposure of internal organs. Avulsions are challenging to repair and should never be considered minor injuries.

Amputation

Amputations differ from avulsions in that they involve the complete loss of a limb, whereas avulsions result in the loss of just a flap of skin (Figure 6). It can occur at any point along an extremity and is usually accompanied by significant arterial bleeding. Despite the seriousness of this injury, a properly cooled and transported amputated limb may sometimes be surgically reattached in a hospital setting.

Puncture and Penetrating Wounds

Puncture and penetrating wounds result from the penetration of a sharp object into the tissue without lateral movement from the point of entry (Figure 7). Puncture wounds can be deceptive, as they may appear small on the surface but extend deeply, potentially damaging the neurovascular structure or internal organs and causing significant internal bleeding or secondary injuries.

Stab wounds from knives or sharp objects, as well as bullet wounds, are examples of penetrating injuries [1,2,3]. Occasionally, the penetrating object may remain logged to the injury and should never be removed without careful assessment by the trauma team, as it might act as mechanical hemostatic and result in further bleeding once removed.

Site of Injury

Injuries can also be classified into three types, depending on the injured site of the body; each entails a different approach to management. Extremity injuries refer to damage inflicted on the blood vessels of the arms or legs. Junctional injuries, on the other hand, involve vascular damage occurring at the junction where the extremities meet the torso, such as the hip, axilla, or base of the neck. Torso injuries often involve non-compressible truncal hemorrhage that occurs anywhere on the torso and involves large blood vessels.

Vascular Injury

Injury to any blood vessel type can result in external bleeding. The specific type of vascular injury can be identified based on the characteristics of bleeding observed [1,2,4].

The following are the distinct types of vascular injuries and their corresponding patterns of bleeding:

Arterial Bleeding

Arterial bleeding typically occurs as a consequence of deep penetrating injuries or amputations. It is distinguished by the forceful ejection of bright red blood from the wound synchronized with each heartbeat [2]. Complete laceration of the artery may trigger spontaneous constriction, which helps to control bleeding. However, if only the artery wall is damaged without complete dissection, it can lead to persistent bleeding.

Indicators of arterial injury are classified into hard signs and soft signs [2]. Identifying hard signs indicates an immediate need for arterial exploration and surgical intervention. To aid in the recollection of these hard signs, the mnemonic “The Broken PIPE” can be employed (Box 1). Conversely, soft signs indicate the necessity for additional investigations such as ankle-brachial index measurement, Duplex Doppler ultrasound, or CT angiography, as determined by clinical assessment. The soft signs can be represented by the mnemonic “NON-Deadly HemorrHage” (Box 2).

Venous Bleeding

Venous Bleeding is characterized by a slower flow of dark red blood out of the wound [2]. However, caution is still recommended in venous bleeding, as it can contribute to significant and rapid bleeding if left untreated [4].

Capillary Bleeding

Capillary Bleeding usually results from damage to subcutaneous capillaries. It is characterized by slow, intermittent bleeding in the form of dots or small oozing [2,4].

Indications of Bleeding Control Techniques

Achieving hemodynamic stability necessitates the effective control of all life- or limb-threatening bleeding. While in most cases of traumatic and non-traumatic resuscitation, emphasis is placed on managing the airway and ensuring proper breathing, in situations of exsanguinating bleeding, prioritizing massive hemorrhage control surpasses the immediate focus on airway and breathing management [1]. The choice of hemostatic technique should be based on the depth and specific location of the injury, as outlined in detail in the “Bleeding Control Techniques” section below.

Contraindications of Bleeding Control Techniques

There are no absolute contraindications to any specific hemostatic method [1]. However, bleeding injuries should not distract the physician from managing concurrent immediate life-threatening conditions. Additionally, immediate wound closure is not recommended in wounds older than 8 hours. Instead, these types of wounds should be cleaned thoroughly, covered with sterile dressing, and closed after 3-5 days if there are no signs of infection. This is referred to as “delayed primary closure” [2,3].

Preparation

Similar to all medical procedures, thorough preparation is essential to ensure efficient hemostasis. This preparation encompasses the healthcare team, equipment, medications, the patient, and the wound.

Team Preparation

The healthcare providers involved in the procedure should possess comprehensive knowledge of indications, contraindications, techniques, and potential complications. The team should wear appropriate personal protective equipment, including face masks, face shields, surgical gowns, gloves, and shoe covers as necessary [3]. This protective gear is crucial to safeguard against blood splashes and potential contact with body fluids, particularly in trauma settings where the patient’s health status may be unknown.

Equipment Preparation

The equipment and medications used for hemostasis must be meticulously prepared and checked for the expiry date and functionality. The required equipment is listed under the corresponding techniques in the “Bleeding Control Techniques” section below.

Patient Preparation

A detailed explanation of the procedure should be provided to the patient, and informed consent should be obtained if applicable. Additionally, securing intravenous access and collecting a blood sample for type and cross-matching and coagulation profile are imperative. Administering analgesics and local anesthetics before procedural maneuvers helps to effectively minimize patient discomfort and disruptive movements.

Wound Preparation

A thorough assessment of the wound should be conducted. Distal movement and neurovascular function should be assessed prior to any manipulation. Contaminated wounds require proper irrigation to remove foreign bodies, followed by sterilization of the surrounding skin using antiseptic solution such as povidone iodine or chlorhexidine. However, wound preparation should not delay definitive hemostatic measures [1,3].

Bleeding Control Techniques

Direct Pressure

The initial step in controlling bleeding involves applying direct pressure to the bleeding wound. This facilitates the formation of a platelet plug and the initiation of the physiologic coagulation cascade, which is typically achievable within 10 to 15 minutes of proper pressure application [1].

Equipment

Sterile gauze pad size 4×4
Compression bandage
Splint\brace

Technique

Ensuring the proper replacement of skin flaps is essential, followed by placing multiple 4×4 sterile gauzes, ideally low adherent type, with equal pressure applied. The wound can be wrapped with a compression bandage if it is in the head or extremities. Following the application of a compression bandage to the extremities, distal mobility, sensation, and perfusion should be checked. Limbs should be placed in a brace to minimize movement and keep it elevated. In body junctions, the wound can alternatively be packed with gauze or hemostatic agents along with topical pressure application [1,2,4].

Precautions

It is important to avoid removing soaked gauze, as this can function as a foreign clot; instead, a new gauze should be applied on top of the existing ones [4]. Compression bandages should be avoided in thoracic wounds, as they can constrict breathing.

Pressure on Arteries

When the source of bleeding cannot be identified, applying proximal pressure can help control the bleeding by reducing blood flow to the injured artery [1]. This is only feasible with extremity wounds and should not be applied to the carotid artery, as this can precipitate ischemic brain insult or vagal stimulation, resulting in bradycardia [4].

Precautions

The time of application is limited to 10 minutes due to the risk of tissue necrosis distal to the pressure point.

Tourniquet

The indication to use tourniquets is severe extremity bleeding that is not controlled by direct pressure application. The concept is constricting arterial flow to the injured area. It is an extremely painful procedure, and proper analgesia should be ensured before applying a tourniquet if time allows.

Equipment

Proper size tourniquet
Alternative: Blood pressure cuff

Technique

Remove any clothing obstructing the tourniquet application site, ensuring it is directly applied to the skin and remains visible. Position the tourniquet approximately 2-3 inches above the wound, avoiding joints (Figure 8). Tighten the tourniquet until the bleeding stops and the pulse distal to the tourniquet is no longer palpable. Note the time of placement on the tourniquet tag or consider using an indelible marker to write it on patient’s skin. [4,5].

If bleeding is not controlled and the distal pulse is still present after applying the first tourniquet, apply a second one just above its location [4]. Increasing the width of the second tourniquet is more effective in controlling bleeding and reducing complications than excessively tightening the initial one. Administer analgesia as needed after the tourniquet is applied.

An alternative to the tourniquet is applying a blood pressure cuff proximal to the wound. The cuff is then inflated 20-30 mm Hg above systolic blood pressure or over 250 mm Hg, and the tubing is clamped with a hemostat [2]. There are many ways to improvise a tourniquet using non-stretchable clothing and a windlass rod like a pen; however, a commercially designed tourniquet is preferable and not likely to loosen easily with patient movement.

To safely remove the tourniquet, apply a pressure dressing directly onto the wound. Then, gradually release the tourniquet while carefully monitoring for any signs of bleeding. If bleeding is successfully controlled, keep the tourniquet loosely secured in case of potential re-bleeding. If bleeding recurs, reapply firm pressure by tightening the tourniquet [5].

Precautions

The maximum duration for tourniquet application is 120 minutes [2]. Prolonged tourniquet application can lead to complications such as nerve injury, tissue necrosis, compartment syndrome, and rhabdomyolysis. However, if the extremity is amputated or if the tourniquet has been applied for more than 6 hours, it should not be loosened as permanent muscle damage occurs after 6 hours and might require amputation.1 Moreover, potential reperfusion injury may occur after 60 minutes of tourniquet use, leading to inflammation-induced damage in local areas and systemic effects on vital organs caused by inflammatory mediators [5].

Topical Hemostatic Agents

Another alternative or adjunct to tourniquet use is topical hemostatic agents. These agents create a platform for platelet deposition and facilitate hemostasis [6]. Examples include [1] oxidized cellulose (e.g., Surgicel), dry gelatin (e.g., Gelfoam, Surgifoam), or cyanoacrylate.

Equipment

Hemostatic agent (e.g., Combat Gauze, Celox Gauze, or ChitoGauze)
Pressure dressing

Technique

The hemostatic gauze is applied with direct pressure for at least 3 minutes. After the field dries, the wound can be sutured, or pressure dressing can be applied. It is important to note that a dry field is required to apply the cyanoacrylate type. Pressure or tourniquet should be used before its application. An alternative to hemostatic gauze is topical thrombin. It can be used directly or diluted with saline and sprayed onto the wound. A concentration of 100 units/mL is effective. In severe bleeding, a concentration of 1000 to 2000 units/mL can be used [1].

Precautions

Potential complications associated with hemostatic agents include excessive granulation tissue and fibrosis with absorbable gelatin agents or foreign body reaction with cellulose [1,7].

Balloon Catheter

Balloon catheters can be used as an improvised tamponade technique to temporarily control severe bleeding from deep injuries, when other conventional methods fail [1,8].

Equipment

Fogarty catheters, Foley catheters, or Sengstaken-Blakemore tubes.
10 cc syringe

Technique

The tube is blindly inserted into the wound, then the ballon is inflated to halt bleeding from deep vascular injuries [1].

Suture Ligation

Suture ligation is used for controlling large bleeding vessels. An effective ligation technique requires careful examination and knowledge of the vascular anatomy to trace and identify the sources of bleeding. A retracted artery can be a potential source of delayed bleeding. Therefore, once an injured vessel is identified, the opposite end should also be traced and ligated [1].

Equipment

Blood pressure cuff
Absorbable suture (e.g., Vicryl, Monocryl, and PDS).
Haemostat
Needle holder
Scissors

Technique

A blood pressure cuff is placed proximally and inflated until the bleeding stops to create a clear field. With gradual deflation of the cuff, large bleeding vessels will start to be visible. Ligation is then completed with suturing in the following steps: [1]

Using a haemostat pinch the free end of the bleeding vessel.
Wrap a proper-sized suture around the vessel.
Tie the suture at the base of the vessel.
Release the haemostat carefully (Figure 9).

if the vessel can not be seen, a figure 8 suture can be applied (Figure 10) [1,3].

Figure 9 - Vessel ligation technique. (1) Grasp the cut end of the bleeding vessel with a haemostat. (2) Pass an appropriately sized suture around the vessel. (3) Tie and secure the suture around the base of the bleeding vessel. (4) Gently release the haemostat from the blood vessel. (Freeman C, Reichman EF. Hemorrhage Control. In: Emergency Medicine Procedures. 6th ed. Elsevier; 2020:112-1. "Control of the Bleeding Vessel that is Visualized." Adapted and redrawn by Tasnim Ahmed, MD).

Cauterization

Cauterization is cost effective and simple haemostatic technique for small vessels measuring less than 2 mm in diameter. Electrical cauterization involves using electrical current to heat an electrode, which then is used to thermally burn the vessel wall and seal it with charred tissue [1,10].

Chemical cauterization can be achieved using silver nitrate (AgNO3). This involves applying the agent to the vessel wall using an applicator, typically a long and small wooden stick tipped with the silver nitrate. Silver nitrate reacts with proteins in the tissue, forming an insoluble deposit that blocks the blood flow. It is only effective when applied to a dry tissue or minimal oozing [1].

Equipment

Blood pressure cuff
Silver nitrate or electric cautery

Technique

Position a blood pressure cuff proximally and gradually inflate it until bleeding stops, to achieve a clear field. Then gently release the pressure, until the smaller bleeding vessels become visible. Use the electrocautery to burn the end of the bleeding vessel or rub the silver nitrate against it to achieve an artificial clot [1].

Vasoconstrictors

In normal conditions, small vessels spontaneously stop bleeding. However, if bleeding persists, local vasoconstrictors mixed with local anaesthetics can be applied. Local anesthetic solutions containing epinephrine, such as lidocaine and bupivacaine, are readily available in the Emergency Department.

Equipment

10 cc syringe
Epinephrine 1:1000
Saline-soaked gauze

Technique

Prepare the diluted epinephrine in a 10 cc syringe. Aspirate prior to injection to ensure that the solution is not injected into a blood vessel. Inject 1 to 2 mL of the solution around the bleeding vessel. Apply direct pressure with saline soaked gauze over the wound. Alternatively, spray the wound with the diluted solution. [1,3]

Precautions

It’s important to avoid using epinephrine or other vasoconstrictors in end-arterial areas like fingers, toes, ears, nose, or penis, to avoid organ ischemia.

Complications

Complications arise when the above-listed techniques are either overused or applied inappropriately. For detailed information regarding the particular complications associated with each technique, please refer to the corresponding technique’s “Precautions” section.

Special Patient Groups

Obtaining hemostasis might be challenging in patients with coagulopathy. Therefore, it is important to remain vigilant and promptly assess the platelet count and plasma coagulation profile (PT/PTT/INR) in patients experiencing external bleeding. The early administration of tranexamic acid, blood products, and cryoprecipitate can aid in achieving hemostasis.

Authors

Tasnim Ahmed

Emergency Medicine Residency graduate from Zayed Military Hospital, Abu Dhabi, UAE. Deputy Editor-in-Chief of the Emirates Society of Emergency Medicine (ESEM) newsletter. Senior Board Member and Website Manager of the Emirates Collaboration of Residents in Emergency Medicine (ECREM). Awarded Resident of the Year twice, at ESEM23 and Menatox23. Passionate about medical education, with a focus on blending art and technology into innovative teaching strategies.

Abdulla Alhmoudi

Dr Abdulla Alhmoudi is a Consultant Emergency Medicine, serving at Zayed Military Hospital and Sheikh Shakhbout Medical City - Abu Dhabi. He pursued his residency training in Emergency Medicine at George Washington University in Washington DC and further enhanced his expertise with a Fellowship in Extreme Environmental Medicine. Dr Alhmoudi's passion for medical education is evident in his professional pursuits. He currently holds the position of Associate Program Director at ZMH EM program and is a lecturer at Khalifa University College of Medicine and Health Sciences. Beyond medical education, he maintains a keen interest in military medicine and wilderness medicine.

Listen to the chapter

References

Chapter 112. Hemorrhage Control. In: Reichman EF. eds. Emergency Medicine Procedures, 2e. McGraw Hill; 2013. Accessed May 22, 2023. https://accessemergencymedicine.mhmedical.com/content.aspx?bookid=683&sectionid=45343754
Spehonja A, Prosen G. Basics of Bleeding Control. In: Cevik AA, ed. International Emergency Medicine Education Project. iEM Education Project; 2018:598-601.
Lammers RL, Smith ZE. Principles of wound management. In: Roberts JR, Hedges JR, eds. Roberts & Hedges’ Clinical Procedures in Emergency Medicine. 6th ed. Philadelphia, PA: Elsevier; 2014:611-634.
Department of the Navy. Bleeding. Brooksidepress.org. 2001. Accessed May 22, 2023. https://www.brooksidepress.org/Products/OperationalMedicine/DATA/operationalmed/Manuals/Standard1stAid/chapter3.html.
Lee C, Porter KM, Hodgetts TJ. Tourniquet use in the civilian prehospital setting. Emergency Medicine Journal. 2007;24(8):584-587. doi:10.1136/emj.2007.046359
Sileshi B, Achneck HE, Lawson JH. Management of surgical hemostasis: topical agents [published correction appears in Vascular. 2009 May-Jun;17(3):181]. Vascular. 2008;16 Suppl 1:S22-S28.
Levy JH. Hemostatic agents and their safety. J Cardiothorac Vasc Anesth. 1999;13(4 Suppl 1):6-37.
Feliciano DV, Burch JM, Mattox KL, Bitondo CG, Fields G. Balloon catheter tamponade in cardiovascular wounds. Am J Surg. 1990;160(6):583-587. doi:10.1016/s0002-9610(05)80750-0
Rudge WB, Rudge BC, Rudge CJ. A useful technique for the control of bleeding following peripheral vascular injury. Ann R Coll Surg Engl. 2010;92(1):77-78. doi:10.1308/rcsann.2010.92.1.77
Kamat AA, Kramer P, Soisson AP. Superiority of electrocautery over the suture method for achieving cervical cone bed hemostasis. Obstet Gynecol. 2003;102(4):726-730. doi:10.1016/s0029-7844(03)00622-7

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Carbon Monoxide Poisoning (2024)

November 29, 2024December 2, 2024 ~ iEM Education Project Team ~ Leave a comment

by Mohammad Issa Naser & Abdulla Alhmoudi

You have a new patient!

A 48-year-old male with a known medical history of hypertension, depression, and prior suicidal attempts was brought into the Emergency Department by EMS after he was found unconscious by his wife after she arrived from work. He was lying down in an enclosed garage at home with the car engine running. She states that her husband was having difficulty breathing when she found him and was not responding to her. She reported that he had been depressed for the last few weeks because of financial problems. Upon arrival at the ED, the patient was unresponsive, with the following vital signs noted: BP 113/74 mmHg, HR 114 bpm, RR 10 bpm, and oxygen saturation at 98%.

What do you need to know?

Importance and Epidemiology

Carbon Monoxide (CO) is often called the “silent killer” as it lacks any warning or alarming signs of its presence. It is a colorless, odorless, tasteless, and non-irritating gas formed by the incomplete combustion of hydrocarbon fuels.

Despite a historical decline in the number of cases, CO continues to be one of the major causes of poisoning-related ED visits, accounting for approximately 50,000 cases every year in the United States, with a mortality rate of 1% to 3% [1]. Although many of these are nonfatal exposures with various degrees of toxicity, an estimated 1,000 to 2,000 patients a year die from severe toxicity [2]. Intentional poisoning cases have higher mortality rates compared to accidental cases and account for two-thirds of deaths [3,4]. Although cases can occur around the year, CO poisoning has a seasonal and geographic relation with cold climates, peaking during winter months, most commonly from faulty furnaces [5].

CO poisoning often has nonspecific toxicologic presentations ranging from minimal symptoms to unresponsiveness. It requires higher suspicion from clinicians to recognize, diagnose, and provide timely and appropriate management to avoid morbidity, mortality, and long-lasting complications. ED physicians should always consider CO poisoning when multiple patients present to the ED from a single location with similar correlating findings [3].

Pathophysiology

CO poisoning causes tissue hypoxia by impairing oxygen delivery and utilization and generating reactive oxygen species. CO can rapidly diffuse into the pulmonary circulation and reversibly bind the iron moiety of heme with approximately 240 times the affinity of oxygen-forming carboxyhemoglobin (COHb). CO impairs heme’s ability to deliver oxygen by directly occupying oxygen-binding sites and causing a conformational change to the other three oxygen-binding sites. This allosteric change increases the affinity of the oxygen binding site and decreases the oxygen delivery to the peripheral tissues, causing a leftward shift in the oxyhemoglobin dissociation curve. The amount of carboxyhemoglobin formed depends on the amount of CO and oxygen in the environment, duration of exposure, and minute ventilation [6].

CO also binds to myoglobin and NADPH reductase, which can worsen the hypoxia of cardiac muscle by affecting the mitochondria and ATP production, potentially leading to atraumatic rhabdomyolysis [2]. Like cyanide, CO inactivates cytochrome oxidase, which is involved in mitochondrial oxidative phosphorylation, causing a switch to anaerobic metabolism, and their combined effects can be synergistic in smoke inhalation [7]. Other effects of CO poisoning include neutrophil degranulation, free radical formation, lipid peroxidation in the brain and other tissues, and cellular apoptosis [2,8]. The half-life of COHb is about 300 minutes; thus, it begins to accumulate in the blood within a short exposure time. With normobaric oxygen (NBO) therapy (which is 100% inhaled oxygen at normal atmospheric pressure), the half-life is decreased to between 50 and 100 minutes; with Hyperbaric oxygen therapy, the half-life can be reduced to 30 minutes [9,10].

Medical History

A thorough history can be very helpful for early recognition of CO-related poisoning. Clinical findings can be variable and highly unspecific. The most common complaint in patients with mild to moderate CO poisoning is headache, present in up to 58% of patients, followed by the wide range of unspecific findings of nausea, dizziness, drowsiness, vomiting, cough or choking, confusion, shortness of breath, syncope, throat and eye irritation and chest pain [3]. It is important for clinicians to inquire about potential CO sources such as residential heating systems, gas appliances, or recent fires. In addition, clinicians should specifically inquire about transient loss of consciousness, as the presence or absence of this finding can be important in determining the severity of the presentation and the need for further interventions like hyperbaric oxygen [6]. Delayed neurological sequelae (DNS) is a well-known complication and can occur in 15 to 40 percent of patients presenting with significant CO poisoning [11]. DNS has been reported to appear 3 to 240 days after apparent recovery, with the majority of cases occurring within 20 days of CO poisoning. Deficits can last a year or more and are typically not found on acute presentation. Patients may present with cognitive impairment, memory deficits, movement disorders, or psychiatric symptoms. Any neurological or neuropsychiatric symptoms persisting beyond the acute phase of CO poisoning should raise suspicion for DNS and warrant appropriate evaluation and management [6]. Risk factors that predict the development of delayed neurologic sequelae include extremes of age and loss of consciousness. Because most CO-poisoned patients reaching the ED survive with minimal intervention, prevention of delayed neurologic and neuropsychiatric sequelae is a primary goal of therapy [12].

Physical Examination

Physical examination in suspected CO poisoning patients should focus on vital signs, cardiac and pulmonary examination, and a thorough neurological assessment. Findings in CO poisoning are usually limited to changes in mental status, tachycardia, and tachypnea in the absence of history of trauma or burns. Symptoms can range from mild confusion to coma [6]. The presence of “cherry-red” skin or mucous membranes may be observed in severe cases or even noted postmortem. However, it’s neither a sensitive nor specific sign, and it does not exclude CO poisoning [13]. Severe CO poisoning can be associated with neurologic, metabolic, and cardiovascular red flags such as seizures, syncope, lactic acidosis, acute myocardial infarction, ventricular arrhythmia, and pulmonary edema [6].

Alternative Diagnoses

Carbon monoxide poisoning can be a “great mimic,” but the early presentations are often nonspecific and readily confused with other conditions, typically a viral syndrome, explaining why influenza is the most common misdiagnosis [14]. CO poisoning can also be misdiagnosed frequently as gastroenteritis, food poisoning, or even colic in infants. Like adults, children tend to develop nonspecific symptoms that complicate the diagnosis [15]. More severe poisoning may be confused with other causes of altered mental status, such as trauma, diabetic ketoacidosis, meningitis, hypoglycemia, and intoxication [16]. The differential diagnosis remains broad without a known exposure source or sick contacts as clues. Cyanide poisoning, especially in patients with smoke inhalation, should also be considered due to the potential for concurrent exposure. In cases of chronic CO exposure, chronic fatigue, mood disorders, sleep disorders, and memory problems should be considered as an alternate diagnosis [17]. Recognizing risk factors for CO poisoning can be crucial in determining the likelihood of CO poisoning; focusing on potential sources of CO poisoning, the presence of multiple individuals with similar symptoms from the same location increases the likelihood of CO poisoning. The CNS is the organ system most sensitive to CO poisoning. Acutely, otherwise healthy patients may manifest headache, dizziness, and ataxia at COHb level as low as 15% to 20%; with higher levels and longer exposures, syncope, seizures, or coma may result [15]. At the same time, history of consuming contaminated food or recent sick contact with flu-like symptoms would make the diagnosis less likely.

Acing Diagnostic Testing

The single most useful diagnostic test to use in a suspected CO poisoning is COHb levels.15 An arterial or venous blood gas analysis with elevated carboxyhemoglobin levels (usually ≥ 3%-4% for nonsmokers or ≥ 10% for smokers) confirms the diagnosis of CO poisoning and provides information about lactate levels and any concurrent metabolic acidosis. It is important to obtain lactate levels to screen for possible concurrent cyanide toxicity (Lactate > 10 mmol/L) if the source of CO was a fire [18]. While an abnormally elevated COHb level indicates CO poisoning, it is important to note that the COHb levels do not accurately represent the severity of the poisoning. This is particularly true if there has been a significant time lapse between the exposure and when the levels were obtained due to CO clearance. Patients with major symptoms such as loss of consciousness altered mental status, or cardiac ischemia should be considered as severe poisoning with any abnormally elevated COHb level. CO poisoning management should focus primarily on the patient’s signs and symptoms rather than relying solely on the COHb level to guide decision-making.

Pulse oximetry (SpO2), a non-invasive bedside test, cannot be used for screening for CO poisoning, as it doesn’t differentiate oxygenated hemoglobin and carboxyhemoglobin and may yield normal values in CO poisoning despite significant tissue hypoxia. Non-invasive CO oximeters measuring COHb and methemoglobin are available and may have a role as a screening test, but their reliability in clinical settings has been questioned [6]. The American College of Emergency Physicians recommends against using pulse CO oximetry for diagnosis of CO toxicity in patients with suspected acute CO poisoning [2].

An electrocardiogram and a measurement of cardiac enzymes should be included due to the possibility of myocardial injury in patients with moderate to severe CO poisoning looking for myocardial ischemia, infarction, or arrhythmias [2,19]. Imaging studies, such as chest radiographs, may be indicated in certain clinical scenarios and can help patients presenting with hypoxia and dyspnea to evaluate for pulmonary edema [20].

Risk Stratification

Significant neurologic manifestations of CO poisoning include findings such as syncope, coma, seizures, altered mental status (GCS <15) or confusion, and abnormal cerebellar function. Metabolic findings such as lactic acidosis may be profound from cellular hypoxia. Cardiovascular findings include acute myocardial ischemia, myocardial injury, ventricular arrhythmia, and pulmonary edema [6].

The clinical policy from the American College of Emergency Physicians concerning the evaluation and management of adult patients with acute carbon monoxide poisoning presents evidence-based recommendations addressing three key clinical questions: the diagnostic accuracy of noninvasive carboxyhemoglobin measurement, the long-term neurocognitive impact of hyperbaric versus normobaric oxygen therapy, and the predictive value of cardiac testing for morbidity and mortality. The policy is based on a systematic literature review, graded using a defined class of evidence system, and offers recommendations for patient management at varying levels of certainty [21].

According to the ACEP’s CO policy, pulse CO oximetry should not be used to diagnose acute carbon monoxide (CO) poisoning due to its low sensitivity. While it offers advantages like being fast, noninvasive, and cost-effective, studies have shown it detects CO toxicity in only about 48% of cases, meaning it misses half of those affected. Similar findings were reported in other studies.

Both hyperbaric oxygen (HBO₂) and high-flow normobaric oxygen therapies are options for treating acute carbon monoxide (CO) poisoning, but it is unclear if HBO₂ is superior in improving long-term neurocognitive outcomes. While HBO₂ reduces carboxyhemoglobin levels and may aid neurologic recovery, its benefits remain debated. Meta-analyses and studies on HBO₂ have shown inconsistent results, with some finding no benefit and others suggesting improved outcomes. Variations in study designs and treatment factors contribute to the uncertainty, highlighting the need for further research.

In moderate to severe carbon monoxide (CO) poisoning, an electrocardiogram (ECG) and cardiac biomarkers should be used to detect acute myocardial injury, a predictor of poor outcomes. Studies have shown that myocardial injury is associated with higher long-term mortality and is an independent predictor of poor prognosis. Further research is needed to explore cardiac testing and interventions in less severe cases and more aggressive cardiac management for high-risk patients.

Management

Initial management starts with assessing and stabilizing the airway, breathing, and circulation. Comatose patients who have severely impaired mental status or who do not have sufficient respiratory effort should be intubated without delay and mechanically ventilated using 100 percent oxygen [6]. Treatment begins with oxygen therapy, and 100% oxygen should be provided as soon as possible with either a non-rebreather mask or endotracheal intubation, which serves two purposes. First, the half-life of COHb is inversely related to PaO2; it can be reduced from approximately 5 hours in room air to 1 hour by providing supplemental 100% oxygen. HBO therapy (at 3 atmospheres) further reduces the half-life to approximately 30 minutes [12]. Oxygen should be continued until the patient is asymptomatic and carboxyhemoglobin levels are ≤ 3%-4% in nonsmokers and ≤ 10% in smokers [2,18,19]. Evidence suggests that hyperbaric oxygen therapy helps prevent delayed neurologic sequelae in acute CO poisoning, but its efficacy decreases with delayed implementation [15]. HBO therapy can be used in patients presenting with a COHb level >25% (>15% if pregnant), unconscious at scene or hospital, reported syncope, persistent altered, mental status, coma, focal neurologic deficit, severe metabolic acidosis (pH <7.25) after empiric cyanide treatment if administered, or evidence of end-organ ischemia (e.g., ECG changes, elevated cardiac biomarkers, respiratory failure, focal neurologic deficit, or altered mental status). A thorough cardiovascular examination should be performed and should focus on signs of contributing cardiogenic shock or hypotension. Establishing IV access and cardiac monitoring are necessary as patients may need IV fluids or inotropes for resuscitation. An ECG and cardiac enzymes should also be included in the evaluation for cardiac ischemia in symptomatic patients at risk. Patients with altered mental status should have a blood glucose check to evaluate for hypoglycemia [6].

Special Patient Groups

Pediatrics

Children may present with subtle and non-specific findings compared to adults, and it is suggested that they can be more sensitive to the effects of CO due to their higher metabolic rates. Fussiness and decreased oral intake may be the only manifestations of CO toxicity. Although children may have higher levels of COHb due to their higher minute ventilation, which should make them more vulnerable to accumulating CO, the long-term outcomes appear favorable as they have lower rates of developing delayed neurological sequelae compared to adults. The diagnosis and management of CO poisoning in young children generally follow the same principles as for other age groups, with no substantial modifications in approach based on age [6].

Pregnant Patients

There is a lower threshold to using HBO therapy in pregnancy due to the greater affinity and the longer half-life of CO that is bound to fetal hemoglobin, the limited capacity to enhance placental perfusion and the direct effects of acidosis and hypoxemia on the fetus. While severe CO poisoning poses serious short- and long-term fetal risk, mild accidental exposure is likely to result in normal fetal outcomes. Because the fetal accumulation of CO is higher and its elimination slower than in the maternal circulation, hyperbaric oxygen may decrease fetal hypoxia and improve outcomes. While these findings provide valuable insights into the effects of CO poisoning and HBO therapy on pregnant patients and their fetuses, the available literature on this subject remains limited [6].

When To Admit This Patient

Hospitalization is warranted in cases where patients exhibit signs of hemodynamic instability, persistent neurologic symptoms, evidence of end-organ damage (including renal injury, rhabdomyolysis, cardiac ischemia, and pulmonary edema), or exposure to methylene chloride. Most patients who do not meet the criteria for HBO therapy and are not clinically ill can typically be managed in the emergency department; generally, patients who become asymptomatic with a carboxyhemoglobin (COHb) level < 5% may be safely discharged home. All patients exposed to CO require close follow-up for delayed neurologic sequelae [18].

Revisiting Your Patient

Our 48-year-old male, who has a history of prior suicidal attempts, was found unconscious in his home garage with his car engine running. The past medical history and his presentation picture put him at risk for carbon monoxide poisoning, and red flags such as his altered mental state and the recognition of a source of carbon monoxide should guide the clinician through the diagnosis and management process. Management started by assessing the airway, breathing, and circulation. The patient was in a state of respiratory arrest and was intubated and ventilated with 100% oxygen. His pupils were dilated and sluggish. The patient was hypotensive, and IV fluids were started while vasopressors were being prepared. A CBC, chemistry, blood glucose, cardiac enzymes, COHb level, and venous blood gas were requested. A Chest XR was also done, which showed no signs of pulmonary edema, and an endotracheal tube was confirmed in place. ECG showed normal sinus rhythm with no ST-T wave changes. COHb level was 38%, blood glucose 139 mg/dl, and cardiac enzymes were within normal range. His blood gas showed a pH of 7.28 and a lactate of 4. A diagnosis of carbon monoxide poisoning was made. The patient was kept on 100% oxygen and was being prepared to be transferred into a hyperbaric oxygen therapy facility.

Authors

Mohammad Issa Naser

Dr Mohammad Naser is currently a Critical Care Medicine Fellow in Sheikh Shakhbout Medical City - Abu Dhabi. He completed his emergency medicine training at Zayed Military Hospital and has obtained both the Emirati and Arab board certifications in Emergency Medicine. Dr. Naser has a profound interest in critical care medicine, particularly in bridging the gap between emergency and intensive care practices. Beyond critical care, He is deeply passionate about medical education, mentoring future healthcare professionals, and developing innovative teaching tools. Additionally, he is actively involved in clinical research, focusing on advancing knowledge and practices in emergency and critical care medicine.

Abdulla Alhmoudi

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References

Rose JJ, Wang L, Xu Q, et al. Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy [published correction appears in Am J Respir Crit Care Med. 2017 Aug 1;196 (3):398-399]. Am J Respir Crit Care Med. 2017;195(5):596-606. doi:10.1164/rccm.201606-1275CI
American College of Emergency Physicians Clinical Policies Subcommittee (Writing Committee) on Carbon Monoxide Poisoning:, Wolf SJ, Maloney GE, Shih RD, Shy BD, Brown MD. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Carbon Monoxide Poisoning. Ann Emerg Med. 2017;69(1):98-107.e6. doi:10.1016/j.annemergmed.2016.11.003
Shin M, Bronstein AC, Glidden E, et al. Morbidity and Mortality of Unintentional Carbon Monoxide Poisoning: United States 2005 to 2018. Ann Emerg Med. 2023;81(3):309-317. doi:10.1016/j.annemergmed.2022.10.011
Rose JJ, Wang L, Xu Q, et al. Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy [published correction appears in Am J Respir Crit Care Med. 2017 Aug 1;196 (3):398-399]. Am J Respir Crit Care Med. 2017;195(5):596-606. doi:10.1164/rccm.201606-1275CI
Centers for Disease Control and Prevention (CDC). Unintentional non-fire-related carbon monoxide exposures–United States, 2001-2003. MMWR Morb Mortal Wkly Rep. 2005;54(2):36-39.
Manaker S, Perry H. (2023) Carbon monoxide poisoning, UpToDate. Available at: https://www.uptodate.com/contents/carbon-monoxide-poisoning (Accessed: 15 May 2023).
Norris JC, Moore SJ, Hume AS. Synergistic lethality induced by the combination of carbon monoxide and cyanide. Toxicology. 1986;40(2):121-129. doi:10.1016/0300-483x(86)90073-9
Dubrey SW, Chehab O, Ghonim S. Carbon monoxide poisoning: an ancient and frequent cause of accidental death. Br J Hosp Med (Lond). 2015;76(3):159-162. doi:10.12968/hmed.2015.76.3.159
Weaver LK, Howe S, Hopkins R, Chan KJ. Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure. Chest. 2000;117(3):801-808. doi:10.1378/chest.117.3.801
Walker AR. Emergency department management of house fire burns and carbon monoxide poisoning in children. Curr Opin Pediatr. 1996;8(3):239-242. doi:10.1097/00008480-199606000-00009
Rose JJ, Wang L, Xu Q, et al. Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy [published correction appears in Am J Respir Crit Care Med. 2017 Aug 1;196 (3):398-399].Am J Respir Crit Care Med. 2017;195(5):596-606. doi:10.1164/rccm.201606-1275CI
Meaden CW, Nelson LS. Inhaled Toxins. In: Rosen’s Emergency Medicine Concepts and Clinical Practice. 10th ed. Elsevier; 2023:666-681.
Harper A, Croft-Baker J. Carbon monoxide poisoning: undetected by both patients and their doctors.Age Ageing. 2004;33(2):105-109. doi:10.1093/ageing/afh038
Dolan MC, Haltom TL, Barrows GH, Short CS, Ferriell KM. Carboxyhemoglobin levels in patients with flu-like symptoms. Ann Emerg Med. 1987;16(7):782-786. doi:10.1016/s0196-0644(87)80575-9
Tomaszewski, C. Carbon Monoxide. IN: Goldfrank’s toxicological emergencies. 9th ed. New York: McGraw-Hill Medical Pub. Division; c2011
Cho CH, Chiu NC, Ho CS, Peng CC. Carbon monoxide poisoning in children. Pediatr Neonatol. 2008;49(4):121-125. doi:10.1016/S1875-9572(08)60026-1
Eichhorn L, Thudium M, Jüttner B. The Diagnosis and Treatment of Carbon Monoxide Poisoning.Dtsch Arztebl Int. 2018;115(51-52):863-870. doi:10.3238/arztebl.2018.0863
Hampson NB, Piantadosi CA, Thom SR, Weaver LK. Practice recommendations in the diagnosis, management, and prevention of carbon monoxide poisoning.Am J Respir Crit Care Med. 2012;186(11):1095-1101. doi:10.1164/rccm.201207-1284CI
Weaver LK. Clinical practice. Carbon monoxide poisoning.N Engl J Med. 2009;360(12):1217-1225. doi:10.1056/NEJMcp0808891
Prockop LD, Chichkova RI. Carbon monoxide intoxication: an updated review.J Neurol Sci. 2007;262(1-2):122-130. doi:10.1016/j.jns.2007.06.037
American College of Emergency Physicians Clinical Policies Subcommittee (Writing Committee) on Carbon Monoxide Poisoning:, Wolf SJ, Maloney GE, Shih RD, Shy BD, Brown MD. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Carbon Monoxide Poisoning. Ann Emerg Med. 2017;69(1):98-107.e6. doi:10.1016/j.annemergmed.2016.11.003

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Documentation (2024)

November 29, 2024January 1, 2025 ~ iEM Education Project Team ~ Leave a comment

by Muneer Abdulla Al Marzooqi

Introduction

Whether rotating in the Emergency Department or elsewhere, one of the critical skills to learn is writing a complete and legible patient record. Documentation in the emergency department is usually challenging, and it may be difficult to adequately capture and note things promptly, especially when dealing with high acuity or critical case scenarios. Even as a medical student or intern, your medical record is essential. It reflects your general approach, thought process, care provided to patients, and potentially identifying gaps in your knowledge and training. Attending physicians, clerkship directors, and faculty usually emphasize and pay attention to how notes are written and may use them for summative or formative assessments and feedback. These documents are also crucial for communication between the emergency department and respective physicians, specialties, and other stakeholders. Appropriate medical documentation improves the quality of communication within an emergency department and aids the quality assurance process.

“It is said that if something is not written in the chart, it never happened.”

A well-organized and legible chart gives auditors and reviewers a clear picture of the physician’s thought processes and actions. It provides a real-time snapshot of a patient’s general condition at any given encounter. There is always room to learn about and improve medical documentation in the emergency department; therefore, this section will review the critical elements used in ED documentation [1,2].

Emergency Medicine Note

Before writing your note, nursing triage notes and vital signs, if available, need to be reviewed. If apparent discrepancies are seen, they need to be verified with the nurse and patient, as they may be errors. In addition, any abnormal vitals in triage must be acknowledged and written in the notes. Like any other medical record, the ED document comprises history, physical examination findings, differential diagnoses, ordered investigations, laboratory and imaging results, assessment, and plan. Each component will be discussed separately, and suitable examples will be provided accordingly [2-4].

History

When writing a patient’s history, one must be clear and thorough yet concise, avoiding lengthy and complex phrases. Ideally, the history should flow in a logical and chronological sequence. Unnecessary details are better avoided, as they serve as distractors and may confuse other readers. Recording the date and time the patient was seen is crucial, especially in critically ill patients. It will help create a timeline for when time-sensitive interventions or medications were administered [3,4].

The components of history

Chief Complaint

This usually includes the presenting complaint, ideally in the patient’s own words, with the duration (e.g., abdominal pain for two days).

History of Present Illness

Generally, there are two formats for writing the history of present illness (HPI): narrative and bullet points [5,6]. Both are acceptable as long as history is written comprehensively, concisely, and coherently. It is valuable to add pertinent negatives and positives when writing the HPI. It would show the physician’s thought process and lead the person reading the chart toward what differential diagnoses to consider and what to rule out depending on what the patient is presenting with. Specific mnemonics may aid in writing a systematic HPI (e.g., OLD CARS or OPQRST).

Example 1:

A 45-year-old man with a history of Coronary Artery Disease and Hypertension presented to the ED with chest pain that started three hours prior. The pain was gradual onset while sitting on his chair, localized in the center of the chest, and lasted for 20 min. It was described as “a heavy boulder on my chest.” It started when he quarreled with his daughter and was relieved with sublingual nitroglycerin. It was associated with nausea and sweating but not vomiting. It was localized and did not radiate into the shoulders or arms. He claimed the pain was moderately intense at 4/10 on the scale. The patient denied shortness of breath, palpitations, dizziness, or abdominal pain.

Example 2:

A 26-year-old male, previously healthy, presents with a sore throat for one week. It is associated with subjective fever and fatigue. It is aggravated whenever he drinks or eats, but he denies any difficulty swallowing or drooling. Also denies any chills, runny nose, cough, night sweats, or shortness of breath. No recent travel history was reported. Has several sick contacts at home with similar symptoms

Review of Systems

Other organ systems and symptoms not mentioned in the HPI must be reviewed to ensure that the patient has no other complaints or organ system involvement. If a review or system (ROS) cannot be obtained because of the patient’s underlying condition (i.e., unconscious, critically ill, or having dementia), this should be noted in the chart. Generally, patients are asked questions from head to toe (e.g., “Do you have a fever, chills, headache, sore throat, chest pain, abdominal pain, urinary symptoms, etc.”). Document all positive ROS symptoms and state the remaining symptoms as otherwise normal [7].

Past Medical/Surgical History, Medications, and Allergies

List any known illnesses that the patient might have had in the past. Include any surgical procedures he had. State what medications he is actively on and whether he has any drug or food allergies.

Family and Social History

Document a brief family history relevant to the chief complaint (e.g., family history of diabetes and cardiac disease in a patient presenting with chest pain). Social history mainly includes questions about smoking habits, alcohol consumption, sexual history, and illicit drug use. It might also be essential and relevant to ask about the patient’s financial and health insurance status, particularly in specific healthcare settings, to avoid ordering unnecessary tests and paying extra costs.

Physical Exam

Recording physical exam findings starts with the patient’s general appearance and vital signs, highlighting abnormal ones. It is important not to document or fabricate any findings that were not examined, as committing to such findings may have medical and medicolegal implications that are best avoided. Document all findings from the examined systems, including inspection, palpation, auscultation, etc. There is no need to document findings not pertinent to the chief complaint (e.g., neurological examination findings in a patient with a sore throat). Include important positive and negative findings for any given case [3].

Example:

A patient with abdominal pain

Important positive findings: Soft, non-tender abdomen, normal active bowel sounds
Important negative findings: No rebound tenderness, guarding, rigidity, or peritoneal signs

Assessment

It should capture the essence of the case and defend the rationale for further investigation. It usually includes an objective case summary, with differential diagnoses based on history and physical examination findings.

Plan

This section includes the investigations, medications, procedures, and consultations to be ordered or performed. The consultation time is crucial; the doctor’s name and recommendations must be promptly documented.

Disposition

This is usually the last part of the note. It indicates whether the patient will be admitted, discharged, or transferred to another facility. If discharged, follow-up and return instructions should be documented clearly [2-4].

Summary of all components in an ED Note

Chief complaint
History of present illness with pertinent positives and negatives
A brief review of systems
A focused past medical and surgical history
Pertinent medications and allergies
Family and social history, if relevant
Vital signs, highlighting any abnormal readings
A focused and appropriate physical exam
Assessment with differential diagnoses
Plan
Disposition

Few helpful suggestions during documentation

Place the date and time on all notes in the medical record.
Write notes clearly and legibly.
If you make a mistake, draw one line through it and sign your initials.
Document a focused but thorough history and physical.
Avoid using unclear abbreviations that are not commonly used.
Document vital signs and address abnormalities.
Document the results of all diagnostic tests that were ordered when appropriate.
When speaking to a consulting service, document the physician’s name and the time the call was made.
Document the patient’s response to therapy.
Document repeat examinations
Document your thought process (medical decision-making)
Avoid writing derogatory comments in the medical record.
Avoid changing or adding comments to medical records after completion. An addendum may be appropriate, but only if appropriately timed and dated.
Document all procedures performed.
If a patient leaves against medical advice (AMA), document that you have explained the specific risks of leaving and that the patient acknowledges and is aware of the risks.
Document plan for outpatient care and follow-up
If using an electronic medical record (EMR) instead of a handwritten one, all of the above sections, components, and suggestions apply [1,8,9].

Sample ED Note

Date & Time: 23/04/2022 at 07:40 AM

Arrival Mode: Private Vehicle

Source of History: Patient and Father

History Limitations: None

Chief Complaint

Abdominal Pain – since 6 hours

History of Present Illness

A 17-year-old male is brought to the ED complaining of abdominal pain since 6 hours of gradual onset. The pain started in the epigastric area and is now localized around the umbilicus. Pain is localized, persistent, and achy, without radiating to the back. It is associated with nausea and two episodes of vomiting. The vomiting is mostly food content and yellowish fluid, with no blood or bile noted. The patient was ill with nasal congestion and throat pain yesterday. He had a subjective fever at home and a decreased appetite. Denies chills, headache, yellowish eye or skin discoloration, diarrhea, or urinary symptoms. He denies eating food from outside in the past two days. No recent travel or sick contacts were reported. Did not try any medications or remedies at home.

Review of Systems

Other than HPI, the review of systems is otherwise normal.

Past Medical History

Unremarkable

Medications and Allergies

No known allergies and not on any regular medications

Family History

Both parents are known to have Hypertension only.

Social History

Denies alcohol consumption or illicit drug use.

Physical Exam

The patient appears to be in moderate pain, holding his abdomen.
Vitals: BP 130/80 mmHg, PR 120 b/min, RR 20 breaths/min, O2 Saturation: 94% on room air
Head and Neck: Dry oral mucosal, no cervical lymphadenopathy
CVS: Symmetrical pulses bilaterally, S1, S2 heard, no murmurs
Lungs: Clear to auscultation bilateral with no crepitations or wheezes
Abdomen:
- Scaphoid abdomen and not distended on inspection,
- tenderness palpable in the epigastrium, umbilical area, and right lower quadrant
- Positive rebound tenderness in the right lower quadrant
- Positive Rovsing’s and Obturator signs
- No palpable masses or hernias
- Negative Murphy’s sign
- Auscultation revealed sluggish bowel sounds
- Rectal exam revealed a normal tone with no blood in the glove
Genital Exam:
- Normal genitalia with no swelling, hernias, or tenderness
- Normal lying testes with no evidence of torsion
- Normal cremasteric reflex on both sides

Assessment

A 17-year-old previously healthy male presented to the ED with a 6-hour history of abdominal pain of gradual onset associated with anorexia, subjective fever, nausea, and vomiting. The physical examination revealed stable vitals, with abdominal examination showing tenderness in the epigastrium and right lower quadrant with rebound tenderness and positive Rovsing’s and obturator signs.

Provisional Diagnosis

Acute Appendicitis

Differential Diagnoses

Acute Gastroenteritis
Food Poisoning
Diabetic Ketoacidosis
Irritable Bowel Disease

Plan

Medications / Treatment:
- 1 Liter IV Normal Saline
- 1g IV Paracetamol for pain
- 10mg IV Metoclopramide for nausea and vomiting
Lab investigations:
- CBC w/Differential count
- Urea & Electrolytes
- Random Serum Glucose
- C-Reactive Protein
- Coagulation Profile
- Type and Screen
- Urine Analysis
Imaging Studies:
- Ultrasound Abdomen
- Possible CT Abdomen in case Ultrasound is inconclusive.
Consultations:
- General Surgery

Author

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.

Listen to the chapter

References

Murphy BJ. Principles of good medical record documentation. Journal of Medical Practice Management. 2001;258-260.
Clerkship Directors in Emergency Medicine (CDEM), Society for Academic Emergency Medicine (SAEM). Medical Student Educators’ Handbook / edited by Robert L. Rogers and Mark Moayedi. 2010.
Carrol S. Documentation | EM Basic [Internet]. Embasic.org. 2016 [cited 25 May 2016]. Available from: http://embasic.org/how-to-give-a-good-ed-patient-presentation/
Carrol S. How to give a good ED patient presentation | EM Basic [Internet]. Embasic.org. 2016 [cited 25 May 2016]. Available from: http://embasic.org/how-to-give-a-good-ed-patient-presentation/
Ronald, Schleifer., Jerry, B., Vannatta. (2011). 4. The Chief Concern of Medicine: Narrative, Phronesis, and the History of Present Illness. doi: 10.1215/00166928-1407531
Adam, Kilian., Laura, A., Upton., John, N, Sheagren. (2020). 2. Reorganizing the History of Present Illness to Improve Verbal Case Presenting and Clinical Diagnostic Reasoning Skills of Medical Students: The All-Inclusive History of Present Illness. doi: 10.1177/2382120520928996
Rui, Zeng. “4. Complete Physical Examination.” (2020). doi: 10.1007/978-981-13-7677-1_50
8. 5 Ways to Improve Medical Documentation in your Emergency Department – Bill Dunbar and Associates [Internet]. Bill Dunbar and Associates. 2014 [cited 25 May 2016]. Available from: http://www.billdunbar.com/2014/02/28/5-ways-to-improve-medical-documentation-in-your-emergency-department/
The Art of Writing Patient Record Notes. Virtual Mentor. American Medical Association Journal of Ethics. 2011;13(7):482-484.

Reviewed and Edited By

Jonathan Liow

James Kwan

Arif Alper Cevik, MD, FEMAT, FIFEM

Toxidromes (2024)

November 29, 2024November 29, 2024 ~ iEM Education Project Team ~ Leave a comment

by Phalguni Sai Preethi Asapu & Thiagarajan Jaiganesh

You have a new patient!

A 24-year-old male university student was brought into the Resuscitation area of the Emergency department via ambulance after his friends found him collapsed and confused on the floor at a party. His friends tell you that this is not the first time and has happened to him in the past. He has had a history of recreational drug usage in the past. No further history is known. On arrival, you notice that the patient is confused, moves to localized pain, and opens their eyes to speech with GCS 12/15. His vitals T = 36.8. C, BP = 82/74 mmHg, HR = 52 bpm, RR = 8 bpm, O2% saturation = 90% on room air. On a quick examination, you notice that the patient has needle marks like train track appearances. His pupils are pinpoint.

What do you need to know?

Importance

Toxidrome, a term coined by Mofenson and Greensher in 1970, refers to a clinical fingerprint that comprises a specific set of characteristic signs and symptoms. These symptoms arise from neurochemical and autonomic processes triggered by exposure to a particular class of toxins [1]. For physicians, recognizing these toxidromes is crucial for saving lives, as they serve as a valuable tool for the prompt detection and management of toxic exposures. Additionally, this recognition aids in differentiating between toxins that may present similarly.

In this chapter, we will discuss the five major toxidromes: Cholinergic, Anticholinergic, Sympathomimetic, Sedative-Hypnotics, and Opioids. However, a detailed examination of each toxidrome is beyond the scope of this chapter.

Epidemiology

A major cause of morbidity and mortality worldwide is both accidental and intentional poisoning from illicit substances. The second most common presentation involves pediatric patients under 6 years of age with accidental poisoning [2].

The American Association of Poison Control Centers reported over two million human exposure calls in 2018. The rates of poisoning cases presented to the emergency department appear to be increasing annually worldwide, with the majority being adults with intentional overdoses [2].

Studies have shown that the most common classes of drugs involved are analgesics, antidepressants, and opioids [3]. Additionally, accidental poisoning from pharmaceuticals, envenomation, and environmental and occupational exposure from either agricultural or industrial agents are also sources of potential toxicity.

Pathophysiology

Cholinergic Toxicity

This particular toxidrome includes nicotinic toxicity, carbachol methacholine bethanechol or pilocarpine overdose, pyridostigmine toxicity, etc., results from inhibition or binding of acetylcholinesterase causes increased levels of acetylcholine in the synaptic clefts leading to an overstimulation of the parasympathetic portion of the autonomic nervous system which maintains the rest and digest functions. The typical presentation of these types of patients includes fluids coming out of every orifice [4,5].

Anticholinergic Toxicity

Anticholinergic toxidrome is frequently encountered because many pharmaceuticals have antimuscarinic properties with drugs such as diphenhydramine, tricyclic antidepressants, doxylamine, and scopolamine. It inhibits the muscarinic cholinergic neurotransmission, therefore blocking the acetylcholine from binding to the receptors, causing an alteration in the normal homeostatic balance between the sympathetic and parasympathetic arms of the autonomic nervous system. This allows the sympathetic side to function unopposed and generates a state of relative sympathomimetics. Therefore, this toxidrome is very similar to sympathomimetic toxicity [4,5].

Sympathomimetic Toxicity

This Toxidrome is defined by increased catecholamines such as epinephrine, norepinephrine, and dopamine, reducing the catecholamine reuptake in the preganglionic synapse. Simply a sympathomimetic excess leading to a fight or flight reaction. This class includes cocaine, amphetamines, phencyclidine hydrochloride (PCP), and lysergic acid diethylamide (LSD) [4,5].

Sedative Hypnotic Toxicity

This toxidrome is frequently encountered in the ED as it includes ethanol intoxication, hence presenting with sedation, and occurs on a spectrum depending on the particular substance, route, and potency. The pathophysiology typically involves an increase in GABA (gamma-aminobutyric acid) neurotransmission in the case of CNS Depressants and enhanced effects of GABA at GABA-A receptor in the case of benzodiazepines [4,5].

Opioid Toxicity

This toxidrome is similar to sedative/hypnotic toxidrome as it also involves sedation and depressed respiratory drive. Opioids stimulate three receptors Mu, Kappa, and Sigma. Receptors are found all over the central and peripheral nervous system producing effects analgesia by inhibiting the nociceptive information to the brain. Increasing the dopamine from the mesolimbic pathway causes euphoria and causing noradrenergic effects in the locus coeruleus producing anxiolysis [4,5].

Medical History

Although intuitive, history is always the key for identifying the etiologies of poisoning; therefore, focused history is paramount. Often, patients are unable and unreliable to provide history due to their clinical state of being obtunded, confused, uncooperative, or even following intentional ingestion. Hence, history must be procured from paramedics, family members, friends, primary care physicians, medical records, and pharmacists as they can offer an in-site that must be correlated with signs and symptoms, physical examination, and laboratory values [6].

The elements that should be focused on during history taking include the type of substance consumed, timing and quantity of ingestion as the management can vary depending on the timing of presentation to the emergency department, intent, whether it was suicidal or homicidal, to be able to obtain all the medications found at the site since multiple drugs can be ingested at once and if there are any forms of chemical exposure or obtaining a product safety protocol.

Physical Examination

Physical examination of poisoned patients provides invaluable clues regarding the agent involved; namely, vital signs, mental status examination, and pupillary size are useful elements. It is also important to examine the skin and mucus membrane with attention to discoloration, moisture levels, track marks, and ulcerations.

A full neurological examination focusing on motor examination should be performed. The Image below highlights the features each patient presents with toxidromes [6,7]:

Alternative Diagnoses

There is a frequent encounter in which the patient presents with some level of delirium. Excluding pathological causes of altered mental status is important, such as acidosis, encephalopathy, electrolyte abnormalities, infection, uremia, trauma, insulin-related seizures/stroke, and psychosis. Identifying reversible causes, such as hypoglycemia and nutritional deficiencies, is vital. Having broad differentials, including toxicological and non-toxicological causes, is crucial for the management of the patient and helps avoid premature conclusions.

Acing Diagnostic Testing

Diagnostic testing in toxicology is guided by clinical findings and suspected toxins in a patient. The following basic tests can be performed in the ED, depending on the presentation.

Electrocardiogram (ECG)

Provides diagnostic and prognostic information; hence, it should be performed on all patients on arrival.
Keeping an eye out for QT prolongation and widening of QRS interval aids in diagnosis as sodium channel blockers (tricyclic antidepressants, cocaine, carbamazepine) and potassium efflux (most antipsychotics and sotalol), respectively [8].

Toxicology Screens [9-11]

It helps to aid diagnosis, although its use can be limited since drugs such as LSD, mushroom, and mescaline are not part of the panel.
Urine toxicology screens are superior to blood toxicology screens as they are more reliable and have a longer period for positive detection, 24-72 hrs. We need to understand that urine toxicology panel is a qualitative measure, not a quantitative test, and false negatives can occur. Hence, it should not delay therapy.
General toxicology panel coverage:
- Amphetamines
- Cocaine
- Ecstasy
- Methamphetamines
- Opiates
- Phencyclidine
- Marijuana
- Benzodiazepines
- Barbiturates
- Methadone
- Tricyclic antidepressants
- Oxycodone

Serum Acetaminophen and Salicylate levels

Serum acetaminophen and salicylate levels should be measured routinely in all patients with suspected drug overdose or substance abuse, as these are among the most commonly implicated substances in acute poisoning cases [12].

Basic Laboratory Testing

Symptomatic patients and those with an unknown/unreliable history should undergo a complete blood count, urinalysis, serum electrolytes, blood urea nitrogen, creatinine, and glucose as a minimum to rule out any pathological cause before a toxic cause.
In severely ill patients, serum ketones, renal function tests, liver function tests, creatinine kinase, ionized magnesium, and calcium should be measured.
If there is suspicion of toxic alcohol ingestion, then additional tests, such as serum osmolality, can be performed [10].

Arterial and Venous Blood Gas Analysis

Blood gas analysis, both arterial and venous, plays a vital role in the evaluation and management of patients presenting with toxidromes. These analyses provide critical insights into acid-base balance, oxygenation, ventilation, and the metabolic status of the patient, all of which can be profoundly affected by various toxic agents.

Routine Pregnancy Tests

Routine pregnancy testing is recommended for all women of childbearing age presenting with suspected poisoning [10], as pregnancy can significantly influence both the clinical presentation and management of toxic exposures.

Radiological Imaging

This is not of much value except in cases of radiopaque toxins, ingested drug packets, non-cardiogenic pulmonary edema, and acute respiratory syndrome due to exposure to certain toxins [10].

Risk Stratification

Risk stratification is essential in managing patients with toxidromes to prioritize care, allocate resources, and guide treatment decisions. It involves assessing the severity of the toxic exposure, identifying life-threatening symptoms, and evaluating patient-specific factors that may influence outcomes. Key considerations include the type and amount of toxin ingested, the time since exposure, and clinical manifestations such as altered mental status, hemodynamic instability, respiratory compromise, or significant acid-base disturbances. Laboratory findings, such as elevated lactate, anion gap metabolic acidosis, or co-oximetry results, provide additional insights into systemic effects of the toxin. Patient factors such as age, comorbidities, and pregnancy status further impact risk categorization. Stratifying patients into low, moderate, or high-risk categories ensures that those with critical conditions receive immediate interventions, such as airway support or antidotal therapy, while lower-risk patients can be managed with observation or symptomatic care. This systematic approach optimizes outcomes by tailoring interventions to the urgency and severity of each case.

Any patient with significant toxicity along with any of the following should be admitted to the ICU [13,14].

CNS depression, lethargy, coma.
Patients with agitation who require either chemical or physical restraints.
If PCO2 >45 mmHg, hypoxia or respiratory failure, endotracheal intubation.
If the patient’s systolic blood pressure is ≤80 mmHg.
Prolonged or recurring seizures.
On an ECG, if a second or third-degree AV block is present.
On an ECG, presence of non sinus cardiac rhythm.
Any significant acid-base disturbances, such as metabolic acidosis with pH ≤7.2.
Any significant metabolic abnormalities requiring either close monitoring or aggressive correction, such as symptomatic hypoglycemia following sulfonylurea or insulin overdose.
Patients with temperatures are at extremes, such as hyperthermia with T >104°F.
Patients who ingest “toxic time bombs” like Ingested drug packets, sustained-release preparations, and ingestion of quantitative level of the drug have unfavorable outcomes.
If the patient needs invasive hemodynamic monitoring such as pulmonary artery catheter, arterial line, or cardiac pacing.
If the patient requires whole bowel irrigation to enhance GI elimination of the toxin.
If the patient is in need of emergency hemodialysis, hemoperfusion, or hemofiltration.
If the patient requires an emergency antidote that requires close monitoring, such as crotalid antivenin, Digi bind, physostigmine, or naloxone drip.
If the patient experiences ischemic chest pain from toxins, namely cocaine and carbon monoxide.
If the patient is exposed to TCA or other drugs with QRS >120 msec or QTc >500 msec.

Management

Optimal management of a poisoned patient depends on various parameters, including the type of poisoning involved, presenting symptoms, severity, and the time elapsed between exposure and presentation. Resuscitation is a crucial initial step for any poisoned patient coming through the ED. Subsequently, a structured risk assessment should identify patients who would benefit from supportive care, decontamination, antidotes, and enhanced elimination techniques. Further assistance can be obtained from a medical toxicologist. The generalized initial evaluation for all poisoned patients in an ED setting includes the following approach.

Primary Survey [15,16]

A: Airway

Assess whether the airway is patent or obstructed.
If not patent: Perform immediate intubation using rapid sequence intubation with pre-oxygenation and neuromuscular blockade.
- Exception: In cases of suspected opioid overdose, administer naloxone to reverse respiratory depression while ensuring adequate oxygenation and ventilation.
Always rule out hypoglycemia as a potential cause before proceeding with intubation.

B: Breathing

Evaluate respiratory rate (RR), effort, chest expansion, presence of abnormal sounds, and oxygen saturation (SpO₂).
Administer high-flow oxygen to all critically ill patients with suspected overdoses, regardless of SpO₂ levels.

C: Circulation

Assess heart rate (HR), blood pressure (BP), central and peripheral pulses, capillary refill time (CRT), and temperature to evaluate circulatory status.

D: Disability (Neurological Status)

Examine Glasgow Coma Scale (GCS), pupil size, and blood glucose levels.
Once Airway, Breathing, and Circulation (ABC) are secured, focus on neurological stabilization.
The traditional “Coma Cocktail” (dextrose, oxygen, naloxone, thiamine) is no longer recommended as a blanket approach. Instead, each component should be administered selectively based on clinical indications [15].

E: Exposure and Environmental Control

Conduct a thorough external examination, assessing for temperature abnormalities, skin findings, injuries, trauma, or signs of transdermal medication patches and external contaminants.
Remove clothing, external contaminants, and concealed items such as drugs or weapons that might provide clues to the history of poisoning.
Manage temperature extremes:
- Severe Hyperthermia (> 40°C): Requires aggressive treatment with sedation, paralysis, and ice bath cooling [17].
- Severe Hypothermia (< 30°C): Requires rapid rewarming. For unconscious patients who achieve return of spontaneous circulation after cardiac arrest, consider therapeutic hypothermia [17].

Secondary Survey

SAMPLE history should be taken, including site, allergies, medications, past medical conditions, last meal, and event history, which have been discussed in this chapter’s history and physical examination section.
A complete neurological examination should be performed.

Management of Patients Depending on The Toxidrome

The general management of a patient after stabilization involves supportive care, which remains the cornerstone of management, decontamination, and specific antidotal therapy when indicated since they do not exist for every potential poisoning.

Anticholinergic Toxidrome Management [18]

Initial management should focus on evaluating and stabilizing cardiovascular and neurological toxicity. If a patient is agitated or having seizures, administer benzodiazepines (lorazepam or diazepam). On an ECG, if the QRS interval is prolonged >120 msec, depicting sodium channel blockade, then Sodium bicarbonate boluses of 50 mEq can be given in adults.

If a patient with anticholinergic toxicity comes to the Emergency department within 2 hours of ingestion and the patient is cooperative, then consider gastrointestinal tract decontamination with activated charcoal. The most common reason for emergency intervention is when the patient presents with delirium, then an antidote, Physostigmine, should be administered since it reversibly inhibits cholinesterase in both central and peripheral nervous systems, allowing acetylcholine accumulation and competition with the antimuscarinic blocking agent occupying the receptor. Its dosage is 0.5 mg – 1 mg IV over 15 minutes, with a maximum of up to 2 mg in the first hours. If more than 3 doses are required in a span of 6 hours, start IV infusion; 1-2 mg followed by 1mg/hr. Reassess after a 12-hour period. Caution: if QRS >100, Na blockade signs and narrow-angle glaucoma, then Physostigmine are contraindicated.

Disposition [19]

Discharge if the patient has minimal symptoms after 6 hours of observation in the ED.
If the patient has had large ingestions, then observe for up to 24-48 hours, even if asymptomatic.
Admission is required if physostigmine is administered since the half-life of physostigmine is often shorter than the ingested drug).
The patient can be discharged if he remains asymptomatic within 6 hours of the last antidote dose.

Cholinergic Toxidrome Management

The management of patients presenting with cholinergic toxicity is directed towards Decontamination, supportive care, and reversal of acetylcholine excess and toxin binding at receptor sites on cholinesterase molecules.

Decontamination includes using universal PPE (full-face air purifying cartilage mask, eye shield, chemical-resistant suites, boots, nitrile/ butyl rubber gloves) to protect the providers due to the contaminant’s dermal absorption. All clothing is removed by thoroughly flushing the skin with water. Activated charcoal or gastric lavage is of no use.

Stabilization and supportive care, Airway management remain crucial due to the high probability of respiratory failure followed by death. Intubation should be considered with either Rocuronium 1mg/kg or Vecuronium, non-depolarizing paralytic agents, since cholinesterases do not metabolize them. Succinylcholine, which is long used in an emergency setting, should be avoided at all times since it is metabolized by cholinesterase and prolongs the duration of effect around 4-6 hours in this particular setting [20].

Antidote therapy is a definitive treatment aimed at reducing the effects and levels of acetylcholine at various receptor sites. Atropine is one of them, and it acts as a competitive inhibitor of acetylcholine at the muscarinic sites. The dosage includes 0.6 – 1 mg atropine can be given. If severely poisoned, then administer 3mg. If there is no response with the first dose, double the dose after 5 minutes until clinical improvement is observed. Sometimes, it may require prolonged administration, which can be done via infusion. The initial loading doses should be followed by an infusion using 20% per hour of the total bolus dose. Note that the endpoint of atropinization includes drying of respiratory secretions, respiratory effort, and normalizing respiratory rate. The second part includes regenerating the acetylcholinesterase function by using an oxime that binds to the organophosphate-cholinesterase complex, leading to a conformational change that allows cholinesterase to function normally. This can be used if there is respiratory depression or failure, seizures, fasciculations, hemodynamic instability, dysthymias, or large amounts of repeated doses of atropine to completely control the signs and symptoms of this type of poisoning. Commonly used agents are Pralidoxime chloride 1-2 g over 30 minutes followed by a continuous infusion at 0.5 to 1 g/hour for several days. Alternatively, Obidoxime can be given in a loading dose of 4 mg/kg over 20 minutes, followed by an infusion of 0.5 mg/kg/hour. It is usually given as 250 mg loading dose in adults followed by 750 mg every 24 hours [20].

Disposition

If the patient is asymptomatic and has had minimal exposure for at least 12 hours after the ingestion, then the patient can safely be discharged.
If there is any evidence of self-harm, consult psychiatry.

Sympathomimetic Toxidrome Management

Patients with this type of toxicity should first undergo stabilization and supportive care, which includes loading the patient with IV fluids to avoid renal failure secondary to rhabdomyolysis. For decontamination, 50 g of activated charcoal can be used if the patient has ingested the toxin within an hour and their airway is protected. Moreover, Benzodiazepines are the key to managing sympathomimetic toxicities as they provide the cleanest pharmacological approach in treating agitated patients because they act by facilitating the binding of the inhibitory neurotransmitter GABA at various GABA receptors throughout central nervous system, such as 10-20 mg oral or IV diazepam or 1-2 mg lorazepam. If the patient remains agitated and has no respiratory depression, then proceed with further boluses via IV. If Oral or IV are unavailable, consider giving via IM 1-2 mg lorazepam or 5-10 mg Midazolam and repeat as necessary.

Another medication is haloperidol (5-10 mg intramuscular), which blocks the postsynaptic dopamine 2 receptors in the mesolimbic system of the brain. It can be used in agitated patients who are unresponsive to two or more doses of benzodiazepines. Ketamine, an N-methyl-D-aspartate receptor antagonist that induces a dissociative state, is used in the setting of uncontrollable agitation in sympathomimetic toxicity [21, 22].

Disposition

Discharge is no symptoms once symptoms resolve after 6 hours of observation.

Opioid Toxidrome Management

Physicians should prioritize stabilizing the airway, oxygenation, and ventilation. Most opioids are extended-release preparation that decreases gastric motility. Activated charcoal can be used, although discouraged due to lack of sufficient evidence to support its use in opioid poisoning. The key management is the use of Naloxone, a competitive opioid antagonist, therefore reversing opioid intoxication effects. Its use is indicated when a patient experiences significant respiratory or central nervous system effects. In general, starting with lower doses and subsequently increasing the doses as needed to alleviate symptoms is an optimal choice. Doses range from 0.04 – 15mg intravenously; starting dose of 0.04 mg is recommended, followed by titration of the subsequent dosages. It can be given via IV, IM, or SC but is ineffective when given orally due to first-pass metabolism [23].

Disposition

If the patient is on long-acting opioids, then admit to an observation unit.
Consider discharge after 6 hours of observation if the patients are asymptomatic.
Asymptomatic body packers should be admitted until the packets are passed or retrieved.

Sedative/Hypnotic Toxidrome Management

Benzodiazepine Toxicity

Initially, patients need to be stabilized, which includes endotracheal intubation with close respiratory and end-tidal carbon dioxide monitoring when obligated, and should not be delayed by the administration of an antidote. Administer activated charcoal (50 g) only if the patient arrives at the emergency department within one hour of ingestion and the patient’s airway is protected. An antidote that can be administered in these cases is Flumazenil, a nonspecific competitive antagonist at the benzodiazepine receptor site, which reverses benzodiazepine sedation after overdose, procedural sedation, and general anesthesia. It is to be noted that Flumazenil reverses the central nervous system depressant effects more than respiratory depression. Flumazenil is not recommended for routine use in the emergency department [23, 24]. It can precipitate acute withdrawal who are chronically dependent on benzodiazepine, leading to status epilepticus. The decision should be based on balancing risk and benefits and the reliability of the user. The dosage includes 0.2 mg IV over 30 seconds. A second dose of 0.2 mg followed by 0.2 mg at a minute interval to a total of 1 mg [25].

Disposition

Asymptomatic patients, after 4 hours of ED observation, can be discharged.
If there is a deliberate overdose, consult psychiatry.

Barbiturates Overdose

Patients with barbiturate toxicity should initially be stabilized by maintaining the airway (Eg. mechanical ventilation), administering IV fluids and vasopressor to eliminate hypotension (Systolic blood pressure >90 mmHg), and adequate urine output, rewarming measures to annihilate hypothermia. There is no specific antidote for barbiturates overdose. Decontamination with 50 g of activated charcoal can be applied if the patient presents within one hour of ingestion and the airway is secured. Dialysis plays a role as enhanced elimination only in patients ingesting phenobarbital, and who are deteriorating despite aggressive supportive care because routine use of it has limited evidence since phenobarbital is a weak acid, alkalization of the urine increases the amount of drug present in ionized form, therefore, minimizing tubular reabsorption and increases drug clearance [25].

Disposition

Consider discharge if the patient shows improvement in the neurological status and vital signs over 6-8 hours.
If symptoms continue after 6 hours, admit the patient.

Special Patient Groups

There aren’t any significant differences in identifying and managing toxidromes in children, pregnant women, or the geriatric population except for the drug dosages. The clinical features remain the same, and the management involves following primary and secondary surveys followed by supportive care, decontamination, antidotes, and enhanced elimination techniques depending on the toxic syndrome involved.

Revisiting Your Patient

Let’s revisit the case discussed at the beginning of the chapter. A patient presents to the ED

collapse and confused on the floor at a party with a history of drug usage of GCS 12/15.

Vitals shows T = 36.8. C, BP = 82/74, HR = 52, RR = 8, O2 sat = 90 on room air. You notice needle track marks on the skin and pinpoint pupils during quick examination. Discussed below is how one should approach this case.

Connect the patient to the monitors and establish two IV access points, along with a 12-lead ECG, to look for abnormal rhythm patterns.
Maintain a clear airway with adequate ventilation since opioids cause respiratory depression.
Administer Naloxone immediately (Begin with small doses of 0.05 mg IV or 0.1 mg IM when the dependence is possible and ventilation can be maintained, then double the dose until respiratory depression is reversed) since the patient’s consciousness level is impaired. Consider referring the patient to the intensive care unit.
Expose the patient and look for transdermal medication patches or concealed drug packets.
Simultaneously with the resuscitative efforts, Obtain the necessary laboratory investigations, such as CBC, U&Es, glucose, LFTs, and CK, a toxic screen, APAP and salicylate levels, and ABG (metabolic acidosis).
Ensure adequate hydration to maintain a good urine output (0.5 mL/kg/hour) and perfusion.
Check for infection at injection sites and for clinical signs of endocarditis, pneumonia, and pulmonary edema.
Discuss testing for HIV and hepatitis in all patients using intravenous drugs.
The secondary survey obtains a thorough history with a neurological examination of the patient.

Authors

Phalguni Sai Preethi Asapu

Dr. Preethi Asapu, is currently a first-year emergency medicine resident at Tawam Hospital, Al Ain, UAE. She graduated with an MBBS from Ras Al Khaimah Medical and Health Sciences University in 2021 and completed her internship at NMC Royal Hospital, Abu Dhabi, UAE. Dr. Asapu is competent researcher with publications to her name. She has Keen interest in Emergency Medicine and Toxicology.

Thiagarajan Jaiganesh

Dr. Jaiganesh is a Chairman and Consultant in Adult and Pediatric Emergency Medicine and serves as an Adjunct Assistant Professor at UAE University. As the former Director of the Emergency Medicine Residency Program at Tawam Hospital in Al Ain, UAE, Dr. Jaiganesh is dedicated to training the next generation of emergency medicine professionals. With a strong academic and professional background, Dr. Jaiganesh has published numerous peer-reviewed articles on emergency medicine and contributes as a Section Editor and Chapter Author for notable medical texts, including the Oxford Handbook for Medical School. A sought-after speaker, Dr. Jaiganesh has been invited to present at numerous national and international conferences and serves as an instructor in various life support courses. Additionally, Dr. Jaiganesh is an expert in medico-legal and clinical negligence matters, providing valuable insights into complex legal and ethical cases in healthcare.