Category: Infectious Problems

Tetanus (2025)

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by Grace Bunemann, Alex Gallaer, Jerry Oommen & Ashley Pickering

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You Have A New Patient!

An 11-year-old female was brought in by ambulance after being attacked by her neighbor’s American Pitbull dog approximately 1 hour prior to arrival. She had attempted to pet the dog and sustained multiple bite wounds to her face and hands. She is crying loudly and is accompanied by her mother and father, who report that she previously had “German Measles” but has no other known medical conditions, though her medical care has been inconsistent. 

The image was produced by using ideogram 2.0.

Her temperature is 37.0°C, pulse is 133/min, and blood pressure is 98/62 mmHg. On examination, she has a dirty, macerated, oozing wound on the left side of her face and multiple deep wounds on her hands and distal arms, all contaminated with soil.

What Do You Need To Know?

Importance

Tetanus is an acute but often fatal disease caused by an exotoxin produced by the bacterium Clostridium tetani. It remains an important public health concern worldwide, particularly in areas with low immunization rates against tetanus [1]. Tetanus infection is characterized by generalized rigidity and convulsive spasms of skeletal muscles [2]. Muscle stiffness typically begins in the head and neck region before becoming generalized.

The CDC reports that in the US, tetanus has been fatal in approximately 11% of reported cases in recent years, while global fatality rates are closer to 50% [2]. In 2019, according to the Global Burden of Disease database, there were nearly 74,000 new worldwide cases of tetanus, corresponding to an incidence rate of 0.95 [3,4]. That same year, there were just under 35,000 deaths attributed to tetanus [3,4]. Since 1990, the global death rate from tetanus has decreased by an astounding 87% [3,4]. This decline is credited to widespread vaccination, improved wound care, and the use of postexposure immunoglobulin.

Epidemiology

A tetanus infection is caused by Clostridium tetani. C. tetani is an anaerobic, spore-forming bacterium that gains access through broken human skin and causes toxin-mediated infection. The spores are found everywhere in the environment, particularly in soil, ash, intestinal tracts/feces of animals and humans, and on the surfaces of skin and rusty tools like nails, needles, or barbed wire[1]. While present worldwide, it is more common in warm, damp climates with rich soil. The organism is sensitive to heat and cannot survive in the presence of oxygen. The spores, in contrast, are extremely resistant to heat and the usual antiseptics [2].

Anyone can get tetanus, but like many diseases, it has a predilection for specific groups. There is an increased risk of tetanus in newborns, pregnant persons with insufficient immunization, intravenous drug users, the elderly, and those lacking primary immunization. Typically, tetanus infections are categorized into the following four categories: generalized (full-body symptoms), localized (symptoms in one area, e.g., leg), cephalic (cranial nerve involvement), and neonatal (history of home birth, soil on umbilical stump, unsterilized instruments) [5].

Pathophysiology

Tetanus is a serious disease caused by the bacterium Clostridium tetani, which produces toxins that disrupt the nervous system, resulting in muscle spasms and rigidity. The pathophysiology of tetanus involves several key stages [6-9]. The process begins when C. tetani spores, which are commonly found in the environment, enter the body through wounds or injuries. These entry points may include minor or unnoticed injuries, burns, surgical sites, intravenous drug use, or unsanitary practices such as umbilical cord cutting in newborns. Once inside the body, the spores encounter anaerobic conditions, often in devitalized tissue, which allow them to germinate into bacteria [7].

The bacteria produce two main toxins: tetanospasmin and tetanolysin [7,8]. Tetanospasmin, a potent neurotoxin, is the primary agent responsible for the clinical features of tetanus. Tetanolysin, a hemolysin, has no clear role in the disease’s pathology. Tetanospasmin enters the lymphatic and circulatory systems, eventually binding irreversibly to receptors at the neuromuscular junctions of the peripheral nervous system. The toxin is then transported retrogradely along nerve axons to the central nervous system (CNS), where it exerts its effects on inhibitory interneurons in the spinal cord and brainstem.

Within the CNS, tetanospasmin blocks the release of inhibitory neurotransmitters such as gamma-aminobutyric acid (GABA) and glycine, disrupting the balance between excitatory and inhibitory signals [5,7,8]. This blockade leads to unregulated muscle activity, characterized by the hallmark symptoms of tetanus: severe muscle spasms and rigidity. The uninhibited release of excitatory neurotransmitters results in continuous muscle contractions, which can be painful and are often triggered by minimal external stimuli like noise, light, or touch. In severe cases, these spasms can cause fractures, tendon ruptures, or respiratory failure [6,8].

Tetanus also affects the autonomic nervous system, leading to symptoms such as fluctuating blood pressure, rapid heart rate, and excessive sweating [6,8]. This autonomic dysfunction results from the toxin’s disinhibitory effects on the sympathetic nervous system. Additionally, the uninhibited release of catecholamines by the adrenal glands contributes to hypersympathetic activity. The effects of the neurotoxin are seen until a new axon terminal is produced which takes 4-6 weeks [2]. The cumulative effects of these pathophysiological processes make tetanus a potentially life-threatening condition that requires prompt recognition and treatment.

Medical History

Tetanus infection should be suspected in any patient presenting for wound management. However, tetanus has an average incubation period of 14 days, though it can range between 3–21 days after exposure. As a result, symptoms of infection are unlikely to be present at the time of initial presentation for an injury. Symptoms of an acute infection may include jaw cramping or the inability to open the mouth, muscle spasms (often in the back, abdomen, and extremities), and sudden painful muscle spasms, which can be triggered by sudden noises. Additional symptoms include trouble swallowing, seizures, headache, fever and sweating, and changes in blood pressure or a rapid heart rate [1].

When assessing a patient for potential tetanus infection, gathering detailed information about their history is essential. Several aspects of the patient’s history can provide crucial insights into the likelihood and severity of tetanus.

Immunization History

Understanding the patient’s vaccination status is critical in evaluating tetanus risk. Key details include the number of vaccine doses received and the timing of the most recent dose. Tetanus commonly occurs in individuals who are unvaccinated, under-vaccinated, or whose immunity has diminished over time. A history of incomplete or absent immunization is a frequent factor in tetanus cases, emphasizing the importance of vaccination in preventing this disease [7,8].

Questions: What is your immunization history against tetanus? Did you receive your childhood vaccinations? When was the last time you received an immunization other than those for flu or COVID? Have you seen a doctor recently for a cut or injury and received an immunization?

  • Important: Most cases occur in patients who are unimmunized or partially immunized.

Wound and Injury History

A thorough wound history is essential in identifying potential entry points for Clostridium tetani spores [6]. Recent injuries, even seemingly minor ones, should be noted, as traumatic wounds are the primary source of infection in most cases [8]. However, tetanus can sometimes develop without any obvious wounds or identifiable source of infection.

Question: How, what, and when did this injury occur?

  • In 70% of patients, a history of injury is present.
  • Most common points of entry include puncture wounds, abrasions, and lacerations.
  • Rare points of entry include chronic wounds, dental procedures, foreign bodies, and corneal abrasions.

Question: Was the object/item clean or dirty?

  • Ask about exposure to soil, ash, intestinal tracts/feces of animals and humans, or rusty tools such as nails, needles, and barbed wire.

Question: Has this happened before?

  • Explore any history of previous tetanus exposure or symptoms.

Wound Characteristics

The type and nature of the wound can provide additional clues. Punctures, lacerations, burns, surgical wounds, or injuries involving intravenous drug use are particularly susceptible to tetanus [8]. Unsanitary practices, such as home deliveries with contaminated tools for umbilical cord cutting, can also introduce the bacterium [8]. Wounds that are heavily contaminated, caused by blunt trauma, or involve animal or human bites carry a higher risk of infection. High-risk wounds include those older than 6 hours, deeper than 1 cm, contaminated, infected, and ischemic.

Incubation Period

The time between the injury and the onset of symptoms (the incubation period) is a key diagnostic factor [7]. A shorter incubation period, typically less than 48 hours, is associated with more severe disease [8]. While the incubation period can range from 1 to 60 days, most cases develop within 7 to 14 days, with an average of 7–10 days [1].

Early Symptoms

Tetanus often begins with subtle symptoms that progress over time. Common early signs include trismus (lockjaw), facial and neck muscle rigidity, and difficulty swallowing (dysphagia) [6,7]. Patients may report a sore throat or localized rigidity around the site of the infection. These early symptoms are often indicative of localized tetanus, where muscle stiffness is confined to a specific area [6].

Symptom Progression

In cases of generalized tetanus, the symptoms typically spread from the face and neck to the rest of the body [7]. Generalized painful muscle spasms and reflex spasms triggered by stimuli such as noise or touch are hallmark signs [8]. 

Risk Factors

Specific risk factors may increase the likelihood of tetanus. These include intravenous drug use, diabetes, recent surgical procedures, or unsanitary childbirth practices [6]. Neonatal tetanus, often resulting from unclean umbilical cord cutting, underscores the importance of the mother’s immunization status and sterile delivery practices [8]. Note that patients with an impaired immune system or a history of poor healing are at increased risk.

Additional Symptoms

Other reported symptoms may include fever, sweating, high blood pressure, rapid heart rate episodes, drooling, involuntary urination or defecation, and severe back arching spasms (opisthotonus) [1,6]. These manifestations often reflect the systemic effects of the tetanus toxin and its impact on the nervous system.

Special Populations

Special populations require targeted questions to better assess risk:

  • Intravenous drug users:
    • Do you share needles?
    • Where are your injection sites?
    • Is there a history of injecting in the neck region?
  • Newborns:
    • What is the mother’s immunization history? Did she receive a Tdap booster during this pregnancy?
    • Was the baby born at home or in a hospital?
    • Was soil applied to the umbilical stump?
    • What instruments were used, if any (applies to both home and hospital births)?
    • Has the neonate received any immunizations?

Finally, it is important to note that not all patients will present with an obvious injury. Approximately 3–5% of patients may have cryptogenic tetanus, where no identifiable entry point can be determined [5,6].

Physical Examination

The physical examination findings in tetanus are pivotal for diagnosis, which is primarily clinical and based on the presence of characteristic signs and symptoms. These features guide timely diagnosis and intervention, as delays in treatment can result in life-threatening complications. Findings vary depending on the type and severity of the infection, but certain hallmark features are common across all forms of tetanus.

General Physical Findings

Tetanus is primarily characterized by muscle rigidity and spasms, which often begin in the jaw and neck before progressing to other parts of the body [2]. A classic early finding is trismus (lockjaw), where patients cannot open their mouths due to masseter muscle spasms [6]. Another distinctive feature is risus sardonicus, a rigid, scornful smile caused by sustained contraction of the facial muscles [6]. Neck stiffness and dysphagia (difficulty swallowing) are other early symptoms caused by pharyngeal and neck muscle spasms [2].

Patients may also exhibit reflex spasms, which are generalized muscle contractions triggered by minimal external stimuli such as noise, light, or touch [6]. Signs of autonomic dysfunction include labile blood pressure, cardiac arrhythmias, and excessive sweating. Fever may be present in some cases, although patients are often afebrile. Importantly, patients with tetanus typically maintain an intact sensorium, remaining conscious and alert unless other brain dysfunction is present [7].

Findings in Generalized Tetanus

In generalized tetanus, muscle spasms follow a descending pattern, starting with the face (trismus and risus sardonicus) and progressing to the neck, back, and extremities [2]. A characteristic posture known as opisthotonus may develop, where the back and legs hyperextend while the arms flex, resembling decorticate posturing [6]. These spasms are often intense and may come in waves. Abdominal rigidity is another common feature, with patients exhibiting tenderness and guarding, sometimes mimicking an acute abdomen [2,7].

Findings in Localized Tetanus

Localized tetanus is marked by persistent muscle contractions confined to the area of the injury [2,6]. Patients may experience localized pain and spasms near the wound [6]. While typically less severe than generalized tetanus, localized tetanus can progress to more widespread symptoms in some cases.

Findings in Cephalic Tetanus

Cephalic tetanus involves dysfunction of the cranial nerves, most commonly the facial nerve. Physical exam findings include cranial nerve palsies, such as deviation of the eyes, eyelid retraction, and facial paralysis. Other associated symptoms include neck stiffness, dysphagia, and a deviated gaze [7].

Findings in Neonatal Tetanus

Neonatal tetanus often presents with poor feeding and difficulty sucking or breastfeeding [6]. Affected infants develop generalized rigidity and spasms, including opisthotonus, along with severe spastic contractions triggered by touch [8]. Additional findings include irritability and excessive crying [1,8].

Specific Diagnostic Tests and Other Findings

The spatula test is a clinical test with high sensitivity and specificity for tetanus [7]. Normally, touching the posterior pharyngeal wall with a spatula induces a gag reflex. In tetanus, it causes a reflex spasm of the masseter muscles, leading to the patient biting down instead of gagging.

Other findings include respiratory distress caused by spasms of respiratory muscles, including the diaphragm and larynx [1,2,8]. Severe muscle contractions can lead to complications such as joint dislocations, long bone fractures, and difficulty breathing [7]. Population studies reveal that lower extremity injuries are the most common antecedent to tetanus, followed by upper extremity and head or trunk injuries.

Alternative Diagnoses

Diagnosis of generalized tetanus is based entirely on the patient’s history and physical examination. Though the majority of cases will involve a preceding injury, making the presentation quite unique, there are aspects of the presentation that may mimic other conditions, which are important to rule out.

The initial presentation could include cranial nerve palsies, particularly in cephalic tetanus. For this reason, it is important to rule out critical conditions, including strokes, neoplasms, infections, or aneurysms. To accurately rule out other diagnoses, it is essential to familiarize yourself with the risk factors and presentations of each condition. Risk factors for stroke include uncontrolled hypertension, diabetes, and hyperlipidemia. Symptomatology may also include headache and localized extremity weakness. Strokes such as venous sinus thrombosis may occur in individuals who are pregnant, have hypercoagulable blood disorders, or use hormones. Neoplasms may present with a more insidious onset and a constellation of symptoms depending on the tumor’s location [6,7], such as headaches, seizures, fatigue, vision changes, gait abnormalities, nausea, and vomiting, in addition to cranial nerve palsy.

Infections will typically have an obvious source near the affected nerve. Parotitis may affect the facial nerve, and otitis media may involve the trigeminal nerve [6,7]. Peritonsillar abscess can cause trismus and neck stiffness, and must be differentiated from tetanus. Meningitis can also lead to cranial nerve palsies but will likely present with preceding neck rigidity, altered mental status, and systemic symptoms concerning for sepsis. Lyme disease may also cause facial nerve palsy and classically follows a tick bite, often occurring after hiking in the Northeastern United States. Botulism is  severe neurological condition caused by a toxin produced by Clostridium botulinum. It presents with flaccid paralysis, dysphagia, and cranial nerve palsies, but does not involve muscle spasms or hypertonia [8].

Muscle spasms and rigidity described in tetanus may also present similarly to other conditions, such as dystonic reactions or neuroleptic malignant syndrome [7,8]. However, these conditions are closely linked to the use of antipsychotic medications and could likely be ruled out after a thorough review of the patient’s medication list [7]. Administration of medications such as diphenhydramine or benztropine would reverse the symptoms in a dystonic reaction but not in tetanus. Strychnine poisoning, a chemical sometimes used in pesticides, is also associated with ingestion and presents with symptoms of hyperreflexia, clonus, and muscle rigidity [6,7]. Critical to this diagnosis is the patient’s history before presentation, as well as the rapid onset of symptoms, typically within 10–20 minutes. Serotonin Syndrome can cause muscle rigidity, and should be considered in the differential diagnosis of tetanus [7]. Low calcium levels can cause muscle spasms, but the autonomic features of tetanus, such as fluctuating blood pressure and heart rate, are usually absent [8].

In addition to contractions and cranial nerve palsies, tetanus may present with systemic symptoms related to autonomic overactivity. These include diaphoresis, tachycardia, cardiac arrhythmias, labile hypertension, and fever. These symptoms might overlap with those seen in sympathomimetic or cholinergic toxicities; however, these toxicities are usually closely tied to the patient’s medications or a reported history of ingestion.

Acing Diagnostic Testing

The diagnosis of tetanus is primarily clinical, relying heavily on the patient’s history and physical examination. There is no single diagnostic test that can definitively confirm or rule out tetanus. However, diagnostic tests may be useful to exclude other potential etiologies that mimic tetanus symptoms.

Bedside Tests

  • Point-of-Care Glucose: Hypoglycemia can mimic certain neurological symptoms, such as cranial nerve palsies, and should be assessed promptly.
  • Spatula Test: This bedside test involves touching the posterior oropharynx with a tongue blade [7].
    • Normal Response: In normal circumstances, this action elicits a gag reflex, and the patient will try to expel the spatula.
    • Positive Test (Tetanus): If tetanus is present, the patient will develop a reflex spasm of the masseter muscles and will bite down on the spatula instead of gagging. A positive response, where the patient bites down rather than gagging, is 94% sensitive and 100% specific for tetanus [6].
  • Electrocardiogram (ECG): If the patient presents with tachycardia, an ECG can help evaluate for arrhythmias and identify other possible underlying causes.

Laboratory Tests

  • Blood Counts and Blood Chemistry: These tests are typically unremarkable in tetanus, meaning they do not show specific changes that help in diagnosing the condition [6]. They can be useful in excluding other causes of a patient’s symptoms.
  • Calcium: Hypocalcemia may cause muscle spasms and cramping, and it is important to rule this out.
  • Creatine Kinase (CK): Prolonged muscle spasms and rigidity in tetanus can result in muscle damage, potentially leading to rhabdomyolysis, making CK levels crucial to monitor.
  • Creatinine: Kidney function should be evaluated, particularly if rhabdomyolysis is suspected, as it can lead to acute kidney injury.
  • Drug Screen: This may help rule out the ingestion of sympathomimetics, such as cocaine, which can cause symptoms similar to tetanus.
  • Wound cultures: Wound cultures can occasionally isolate Clostridium tetani, but they are not a reliable diagnostic tool for tetanus. Cultures are positive in only about 30% of confirmed tetanus cases, and the organism can sometimes be isolated from wounds of individuals who do not exhibit any symptoms of tetanus. Additionally, the challenges in culturing C. tetani and the possibility of isolating non-toxigenic strains further limit the diagnostic utility of this method [2,7,8]. 
  • The antitoxin assay measures serum levels of tetanus antitoxin. While not widely available, a serum antitoxin level of 0.01 IU/mL or higher is typically considered protective and reduces the likelihood of tetanus. However, this test is not consistently reliable and is not commonly utilized for diagnostic purposes.

Imaging

  • CT of the Head: A head CT scan can help exclude intracranial pathologies, such as stroke or mass lesions, that may mimic tetanus symptoms, especially in cases involving cranial nerve palsies.
  • CT of the Abdomen: In cases of localized tetanus affecting the abdomen, a CT scan might be necessary, as the presentation can resemble an acute abdomen.

Risk Stratification

The severity of a tetanus infection is multifactorial. Factors such as age, immunity, location of injury, depth of injury, and ultimately the quantity of tetanus toxin contribute to the development of generalized tetanus. A longer interval between symptom onset and the appearance of spasms has been linked to milder features. Ultimately, risk stratification after the onset is difficult to accurately assess, as all forms of tetanus may develop into generalized tetanus. Therefore, prevention via immunization and subsequent boosters for high-risk wounds is crucial.

Management

In severe cases of tetanus, critical patients should be managed systematically using the ABCDE approach [5]. This approach ensures comprehensive assessment and treatment of the patient’s condition.

Airway and Breathing

Early intubation and mechanical ventilation should be strongly considered to manage airway compromise caused by trismus, laryngospasm, and neck and chest wall rigidity, which can impair airway access and create ventilation challenges [5]. The use of succinylcholine and other depolarizing paralytic agents should be avoided due to the risk of hyperkalemia.

Circulation

For patients exhibiting systemic illness, standard sepsis treatment should be initiated, including the administration of intravenous fluids, blood cultures, and broad-spectrum antibiotics [5].

Antimicrobial therapy options include:

  • Metronidazole 500 mg intravenously every 6 to 8 hours (first-line therapy).
  • Penicillin G 2 to 4 million units intravenously every 4 to 6 hours (second-line therapy).
  • Doxycycline 100 mg intravenously every 12 hours.

To neutralize unbound tetanus toxin, the following measures are recommended:

  • Human Tetanus Immune Globulin (HTIG) 500 units intramuscularly [9]:
    • Administer a portion of the dose at a different site from the tetanus toxoid vaccine.
    • Inject part of the dose directly around the wound.
    • This dosage is the same for adults and pediatric patients.
  • If HTIG is unavailable, intravenous immune globulin should be used.

In cases of autonomic dysfunction, pharmacological interventions include:

  • Labetalol (0.25 to 1 mg/minute) to block adrenergic responses through dual alpha- and beta-blockade. Note that beta-selective blockers should be avoided due to increased associated mortality [5].
  • Magnesium sulfate:
    • Loading dose: 40 mg/kg over 30 minutes.
    • Continuous infusion: 2 g/hour for patients >45 kg or 1.5 g/hour for patients ≤45 kg.
    • This is considered first-line or adjuvant therapy to reduce muscle spasms,

and toxicity monitoring should include checking for hyporeflexia.

  • Morphine (0.5 to 1 mg/kg/hour) can be used as a continuous infusion for managing autonomic dysfunction and sedation.

Disability: Control of Muscle Spasms

Effective spasm control is essential to prevent complications such as rhabdomyolysis, fractures, and apnea [5]. Recommended treatments include:

  • Benzodiazepines:
    • Diazepam: 10–40 mg intravenously every 1 to 4 hours as needed.
    • Midazolam: Continuous infusion at 5–15 mg/hour.
  • If benzodiazepines fail, neuromuscular blockade may be necessary. This requires endotracheal intubation and the use of:
    • Vecuronium: Initial bolus dose of 0.08 to 0.1 mg/kg, followed by continuous infusion at 0.8 to 1.7 µg/kg/minute.
    • Rocuronium: Initial bolus dose of 0.6 to 1 mg/kg, followed by continuous infusion at 8 to 12 µg/kg/minute.
    • Consider intravenous propofol or intrathecal baclofen for refractory spasms.

Exposure: Identifying and Managing the Source

A thorough skin examination is necessary to identify potential sites of inoculation, including acute skin breaks and chronic wounds. Proper wound care includes cleaning and debridement to remove the source of infection.

To minimize muscle spasms triggered by sensory stimuli, patients should be admitted to the ICU with precautions such as:

  • Reducing exposure to loud noises, bright lights, and sudden movements.
  • Avoiding other forms of sensory stimulation.

In cases where a tetanus infection is possible, but no clinical signs or symptoms are present, the patient should undergo thorough wound irrigation and debridement. In addition, the patient’s immunization record should be reviewed. If it is unclear whether the patient has ever received their initial series of tetanus shots (part of the WHO-recommended childhood immunization series), proceed with a primary series of 3 tetanus shots and boosters every 10 years. If the patient presents with high-risk wounds and their last booster was received more than 5 years prior, provide a booster.

Patients who are unimmunized, incompletely immunized, or for whom immunization history is unclear should also receive Human Tetanus Immunoglobulin (HTIG). HTIG neutralizes the tetanus toxin and provides passive immunization for 3–4 weeks while the tetanus immunization series begins to provide immunity [9]. People with severe immunodeficiency or HIV infection presenting with high-risk wounds should also receive tetanus immune globulin, regardless of vaccination history [2].

This medication is administered by intramuscular injection. A dose of 250 IU (250 IU/ml, 1 ml) is given for wounds sustained within 24 hours, or 500 IU (250 IU/ml, 2 ml) for wounds older than 24 hours [9]. HTIG is also given for the treatment of tetanus once symptoms arise, to bind any circulating tetanus toxoid not bound to neurons and prevent further binding [2]. The treatment dose is 500 IU as a single dose, to be injected into 2 different sites, for all ages, from neonates through adults [10].

Medications

Human Tetanus Immunoglobulin (HTIG)

Dosage and Administration

For wound prophylaxis, the recommended dosage of Human Tetanus Immunoglobulin (HTIG) is based on the time elapsed since the injury [9]:

  • Within 24 hours: 250 IU (250 IU/mL, 1 mL).
  • After 24 hours: 500 IU (250 IU/mL, 2 mL).

HTIG is administered as a single dose via intramuscular (IM) injection. It should not be given intravenously to avoid complications.

Use During Pregnancy and Breastfeeding

HTIG is considered safe in pregnancy and breastfeeding and is categorized as Category C for all trimesters [10]. A small number of case reports suggest that IgG and IgM antibodies may transfer into colostrum and breast milk [10].

Cautions and Considerations
  1. Allergic Reactions: Although rare, allergic reactions may occur. HTIG should not be administered to patients with a known allergy to the immunoglobulin.
  2. Injection Technique: Proper technique is critical to avoid complications:
    • Ensure the injection does not enter a blood vessel, as this can lead to shock. To confirm, aspirate prior to administering the dose.
  3. General Precautions: Monitor the patient for any signs of an adverse reaction following administration.

Special Patient Groups

Pediatrics

Primary immunization is key in this group. Passive immunization from a fully vaccinated mother provides protection before infant vaccines are begun. Additionally, living environments free from high-risk exposures (e.g., rusty nails, fences) is important. Dtap is used for children ≤7 years old, while Tdap or Td is recommended for children >7 years old and adolescents [2].

Pregnant Patients

All pregnant women should receive a tetanus booster during every pregnancy, regardless of prior vaccination history, with Tdap vaccination recommended between 27–36 weeks of gestation [2,6]. This protects the newborn from pertussis, tetanus, and diphtheria by transferring maternal antibodies for passive immunity. If the childhood immunization series was completed but the last booster was over 10 years ago, a single booster dose is recommended. For unvaccinated or incompletely vaccinated individuals, at least two doses of a tetanus toxoid-containing vaccine (one of which must be Tdap) should be administered during pregnancy, with the series completed postpartum [2]. Preventive strategies to reduce neonatal tetanus risk include clean delivery practices and proper umbilical cord care, as unsanitary home deliveries or contaminated tools are common causes of neonatal infections [1,8]. For wound management, Tdap is indicated if more than five years have elapsed since the last dose, and TIG is recommended for tetanus-prone wounds in inadequately vaccinated women. Vaccination during pregnancy is safe, with no evidence of adverse outcomes, and plays a critical role in global efforts to eradicate maternal and neonatal tetanus.

Geriatrics

Tetanus in geriatric populations presents unique challenges due to waning immunity, comorbidities, and increased disease severity [6]. Older adults face a higher incidence of tetanus, with mortality rates significantly greater than in younger populations. For example, in the U.S., individuals aged 65 years or older have an incidence rate of 0.23 cases per 1 million, compared to 0.08 cases per 1 million in those under 65, and they account for the majority of tetanus deaths [6]. Waning immunity is a major factor, with only 28% of adults over 70 years immune. Clinical presentations often include trismus, rigidity, and spasms, but geriatric patients are at greater risk for complications such as respiratory failure, cardiac arrhythmias, and aspiration pneumonia, leading to poor prognosis [2]. Individuals in this group need to receive booster doses every 10 years and should have living environments free from high-risk exposures [2,6]. Intensive care management, supportive care, and public health education are crucial to improving outcomes [5,8].

When To Admit This Patient

Tetanus carries a significant burden of morbidity and mortality for patients who experience an infection. Accordingly, it is appropriate to maintain a low threshold to admit any patient in whom you suspect an acute tetanus infection.

In individuals presenting with signs or symptoms of tetanus infection, or in individuals deemed to be at high risk of developing tetanus who did not receive prophylactic vaccination or immunoglobulins after initial exposure, admission to the Intensive Care Unit (ICU) or a similarly capable unit with ventilator support is recommended. For hospitals without an ICU, it is recommended to pursue transfer to a facility with higher-level care whenever possible.

In individuals presenting immediately following exposure to tetanus toxins, risk stratification should be performed as outlined earlier, with vaccination status playing a significant role in determining intervention. Asymptomatic patients who are exposed to tetanus toxins but are adequately vaccinated or receive immunization with or without tetanus IVIG in the emergency department may be safely discharged. For discharged patients, extensive teaching about the signs and symptoms of tetanus infection should be provided, along with strict instructions to return immediately to the Emergency Department if any symptoms develop.

Revisiting Your Patient

The image was produced by using ideogram 2.0.

A thorough physical exam reveals a 4 cm, linear wound on the left cheek that is oozing dark blood and contains soil. There is no disruption of the underlying buccal mucosa. Additionally, there are multiple deep, penetrating wounds to the bilateral hands and distal forearms that also contain dirt and soil but are currently hemostatic. No evidence of other injuries is observed. Visual acuity is intact in both eyes. A neurologic exam, including cranial nerves, is diffusely within normal limits. The patient is neurovascularly intact in all extremities, with no signs of cyanotic tissue. The wounds are copiously irrigated and cleansed while further information is gathered.

The patient’s parents report that she has received inconsistent medical care since birth because “she has been healthy.” They also state that they do not believe she has received standard childhood vaccinations. X-rays of the bilateral wrists and forearms do not demonstrate foreign bodies or bony injuries.

This patient is hemodynamically stable with hemostatic wounds. Based on the findings from the history and physical exam, you decide that this patient should receive tetanus immunization as well as tetanus immunoglobulin therapy. Red flags in this patient’s case include the history of inconsistent medical care, previous infection with “German Measles” (Rubella), which children are routinely vaccinated against in many countries, and the presence of deep, contaminated wounds.

Moreover, due to this child’s lack of vaccination history, it is recommended that she receive a full 3-dose primary tetanus vaccination series. Wound care should also be initiated, and sutures are likely indicated for this patient.

Authors

Picture of Grace Bunemann

Grace Bunemann

Grace Bunemann, DO is an emergency medicine resident at Rush University Medical Center in Chicago, Illinois. She currently serves on the Emergency Medicine Residents’ Association Board of Directors as Director of Leadership Development. She also assists with the EMRA Global Emergency Medicine Student Leadership Program. She plans to pursue a global emergency medicine fellowship after finishing residency with a focus in equitable health systems and medical education.

Picture of Alex Gallaer

Alex Gallaer

Alex Gallaer, MD is an Emergency Medicine resident in the Global Health track at the University of Utah. He is a facilitator for EMRA’s Global Emergency Medicine Leadership Program and has interests in equitable medical care, establishment of global health infrastructure, prehospital/disaster medicine, and medical education.

Picture of Jerry Oommen

Jerry Oommen

Jerry Oommen, DO is a global emergency medicine fellow at The George Washington University and a fellow co-director of ACEP's Global Emergency Medicine Student Leadership Program. Primary areas of global health interest include medical education and capacity building. 

Picture of Ashley Pickering

Ashley Pickering

Before medical school I had a diverse career path, which included biomedical engineering, outdoor education, working as an EMT on a Colorado ski patrol, and critical care nursing. I lived out west for 15 years, mainly in CO, and went to medical school at University of Arizona in Tucson before moving to Baltimore for residency at University of Maryland. Currently I am a Global Emergency Medicine Fellow at University of Colorado. Throughout my training I have found ample opportunities to pursue my interest in building emergency care globally. I have researched the barriers to accessing emergency care in rural Uganda, helped to provide emergency care training in Sierra Leone and Liberia and am currently the Executive Director of Global Emergency Care a non-profit training non-physician clinicians in Uganda. My current focus is on quality of emergency care in LMICs. I am working on an WHO Emergency Care Toolkit implementation project which explores the impact of basic emergency care educational and process improvements on clinical indicators of quality, as well as the experiences patients and staff.

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References

  1. World Health Organization. Tetanus.  https://www.who.int/news-room/fact-sheets/detail/tetanus. Published July 12, 2024. Accessed April 5, 2023.
  2. Centers for Disease Control and Prevention. Chapter 21: Tetanus. In: Epidemiology and Prevention of Vaccine-Preventable Diseases. Updated April 25, 2024. Accessed January 7, 2025. https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-21-tetanus.html
  3. Behrens H, Ochmann S, Dadonaite B, Roser M. Tetanus. Our World in Data. Published March 2019. Updated January 2024. Accessed January 7, 2025. https://ourworldindata.org/tetanus
  4. Li J, Liu Z, Yu C, et al. Global epidemiology and burden of tetanus from 1990 to 2019: A systematic analysis for the Global Burden of Disease Study 2019. Int J Infect Dis. 2023;132:118-126. doi:10.1016/j.ijid.2023.04.402
  5. Jain Rupal, Felipe Naillid. EM:RAP. Tetanus. In: CorePendium. Accessed January 7, 2025. https://www.emrap.org/corependium/chapter/recGn75URBGNVcZTD/Tetanus
  6. Yabes JM Jr. Tetanus. Medscape. Updated December 15, 2024. Accessed January 7, 2025. https://emedicine.medscape.com/article/229594-overview
  7. Bae C, Bourget D. Tetanus. [Updated 2023 May 31]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459217/
  8. George EK, De Jesus O, Tobin EH, et al. Tetanus (Clostridium tetani Infection) [Updated 2024 Feb 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482484/
  9. Médecins Sans Frontières. Human Tetanus Immunoglobulin (HTIG). In: MSF Medical Guidelines. Accessed January 7, 2025. https://medicalguidelines.msf.org/en/viewport/EssDr/english/human-tetanus-immunoglobulin-htig-16688425.html
  10. Physician’s Desk Reference: Tetanus Immune Globulin Human. HyperTET S/D (tetanus immune globulin (human)) dose, indications, adverse effects, interactions… from PDR.net. https://www.pdr.net/drug-summary/HyperTET-S-D-tetanus-immune-globulin–human–2085.1437. Accessed April 5, 2023.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Sepsis (2024)

~ iEM Education Project Team ~ Leave a comment

by Tina Samsamshariat, Ardeshir Kianercy, & Elizabeth DeVos

Authors
Listen

You Have A New Patient!

A 75-year-old female with a history of diabetes, hypertension, and tobacco use disorder is brought to the emergency department by her granddaughter due to increasing confusion. The patient was diagnosed with influenza two weeks ago by her primary care physician. Yesterday, she began to complain of a productive cough and shortness of breath. Her current medications include lisinopril, metoprolol, and metformin.

Upon examination, the patient is oriented only to herself. Her blood pressure is 94/48 mm Hg, heart rate is 128 beats per minute, respiratory rate is 30 breaths per minute, and her temperature is 39°C. Oxygen saturation is 88% on room air. The physical exam shows increased work of breathing, rales, and cool, clammy skin.

The image was produced by using ideogram 2.0.

What Do You Need To Know?

Importance

Sepsis is a critical medical condition that demands urgent attention due to its significant impact on patient outcomes and healthcare systems. Early detection and treatment of sepsis are crucial, as they can substantially reduce mortality rates, treatment delays, and improve appropriate care. In intensive care units (ICUs), sepsis poses a considerable challenge, with its management requiring substantial resources and expertise. Moreover, sepsis has far-reaching consequences beyond immediate patient care, affecting healthcare costs and long-term patient outcomes.

Epidemiology [1-3]

In 2017, there were an estimated 48.9 million incident cases of sepsis and 11 million sepsis-related deaths, accounting for approximately 20% of all global deaths. The global burden of sepsis is challenging to quantify, with low- and middle-income countries bearing the highest burden of cases and deaths. Sepsis can arise from infections in both community and healthcare settings, with diarrheal diseases and lower respiratory infections being the leading contributors to sepsis cases and mortality. Additionally, noncommunicable diseases and injuries significantly contribute to the sepsis burden. Despite these challenges, sepsis is treatable when identified and managed promptly. To address this, the World Health Organization has emphasized the importance of strengthening global efforts in the prevention, identification, diagnosis, and clinical management of sepsis.

Definitions

Term

Definition

 

Sepsis

Life-threatening organ dysfunction from dysregulated host response to infection

 

Organ Dysfunction

An acute change in the total Sequential Organ Failure Assessment (SOFA) score ≥2 points from baseline

 

Septic Shock

Sepsis with circulatory and metabolic abnormalities are profound enough to substantially increase mortality.

SIRS (systematic inflammatory response syndrome)

At least 2 of the following:

  • Heart rate > 90 beats/min
  • Respiratory rate > 20 cycles/min or PaCO2 <32 mm Hg
  • Temperature > 38°C or < 36°C
  • WBC > 12,000/mm3, < 6,000/mm3 or > 10% bandemia

qSOFA (adapted SOFA score tool to assess risk of poor outcome in sepsis):

At least 2 of the following indicates higher rate of mortality:

  • Respiratory rate ≥ 22/min
  • Altered mentation (GCS < 15)
  • Systolic blood pressure < 100 mm Hg

Pathophysiology [3-6]

Sepsis is a syndromic response to infection with biological, biochemical, and physiologic manifestations. The sepsis response exists on a spectrum ranging from infection to septic shock. The definition continues to evolve as the pathophysiology is better understood. The previous definitions of sepsis emphasized at least two of the four SIRS criteria (see Table above). Multiple inflammatory processes can cause SIRS and is not specific to sepsis. The SIRS criteria have been removed from the current definition of sepsis because they do not appropriately capture the life-threatening organ dysfunction critical to the pathophysiology. Thus, severe sepsis, previously defined as sepsis complicated by organ dysfunction, has also been removed because of redundancy.

The newest definition of sepsis goes beyond SIRS to account for the early activation of pro- and anti-inflammatory responses as well modifications in non-immune modulated pathways. Furthermore, it is recognized that the clinical and biological manifestations of sepsis are heterogeneous depending on age, comorbidities, sex, and source of infection. A higher SOFA score is associated with an increased probability of mortality. The quick SOFA or qSOFA has been adapted for rapid bedside assessment of patients with infection, prompting further workup for organ dysfunction. While a positive qSOFA should alert clinicians to possible sepsis, it is not recommended to be used as a single screening tool because of its poor sensitivity. Artificial intelligence (AI) systems alert clinicians to a patient’s risk of sepsis, which may improve patient outcomes compared to traditional methods in hospitals where AI is adopted. The role of machine learning in detecting sepsis continues to be an area of research.

Sepsis progresses to septic shock when a patient displays hypotension requiring vasopressors to maintain MAP ≥65 mm Hg and hyperlactatemia (lactate > 2 mmol/L [18 mg/dL]) after volume resuscitation. Hospital mortality exceeds 40% when septic shock criteria are met.

If patients are suspected to be septic, rapid source identification, assessment, and management of their clinical status is crucial to prevent acute deterioration and progression to septic shock and death.

Medical History [7,8]

Recognizing risk factors for sepsis is important, as they significantly contribute to its incidence and associated mortality.

Key risk factors for sepsis incidence and mortality

  • Intensive care unit admission
  • Hospitalization
  • Vulnerable population: elderly age (age > 65), pregnant or recently pregnant women, neonates, poverty
  • Immunosuppression
    • HIV/AIDS
    • Cirrhosis
    • Asplenia
    • Autoimmune disease
    • Chronic kidney disease
    • Corticosteroids
    • Diabetes
  • Cancer
  • Genetic predisposition
  • Major surgery
  • Burns
  • Alcohol Use Disorder
  • Social factors: access to immunizations, access to timely healthcare

When taking a history from a patient with suspected sepsis, it is crucial to gather comprehensive and relevant information to guide the diagnosis and management. Here are key areas to focus on:

Recent Illness or Infection

  • Ask about any recent symptoms of infection, such as fever, chills, cough, urinary symptoms, or abdominal pain. Determine the duration and progression of these symptoms.

Medical History

  • Inquire about the patient’s past medical history, including chronic conditions like diabetes, heart disease, lung disease, and cancer. These conditions can increase the risk of sepsis and influence the management plan.

Immune Status

  • Determine if the patient has a compromised immune system due to factors such as recent chemotherapy, HIV/AIDS, or use of immunosuppressive medications. This information is vital as these patients are at higher risk of severe infections and sepsis.

Recent Procedures or Hospitalizations

  • Ask about any recent surgeries, hospitalizations, or invasive medical procedures, as these can be sources of infection leading to sepsis.

Current Medications

  • Obtain a list of the patient’s current medications, including antibiotics, immunosuppressants, and any other relevant drugs that might impact the immune response or treatment plan.

Symptoms of Sepsis

  • Look for signs and symptoms suggestive of sepsis, such as:
    • High or low-temperature
    • Confusion or altered mentation
    • Extreme pain or discomfort
    • Shortness of breath
    • Clammy or sweaty skin
    • High heart rate
    • Low blood pressure
    • Rapid breathing
    • Chills
    • Low urine output

Exposure History

  • Ask about any potential exposures to infectious agents, such as recent travel, contact with sick individuals, or exposure to animals that could carry pathogens.

Social and Lifestyle Factors

  • Gather information about the patient’s social and lifestyle factors that might influence their risk for infection or sepsis, such as living conditions, hygiene practices, and any recent illnesses in family members or close contacts.

Physical Examination [2,7-9]

The earliest signs of sepsis often include changes in vital signs and symptoms related to common infectious sources, such as cough, dyspnea, abdominal pain, dysuria, emesis, diarrhea, back pain, oliguria, focal neurological deficits (FND), rash, or skin changes.

Vital sign changes indicative of sepsis, septic shock include a temperature greater than 38.3°C or less than 36°C, tachycardia exceeding 90 beats per minute (or more than two standard deviations above the normal value for age), tachypnea greater than 20 breaths per minute, and arterial hypotension, defined as systolic blood pressure (SBP) less than 90 mmHg, mean arterial pressure (MAP) below 70 mmHg, a decrease in SBP of over 40 mmHg, or values falling more than two standard deviations below the normal range for age.

Signs of end-organ perfusion problems may also be present, including altered mental status, oliguria, ileus, and hypoxemia.

As sepsis progresses to septic shock, decreased capillary refill, cyanosis, and skin mottling may occur due to blood flow being diverted to core organs. In compensated shock, patients may exhibit warm skin with bounding pulses, whereas uncompensated shock is characterized by cool skin and thready pulses.

Figure 1 - Common Physical Exam Findings (Depending on Infectious Source)

Alternative Diagnoses [7-8]

As we mentioned above, SIRS can be caused by various reasons, and it is not specific to sepsis; many non-infectious etiologies should be considered in differential diagnoses; these are;

Shock Causes

  • Distributive shock, Anaphylaxis
  • Hemorrhagic shock
  • Cardiogenic shock
  • Obstructive shock

Cardiac/pulmonary

  • Acute respiratory distress syndrome
  • Pulmonary embolism

Endocrine

  • Adrenal Crisis
  • Pancreatitis
  • Diabetic ketoacidosis

Hematologic

  • Disseminated Intravascular Coagulation
  • Anemia

Other

  • Toxic Shock Syndrome
  • Drug Toxicity

Acing Diagnostic Testing

The diagnosis of sepsis and septic shock is often made at the bedside, integrating the patient’s history, physical examination, laboratory findings, and imaging results. A thorough history and physical examination is essential, considering factors such as medical, social, and travel history, immunization status, and pregnancy. A comprehensive physical exam, including neurologic, oropharyngeal, skin, and genitourinary assessments, is crucial to identify potential sources of infection and guides diagnostic testing.

Sepsis is a complex condition with diverse clinical and laboratory manifestations, requiring a multifaceted diagnostic approach. Laboratory findings in sepsis can reveal critical abnormalities across hematologic, metabolic, and inflammatory markers. Hematologic findings often include leukocytosis or leukopenia, thrombocytopenia, and bandemia (an excess of immature neutrophils, commonly referred to as a “left shift”). Coagulation abnormalities are also frequently observed. Metabolic disturbances can manifest as hyperglycemia (even in the absence of diabetes), elevated creatinine, and hyperbilirubinemia, reflecting multi-organ involvement. Elevated inflammatory markers, such as C-reactive protein (CRP) and procalcitonin, are common, along with hyperlactatemia, which often indicates tissue hypoperfusion and metabolic stress. Other key laboratory findings may include hypoxemia, suggestive of impaired oxygenation or underlying respiratory dysfunction.

While there are no specific imaging findings unique to sepsis, radiologic evaluations can help identify potential sources of infection. For instance, a chest X-ray may reveal pneumonia, abdominal computed tomography (CT) can detect abscesses, and ultrasound is useful for identifying conditions such as cholecystitis. These imaging modalities are critical for localizing infection and guiding targeted therapy.

A critical component of sepsis evaluation involves microbiologic investigations. Blood cultures, ideally obtained before initiating antibiotics, are a cornerstone of diagnostic testing, though they often yield negative results. Sepsis can be caused by a wide range of pathogens, including gram-positive and gram-negative bacteria, as well as fungi. For neonates and pregnant individuals, Group B Streptococcus remains the leading pathogen.

Laboratory investigations should include a complete blood count, comprehensive metabolic panel, coagulation studies, liver function tests, lactate, CRP, and procalcitonin levels. Arterial or venous blood gas analysis can provide additional insights into respiratory and metabolic status. Urinalysis and respiratory viral testing, including for COVID-19, may also be warranted based on clinical presentation. Culture collection, such as blood, urine, sputum, tracheal aspirates, wound swabs, or cerebrospinal fluid (CSF), is essential for pathogen identification, with at least two sets of blood cultures recommended before antibiotic administration.

Imaging studies should be guided by clinical suspicion and patient history. Chest X-rays, CT scans, magnetic resonance imaging (MRI), and ultrasound can help identify the infection’s origin and extent, facilitating more accurate and timely treatment decisions.

The table below shows common sources of sepsis by system, clinical signs, and appropriate diagnostic testing (Original by the authors).

 

System

 

 

Possible Diagnoses

 

Signs / Symptoms

 

Potential Testing

Pulmonary

Pneumonia, Lung Abscess

 

Cough, dyspnea, sputum production, rales, effusion

CXR, lung ultrasound, culture

Skin/Soft tissue

Indwelling Catheters, Cellulitis, necrotizing fasciitis

 

Erythema, warmth, necrosis, pain, petechiae, rash

Site cultures, CT, ultrasound

Intraabdominal           

Cholecystitis, cholangitis, appendicitis, diverticulitis, spontaneous bacterial peritonitis, Clostridium difficile

Abdominal pain, jaundice, nausea, emesis, diarrhea, guarding, rigidity

CT, ultrasound, KUB, stool culture

Cardiac

Endocarditis, myocarditis

Murmurs, history of valve disease

Echocardiogram, blood culture

Genitourinary

Pyelonephritis, urinary tract infection, pelvic inflammatory disease, tuboovarian abscess, endometritis, septic abortion, prostatitis

Dysuria, urinary hesitancy, flank pain, vaginal discharge, genital pain

CT, UA, urine culture, blood culture 

Neurologic

 

Meningitis, cerebral abscess, epidural abscess 

Nuchal rigidity, altered mental status (AMS), FND

CT, CSF culture, MRI

Orthopedic

Osteomyelitis, septic arthritis, indwelling hardware

AMS, pain

XR, CT, culture

Otolaryngologic

Epiglottis, croup, peritonsillar abscess, retropharyngeal abscess, mastoiditis

Stridor, trismus, swelling, temporal bone tenderness

CT, culture

Risk Stratification [9-11]

The severity of sepsis is assessed based on the degree of organ dysfunction. Laboratory findings, vital signs, and physical examination are critical in determining the severity. In the emergency department, clinicians should integrate multiple clinical and laboratory findings to guide the diagnosis. Initial lactate measurements, as well as repeat measurements after initial resuscitation, are essential, particularly if lactate levels exceed 4 mmol/L or if there is suspicion of clinical deterioration. The Sequential Organ Failure Assessment (SOFA) score is a valuable tool for evaluating organ dysfunction.

Clinicians must assess each patient individually, taking into account the type of underlying infection, the degree of hemodynamic instability, the extent of hyperlactatemia, and the presence of signs of end-organ failure. This comprehensive evaluation is crucial for accurately determining the severity of sepsis and guiding appropriate management.

Management [7-9, 12-14]

Immediate Actions in the Emergency Department

Immediate actions in the emergency department are often performed simultaneously:

  1. Stabilize the Airway: Administer supplemental oxygen to maintain oxygen saturation levels at ≥92%.
  2. Cardiac Monitoring: Place the patient on a cardiac monitor to assess rhythm and hemodynamic status.
  3. Intravenous Access: Establish intravenous access and anticipate the need for a central venous catheter and invasive blood pressure monitoring if necessary.
  4. Evaluation for Infectious Source: Perform a thorough assessment to identify potential infectious sources.

Initial Resuscitation

Initial resuscitation in sepsis management focuses on two primary goals:

  1. Restoring Tissue Perfusion
  2. Initiating Antimicrobial Therapy

Restoring Tissue Perfusion

Fluids:

  • Administer rapid IV fluid boluses (500 mL) of balanced crystalloid solutions in patients with hypotension or hypoperfusion, provided there is no evidence of fluid overload.
  • Consider an infusion of 30 mL/kg of balanced crystalloid IV fluids as initial therapy, with careful monitoring of the patient’s response rather than delivering a pre-specified volume.
  • Balanced crystalloid solutions (e.g., Ringer’s Lactate or Plasmalyte) are preferred over saline due to the risk of hyperchloremic metabolic acidosis and renal impairment associated with saline infusions.

Vasopressors:

  • Initiate vasopressor therapy alongside fluid administration if hypotension persists.
  • Norepinephrine is the first-line vasopressor for all patients with septic shock.
  • Vasopressin (0.03 to 0.04 U/min) may be used as an adjunct to norepinephrine.
  • Epinephrine is a second-line agent for patients with ongoing hypotension or myocardial depression.
  • Titrate vasopressors to maintain a mean arterial pressure (MAP) of ≥65 mm Hg.
  • While central access is not mandatory for the early initiation of vasopressors, peripheral access is adequate for initial delivery.

Antimicrobial Therapy

Choice of Antibiotics:

  • Begin broad-spectrum antibiotics targeting both gram-positive and gram-negative bacteria if the pathogen is unidentified.

Timing:

  • Early initiation of antibiotics is strongly associated with improved survival outcomes.
  • Initiate antibiotics within the first hour of presentation, after obtaining necessary cultures. Do not delay antibiotic administration for testing.

Antivirals and Antifungals:

  • Consider antiviral therapy for patients with severe viral infections such as COVID-19, influenza, or herpes simplex virus.
  • Initiate antifungal therapy in high-risk patients when indicated.

Source Control

Early source control is critical in managing sepsis:

  • Identify and treat infectious sources promptly.
  • Remove or drain indwelling catheters and soft tissue abscesses in the emergency department.
  • Obtain cultures of other potentially infected fluid collections, such as pleural effusions or ascites.
  • Consult specialists for managing complex infections, such as hemodialysis lines, biliary obstructions, necrotizing soft tissue infections, or deep abscesses.

Continued Management

Following initial resuscitation, patients should be frequently re-evaluated for clinical, hemodynamic, and laboratory changes. Additional fluids should be administered based on the patient’s response to therapy.

Evaluating Fluid Response:

  • Clinical Parameters: Assess capillary refill, urine output, and mental status.
  • Quantitative Parameters: Use tools such as central venous pressure, passive leg raise tests, or inferior vena cava (IVC) collapsibility on point-of-care ultrasound (POCUS).
  • Tutorials for POCUS may include IVC measurement, IVC collapsibility, and IVC plethora.

Other Treatments

  • Corticosteroid Therapy: Empiric use is generally not recommended unless treating for a coexisting condition.
  • Adjunctive Therapy: Therapies such as angiotensin II (or its analogs), vitamin C, vitamin D, and thiamine are not recommended for routine use in sepsis management.

Special Patient Groups

Pediatrics [15-17]

Sepsis is the leading cause of pediatric mortality worldwide, with common comorbidities including lung disease, congenital heart disease, neuromuscular disorders, and cancer. Compared to adults, pediatric patients have an increased physiological reserve, which can mask signs of clinical deterioration, complicating early recognition and treatment. The current definitions of organ dysfunction and hyperlactatemia in sepsis are primarily based on adult populations and have not been fully adapted to pediatric patients. Pediatric sepsis is still defined as the presence of infection along with at least two out of four systemic inflammatory response syndrome (SIRS) criteria, while pediatric septic shock is characterized by severe infection resulting in cardiovascular dysfunction. Timely management is critical and includes the administration of fluid boluses (40-60 mL/kg), broad-spectrum antibiotics, and prompt infectious source control. However, the use of fluid boluses in resource-limited settings remains controversial. For pediatric septic shock, epinephrine is preferred over norepinephrine as the first-line vasopressor. Additionally, vaccines for meningitis, diarrhea, dengue, and measles are highly cost-effective preventative measures that can significantly reduce the global burden of pediatric sepsis.

Pregnant Patients [18]

Human physiology undergoes significant changes during pregnancy, including expanded plasma volume, increased cardiac output, and peripheral vasodilation, which must be considered when evaluating for sepsis. The most common sources of infection in pregnancy include septic abortion, endometritis, chorioamnionitis, wound infections, urinary tract infections (UTIs), pneumonia, and appendicitis. Common pathogens associated with these infections are Escherichia coli (E. coli), Group A Streptococcus, and Group B Streptococcus. Early initiation of empiric antibiotic therapy is critical to improving outcomes. Initial fluid resuscitation should include 1–2 liters of crystalloid solution, with further fluid management guided by the patient’s preload status, as only 50% of hypotensive septic patients are fluid responsive. Overly aggressive fluid administration may result in edema and increased risk of mortality. Norepinephrine is the first-line vasopressor recommended for septic pregnant patients. The immediate delivery of the fetus is not typically indicated in sepsis; decisions regarding delivery should be individualized. Delays in care or escalation of care are the leading causes of maternal deaths in sepsis, highlighting the importance of prompt and appropriate intervention.

COVID-19 [19,20]

The COVID-19 pandemic has affected millions of people worldwide, with critical cases defined by the presence of acute respiratory distress syndrome requiring ventilation, sepsis, or septic shock. Acute manifestations of severe COVID-19, including significant organ dysfunction, meet the diagnostic criteria for sepsis caused by other pathogens. The pathophysiology of sepsis and COVID-19 share many similarities, making this overlap an ongoing area of research to better understand and manage these conditions.

Geriatrics [21,22]

Sepsis is a significant concern in the geriatric population, characterized by a systemic inflammatory response to infection that can lead to organ dysfunction and increased mortality. Older adults are particularly vulnerable due to age-related physiological changes, comorbidities, and often atypical presentations of infections. Studies indicate that sepsis is a leading cause of morbidity and mortality among older individuals, with a higher incidence of severe outcomes compared to younger populations. Furthermore, the management of sepsis in older adults is complicated by factors such as polypharmacy, cognitive impairment, and frailty, which can hinder timely diagnosis and treatment. Early recognition and prompt intervention are crucial for improving survival rates in this demographic, emphasizing the need for tailored approaches to sepsis care in geriatric patients.

When To Admit This Patient [23,24]

All diagnosed sepsis patients required admission. Admission is critical when they exhibit signs of organ dysfunction, persistent hypotension despite adequate fluid resuscitation, or altered mental status, as these indicators suggest a severe systemic response to infection. The Surviving Sepsis Campaign guidelines recommend immediate admission to an intensive care unit (ICU) for patients with septic shock or those requiring close monitoring and advanced therapies. Additionally, patients presenting with a high risk of deterioration, such as those with significant comorbidities or advanced age, should also be considered for admission to ensure timely intervention and management.

Revisiting Your Patient

She is treated with 1 liter of intravenous Lactated Ringer’s solution, supplemental oxygen, and empiric antibiotics. Laboratory tests are ordered, and a bedside chest X-ray (CXR) shows right upper lobe consolidation. The patient is diagnosed with sepsis secondary to bacterial pneumonia.

Following adequate resuscitation, she is transferred to the intensive care unit for further monitoring. Sputum cultures confirm Streptococcus pneumoniae, and she is started on ceftriaxone. Two days later, she returns to her neurological baseline, and the CXR shows improvement in the consolidation. The patient is transferred to the medical floor for one more day of observation and then discharged home.

Authors

Picture of Tina Samsamshariat

Tina Samsamshariat

Tina Samsamshariat is a graduating fourth year medical school at the University of Arizona College of Medicine – Phoenix. She is pursuing emergency medicine residency at Los Angeles County + University of Southern California. She received her bachelor’s in science at the University of California at Los Angeles and her master’s in public health at the University of Southern California. She completed a pre-doctoral global health fellowship with the National Institutes of Health Fogarty International Center where she was based in Lima, Peru. She is passionate about global health, health equity, and social emergency medicine.

Picture of Ardeshir Kianercy

Ardeshir Kianercy

Picture of Elizabeth DeVos

Elizabeth DeVos

Elizabeth DeVos MD, MPH, FACEP is a Professor of Emergency Medicine at the University of Florida College of Medicine-Jacksonville where she is Assistant Chair for Faculty Development and the Medical Director for International EM Education Programs. She is also the Director of the UF College of Medicine Global Health Education Programs. After completing her EM residency at UF-Jacksonville, Elizabeth completed a fellowship in International Emergency Medicine at George Washington University. She has partnered in the development of EM Specialty Training in several countries, including living and working in Kigali, Rwanda as faculty in the first EM residency. Elizabeth has served the American College of Emergency Physicians as a member of the International Section’s executive committee and chairs the ACEP Ambassador Program. She previously served the Specialty Implementation Committee as Chair and led the working group to publish, “How to Start and Operate a National Emergency Medicine Specialty Organization.”

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References

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  21. Kumar A, et al. Sepsis in the Elderly: A Review. J Geriatr Emerg Med. 2020;21(3):145-153.
  22. Klein MJ, et al. Challenges in the Management of Sepsis in Older Adults. Age Ageing. 2021;50(4):120
  23. Rhodes A, Evans LE, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Crit Care Med. 2017;45(3):486-552. doi:10.1097/CCM.0000000000002255.
  24. Weinberg J, et al. The impact of comorbidities on sepsis outcomes: a systematic review. J Crit Care. 2018;47:238-244. doi:10.1016/j.jcrc.2018.07.002

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

How to Interpret C-Spine X-ray (2024)

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by Maitha Mohammed Alneyadi & Mansoor Masarrat Husain

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Introduction

Cervical spine x-ray interpretation is a vital skill in emergency medicine. This is particularly important as cervical spine injuries can leave patients with permanent neurological damage or death. While CT scans have overtaken X-rays as the primary form of cervical spine imaging, X-rays can be handy in rural areas or areas with limited resources. If in doubt, always ask for an expert opinion.

Cervical spine injuries commonly arise from motor vehicle accidents or falls from heights. They more commonly occur in men, and worse outcomes often happen to patients with underlying degenerative changes. Mechanisms of injuries causing fractures include flexion, extension, rotational, or vertical compression—these will be elaborated on further in this chapter. Cervical spine x-rays are somewhat useful if the patient is awake, stable, and has isolated injuries. In addition, they can be ordered in patients with upper airway obstruction symptoms, to look for soft tissue infections, foreign body demonstration, or if there is neck pain with no significant trauma.

Remember, cervical spine x-rays require manipulation of the neck to get clear views. Consider an alternative diagnostic choice like CT (Computed Tomography) or MRI (Magnetic Resonance Imaging) if cervical spine movement is restricted by a cervical collar. X-rays are also not advisable when neurological symptoms are present following trauma, in an uncooperative patient, or when a more accurate radiological modality is easily available.

Plain radiographs that display the lateral projection of the cervical spine, along with an open mouth view, are quite effective at identifying cervical spine fractures. Statistics indicate that the risk of overlooking a significant fracture is less than 1%. Including the anteroposterior (AP) projection raises the sensitivity to almost 100%. All three essential projections mentioned above can be seen in the figure below.

C-spine x-ray - 3 views - Lateral view with normal slight lordosis (A), Odontoid or open mouth view of the atlas and axis (B), Standard anteroposterior or AP view with open mouth, it can also be taken with closed mouth (C).

Before analyzing cervical radiographs, some additional facts need to be presented. Most spinal injuries occur at the junctions of the spine: craniocervical, cervicothoracic, thoracolumbar, and lumbosacral.

The only c-spine radiograph one should be satisfied with is the one showing all seven cervical vertebrae (C1–Th1). The C7–Th1 vertebrae may be obscured in muscular or obese patients, or in patients with spinal cord lesions that affect the muscles that normally depress the shoulders. Such lesions, which leave the trapezius muscle unopposed, occur in the lower cervical region. Shoulders can be depressed by pulling the arms down slowly and steadily or, if the patient is capable, by asking them to depress one shoulder and lift the other hand above their head to achieve the swimmer’s position, which better visualizes the lower vertebrae.

Two examples of a cervical x-ray that is not good enough for the evaluation of the possible injury of the neck.

We will now present a systematic method for interpreting cervical spine x-rays. First, identification—make sure details are correctly matched to the patient by name, date of birth, record number, and the time the scan was done. Use an old x-ray of the patient as a comparison if the study has been done previously.

Interpretation

We utilize the ABCD system to comprehensively interpret cervical spine X-rays.

A: Alignment and adequacy
B: Bones
C: Cartilages
D: Dense soft tissue

Cervical spine X-rays typically include three views: the lateral view (or cross-table view), the odontoid view (or open mouth view), and the anterolateral view. If the lateral view is inadequate, an additional view called the “Swimmer’s view” may be requested to visualize the C7 and T1 vertebrae.

Lateral View

Example of a slightly rotated not ideal lateral projection of the cervical spine in (A) and an x-ray of an ideal lateral projection in (B).

A: Adequacy and Alignment

Lateral view - Adequacy and Alignment
Always assess (AV) anterior vertebral, (PV) posterior vertebral and (SL) spinolaminar lines, they should run smooth, without any disruptions, and should form a slight lordotic shape. All three lines should form a smooth and lordotic curve of the cervical spine. Any disruption in the flow of these lines suggests either a bony or a ligamentous injury.

An adequate image includes the base of the skull to the upper border of T1.

There are four parallel lines to note, from front to back (See image on the left, Courtesy of Dr Hussain Aby Ali). The front line (in purple), referred to as the anterior longitudinal line, runs along the anterior border of the vertebrae.

The second line, or the middle line, referred to as the posterior longitudinal line (in yellow), runs along the posterior border of the vertebrae.

Next, the spinolaminar line (in green) runs between the spinous process and lamina, along the anterior edge of the spinous process.

Lastly, the posterior spinous line (in blue) runs smoothly along the tips of the spinous processes.

The spinal cord lies between the posterior spinous and spinolaminar lines. Disruption of any of these lines indicates a fracture [1].

The image reveals disruption of the normal alignments as indicated with a step-off in C2. This has shifted all the lines forward as seen in a hangman’s fracture. Hurley CM, Baig MN, Callaghan S, Byrne F. Cervical spine hangman fracture secondary to a gelastic seizure. BMJ Case Reports. 2019;12(8):e230733. doi: https://doi.org/10.1136/bcr-2019-230733
Disruption in the shape of the AV line, that indicates injury, and in this case a fracture of the body of C7.

An important exception to the usual guidelines involves pseudo-subluxation of C2 and C3 in the pediatric population, which can lead to confusion. In these cases, it is essential to examine the spino-laminar line from C1 to C3. Be cautious of injury if the base of the C2 spinous process is more than 2 mm away from this line. Additionally, correlate your findings with any relevant soft tissue observations (see below under “D”).

On the lateral view, also assess the predental space, which is the distance between the anterior surface of the odontoid process and the posterior aspect of the anterior ring of C1. This distance should not exceed 3 mm in adults or 5 mm in children (see image below).

B: Bones

Examine the vertebrae for a normal bony outline and bone density. It is important to note any subtle changes in bone density, as these may indicate a compression fracture. Areas with decreased bone density are more vulnerable to fractures and are often seen in patients with conditions such as rheumatoid arthritis, osteoporosis, or metastatic osteolytic lesions. Acute compression fractures, in contrast, typically present as areas of increased bone density.

Integrity of the vertebrae - Image on the left (Courtesy of Hussain Aby Ali), Image on the right (Courtesy of Yvette Mellam, [3] - Gaillard F. Cervical spine fractures. Radiology Reference Article. Radiopaedia.org. Radiopaedia. https://radiopaedia.org/articles/cervical-spine-fractures)

To check the integrity of the vertebrae, we must trace each vertebra individually. If there are any irregularities in the cortex of the bone, there may be a fracture.

As you trace the vertebrae on the right side (the image above), you may note that the sixth vertebra has slipped forward and is not continuous, which is an example of a vertebral fracture.

This is followed by scanning vertebrae C3–C7 in the usual manner, with no specific shadows or rings. The rest of the vertebral spaces must be equal, with a rectangular shape. Follow the spinous processes to look for any fractures [1].

Other examples are given below. See the fracture on 7th vertebral body (image A below), and fracture on spinous process of the 7th vertebrae (image B below).

Watch for a non-disrupted bony outline. Disruption, as in the above examples means fracture of the bone structure. Also search for any hypo- or hyper-dense areas in the bone, as it may be the only indication of the compression fracture. In (A) slight widening of the soft tissue is visible just in front of the fracture, under the white arrow, which may indicate that this is an acute injury.

Let us zoom in into the same image and focus on C1 and C2.

Coffee bean and C1 and C2

Start your day with a coffee—or rather, a coffee bean shadow—when interpreting c-spines. This shadow corresponds to the anterior arch of the atlas found in C1. Bear in mind that the peg might get in your way. With that, make sure the coffee bean shadow is adjacent to the odontoid peg. If not, think of a fracture!

When looking at C2, trace the ring, referred to as Harris’ ring (black color in the image above), which is the lateral mass of the vertebra. Discontinuity of the ring demonstrates a fracture.

C: Cartilage space assessment

n the assessment, examine the disc spaces, facet joint spaces, and interspinous spaces for any misalignments or increased space. Subluxations or facet dislocations can be identified by disruptions in the demarcated boxes, while any interspinous height exceeding 50% of the vertebral body indicates ligament disruption. On a good-quality lateral view x-ray of a healthy person, uniform intervertebral spaces should be evident.

An emergency physician may diagnose subluxations and dislocations of the facet joints by assessing the cartilage space between the vertebral corpora, facet joints, and spinous processes. However, increased interspinous distance by more than 50% suggests a ligamentous injury, and protective muscle spasms may complicate interpretation.

Uniform intervertebral cartilage spaces, also facet joints must be inspected, for any unusual alignment or increased space.

D: Dense soft tissue

Subsequently, we check the prevertebral space (in yellow), with the trachea sitting right in front of it (in red) (see the image below, courtesy of Hussain Aby Ali). Take C4 as your reference point (in purple). As a rule of thumb, the prevertebral space at or above C4 should be less than one-third the width of the vertebral body, while below C4 it should measure less than the width of the adjacent vertebra. In pediatrics, the prevertebral space at C4 is 7 mm, and at C6 it measures 14 mm or less, depending on age. In adults, the prevertebral space at C6 measures 22 mm. Enlarged measurements may indicate a hematoma related to a fracture, although normal measurements do not rule out a fracture [1].

The prevertebral soft tissues can serve as an indicator of acute swelling or hemorrhage resulting from an injury, and in some cases, may be the only indicator of an acute injury visible on an x-ray. The normal width of the prevertebral tissue decreases from C1 to C4 and increases from C4 downward. Normal measurements are less than 7 mm from C1 to C4 (less than half the vertebral body width at this level) and less than 22 mm below C5 (less than the vertebral body width at this level, as shown in Figure 9). The presence of air within the soft tissue could suggest a rupture of the esophagus or trachea.

Retro-pharyngeal soft tissue, narrows down from C1 to C4, and should not exceed more than 7mm (less than third of the vertebral body). Bellow the C4 soft tissue starts widening, but should not exceed 22mm (for easier thinking, should not exceed the width of the body of the vertebrae.

Odontoid – Open Mouth View

A: Adequacy and Alignment

The odontoid x-ray is typically the second standard view obtained in the emergency department. Its primary goal is to visualize the odontoid process of the C2 vertebra and the C1 vertebra. This view can be taken with the patient’s mouth either open or closed.

When examining the odontoid x-ray, two key aspects are assessed: first, the distance between the odontoid process and the lateral masses of the C1 vertebra should be equal. If there is an inequality, it may indicate a slight rotation of the head. Second, considering the previous point, the margins of the C1 and C2 vertebrae should remain aligned.

The distance between the odontoid process and the lateral masses of the C1 should be equal, if not inequality may be due to the slight rotation of the head. (If the patient has the upper central incisor teeth, we can check if the space between those two teeth aligns with the middle of the odontoid process, this might give the slight idea about rotation in case process itself is not broken and misaligned). Even with the slight rotation of the head we can still check alignment by looking at the lateral margins of the C1 and C2, which should remain aligned.

B: Bones

The odontoid view is most helpful for assessing peg fractures and examining the lateral masses and spaces at C1 and C2. Start by drawing a line from the end of the lateral mass (in purple), along the shaft, up around the odontoid peg, and down to the other lateral end (in green), which marks C2. Next, demarcate C1’s lateral masses on each side and look for any irregularities or fractures.

C: Cartilage space assessment

The space between the peg and C1’s lateral masses must be equal (green asterisks), as should the spaces between C1 and C2 lateral masses (blue asterisks). Unequal lateral mass spaces could raise suspicion of subluxation, which may indicate that the transverse ligament holding the peg in place is torn. Alternatively, consider a Jefferson fracture, which will be discussed later in this chapter.

Draw an imaginary line along the lateral edges of C1 and C2, and check for any misalignment or displacement (red circles). It is important to note that when a patient’s cervical spine is rotated, the images may be inaccurate due to artifacts, which could be misconstrued as fractures, as shown in the image below [1].

An inappropriate imaging angle can result in an inconclusive image. In such cases, you may notice unequal spaces between the odontoid and C1 lateral masses, even when no underlying fractures are present. This situation should prompt a discussion with the radiologist or the consideration of further imaging, such as a CT scan or MRI.

Beware of the Mach effect!
The Mach effect is an optical illusion that can occur during imaging interpretation. It creates the appearance of a lower density at specific levels of the odontoid peg, which may falsely mimic an odontoid fracture. This illusion arises from the way edges and contrasts in the image are perceived by the human eye, often giving the impression of a discontinuity or fracture when none is present. It is crucial to recognize this phenomenon to avoid misdiagnosis, especially when interpreting odontoid fractures on radiographs. Careful examination and, if needed, correlation with additional imaging modalities such as CT or MRI can help confirm the true nature of the findings.

[4] - Czarniecki M, Niknejad M. Mach effect - mimicking odontoid fracture. Radiopaediaorg. Published online November 24, 2012. doi: https://doi.org/10.53347/rid-20528

Anteroposterior View

A: Adequacy and Alignment

Images taken in this projection are usually less clear than the two mentioned above. The tips of the spinous processes should lie in a straight line along the midline, and the distances between the spinous processes should also be checked. Anomalies, such as bifid spinous processes, can complicate interpretation. The laryngeal and tracheal shadows should align down the middle, and the alignment of the lateral masses of the vertebrae should also be assessed.

Blue line connects the spinous processes, they should lie mid-line and have an equal amount of space between. Red-line should smoothly connect the lateral masses of the vertebrae. Always check the edges of the picture, in most cases, apexes of the lungs are visible, check for pneumothorax.

An adequate image includes the vertebral bodies of the cervical vertebrae along with the superior border of the thoracic vertebrae. Vertical lines running across and along the spinous processes and vertebral bodies help assess alignment. Three lines are particularly important: the spinous process line (in blue), which runs through the spinous processes of C1 to C7, ensuring vertical alignment, and two lateral lines (in green), which run smoothly along the transverse processes, confirming their normal alignment.

B: Bones

The anteroposterior (AP) view of the cervical spine is one of the standard projections used during imaging. It is taken with the x-ray beam directed from the front (anterior) to the back (posterior) of the neck. While it provides a general overview of the alignment of the vertebrae and highlights features such as the spinous processes and transverse processes, this view may not always clearly demonstrate fractures.

Fractures, especially those involving the odontoid peg, vertebral bodies, or certain types of subtle cortical disruptions, can be challenging to detect due to the overlapping structures in this projection. Additionally, anomalies such as misalignment or crowding of the spinous processes might not be easily discernible. As a result, this view is often supplemented with lateral or oblique views and, in cases of doubt, with advanced imaging techniques like CT or MRI for a more definitive diagnosis.

The AP view remains an important tool for assessing gross abnormalities, vertebral alignment, and pathological conditions, such as tumors or significant bone density changes. However, its limitations in detecting subtle fractures underscore the need for careful correlation with clinical findings and additional imaging.

C: Cartilage space assessment

In an AP cervical spine x-ray, the assessment of cartilage spaces is crucial for evaluating alignment and potential injuries. A key rule to follow is the 50% rule: any increase in the cartilage space by more than 50% compared to adjacent spaces suggests anterior cervical dislocation. This finding is often associated with trauma, such as ligamentous injury or vertebral subluxation, but it is important to note that the 50% rule does not apply in cases of muscle spasm, particularly when the neck is in a flexed position.

To confirm the diagnosis and exclude vertebral slippage, it is essential to examine the lateral view. The lateral view provides additional details regarding the vertebral alignment, anterior displacement, and associated injuries that may not be visible on the AP view. Ensuring that the vertebrae are properly aligned without slippage is vital for accurate assessment and diagnosis.

By correlating findings from both the AP and lateral views, a clearer picture of cervical spine integrity can be obtained, helping to differentiate between conditions caused by trauma and those related to positional factors or muscle spasms.

D: Dense soft tissue

In the AP cervical spine view, it is important to assess for the presence of surgical emphysema or pneumothorax, as these findings can indicate significant underlying trauma.

Surgical Emphysema: Look for evidence of air trapped in the soft tissues of the neck. This appears as dark, radiolucent (black) streaks in areas where soft tissues should normally appear opaque. Surgical emphysema in the cervical region can result from tracheal or esophageal injury, penetrating trauma, or fractures that disrupt the airways. Its presence warrants immediate attention and further investigation to locate the source of the air leakage.

Pneumothorax: Although primarily evaluated using a chest x-ray, a pneumothorax might be visible on an AP c-spine x-ray, especially if significant. This is seen as an absence of lung markings on the affected side, with a radiolucent (black) space outlining the lung. Pneumothorax may occur in association with rib fractures or blunt trauma extending to the thoracic region and can contribute to respiratory distress.

Other Views

Swimmer’s view

When C7 or T1 is not clearly visible on the lateral view due to dense body musculature, obtaining a “Swimmer’s view” can be helpful. This imaging technique specifically focuses on the alignment of C7 and T1 at the cervico-thoracic junction. To achieve this view, patients are instructed to lower the shoulder on the same side as the area being examined [5].

Murphy A, Normal cervical spine radiographs with swimmer's view. Case study, Radiopaedia.org (Accessed on 07 Dec 2024) https://doi.org/10.53347/rID-48418 - https://radiopaedia.org/cases/48418

Flexion and Extension Views

Oblique and flexion/extension views are not recommended in the emergency department setting as they can lead to further neurological injuries caused by manipulation. These views are only useful when interpreted by an experienced physician. Flexion and extension views are often contraindicated due to suspected unstable trauma or are impossible to perform because of spastic musculature following the injury (see Figure below). Additionally, unsupervised or forced flexion or extension in a patient with ligamentous injury can result in significant neurological damage. Therefore, other imaging modalities are necessary when a suspected injury is present.

Straightened normal lordotic curvature of the c-spine, may be due to the muscle spasm as a protective mechanism, what also makes flexion and extension views hard to capture.

Abnormal findings on cervical spine x-rays

C1 (Jefferson) fracture

A C1 fracture, also known as a Jefferson fracture, is best visualized on the odontoid view. This type of fracture typically results from axial loading, such as a heavy blow to the top of the head. The force compresses the cervical spine, leading to fractures in both the anterior and posterior arches of C1. These fractures are considered unstable because the transverse ligament, which stabilizes the relationship between the odontoid peg (dens) and the lateral masses of C1, is often disrupted.

Key imaging findings include widened spaces between the odontoid peg and the lateral masses of C1 (marked by orange asterisks). Additionally, the lateral masses of C1 may appear misaligned with those of C2 (marked by green circles), indicating instability [6]. The widening of these spaces and misalignment reflects the ligamentous injury and mechanical instability associated with this fracture.

Due to its unstable nature, a Jefferson fracture requires prompt recognition and further imaging, such as CT scans, to confirm the diagnosis and assess the extent of injury. Management often involves immobilization or surgical intervention, depending on the severity of the ligament disruption and alignment abnormalities.

C2 fractures

Odontoid peg fracture

To identify a C2 fracture, it is essential to evaluate both the open mouth (odontoid) view and the lateral view, as these complementary perspectives provide critical information about the integrity of the C2 vertebra.

  1. Open Mouth (Odontoid) View:
    This view is particularly useful for assessing the odontoid peg, also known as the dens. A discontinuity of the peg process, as shown in the image above, is a hallmark feature of a C2 fracture. This disruption indicates a break in the odontoid peg, which is often caused by significant trauma. The open mouth view allows for a clear examination of the alignment and spacing between the odontoid peg and the lateral masses of C1, helping to confirm the fracture.

  2. Lateral View:
    The lateral view provides additional details about the alignment and integrity of the C2 vertebra. In cases of a C2 fracture:

    • Alignment Disruption: The normal alignment of the vertebral bodies is disturbed, indicating instability.
    • Harris Ring Discontinuity: The Harris ring, a radiographic marker of the lateral mass of C2, appears interrupted, further confirming the presence of a fracture.
    • Posterior Displacement of the Odontoid Peg: The odontoid peg may be displaced posteriorly, which can compromise the spinal canal and potentially compress the spinal cord.

Types of Odontoid Fractures

The graphical presentation above illustrates the three types of odontoid fractures, as labeled below:

Type I:

  • Location: Fracture at the tip of the dens.
  • Associated Injury: Alar ligament avulsion.
  • Stability: This is considered a stable fracture.

Type II:

  • Location: Fracture at the base of the odontoid process.
  • Stability: This is an unstable fracture. It is the most common type of odontoid fracture and is associated with a high risk of nonunion due to poor blood supply at the fracture site.

Type III:

  • Location: A fracture extending through the body of the axis (C2), curving laterally from one end to the other.
  • Stability: This is also considered an unstable fracture. These fractures may disrupt the lateral masses of C2, further compromising spinal stability.

Recommended Management

  • CT Scan: If any of these fractures are suspected or identified on plain x-rays, a CT scan is recommended for further evaluation to define the fracture line and assess the extent of bony disruption.
  • Immobilization: The cervical spine should be immobilized using a cervical collar (c-collar) to prevent further injury.
  • Consultation: Immediate consultation with neurosurgery is advised, as surgical intervention may be required, especially for unstable fractures (Type II and III).

These fractures, particularly Type II and III, have significant clinical implications due to their instability and proximity to critical neural structures, necessitating prompt diagnosis and intervention.

Odontoid fracture - type 2 (Courtesy of Dejvid Ahmetovic)
Suspected fracture of the odontoid process, but with closed mouth teeth might affect the view.
Same patient, but with open mouth view, and the fracture through the body of C2 is visible, also note misalignment of lateral borders of C1 and C2 and difference in space between odontoid process and lateral masses of C2 on both sides.
Hangman's fracture

A Hangman’s fracture is a bilateral fracture of the pars interarticularis of the C2 vertebra, often resulting in cervical spine instability. This type of fracture is best visualized on a lateral view, which reveals key findings:

Loss of Smooth Anterior Alignment

  • The normal, smooth anterior alignment of the cervical spine is disrupted and replaced by a visible step, indicating displacement.

Cortical Discontinuity

  • The fracture causes a break in the cortical bone, further demonstrating structural instability of the vertebra.
Hangman's fracture
Hangman's fracture

Mechanism of Injury

  • Hyperextension Trauma
    • This fracture is commonly caused by hyperextension injuries, such as those sustained in motor vehicle accidents.
    • It is also seen in diving accidents, where a diver’s head strikes the pool floor upon impact.

Clinical Significance

  • Hangman’s fracture is classified as unstable, as it compromises the integrity of the C2 vertebra and its supporting structures, potentially endangering the spinal cord.

Management

  • Immediate immobilization of the cervical spine with a cervical collar is essential. Advanced imaging (CT or MRI) is recommended to further evaluate the extent of the injury and rule out associated soft tissue or ligamentous damage.
  • Consultation with a neurosurgeon is critical for determining the need for surgical stabilization.

Importance of Recognizing C2 Fractures

C2 fractures, such as odontoid fractures or hangman’s fractures, are critical injuries due to their proximity to the spinal cord and brainstem. Prompt recognition using the open mouth and lateral views is vital to avoid neurological complications. Advanced imaging techniques, such as CT or MRI, are often required for further evaluation and to guide management strategies, which may include immobilization or surgical intervention.

Extension Teardrop Fracture

An extension teardrop fracture is a specific type of cervical spine injury in which a portion of the antero-inferior corner of the vertebra is fractured, resembling a teardrop shape. This injury is most commonly observed at C3 and is highly significant due to its association with instability and potential neurological compromise.

Fracture Appearance

  • The fracture is located at the antero-inferior corner of the vertebral body, creating a teardrop-shaped fragment.
Extension Teardrop Fracture - AlJahdali S, Extension teardrop fracture. Case study, Radiopaedia.org (Accessed on 07 Dec 2024) https://doi.org/10.53347/rID-76901 - https://radiopaedia.org/cases/76901

Mechanism of Injury

  • Caused by sudden hyperextension of the neck, which disrupts the anterior longitudinal ligament.
  • Often occurs in activities like diving, particularly when the diver strikes their head against a hard surface such as the pool floor.

Associated Injuries

  • This type of fracture is frequently associated with central cord syndrome, a neurological injury caused by compression of the spinal cord, leading to weakness more pronounced in the upper limbs than the lower limbs.

Management

  • Immediate Stabilization
    • Apply a cervical collar (C-collar) to immobilize the spine and prevent further injury.
  • Imaging
    • A CT scan is the imaging modality of choice to confirm the diagnosis, evaluate the extent of the fracture, and assess for additional injuries or spinal canal compromise.
    • Consultation
      • Immediate consultation with a neurosurgeon is essential for determining the best treatment approach. Depending on the severity, surgical intervention may be necessary.

Flexion Teardrop Fracture

A flexion teardrop fracture is a severe and unstable cervical spine injury resulting from high-energy flexion trauma, frequently occurring at the C5/C6 level. This type of fracture is significant due to its association with spinal instability and neurological damage.

Radiographic Findings (Lateral View):

  • The three longitudinal lines (anterior, posterior, and spinolaminar lines) are disrupted, indicating misalignment and instability.
  • A teardrop-shaped fragment is seen at the antero-inferior corner of the vertebral body, representing the avulsed piece of bone.
[7] Flexion Teardrop Fracture - El-Feky, Mostafa & Munir, Muhammad. (2020). Flexion teardrop fracture. 10.53347/rID-78890.

Mechanism of Injury

  • Caused by hyperflexion of the neck, which exerts excessive force on the cervical spine.
  • This leads to a disruption of the posterior longitudinal ligament, further contributing to instability.

Neurological Association

  • The injury often results in anterior cervical cord syndrome, characterized by loss of motor function and pain/temperature sensation below the level of injury, with preserved proprioception and vibration senses.

Management

  • Immediate Stabilization
    • Apply a cervical collar (C-collar) to immobilize the cervical spine and prevent further injury.
  • Advanced Imaging
    • A CT scan is the preferred imaging modality to confirm the diagnosis, evaluate the extent of the fracture, and identify associated injuries such as spinal canal compromise or ligamentous disruption.
    • MRI may be indicated to assess soft tissue and spinal cord involvement.
  • Consultation
    • Urgent consultation with a neurosurgeon is essential due to the unstable nature of this fracture. Surgical stabilization is often required to restore spinal alignment and prevent further neurological deterioration.

Clinical Importance

The flexion teardrop fracture is considered one of the most unstable cervical spine injuries. Prompt recognition, immobilization, and appropriate surgical management are critical to improving patient outcomes and minimizing long-term neurological deficits.

Clay Shoveler's Fracture

A Clay Shoveler’s fracture is a stable fracture that involves an avulsion of the spinous process, typically occurring in the lower cervical or upper thoracic spine (most commonly at C6, C7, or T1).

Clinical Presentation

  • Patients present with localized pain and tenderness over the affected area.
  • The pain is often exacerbated by movement or palpation of the spine.

Stability

  • This is considered a stable fracture as it does not involve the vertebral body, spinal canal, or neurological structures. However, the injury can still cause significant discomfort and impair mobility.
Clay Shoveler's Fracture The spinous process of C6 is displaced from the vertebra.- Radswiki T, Botz B, Baba Y, et al. Clay-shoveler fracture. Reference article, Radiopaedia.org (Accessed on 07 Dec 2024) https://doi.org/10.53347/rID-13207 - https://radiopaedia.org/articles/13207
Clay Shoveler's Fracture (Courtesy of Dejvid Ahmetovic)

Examination and Management

  • Neurological Assessment
    • A neurological examination should always be performed to rule out any associated injuries or deficits, even though this fracture typically does not affect the spinal cord or nerves.
  • Immobilization
    • The patient should be placed in a cervical collar (c-collar) to immobilize the spine and alleviate pain during the acute phase of the injury.
  • Imaging
    • A lateral cervical x-ray is often sufficient to diagnose the fracture, but a CT scan can provide additional details if needed.
  • Treatment
    • Since this is a stable fracture, management is typically conservative, including pain control, immobilization, and physical therapy as needed.

Clay Shoveler’s fractures are generally associated with good outcomes, and patients can recover fully with appropriate care and immobilization.

Retropharyngeal abscess

Patients with a retropharyngeal abscess often present with:

  • Sore throat and fever.
  • Torticollis: The head is tilted to one side due to neck stiffness and discomfort.
  • Dysphagia: Difficulty swallowing.
  • Respiratory Distress: Severe cases may manifest with stridor, drooling, or increased breathing effort with retractions, indicating a compromised airway.

Management

  • Immediate Interventions
    • Patients in respiratory distress should be closely monitored as the airway may become obstructed, necessitating emergency airway management, including the potential need for a surgical airway (e.g., tracheostomy).
  • Specialist Consultation
    • A prompt otolaryngology consult is warranted for evaluation, incision and drainage (I&D) of the abscess, and initiation of intravenous antibiotics.
  1.  

Radiographic Assessment

  • Measuring the Retropharyngeal Space
    • The retropharyngeal space is evaluated using lateral cervical spine x-rays.
    • Between C2 and C4, the vertebral bodies can be divided into thirds. The retropharyngeal space should not exceed one-third the width of the corresponding vertebral body.
    • At C4 and below, the vertebral bodies should be divided in half, with the prevertebral space width being approximately equal to the anterior half of the vertebral body [8].
  • Signs of Retropharyngeal Abscess
    • Widening of the retropharyngeal space beyond normal parameters is highly suggestive of an abscess.
    • Additional findings may include air-fluid levels, soft tissue swelling, or displacement of adjacent structures.

Epiglottitis

Epiglottitis is a rapidly progressive and potentially life-threatening disease that primarily affects the upper airway. Patients often present with:

  • Fever and sore throat as initial symptoms.
  • Drooling and difficulty swallowing (dysphagia).
  • Inspiratory stridor, indicating partial airway obstruction.

These symptoms suggest an urgent need for airway evaluation and management.

  1.  

Lateral Neck X-ray

  • The hallmark finding is the “thumb sign”, which represents the swollen epiglottis.
  • Swelling of the epiglottis and aryepiglottic folds is characteristic of this condition.
  • The epiglottis appears enlarged and rounded, resembling the shape of a thumb.

Importance of Early Recognition

  • Epiglottitis can rapidly progress to complete airway obstruction, particularly in children.
  • It is critical to recognize these findings on a lateral neck x-ray and act promptly to secure the airway.

Management

Patients showing signs of airway obstruction require immediate attention, with priority given to securing the airway. In severe cases, this may involve intubation, preferably using fiberoptic intubation in a sitting position, or tracheostomy if necessary. This procedure should be performed collaboratively with ENT surgeons and anesthesia professionals in a controlled environment.

As a temporary measure, nebulized racemic epinephrine can be administered to reduce airway swelling, and broad-spectrum antibiotics should be started promptly to treat the underlying infection. Supportive care, such as humidified oxygen, may also be beneficial. Additionally, a nasopharyngoscopy should be performed to directly visualize the epiglottis and assess the extent of swelling.

Laryngotracheobronchitis (Croup)

Laryngotracheobronchitis, commonly referred to as croup, presents with characteristic symptoms including:

  • Barking cough, often likened to a seal’s bark.
  • Inspiratory stridor, indicating upper airway obstruction.
  • Drooling or dysphagia, in some cases.
  • Signs of increased work of breathing, such as retractions and nasal flaring.

These symptoms are typically caused by inflammation and narrowing of the subglottic airway, often following a viral infection.

Radiographic Findings

  • An anteroposterior (AP) neck x-ray may reveal the steeple sign, which represents narrowing of the subglottic trachea [10].
  • The steeple sign is considered pathognomonic for croup, though it is also occasionally observed in bacterial tracheitis.
  • A neck x-ray is not required for diagnosing croup but may be helpful to confirm the diagnosis when the patient is stable and cooperative [11].
[10] - Gaillard F, Kearns C, Murphy A, et al. Croup. Reference article, Radiopaedia.org (Accessed on 07 Dec 2024) https://doi.org/10.53347/rID-1185 - https://radiopaedia.org/articles/1185

While croup is usually a clinical diagnosis, imaging may be considered in atypical presentations or to rule out other conditions like epiglottitis or retropharyngeal abscess. Prompt recognition of croup and appropriate management can prevent complications associated with airway obstruction.

Clinical Decision Rule

There are two widely used scoring systems for neck injuries, primarily for diagnostic purposes: the National Emergency X-Radiography Utilization Study (NEXUS) criteria and the Canadian C-spine rules (CCR). Both have high sensitivity (89% and 98%, respectively) but low specificity (39% and 16%, respectively) [12]. Neither tool is used for patients over 65 years of age.

The NEXUS criteria can be easily remembered using the mnemonic NSAID:

  • N: Neurological deficit
  • S: Spine tenderness, midline
  • A: Altered mental state
  • I: Intoxicated
  • D: Distracting injury

A positive finding in any of these categories requires imaging.

The Canadian C-spine rule, on the other hand, categorizes patients into two groups based on severity: high risk and low risk. It uses a stepwise, question-based approach. Patients who are 65 years or older, those with a high-risk mechanism of injury, or those presenting with neurological symptoms always require imaging.

Refer to the diagram for a simplified explanation.

Specific Patient Groups

Pediatrics

Younger patients have anatomical differences compared to adults, including a larger head, incomplete ossification of the vertebrae, and firm attachment of the ligaments to the spine, which predispose them to injuries. Poor balance and a flexible spine further increase the risk of injury. As children reach the age of 8, their balance improves, and the injury rates decrease.

Nevertheless, pediatric patients can sustain spinal cord syndromes similar to those in adults, which may cause lifelong disabilities. Examples include central cord syndrome, anterior cord syndrome, posterior cord syndrome, Brown-Séquard syndrome, and spinal shock. The decision to perform imaging and the modality chosen are based on criteria similar to those used for adults.

In pediatric trauma patients, the ABCDE trauma evaluation must be followed, as with adults. An important entity to consider is SCIWoRA (Spinal Cord Injury Without Radiographic Abnormality), which is defined specifically for children under 8 years of age. This condition occurs when hyperextension forces injure the neck, leading to neurological deficits without abnormalities detected on x-rays or CT scans. MRI is required to assess the severity and prognosis. Favorable MRI findings include small hematomas and edema, whereas large hematomas or spinal cord transections are considered unfavorable [13].

Geriatrics

Motor vehicle accidents and falls from standing or sitting positions remain the two most common causes of cervical spine injuries in geriatric patients [14]. Due to anatomical degenerative changes and low bone density, even low-energy mechanisms can result in high-impact injuries. CT scanning is recommended for evaluating suspected cervical spine injuries in geriatric patients, who should always be considered trauma patients.

Pregnant Patients

Pregnant individuals involved in trauma require standard trauma protocols for evaluation and treatment, including CT imaging. Although CT imaging exposes both the mother and fetus to radiation, this exposure is not associated with an increased risk of fetal anomalies. However, the use of CT imaging should be carefully considered, with discussions involving the patient or their family, the radiologist, and a senior physician [15].

Authors

Picture of Maitha Mohammed Alneyadi

Maitha Mohammed Alneyadi

Emergency Medicine Department, Tawam Hospital, Al Ain, United Arab Emirates

Picture of Mansoor Masarrat Husain

Mansoor Masarrat Husain

Emergency Medicine Department, Tawam Hospital, Al Ain, United Arab Emirates

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References

  1. Raby N, Berman L, Morley S, Gerald De Lacey. Accident & Emergency Radiology: A Survival Guide. Saunders; 2015, P. 171-198
  2. Hurley CM, Baig MN, Callaghan S, Byrne F. Cervical spine hangman fracture secondary to a
    gelastic seizure. BMJ Case Reports. 2019;12(8):e230733. doi: https://doi.org/10.1136/bcr-2019-230733
  3. Gaillard F. Cervical spine fractures. Radiology Reference Article. Radiopaedia.org. Radiopaedia. https://radiopaedia.org/articles/cervical-spine-fractures
  4. Czarniecki M, Niknejad M. Mach effect – mimicking odontoid fracture. Radiopaediaorg. Published online November 24, 2012. doi: https://doi.org/10.53347/rid-20528
  5. Murphy A. Cervical spine (swimmer’s lateral view). Radiopaediaorg. Published online October 7, 2016. doi: https://doi.org/10.53347/rid-48437
  6. Erskine J Holmes, Misra RR. A-Z of Emergency Radiology. Cambridge University Press; 2006, P. 23-31
  7. Harvey H. Flexion teardrop fracture. Radiology Reference Article. Radiopaedia.org. Radiopaedia. https://radiopaedia.org/articles/flexion-teardrop-fracture-1?lang=us
  8. Sheikh Y, Bickle I. Retropharyngeal abscess. Published online July 13, 2014. doi:https://doi.org/10.53347/rid-30018
  9. Sutton AE, Guerra AM, Waseem M. Epiglottitis. In: StatPearls. Treasure Island (FL): StatPearls Publishing; October 5, 2024.
  10. Murphy A, Gaillard F. Croup. Radiopaediaorg. Published online May 2, 2008. doi: https://doi.org/10.53347/rid-1185
  11. Gaillard F. Steeple sign (trachea). Radiology Reference Article. Radiopaedia.org. Radiopaedia. https://radiopaedia.org/articles/steeple-sign-trachea?lang=us
  12. Vazirizadeh-Mahabadi M, Yarahmadi M. Canadian C-spine Rule versus NEXUS in Screening of Clinically Important Traumatic Cervical Spine Injuries; a systematic review and meta-analysis. Arch Acad Emerg Med. 2023;11(1):e5. Published 2023 Jan 1. doi:10.22037/aaem.v11i1.1833
  13. Szwedowski D, Walecki J. Spinal Cord Injury without Radiographic Abnormality (SCIWORA) – Clinical and Radiological Aspects. Pol J Radiol. 2014;79:461-464. Published 2014 Dec 8. doi:10.12659/PJR.890944
  14. Lomoschitz FM, Blackmore CC, Mirza SK, Mann FA. Cervical spine injuries in patients 65 years old and older: epidemiologic analysis regarding the effects of age and injury mechanism on distribution, type, and stability of injuries. AJR Am J Roentgenol. 2002;178(3):573-577. doi:10.2214/ajr.178.3.1780573
  15. Irving T, Menon R, Ciantar E. Trauma during pregnancy. BJA Educ. 2021;21(1):10-19. doi:10.1016/j.bjae.2020.08.005

FOAM and Further Reading

http://radiologymasterclass.co.uk/tutorials/musculoskeletal/x-ray_trauma_spinal/x-ray_c-spine_normal

http://reference.medscape.com/features/slideshow/c-spine#8

http://www.slideshare.net/Rajaoct/x-ray-cspine

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Fever in Children (2024)

~ iEM Education Project Team ~ Leave a comment

by Camilo E. Gutierrez

Authors
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Disclaimer: The guidelines for evaluating febrile infants in this publication are based on current U.S. practices and epidemiology. These may not apply to other regions, particularly low- and middle-income countries, where vaccination rates, healthcare access, and local factors may differ. Local guidelines should be consulted in those settings.

You have new patients!

You are working in an emergency department, and during your shift, you see a number of different patients.

Bed 1

In bed 1, a parent brings a full-term 2-month-old male infant who has been complaining of fever at home for 1 day. The child has been drinking well, has normal urine output, and has no associated symptoms.

Prenatal care was normal, infant was born by normal vaginal delivery with no complications and went home with mom after a couple of days. Of note, the mother had a fever during delivery and received antibiotics—no sick contacts at home.

The male infant is vigorous and appears well during your examination. Currently afebrile with normal vital signs.

Bed 2

In bed 2, you find a well-appearing 2-month-old female infant with complaint of fever at home. This child has had fever for 1 day. She also has a runny nose and a couple of episodes of vomiting after feeding. The family is visiting from out of town and has no way to contact their pediatrician.

Prenatal care was normal, infant was born by normal vaginal delivery with no complications and went home with mom after a couple of days—no sick contacts at home.

The female infant is vigorous and well-appearing during your examination. Currently afebrile with normal vital signs.

Bed 3

In bed 3, you have a 3-year-old fully vaccinated boy who has had fever of up to 38.5°C every day for the last week. Aside from the fever, there were no significant respiratory symptoms, vomiting, or diarrhea. He has been able to drink well, although not eating his usual amount.

Vital signs are remarkable for fever of 39°C, mild tachycardia to 120 bpm, and respiratory rate of 32 rpm. On exam, he has mildly injected conjunctiva, cervical adenopathy, and some peeling of his fingers.

How will you approach each of these patients?

Introduction

Fever is a common childhood complaint frequently encountered in emergency medicine [1]. It is a symptom of an underlying illness or infection and occurs when the body’s temperature rises above its normal range [2]. In children, a fever is generally defined as a temperature of 38°C (100.4°F) or higher in infants under 3 months and 38.5°C (101°F) in older toddlers and children [3].

Many causes of fever in children include viral or bacterial infections, autoimmune disorders, allergies, and reactions to medication. In some cases, the cause of the fever may be difficult to determine [2].

In emergency medicine, the primary concern with fever in children is identifying the underlying cause and treating it appropriately. This may involve a thorough physical examination, blood tests, imaging studies, or other diagnostic tests to help identify the cause of the fever.

In addition to treating the underlying cause of the fever, several measures can be taken to help manage the symptoms of fever in children. These may include administering acetaminophen or ibuprofen to help lower the child’s temperature, ensure adequate hydration, and closely monitor the child’s temperature and other vital signs  [4].

It is important to seek medical attention promptly if your child has a fever accompanied by other symptoms such as difficulty breathing, severe headache, rash, or lethargy. With prompt diagnosis and treatment, most cases of fever in children can be successfully evaluated and managed in the emergency department.

Temperature should ideally be measured rectally in infants [5]. In older toddlers and children, oral or axillary measurements are acceptable, understanding there is an approximate 0.5°C difference between the latter and rectal temperatures [6]. Also, rectal or oral measurements might be contraindicated in patients with immunodeficiency or neutropenia.

The pathophysiology of fever is associated with the liberation of cellular mediators such as interleukins, tumor necrosis factor, and interferon and their impact on prostaglandins at the hypothalamic level, raising the endogenous thermostat [7]. Fever is thought to be a benign and useful mechanism to stimulate the immune system, although it does increase metabolic demands, which can affect homeostasis at various levels [8].

This chapter will review the evaluation of febrile children in the emergency department.

What do you need to know?

Fever in infants

The American Academy of Pediatrics (AAP) recently updated its guidelines [9] for evaluating and managing fever in infants, providing evidence-based recommendations for healthcare providers.

According to the new guidelines, any infant younger than 60 days of age with a fever (rectal temperature of 38°C or higher) should be evaluated promptly. Fever in this age group can be a sign of a serious bacterial infection or invasive infection that requires urgent medical attention. The evaluation should include a complete physical examination, blood tests, urine tests, and possibly a lumbar puncture.

The guidelines also emphasize the importance of assessing the infant’s overall clinical appearance, including their hydration status, activity level, and interaction with caregivers. Any infant who appears ill, dehydrated, or has other concerning symptoms should be evaluated and managed as an inpatient.

Overall, the AAP guidelines aim to provide a systematic approach to evaluating and managing fever in infants, focusing on early recognition and treatment of serious bacterial infections while minimizing unnecessary diagnostic testing and hospitalization. It is important for healthcare providers and parents to be aware of these guidelines and to seek prompt medical attention if an infant develops a fever.

Prenatal risk factors should be assessed and include prematurity, prenatal care, maternal infections such as Group B Streptococcus and herpes, prolonged rupture of membranes, birth by C-section of normal vaginal delivery, maternal fever, and need for peripartum antimicrobial administration. Postnatal factors may include admission to the neonatal intensive care unit, the presence of respiratory support, central or peripheral lines, exposure to sick contacts, or the use of antibiotics as a newborn. Social determinants of health, such as access to healthcare, education, adequate environment, economic stability, and social and community support, play a key role in the decision-making process considering the disposition of the febrile infant once assessed in the emergency department.

Clinical prediction rules have been developed and validated, and guidelines have been adapted to include their use. Currently, the Step-by-step and the PECARN prediction rules offer a high sensitivity (96.7% and 92%, respectively) for the detection of SBI/IBI in infants and, more importantly, a very high negative predictive value (>99%) by which if all the high-risk lab criteria, including inflammatory markers, are negative, the presence of IBI/SBI is extremely unlikely [10] [11].

Infants < 21 days of age

The risk of serious bacterial infection (SBI), which includes bacteremia, urinary tract infection, and meningitis in infants younger than 21 days of age, is very high, and clinical examination parameters are not sensitive or specific enough to determine which infants are not at risk of sepsis. Patients at this age with a fever > 38°C, hypothermia, bradycardia, or apnea have a high risk of sepsis and septic shock. Infants under 21 days of age require thorough evaluation, including complete blood cell counts (CBC), blood culture, catheterized urine sample for microscopic urinalysis and urine culture, and a spinal puncture (LP) for evaluation and culture of cerebrospinal fluid. In addition, these patients should receive parenteral antibiotics such as Ampicillin, Gentamycin, and/or Cefotaxime as per local guidelines. For patients of this age, it is important always to consider the possibility of herpes simplex virus (HSV) infection, and parenteral acyclovir should be considered pending results of HSV nucleic amplification tests (HSV DNA PCR) or viral culture studies [12]. These patients should be admitted to an inpatient level of care for close monitoring and pending results of blood, urine, and CSF cultures.

Infants 22-28 days

It is important to understand that any current guidelines for evaluating febrile infants apply to well-appearing children. Suppose there is any concern or clinical finding regarding an ill-appearing infant. In that case, a thorough examination and laboratory testing, including blood, urine, CSF cultures, broad-spectrum antibiotics, and admission to a hospital service, are indicated [13].

Infants in this age range are still considered at high risk for serious invasive infections, especially if there are any risk factors, as described above. Current guidelines still strongly recommend considering full evaluation of the patients 22 to 28 days old, strongly consider antibiotic management pending culture results, and possible admission to a hospital.

However, in select infants of this age range, a more conservative approach has been suggested: obtaining catheterized urine samples, a complete blood count, urine and blood cultures, and introducing inflammatory markers. Currently studied and available inflammatory markers include c-reactive protein (CRP), Procalcitonin, and absolute neutrophil count (ANC). These tests’ recommended cut-offs are CRP > 20 mg/L, Procalcitonin > 0.5 ng/ml, and ANC > 4000/µL or <1000/µL, respectively.

If a well-appearing infant has normal urinalysis, normal WBC, and negative inflammatory markers, one possibility would be admission to a hospital service with or without obtaining a lumbar puncture. However, this opens the opportunity to admit without giving antimicrobial agents and observing pending culture results [14]. However, if any of the screening labs or inflammatory markers are elevated, antibiotics and admission are necessary. Still, the possibility of HSV infection should be considered at this age.

Infants 29-60 days

For this age group, for well-appearing infants with a temperature >38°C, the recommendation is to obtain urine and blood, including cultures and inflammatory markers [15]. At this age, obtaining a lumbar puncture is no longer mandatory for a well-appearing child with otherwise normal laboratory evaluation and negative inflammatory markers. If inflammatory markers are elevated in the absence of a positive urinalysis, a lumbar puncture is indicated to rule out meningitis. If the urinalysis is positive and inflammatory markers are below the threshold, there is no clear indication to perform a spinal tap, and the infant can be treated for a urinary tract infection potentially with oral antimicrobials and can be considered a candidate to be discharged home with close follow up within 24 hours. Suppose all the screening labs and inflammatory markers are within normal limits. In that case, there is no indication for antibiotic treatment, and the patient can be observed at home with close follow-up in 24 hours [16]. Recent literature suggests that well-appearing infants with an uncomplicated urinary tract infection (UTI) have a very low risk of bacteremia and an even lower risk of meningitis.

In order to discharge an infant home, the clinician must ensure that the parents understand the degree of risk, the importance of prompt follow-up within 24 hours, the capacity and ability to return to medical care, and the understanding to return immediately if there is any deterioration in the infant’s status. If not all of these criteria can be fulfilled, and there are social, language, or intellectual barriers to healthcare, the patient should be admitted to the hospital for observation.

In infants older than 30 days of age, antimicrobial regimens can include ceftriaxone for the treatment of bacteremia and/or urinary tract infections, with the consideration of ceftazidime or vancomycin for the treatment of bacterial meningitis. Oral regimens of first or second-generation cephalosporins can be considered for uncomplicated urinary tract infections. Always consider the local flora, antibiograms, and susceptibility to antibiotics before prescribing antimicrobial courses.

Also, it’s important to remember that if there is any concern, a full septic workup should be obtained, and broad-spectrum antibiotics should be used pending the culture results.

Infants older than 2 months of age

Vaccination has significantly reduced the incidence of bacterial infections in children, including serial bacterial infections. For example, the Haemophilus influenzae type b (Hib) vaccine has been highly effective in reducing the incidence of invasive Hib disease, which can cause meningitis, pneumonia, and other serious infections in young children. The introduction of the pneumococcal conjugate vaccine (PCV) has also led to a significant reduction in the incidence of invasive pneumococcal disease, including pneumonia and meningitis. E. coli has become the most common pathogen responsible for IBI in infants, bacteremia, and meningitis.

Furthermore, vaccination can indirectly reduce the incidence of serial bacterial infections by reducing the overall burden of bacterial infections in the community. When fewer people are infected with a particular bacterium, there is less opportunity for that bacteria to be transmitted from person to person, known as herd immunity, reducing the risk of serial infections for the general population.

Vaccination has significantly reduced the incidence of bacterial infections in children, including serial infections. Vaccination is a safe and effective way to protect children from serious bacterial infections and is an important part of routine healthcare for children.

For the evaluation of well-appearing, febrile infants older than 2 months of age, the main recommendation is always to consider the possibility of a urinary tract infection (UTI). The incidence of bacteremia and meningitis in areas with adequate vaccination coverage has decreased to approximately 1% risk of bacteremia and <0.5% risk of bacterial meningitis. However, the risk of UTI remains at 10-20% risk.

In general, the risk of UTI is similar in females and males up to 6 months of age. However, it drops for circumcised males after 6 months. The prevalence of UTI remains high in females up to 24 months of age.

As discussed above, if there is any concern about a high fever or a child who is not well-appearing, a more aggressive evaluation should be undertaken, and appropriate antimicrobial therapy should be considered.

The need to obtain a lumbar puncture (LP) in a well-appearing infant in this age group is of less debate currently as the incidence of bacterial meningitis is so rare, especially with a reassuring examination and low-risk screening labs.

After 2 months of age, it is important to consider the prevalence of viral infections. Common viral infections such as Respiratory Syncytial Virus (RSV), Influenza Virus, Rhinovirus, Enterovirus, Metapneumovirus, and Coronavirus, including SARS-COVID-2 virus, are prevalent in infants, and studies reveal that the presence of these viral infections is related to less possibility of serious invasive bacterial etiology perhaps with the exception of UTI’s. The incidence of UTIs in children with associated RSV infection is still high and warrants evaluation. However, it is important always to be vigilant of the possibility of HSV disease, a thorough maternal history, exposure, and physical examination is important, as well as considering obtaining blood, skin, mucosal, and CSF samples to send for culture or nucleic acid amplification and consider starting antiviral therapy presumptively due to the severity of these infections in infants, specially central nervous system or disseminated disease, which carry high morbidity and mortality.

Recent antimicrobial use also needs to be considered in infants within this age group. If any oral antimicrobials have been administered within 72 hours, the clinician should consider the possibility of partially treated infection or masking of signs and symptoms of bacterial infection. In this scenario, obtaining urine and blood cultures should be strongly considered.

There is poor evidence regarding the extent of evaluation in recently immunized infants. Recent immunizations are generally considered vaccinations administered in the previous 24 to 48 hours. In general, for a well-appearing infant older than 2 months, with a normal physical examination after a recent immunization less than 24 hours prior to the evaluation, the general consensus is not necessarily to obtain any testing but to direct the patient for a follow-up evaluation in the next 24 hours to ensure fever is not further present within 48 hours after vaccinations. However, the clinician should consider the possibility of catheterized urine evaluation within 48 hours of immunization due to the prevalence of UTI.

Invasive Bacterial Infections (IBI)

IBI is used to discuss the evidence of localized bacterial infections in infants and toddlers. A thorough physical examination should provide a clue of the presence of any of these disease processes. The term usually includes acute otitis media, cutaneous cellulitis or omphalitis around the umbilicus in infants, bacterial arthritis, skin abscess, and mastitis. Occult causes of IBI are less evident by physical examination and require a high index of suspicion, and the likely need for laboratory or imaging evaluation includes bacterial pneumonia, osteomyelitis, epidural abscess, brain abscess, or meningitis. Ill-appearing infants with focal infections do require a thorough evaluation, including cultures of abscess drainage, fluid aspirates, and skin or mucosal discharge [17].

Hyperpyrexia

The literature describes a linear correlation between high fever and serious bacterial infection. Hyperpyrexia is defined as rectal temperature ≥40°C (104°F) and is uncommon among febrile infants but is highly associated with invasive bacterial infection. If an infant presents with hyperpyrexia, blood cultures should be obtained and treated with broad-spectrum antimicrobials pending the blood culture results.

Fever of unknown origin / Fever without a source

Fever of unknown origin (FUO) is generally defined as a temperature >38.3°C (101°F), at least once daily, that lasts for at least 8 days and for which the cause cannot be identified after an initial workup. FUO can be challenging to diagnose, especially in children, as it can be caused by a variety of infectious, inflammatory, and neoplastic diseases, usually in this order of prevalence. Fever without a source (FWS) is generally defined as fever for less than 1 week without adequate explanation after a thorough history and physical examination.

The evaluation of FUO in children typically involves a comprehensive history and physical examination, as well as laboratory tests, imaging studies, and sometimes more invasive procedures [18]. It is important to understand the local distribution of infectious agents and the regional or ethnic presentation of specific inflammatory or rheumatologic conditions. Still, there is a small minority of patients in whom, after thorough evaluations, no cause is identified.

The following is a general approach to the evaluation of FUO in children:

History and physical examination: A thorough history and physical examination are critical in identifying any clues that may help narrow down the potential causes of the fever. Important details to gather include the child’s age, travel history, recent infections, medication use, and exposure to animals or sick contacts. Concerning fever, it is important to verify its height, duration, pattern, if it is documented or subjective, and any other associated symptoms surrounding febrile spikes. Associated complaints or symptoms can be useful in helping establish a correlation. Respiratory symptoms, gastrointestinal complaints, bone and muscle aches, and skin rashes may suggest specific etiologies that may present with prolonged fevers. Travel and exposure are key questions that can help narrow the possibility of etiologic agents. Contact with sick individuals, pets, farms, and other animals can point to specific infectious etiologies. It is easy to find lists of common infectious diseases by geographic location.

Vital signs should be documented, and discrepancies should be analyzed. For example, fever and bradycardia might suggest a few specific conditions (tick-borne or mosquito-related illnesses, legionella, Leptospira). Weight loss might suggest systemic diseases or malignancy.

The physical examination should include a detailed examination of all organ systems. Detailed skin evaluation might suggest dermatologic manifestations, as skin rashes can be associated with specific infectious or rheumatologic diseases. Examination of mucosal surfaces, including conjunctiva, mouth, and genitalia, might provide clues to systemic, rheumatologic, infectious, or inflammatory diseases. Lung and cardiovascular exam might reveal evidence of effusions or endocarditis. Attention to typical and atypical lymphadenopathy, organomegaly, or bone or muscle tenderness that might suggest infiltrative disease, inflammatory or infectious process. The genitourinary examination should be considered to exclude sexually transmitted diseases, pelvic masses, and inflammatory or malignant etiologies. Finally, a detailed neurological assessment might suggest subtle neuro deficits that might point to neuropathies, spinal pathology, medication, or toxic overdoses.

The physical exam should be repeated frequently in children, as it often evolves and changes according to disease progression.

Often, the initial assessment will be performed by a primary care clinician in an outpatient setting unless the child has become ill, has rapidly progressing symptoms or deterioration, or initial common studies have been performed and need for more complex testing needs to be performed.

Laboratory tests: A complete blood count with differential cell count, blood cultures, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), liver and renal function tests, and urinalysis should be obtained as part of the initial workup. Depending on the clinical presentation and suspected etiology, additional tests such as serologic studies, viral cultures, and molecular diagnostic tests may be indicated. Leukocytosis, cytopenia, anemia, thrombocytosis or thrombocytopenia, and atypical cell lines such as atypical leukocytes, bandemia, eosinophilia, can all point to various infectious etiologies, and might suggest viral, fungal, parasitic, rickettsial, and chronic disease or malignancy. Inflammatory markers are non-specific but can help the clinician trend the progression of a disease process.

Secondary-tier testing may involve ANAs, cryoglobulins, immunoglobulins, ferritin, and targeted rheumatologic and immunologic tests to help identify a more specific etiology. Additionally, tumor markers and specialized viral and infectious testing—such as DNA and RNA viral profiles, serologies for viral, bacterial, or rickettsial infections, and RPR or VDRL for presumed syphilis—can be utilized. Stool studies can reveal infectious etiologies, and calprotectin or occult blood can suggest inflammatory pathology.

Imaging studies: Chest X-ray, abdominal ultrasound, and/or computed tomography (CT) scans may be necessary to evaluate for pulmonary, abdominal, or pelvic pathology. Plain films can help evaluate bony malignancy or infections, soft tissue calcifications, and bone density. Magnetic resonance imaging (MRI) or positron emission tomography (PET) scans may be helpful in identifying occult infections or tumors. A conscious balance between radiation, costs, risks and benefits should guide imaging studies. A discussion with radiology experts might help direct the imaging study of choice and the need for contrast material.

Invasive procedures: Depending on the clinical presentation and initial workup, invasive procedures such as bone marrow biopsy, lymph node biopsy, or liver biopsy may be necessary to establish a diagnosis.

It is important to note that the evaluation of FUO in children should be individualized based on the patient’s clinical presentation and suspected etiology. A multidisciplinary approach involving infectious disease specialists, hematologists/oncologists, and rheumatologists may be necessary to establish a diagnosis and guide management.

Revisiting Your Patient

In bed 1, the 2-month male infant with fever at home for 1 day with history of maternal fever during delivery underwent a full septic workup due to the risk factors, received a dose of ceftriaxone and was admitted to the hospital for observation for 24 hours, until urine, blood, and CSF cultures were negative.

In bed 2, your 2-month-old female infant with fever at home only underwent a catheterized urine sample that was unremarkable. Because the mom had no good follow-up with a primary care provider, the infant was admitted to the hospital for 24 hours with no antibiotics until the urine culture was negative for 24 hours.

In bed 3, you have a 3-year-old fully vaccinated child who has had fever of up to 38.5◦C every day for the last week—examination with fever, conjunctivitis, and skin peeling.

This child underwent laboratory workups, including inflammatory markers, blood counts, chemistry, and liver function tests. He was admitted to the hospital for consultation with Cardiology and infectious Diseases to consider further evaluation for Kawasaki disease.

Author

Picture of Camilo E. Gutierrez

Camilo E. Gutierrez

Dr. Gutiérrez is an Associate Professor of Pediatrics and Emergency Medicine at George Washington University School of Medicine and Health Sciences, practicing Pediatric Emergency Medicine at Children’s National Hospital in Washington, DC. He is a renowned Pediatric Emergency Physician with extensive experience in clinical care, education, and global health. He leads international initiatives to improve pediatric emergency systems, having served in leadership roles for various global organizations. With over 90 international lectures, 30 publications, and a focus on pediatric trauma, critical care, and ultrasound, he is a key advisor in developing acute care systems worldwide.

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References

  1. Courtney, L., Franklin., Bernie, Carter., David, Taylor-Robinson., E., Carrol. “P09 Understanding the reasons behind paediatric attendances to emergency departments for febrile illness in the UK: A qualitative study.” JECH (2023). doi: 10.1136/jech-2023-.
  2. Jayashree M, Parameswaran N, Nallasamy K, et al. Approach to fever in children. Indian J Med Microbiol. 2024;50:100650. doi:10.1016/j.ijmmb.2024.100650
  3. Rajesh, Kasbekar., Aftab, Naz., Lorenzo, Marcos., Yingjie, Liu., Kristine, Hendrickson., James, C, Gorsich., Matt, Baun. “Threshold for defining fever varies with age, especially in children: A multi-site diagnostic accuracy study..” (2021).:2705-2721.
  4. “The management of fever in children.” Minerva pediatrics, 74 (2022). doi: 10.23736/s2724-5276.22.06680-0.
  5. Luis, Ángel, Bolio, Molina., Gabriela, Toledo, Verónico. “1. New Technique to Verify Permeability and Anorectal Malformations, and Take Rectal Temperature in Neonates And Infants.” (2023). doi: 10.33425/2689-1085.1057.
  6. Mohammed, Baba, Abdulkadir., W, B, Johnson. “6. A comparative study of rectal tympanic and axillary thermometry in febrile children under 5 years of age in Nigeria.” Paediatrics and International Child Health (2013). doi: 10.1179/2046905513Y.00.
  7. Soszyński D. Mechanizmy powstania i znaczenie goraczki [The pathogenesis and the adaptive value of fever]. Postepy Hig Med Dosw. 2003;57(5):531-554.
  8. Norbert, J., Roberts., Juan, C., Sarria. “4. Recognizing the Roles of Fever in Host Survival and in Medical Intervention in Infectious Diseases..” The American Journal of the Medical Sciences, (2024). doi: 10.1016/j.amjms.2024.05.013.
  9. https://www.aap.org/
  10. Tahir, Hameed., Sereen, AlMadani., Walaa, Shahin., Husam, Ardah., Walaa, A, Almaghrabi., Mohammed, Alhabdan., Ahmed, Mohammed, Alfaidi., Asma, Abuthamerah., Mamdouh, Al‐Ahmadi., Majed, Almalki., Mona, Al-Dabbagh. “1. Application of the Pecarn Prediction Rule for Febrile Infants up to 90 Days of Age: A Multi- Center Study. doi: 10.21203/rs.3.rs-4761730/v1.
  11. Natalia, Sutiman., Zi, Xean, Khoo., Gene, Yong-Kwang, Ong., Rupini, Piragasam., Shu-Ling, Chong. “2. Validation and comparison of the PECARN rule, Step-by-Step approach and Lab-score for predicting serious and invasive bacterial infections in young febril. e infants..” Annals Academy of Medicine Singapore (2022). doi: 10.47102/annals-acadmedsg.2022193.
  12. Stacy, Lund., Tine, Brink, Henriksen., Anja, Poulsen., Kia, Hee, Schultz, Dungu., Emma, Louise, Malchau, Carlsen., Bo, Mølholm, Hansen., Lise, Aunsholt., Ulrikka, Nygaard. “1. [Herpes simplex virus infection in newborns]..” Ugeskrift for Læger, 2022.
  13. Pantell RH, Roberts KB, Adams WG, et al. Evaluation and Management of Well-Appearing Febrile Infants 8 to 60 Days Old [published correction appears in Pediatrics. 2021 Nov;148(5):e2021054063. doi: 10.1542/peds.2021-054063]. Pediatrics. 2021;148(2):e2021052228. doi:10.1542/peds.2021-052228
  14. Rajendra, Prasad, Anne., Sourabh, Dutta., Haribalakrishna, Balasubramanian., Ashutosh, N., Aggarwal., Neelima, Chadha., Praveen, Kumar. “2. Meta-analysis of Cerebrospinal Fluid Cell Count and Biochemistry to Diagnose Meningitis in Infants Aged < 90 Days.”. American Journal of Perinatology. (2024), doi: 10.1055/a-2095-6729.
  15. Jamie, M., Pinto., Vaidehi, Patel., Anna, Petrova. “Role of viral pathogen(s) detection in hospital-based management of 29-90-day-old infants with unexplained fever..” MINERVA Pediatrica. (2023). doi: 10.23736/S2724-5276.23.07207-5.
  16. Rachel, G., Greenberg., Tamara, I., Herrera. “4. When to Perform Lumbar Puncture in Infants at Risk for Meningitis in the Neonatal Intensive Care Unit.” (2019). doi: 10.1016/B978-0-323-54391-0.00008-4.
  17. Dana, M., Foradori., Michelle, A., Lopez., Matthew, Hall., Andrea, T., Cruz., Jessica, L., Markham., Jeffrey, D., Colvin., Jennifer, A., Nead., Mary, Ann, Queen., Jean, L., Raphael., Sowdhamini, S., Wallace. “2. Invasive Bacterial Infections in Infants Yo. unger Than 60 Days With Skin and Soft Tissue Infections. Pediatric Emergency Care, doi: 10.1097/PEC.0000000000001584.
  18. Sandra, Trapani., Adele, Fiordelisi., Mariangela, Stinco., Massimo, Resti. “1. Update on Fever of Unknown Origin in Children: Focus on Etiologies and Clinical Approach.” Children (Basel), (2023). doi: 10.3390/children11010020.

Reviewed and Edited By

Picture of Jonathan Liow

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.

Picture of James Kwan

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.

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Gastroenteritis and Dehydration In Children (2024)

~ iEM Education Project Team ~ Leave a comment

by Neha Hudlikar & Abdulla Alhmoudi 

Authors
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You have a new patient!

14-month-old Zoey is brought to A&E by her mother with complaints of vomiting and diarrhea for one day. She has had six episodes of vomiting and eight episodes of loose stools since last night. She has also not had a wet diaper for almost 12 hours now. In triage, her vitals are HR 165 b/min, RR 45 br/min, Temperature 38.5 C, SpO2 97% CR 3 seconds. The nurse in triage notes that she has a glazed look. She is otherwise fit and well, with no past medical history. Zoey’s weight – 10 kg.

What will be your approach for this patient?

a-photo-of-a-baby (image produced by using ideogram2.0)

What do you need to know?

Importance

Acute gastroenteritis is one of the most common reasons for visits to pediatric emergency departments [1]. The World Health Organization (WHO) defines diarrhea as the passage of three or more liquid stools per day, or a more frequent passage than what is normal for the individual. When diarrhea occurs alongside vomiting, it is referred to as acute gastroenteritis (AGE).

Diarrhea can be categorized into three clinical types based on the presence or absence of blood and the timing of symptoms:

1. Acute watery diarrhea – lasts from hours to several days, but less than 14 days.
2. Acute bloody diarrhea – also known as dysentery, lasts less than 14 days.
3. Persistent diarrhea – lasts longer than 14 days.

Infectious gastroenteritis can be caused by various pathogens, including viruses, bacteria, and parasites. Rotavirus is the most common causative agent worldwide, responsible for 37% of diarrhea-related deaths in children under five years of age.

Epidemiology

Gastroenteritis is the second leading cause of death in children below the age of 5 and a leading cause of malnutrition in this age group. Globally, there are approximately 1.7 billion cases of childhood diarrheal diseases yearly, and the burden is substantial [2]. There is a direct impact of admission costs on the hospital budget and direct and indirect societal costs when children are admitted to hospitals.

In low-income countries, children under three years old, on average, have three episodes of diarrhea every year. This puts them at risk of malnutrition and, in turn, makes them vulnerable to further episodes of infectious diarrhea.

Pathophysiology

The loss of water and electrolytes via stools, vomit, sweat, and urine without adequate replacement leads to dehydration, a serious complication of gastroenteritis. Physiologic factors that predispose children to serious complications from dehydration include limited stores of fat and glycogen, relatively larger extracellular fluid compartments, and a limited ability to conserve water through their kidneys compared to adults.

Bicarbonate loss in stools, decreased tissue perfusion leading to anaerobic metabolism and lactic acid production, ketosis due to starvation, and decreased excretion of hydrogen ions due to poor renal perfusion are some of the mechanisms contributing to metabolic acidosis in pediatric dehydration due to acute gastroenteritis.

The exact pathophysiology depends on the causative agent. Infectious agents cause diarrhea via adherence, mucosal invasion, enterotoxin, and cytotoxin production.S. aureus and Bacillus cereus produce heat-stable enterotoxins in the food, which once consumed, lead to rapid onset of symptoms and are usually self-limiting. C. Perfingens, Enterotoxigenic E.coli produce enterotoxins in the small intestine leading to watery diarrhea. Other pathogens like enterohemorrhagic E. Coli (EHEC), Salmonella, Shigella, and Campylobacter jejuni produce toxins that directly invade the bowel leading to inflammatory diarrhea. Viruses often destroy the villus surface of the intestinal mucosa, and parasites often adhere to the mucosa.

Medical History

A focused and detailed history is essential to narrowing our differential diagnoses and guiding management. The history should include the timing, frequency, and severity of symptoms. We should also ask about any contact with someone with similar symptoms, known or suspected outbreaks in school or nursery, and recent travel.

All patients with acute gastroenteritis are at risk of dehydration, and the initial evaluation should include questions to assess its severity. The child’s oral intake, amount of urine passed, mental status (lethargy/irritability), etc., should be asked for in the initial evaluation. 

It is also important to ask for associated symptoms such as fever, abdominal pain, blood in the stools, and rash. Children with inflammatory diarrhea can develop serious illnesses like hemolytic uremic syndrome (HUS) with renal involvement. 

Other important questions in history include the child’s vaccination status, recent hospitalization/antibiotic use, and whether the child has any underlying chronic medical conditions/immunosuppression.

Physical Examination

Examining the child should be systematic, looking for the severity of dehydration and differentiating gastroenteritis from other causes of vomiting and diarrhea in children.

General examination should include the child’s appearance, alertness, lethargy, irritability, and weight. Vital signs should be assessed relative to the age. Physicians should look for explicit signs of dehydration, such as dry mucous membranes, sunken eyes, depressed fontanelle, and the presence/absence of tears. The cardiovascular exam should include heart rate, quality of pulses, and central and peripheral capillary refill times. Deep, acidotic breathing suggests severe dehydration. An abdominal examination assesses tenderness, bowel sounds, guarding, and rebound. Flank tenderness increases the likelihood of pyelonephritis. Examine the skin to check skin turgor, peripheral temperature, and other signs such as jaundice/rash.

Abnormal skin turgor, prolonged capillary refill time, and abnormal respiratory pattern are the three most useful examination findings in children with more than 5% dehydration [3]. It is important to note that these signs can be subtle, and determining the severity of dehydration accurately is challenging for physicians.

Alternative Diagnoses

Dehydration most commonly results from acute gastroenteritis in children. However, other diagnoses should be considered based on physical examination and history. Children with fever who are very ill-looking should have sepsis as one of the differential diagnoses. Other diagnoses to consider are urinary tract infection, appendicitis, hemolytic uremic syndrome, intussusception, and diabetic ketoacidosis. Symptoms immediately after ingestion should prompt physicians to consider ingestion of a foreign body or toxic substance. 

Vomiting and diarrhea are two important components that ED practitioners need a careful evaluation to rule in or out various diseases.

When evaluating vomiting in children, it is essential to consider a wide range of differential diagnoses spanning several systems. Central nervous system causes include space-occupying lesions, hydrocephalus, and infections. Cardiac-related vomiting may be attributed to congestive heart failure from various etiologies. Gastrointestinal conditions such as intussusception, midgut volvulus, pyloric stenosis, appendicitis, and esophageal or hepatic disorders are significant considerations. Renal issues like urinary tract infections, pyelonephritis, renal insufficiency, and renal tubular acidosis can also manifest as vomiting. Furthermore, metabolic and endocrine abnormalities, including diabetic ketoacidosis, Addisonian crisis, congenital adrenal hyperplasia, and inborn errors of metabolism, are key causes. Infectious conditions such as sepsis, pneumonia, otitis media, streptococcal pharyngitis, and gastroenteritis must also be included in the diagnostic workup.

Diarrhea in children can arise from diverse causes. Gastrointestinal disorders such as intussusception, Hirschsprung’s disease with toxic megacolon, inflammatory bowel disease, and appendicitis are prominent. Renal conditions, including urinary tract infections and pyelonephritis, can also lead to diarrhea. Infectious etiologies like sepsis, pneumonia, gastroenteritis, and pseudomembranous colitis are frequent contributors. Other causes include drug effects or overdose, hemolytic uremic syndrome, and congenital secretory diarrhea.

Understanding these potential causes is essential for accurate diagnosis and effective management.

Acing Diagnostic Testing

The workup should be guided by history and physical examination to determine the level of dehydration. In most cases, it is a self-limiting disease, and the principal goal of testing in ED should be to identify and correct fluid, electrolyte, and acid-base deficits. 

Most children with mild to moderate disease require no diagnostic testing. Children requiring IV hydration should have blood gas, serum electrolytes, bicarbonate, urea, and creatinine levels tested. It is common for young children to have hypoglycemia, and checking serum glucose levels is important. In children presenting with fever or mucous/blood in their stools, consider testing for fecal leucocytes to support a diagnosis of invasive diarrhea. A positive test should be followed by a stool culture, and it is important to note that a negative test does not rule out invasive disease.

Consider additional testing, such as blood and urine cultures, chest X-rays, and lumbar puncture, in immunosuppressed patients, infants less than 2 months old, or children with suspicion of bacteremia or localized invasive disease. 

Risk Stratification

The Gorelick scale and The Clinical Dehydration Score (CDS) are two of the most widely used scoring systems to predict the presence and severity of dehydration in the pediatric population. It is important to note that neither can definitively rule in or out dehydration in children and infants. Physicians should continue to use a structured approach to patients presenting with acute gastroenteritis and use these scores to aid clinical decision-making [4,5,6].

Clinical Dehydration Scale

 

0

1

2

 

0: No dehydration (<3%)

1-4: Some dehydration (≥3%- <6%)

5-8: Moderate dehydration (≥6%)

General appearance

Normal

Thirsty, restless or lethargic but irritable when touched

Drowsy, limp, or comatose

Eyes

Normal

Slightly sunken

Very sunken

Mucous membranes

Moist

“Sticky”

Dry

Tears

Present

Decreased

Absent

 

Gorelick Scale for Dehydration

characteristic

no or minimal dehydration

moderate to severe dehydration

general appearance

alert

restless, lethargic, unconscious

capillary refill

normal

prolonged or minimal

tears

present

absent

mucous membrane

moist

dry, very dry

eyes

normal

sunken; deeply sunken

breathing

present

deep; deep and rapid

quality of pulses

normal

thready; weak or impalpable

skin elasticity

instant recoil

recoil slowly; recoil > 2 s

heart rate

normal

tachycardia

urine output

normal

reduced; not passed in many hours

Evaluating dehydration with Gorelick scale [6];

4-Point Scale (Italics):

  • 4 points: Presence of 2 or more clinical signs correlating with ≥5% body weight loss from baseline.
  • 4 points: Presence of 3 or more clinical signs correlating with ≥10% body weight loss from baseline.

10-Point Scale (Based on All Signs and Symptoms):

  • ≥3 clinical signs: Associated with ≥5% body weight loss from baseline.
  • ≥7 clinical signs: Associated with ≥10% body weight loss from baseline

Some groups are at higher risk of developing complications from acute gastroenteritis. These include premature infants, very low birth weight infants, and infants below the age of 3 months. Children who are malnourished, immunosuppressed, and with chronic underlying medical conditions are also at higher risk of developing complications.

Indications for inpatient management of children presenting with acute diarrhea have been proposed, and the Table below summarizes these recommendations.

Indications for Inpatient Management of Children with Acute Diarrhoea

  • Difficulties in administrating oral rehydration therapy (patient refusal, intractable vomiting)
  • History of premature birth, chronic medical conditions, or concurrent illness, very young age
  • Parental/caregiver concern about continuing ORT at home/unable to provide adequate care
  • Persistent vomiting, high output diarrhoea, persistent dehydration
  • Uncertainty of diagnosis warranting further observation
  • Progressive symptoms or unusual irritability/drowsiness
  • Lack of easy access to hospital care if needing to return

Adapted from King CK, Glass R, Bresee JS, Duggan C; Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. 2003;52(RR-16):1-16.

Management

Management in the Emergency Department should initially focus on correcting dehydration. Oral rehydration solution (ORS) is recommended for all children with mild to moderate dehydration.

To calculate the volume of oral replacement therapy (ORT), the first step is to estimate the degree of dehydration based on history and physical examination findings (see Table below). The desired volume of ORS is then calculated based on the degree of dehydration (30 to 50 mL/kg for mild and 60 to 80 mL/kg for moderate dehydration). 25% of the calculated volume of ORS is given every hour for the first four hours and ongoing losses can be replaced at 10 mL/kg for each stool and 2 mL/kg for each emesis. The patient needs reassessment at the end of the first few hours and those with no clinical deterioration may have a 2 to 4-hour trial with ORT. If the child is unable to keep up with ongoing losses and if volume replacement is not adequate at the end of 8 hours, IV rehydration is recommended. Ondansetron is a selective 5-hydroxytryptamine type 3 receptor antagonist, a useful adjunct in treating AGE. It acts on peripheral and central chemoreceptors to alleviate nausea. It has been shown to decrease vomiting, improve oral intake, and reduce the need for intravenous fluid resuscitation and hospital admissions [7].

Assessment of Degree of Dehydration

Mild dehydration (3%-5%)

Moderate dehydration (5%-10%)

Severe dehydration (> 10%)

Mental status

Alert

Irritable

Lethargy

Heart rate

Normal

Increased

Increased

Quality of pulses

Normal

Normal to decreased

Decreased to thready

Mucous membranes

Wet

Slightly dry

Dry

Capillary refill

< 2 seconds

> 2 seconds

> 2 seconds

Blood pressure

Normal

Normal

Normal to decreased

Respirations

Normal

Tacypnea

Tachypnea, deep

Fontanelle

Normal

Sunken

Sunken

Eyes

Normal

Slightly sunken, decreased tears

Sunken, cries without tears

Urine output

Normal to decreased

Decreased

Oliguric or anuric

Skin turgor

Normal

Slightly reduced

Reduced

Children with severe dehydration, signs of shock, failed attempts with oral rehydration therapy, intractable vomiting, hypoglycemia, or electrolyte derangements require intravenous fluid resuscitation, which is often initiated as a 20 mL/kg bolus of 0.9% of sodium chloride in ED. These patients need frequent re-evaluation to review their response to IV hydration. Improvements in mental status, tachycardia, capillary refill time, and urine production are some signs that signal a good response to intravenous resuscitation. After initial resuscitation, patients will need an evaluation of their maintenance fluid needs, which could be either intravenous fluid therapy or ORT, depending on the patient’s clinical status. Maintenance fluids are calculated based on the child’s weight using the 4-2-1 Holliday-Segar Rule.

Holliday-Segar Rule for Maintenance Fluid Calculation

Body Weight

mL/kg/hr

mL/kg/day

First 10 kg

4

100

Second 10 kg

2

50

Each additional kg

1

20

Children who require multiple fluid boluses without signs of improvement should be investigated for other serious conditions such as adrenal insufficiency, cardiogenic or septic shock, etc. It is important to note that rapid correction of serum sodium levels can lead to osmotic demyelination syndrome in hyponatremia and cerebral edema in hypernatremia.

In children with hypoglycemia, glucose can be replaced as per the “rule of 50,” where the percent dextrose multiplied by the number of mL per kilogram equals 50. Neonates often get 10% dextrose solution at 5mL/kg, children between 1 month to 8 years of age (or 25 kg weight) can be given 2mL/kg of 25% dextrose. 50% of dextrose at 1mL/kg can be used safely in older children. The higher tonicity of 25% and 50% dextrose solutions poses a risk of tissue necrosis if extravasation occurs during peripheral IV infusion.
 
Antibiotics are not indicated in viral gastroenteritis and most cases of uncomplicated bacterial gastroenteritis. Considerations can be made for very young infants, immunocompromised, and those with chronic underlying medical conditions. The WHO recommends zinc supplementation for children under 5 years suffering from AGE in developing countries [8]. Studies showing the efficacy of probiotics are inconclusive and further research is needed to establish the safety and efficacy of probiotics in children with AGE [9].

When To Admit This Patient

Most cases of AGE are self-limiting and can be managed on an outpatient basis after a brief period of observation in the ED. Parents and caregivers should be given appropriate discharge instructions emphasizing hygiene and hand-washing techniques to prevent the further spread of the illness. Breastfeeding/routine diet should be continued at home, and supplemental electrolyte solutions may be recommended. Parents and caregivers should be educated to recognize the signs of dehydration and advised to bring the child back to the ED for these. Children with intractable vomiting, severe dehydration, failure to maintain oral hydration, electrolyte derangements, deteriorating clinical status, and those at high risk for complications (very low birth weight infants, < 3 months old, immunosuppressed, and children with chronic medical problems) should be admitted to hospital.

Revisiting Your Patient

History-taking reveals that Zoey has not had much to drink or eat in the past 12 hours, and there has been an outbreak of gastroenteritis in the nursery that she attends. There has been no blood in the stools, and Mum says that Zoey has been very sleepy for the last few hours. Her vaccinations are up to date, and she has no other medical history of note.

On examination, she is irritable when you approach her, and your systematic examination reveals the following:
CNS – Irritable, no signs of meningism, anterior fontanelle closed
HEENT – Dry mucous membranes, slightly sunken eyeballs
Respiratory – Mild tachypnea, bilateral air entry with clear breath sounds
CVS – Central capillary refill 3 seconds, tachycardia, BP 88/50
Abdomen – Soft, lax and non-tender. Bowel sounds ++, no mass palpable
Skin – Slightly reduced skin turgor, no rash

Next steps?

Your examination reveals no red flags of meningitis/sepsis or surgical abdomen. Given the recent outbreak of gastroenteritis in her nursery, you make a provisional diagnosis of acute gastroenteritis for Zoey. Your clinical assessment estimates the degree of dehydration to be moderate (5-10%), and you calculate her fluid depletion to be between 600 to 800 mL (60 to 80 mL/kg). You start the patient on oral rehydration therapy aiming for at least 200 mL to be given slowly over the next hour. You guide the mother in letting the staff know if Zoey vomits or has another episode of diarrhea while in the Emergency Department.

Investigations?

You ask for a random blood sugar to rule out hypoglycemia and a urine dipstick to rule out urinary tract infection.

Review
After an hour, Zoey tolerated 250 mL of oral rehydration solution and had one episode of vomiting but no diarrhea. Her blood sugar was 4 mmol/l. She has perked up significantly and is more alert than before. Her vital signs show improvement, and you decide to give her Ondansetron and continue the ORT.

After two hours, Zoey has tolerated around 400 mL of ORS and is more alert and interactive now. Her vitals are normal, and she has not had any further episodes of diarrhea or vomiting. She has also passed some urine, which has been tested and found to be negative for infection.

Mum was advised to continue oral hydration at home as well as the slow introduction of a regular diet and to come back to ED if Zoey could not tolerate orally, had intractable vomiting, any blood in her stools, high-grade fever, or change from her baseline mental status. Zoey was discharged from the ED and would follow up with her primary physician in the community.

Authors

Picture of Neha Hudlikar

Neha Hudlikar

Emergency Department, Zayed Military Hospital, Abu Dhabi

Picture of Abdulla Alhmoudi

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.

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References

  1. McDermott KW, Stocks C, Freeman WJ. Overview of Pediatric Emergency Department Visits, 2015. In: Healthcare Cost and Utilization Project (HCUP) Statistical Briefs. Rockville (MD): Agency for Healthcare Research and Quality (US); August 7, 2018.
  2. Hartman RM, Cohen AL, Antoni S, et al. Risk Factors for Mortality Among Children Younger Than Age 5 Years With Severe Diarrhea in Low- and Middle-income Countries: Findings From the World Health Organization-coordinated Global Rotavirus and Pediatric Diarrhea Surveillance Networks [published correction appears in Clin Infect Dis. 2023 Jan 6;76(1):183]. Clin Infect Dis. 2023;76(3):e1047-e1053. doi:10.1093/cid/ciac561
  3. Steiner MJ, DeWalt DA, Byerley JS. Is this child dehydrated?. JAMA. 2004;291(22):2746-2754. doi:10.1001/jama.291.22.2746
  4. Falszewska A, Szajewska H, Dziechciarz P. Diagnostic accuracy of three clinical dehydration scales: a systematic review. Arch Dis Child. 2018;103(4):383-388. doi:10.1136/archdischild-2017-313762
  5. Freedman SB, Vandermeer B, Milne A, Hartling L; Pediatric Emergency Research Canada Gastroenteritis Study Group.
  6. Pringle K, Shah SP, Umulisa I, et al. Comparing the accuracy of the three popular clinical dehydration scales in children with diarrhea. Int J Emerg Med. 2011;4:58. Published 2011 Sep 9. doi:10.1186/1865-1380-4-58
  7. Tomasik E, Ziółkowska E, Kołodziej M, Szajewska H. Systematic review with meta-analysis: ondansetron for vomiting in children with acute gastroenteritis. Aliment Pharmacol Ther. 2016;44(5):438-446. doi:10.1111/apt.13728Diagnosing clinically significant dehydration in children with acute gastroenteritis using noninvasive methods: a meta-analysis. J Pediatr. 2015;166(4):908-16.e166. doi:10.1016/j.jpeds.2014.12.029
  8. Goldman RD. Zinc supplementation for acute gastroenteritis. Can Fam Physician. 2013;59(4):363-364.
  9. Cameron D, Hock QS, Kadim M, et al. Probiotics for gastrointestinal disorders: Proposed recommendations for children of the Asia-Pacific region. World J Gastroenterol. 2017;23(45):7952-7964. doi:10.3748/wjg.v23.i45.7952

Additional Resources

King CK, Glass R, Bresee JS, Duggan C; Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. 2003;52(RR-16):1-16.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

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Meningitis (2024)

~ iEM Education Project Team ~ Leave a comment

by J. Austin Lee

Authors
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You have a new patient!

A 21-year-old male presented to a clinic. He is a refugee and has been here with a high-grade fever and a severe headache for the past three days. The patient had been working as a laborer in construction sites in the area for the past six months. At triage, his vital signs are as follows: temperature of 39.1°C (102.5°F), blood pressure of 110/70 mmHg, heart rate of 110 beats per minute, and respiratory rate of 22 breaths per minute.

Further examination reveals that the patient is quite photophobic. You note that he prefers to sit still, and when you examine him further, you feel that his neck is quite uncomfortable when flexed, and there is discomfort with flexed hips and passive knee extension. The patient was accompanied by a co-worker who reported that this morning, the patient was vomiting and had been confused. The patient had no history of recent travel or vaccination.

What do you need to know?

Importance

Meningitis is an important infectious disease with severe consequences if not promptly recognized and treated. Meningitis is caused by inflammation of the meninges, the membranes covering the brain and spinal cord. It can be caused by a bacterial, viral, fungal, or parasitic infection. Moreover, meningitis can be triggered by physical injury, autoimmune disorders, cancer, or certain drugs that can cause meningitis. Generally, when discussing meningitis, we are primarily concerned with infectious etiologies. In addition to the high mortality associated with meningitis, survivors may suffer from long-term sequelae, such as hearing loss, cognitive impairment, and neurologic deficits [1]. Infants, children, and immunocompromised patients are at a higher risk of developing meningitis, and outbreaks can occur in crowded living conditions, with classic examples including crowded urban areas (including slums), university dormitories, and military barracks [2]. Prompt recognition and treatment with appropriate antibiotics or antivirals are critical for improving outcomes in patients with meningitis [3].

Epidemiology

Meningitis is a significant global health problem, particularly in low- and middle-income countries. According to the World Health Organization (WHO), there are an estimated 1.2 million cases of bacterial meningitis each year, resulting in 250,000 deaths [4]. According to the Global Burden of Disease study, meningitis is responsible for an estimated 21.9 million disability-adjusted life years (DALYs) globally [5]. The burden of meningitis is particularly high in sub-Saharan Africa, where large-scale epidemics of meningococcal meningitis occur. In these regions, outbreaks are often associated with overcrowding, malnutrition, and poor sanitation, and can cause high rates of mortality and long-term disability. While vaccination has helped to reduce the burden of meningitis in many parts of the world, there is still a need for continued surveillance and control measures, particularly in high-risk populations.

Pathophysiology

Bacteria (and viruses and chemicals) can cross the blood-brain barrier to infect or inflame the meninges by spreading from the bloodstream. Pathogens can also spread from contiguous infection (from a source such as the sinuses or middle ear), trauma, neurosurgery, or indwelling medical devices [6]. Nasopharyngeal colonization from infected droplets of respiratory secretions or distant localized infection (lungs, urine) with subsequent bloodstream invasion are other sources of infection [6].

Once the pathogen reaches the meninges, it triggers an immune response, releasing pro-inflammatory cytokines, which attract immune cells to the site of infection. This immune response leads to the characteristic symptoms of meningitis, including fever, headache, neck stiffness, and altered mental status. In severe cases, the inflammation can lead to increased intracranial pressure, cerebral edema, and brain herniation, which is life-threatening and frequently fatal [6].

Bacterial meningitis poses an emergent risk to the neurological system; progression can result in rapid fatality. Furthermore, bacterial meningitis has the potential to cause long-term complications, including hearing and vision impairment, memory and concentration issues, epilepsy, coordination and balance difficulties, learning challenges, and behavioral disorders [6]. In community-acquired meningitis, S. pneumoniae has become the most common pathogen since routine immunization of infants against H. influenzae type B [7]. It’s important to note that the most common causes of meningitis can vary depending on the patient’s age, geography, and immune status [8]. Table 1 summarizes most common pathogens of meningitis.

Table 1: Common Infectious Causes of Meningitis [7-14].

Pathogen

Common Etiologies

Bacteria

Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae, Listeria monocytogenes

Viruses

Enteroviruses (e.g. Coxsackie virus, Echovirus), Herpes simplex virus, Varicella-zoster virus, Mumps virus

Fungi

Cryptococcus neoformans, Histoplasma capsulatum, Coccidioides immitis

Parasites

Naegleria fowleri, Acanthamoeba species

Medical History

Key features in the medical history of meningitis include the onset and duration of symptoms, recent travel or exposure to infectious agents, immunization status, underlying medical conditions, and medication use. It is important to obtain a detailed history of present illness, including the timing and progression of symptoms such as fever, headache, neck stiffness, altered mental status, and rash. Patients may also report symptoms such as nausea, vomiting, photophobia, and seizures. Recent travel or exposure to individuals with known or suspected meningitis can help identify potential infectious agents. Immunization status, particularly regarding vaccines against meningococcal and pneumococcal infections, is also important to determine. Patients with chronic medical conditions or who are taking immunosuppressive medications may be at increased risk for certain pathogens or complications.

Physical Examination

The physical exam findings in a patient with meningitis include vital signs, general appearance, and specific neurological findings. Vital signs such as fever, tachycardia, and hypotension are common. Patients may appear acutely ill, with a lethargic or altered mental status. They may exhibit signs of meningeal irritation, such as photophobia, neck stiffness, and a positive Kernig or Brudzinski sign. Kernig’s sign is the inability to straighten the leg when the hip is flexed to 90 degrees; Brudzinski’s sign is positive when forced flexion of the neck elicits a reflex flexion of the hips [6]. Both Kernig and Brudzinski have reported low sensitivity (5%) but high specificity (95%) [6]. Neurological findings such as altered level of consciousness, focal neurologic deficits, and seizures may also occur or be present. Skin findings such as a petechial or purpuric rash may present in meningococcal meningitis patients. In infants, bulging fontanelles and poor feeding are concerning. Jolt accentuation testing can provide additional value: the patient horizontally rotates the head at two to three rotations per second [15]. The worsening of an existing headache indicates a positive result, though the sensitivity of jolt accentuation for diagnosing meningitis varies widely, with estimates ranging from 40-96% [15].

Table 2: Common signs/symptoms of meningitis, with sensitivity [8-10]

Sign / Symptom

Sensitivity

Neck stiffness

30-100

Headache

70-100

Photophobia

50-90

Nausea/vomiting

50-90

Altered mental status

50-80

Jolt accentuation

40-90

Fever

70-80

Seizures

10-30

Focal neurological deficits

<10

Alternative & Differential Diagnoses

  • Encephalitis: inflammation and swelling of the brain parenchyma; encephalitis tends to cause more neurological symptoms such as confusion, seizures, and changes in behavior or personality.
  • Chemical meningitis (e.g., due to contrast agents, medications, or illicit drugs): The patient should have a history of exposure to a triggering agent, such as a medication or contrast dye.
  • Carcinomatous meningitis (e.g., metastatic cancer cells in cerebrospinal fluid); history or imaging with evidence of metastatic disease.
  • Aseptic meningitis (e.g., due to autoimmune disorders, sarcoidosis, or drug reactions) symptoms are usually milder. They may include fever, headache, and neck stiffness, often including other symptoms such as rash or joint pain.
  • Cerebral vasculitis is inflammation and damage to the blood vessels that supply the brain. It may have a more insidious onset and a chronic or recurrent course.
  • Traumatic meningitis (e.g., due to head injury or neurosurgical procedures)
  • Brain abscess or subdural empyema; likely to include more focal neurological symptoms/deficits such as weakness or paralysis, seizures, or speech and vision problems.
  • Subarachnoid bleeding is commonly associated with sudden, severe headaches, nausea, vomiting, and, at times, syncope.
  • Tetanus is commonly associated with other symptoms such as jaw stiffness, diffuse muscle rigidity/spasm, difficulty swallowing, and respiratory distress.
  • Malaria, particularly cerebral malaria, is typically found in areas with high transmission rates of malaria, and cerebral malaria typically has a more gradual onset. It can progress over several days to weeks.

Acing Diagnostic Testing

Acute diagnostic testing is crucial in managing meningitis as it allows for early detection and appropriate treatment. The accepted gold standard for diagnosing meningitis is cerebrospinal fluid (CSF) analysis, obtained through a lumbar puncture [6,16]. CSF analysis includes cell count, protein and glucose levels, culture, and gram stain [16]. Elevated CSF white blood cell count and protein levels are common findings in meningitis, while glucose levels are often decreased. CSF culture and gram stain are essential to identify the causative organism, guide antimicrobial therapy, and can be used to monitor response to treatment.

In addition to CSF analysis, imaging studies such as computed tomography (CT) or magnetic resonance imaging (MRI) may also be obtained to evaluate for complications of meningitis, such as hydrocephalus, cerebral edema, or abscess formation. However, these imaging studies are typically not used for the initial diagnosis of meningitis. CT is a strong consideration to be performed before lumbar puncture (LP) to exclude increased intracranial pressure (ICP) or mass lesion when CT is available and a patient has any of these criteria: immunocompromised state, history of CNS disease, new-onset seizure, papilledema, severe decreased consciousness (GCS<12) or focal neurologic deficit [6].

Blood cultures may also be obtained to help identify the causative organism and determine appropriate antimicrobial therapy. In particular, meningococcemia can rapidly lead to shock and multiorgan failure. Other laboratory tests, such as complete blood count (CBC), chemistry panel, and coagulation studies, are also routinely obtained to evaluate potential complications or comorbidities.

Rapid diagnostic tests, such as polymerase chain reaction (PCR) or antigen tests, may also be available in some settings. These tests can help quickly identify some causes of meningitis, such as bacterial or viral meningitis. They can provide near real-time speciation of the causative organism and help tailor appropriate treatment.

Table 3: CSF Testing Characteristics [9-11, 17-19]

Test

Normal Results

Bacterial Meningitis Results

Viral Meningitis Results

Fungal Meningitis Results

Appearance

Clear, colorless

Cloudy or turbid

Clear to slightly cloudy

Cloudy or turbid

WBC count

<5 cells/microliter

Elevated

Elevated, often lymphocytic

Elevated, often lymphocytic

Glucose

40-70 mg/dL

Decreased

Normal or slightly decreased

Decreased

Protein

15-45 mg/dL

Elevated

Normal to slightly elevated

Elevated

Gram stain

No organisms

Gram-positive or gram-negative organisms

Negative for bacteria, positive for virus

Negative for bacteria and virus

Culture

Negative

Positive for bacterial growth

Negative for bacteria, positive for virus

Positive for fungal growth

Risk Stratification

Several features in the history, physical examination, and testing can indicate a worse outcome in a patient with meningitis. Some of these include advanced age, altered mental status, presence of seizures, hypotension, tachycardia, high cerebrospinal fluid (CSF) protein and low glucose levels, high white blood cell count in CSF, and delayed initiation of appropriate antimicrobial therapy.
Various risk stratification tools have been developed for meningitis, such as the Glasgow Meningococcal Septicemia Prognostic Score (GMSPS), which is used to predict mortality in meningococcal disease. This tool includes variables such as age, Glasgow Coma Scale score, presence of meningismus, and presence of shock. This tool is most helpful in identifying the most sick cases, which are likely to be evident based on the clinical history and exam. Although this score exists, it is not routinely used in clinical practice. Another tool is the Bacterial Meningitis Score (BMS), which helps clinicians differentiate bacterial from aseptic meningitis based on the presence of certain clinical and laboratory features. The BMS includes age, cerebrospinal fluid protein level, cerebrospinal fluid neutrophil count, and peripheral blood absolute neutrophil count.

Management

In patients with whom you have concerns about meningitis, stabilization of an unstable patient is the priority. Assess the airway and breathing, including monitoring the respiratory rate and saturation levels. Administer supplemental oxygen if necessary. Evaluate circulation by checking the pulse, capillary refill time, and blood pressure. Provide fluids or administer medications as required. Next, the neurological function can be evaluated using tools like the Glasgow Coma Scale or AVPU (Alert, Verbal, Painful, Unresponsive) scale. Additionally, glucose levels and the presence of focal neurological signs, seizures, and papilledema should be assessed.

Empiric antibiotics should be started as soon as possible, even before the results of CSF culture and sensitivity are available, in order to reduce the risk of mortality and morbidity. In addition, supportive measures such as fluid and electrolyte management, seizure prophylaxis, and management of increased intracranial pressure are essential in managing meningitis. Patients with severe disease or complications may require ICU admission. Close follow-up with repeat CSF analysis and neuroimaging may be necessary to monitor response to treatment and identify potential complications.

Empiric treatment for bacterial meningitis typically involves using third-generation cephalosporins, such as ceftriaxone or cefotaxime, with or without vancomycin to cover for potential penicillin-resistant strains of Streptococcus pneumoniae. In infants under 1 month of age and patients over 50 years, ampicillin is often added to cover for Listeria monocytogenes [2]. Dexamethasone, a corticosteroid, is also given prior to or at the time of antibiotic initiation in adults and children with suspected or confirmed bacterial meningitis to reduce the risk of neurologic sequelae. The administration of corticosteroids has been shown to significantly reduce hearing loss and neurological complications in patients with meningitis.

However, using corticosteroids has not significantly impacted overall mortality rates [20]. The management of viral meningitis is mainly supportive. Antiviral treatment may be considered for specific viral pathogens, such as acyclovir for herpes simplex virus (HSV) or ganciclovir for cytomegalovirus (CMV). However, empiric antiviral treatment is not recommended in most cases of viral meningitis. The use of corticosteroids, such as dexamethasone, is controversial in viral meningitis and is not generally recommended [20].
Pre-exposure prophylaxis, though intrapartum prophylaxis of group B streptococcus in pregnant women, has significantly reduced the risk of early-onset group B strep meningitis [21]. Post-exposure prophylaxis is also an important consideration in contacts of patients diagnosed with meningitis; close contacts are defined as individuals who have had prolonged close contact with the index case, such as household contacts, healthcare workers, or individuals who shared a room or had direct contact with respiratory or oral secretions. Antibiotic prophylaxis is typically recommended within 24-48 hours of identification of the index case and may include rifampin, ciprofloxacin, or ceftriaxone, depending on the age and health status of the contact. In addition to antibiotics, vaccination with the meningococcal conjugate vaccine may be recommended for close contacts, particularly those at increased risk.

The recommended antibiotic prophylaxis is usually a single dose of intramuscular ceftriaxone (250 mg for adults and children weighing > 45 kg and 125 mg for children weighing < 45 kg). Alternatively, oral antibiotics such as rifampin, ciprofloxacin, or azithromycin can be used as alternatives. For exposure to Streptococcus pneumoniae, oral amoxicillin is recommended for prophylaxis, and for exposure to Haemophilus influenzae type b (Hib), rifampin or ceftriaxone is recommended.

Special Patient Groups

Elderly individuals, particularly those over 65, may present with atypical meningitis characterized by lethargy, minimal signs of meningismus, and the absence of fever. Conversely, younger individuals such as neonates, infants, and children often present with symptoms such as poor feeding, irritability, fever, and in babies, a shrill cry, decreased appetite, rash, and vomiting. In young children, the presentation of meningitis can mimic flu-like symptoms, including cough or respiratory distress, and it is not uncommon for them to have a history of respiratory tract infection. Seizures are also more frequently observed in this age group with meningitis. When evaluating a febrile child who appears unwell, it is crucial to consider bacterial meningitis as a potential diagnosis until ruled out. It is worth noting that blood and cerebrospinal fluid results may appear normal, especially in extremely young or old age groups.

When To Admit This Patient

Patients with suspected meningitis should be admitted to the hospital from the emergency department, as this is a potentially life-threatening condition that requires urgent evaluation and treatment. Admission should be considered for patients with a high likelihood of meningitis based on clinical presentation and laboratory findings. Patients with severe symptoms such as altered mental status, seizures, or signs of sepsis are particularly high-risk and should be admitted promptly. Patients with risk factors such as immunocompromised status, recent head trauma, or history of neurosurgical procedures should also be admitted.

Patients with meningitis who present with severe symptoms or complications such as altered mental status, seizures, respiratory distress, or signs of sepsis should be considered for admission to the intensive care unit (ICU). In addition, patients with bacterial meningitis or other severe forms of meningitis, such as fungal or tuberculous meningitis, and those immunocompromised should also be admitted to the ICU for close monitoring and aggressive treatment. Patients with a high risk of developing cerebral edema or increased intracranial pressure, such as those with hydrocephalus or brain abscess, may also require ICU admission. Close monitoring of vital signs, neurologic status, and laboratory parameters, such as blood glucose and electrolytes, is likely best done in an ICU.

Revisiting Your Patient

Let’s go back to the clinical presentation of your 21-year-old male refugee. He has fever, tachycardia, vomiting and confusion, and meningitis was suspected. You performed a lumbar puncture, and the cerebrospinal fluid analysis showed a white cell count of 1500 cells/µL with predominant neutrophils, protein level of 150 mg/dL, and glucose level of 30 mg/dL. The patient was started on treatment with intravenous ceftriaxone and vancomycin and admitted to the hospital. The patient was diagnosed with bacterial meningitis and was continued on intravenous antibiotics for a total of 14 days.

The patient responded well to the treatment and was discharged after completing the course of antibiotics. Appropriate public health notification was made, and the patient was scheduled for post-discharge follow-up care and vaccination.

Author

Picture of J. Austin Lee, MD MPH DTMH

J. Austin Lee, MD MPH DTMH

Austin Lee, MD MPH DTMH, is a practicing emergency medicine doctor in the United States. He currently works with Indiana University Health, across several hospital sites. Dr. Lee obtained an MPH at the George Washington University before going to medical school at Indiana University. He completed his emergency medicine residency at the University of Virginia, and then worked at Brown University where he was a part of the Global Emergency Medicine fellowship. Austin has worked on a number of international emergency medicine projects, and is actively engaged in supporting the development of emergency medicine in Kenya.

Listen to the chapter

References

  1. Tunkel AR, Scheld WM. Acute meningitis. In: Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 20th ed. Vol 1. New York, NY: McGraw-Hill Education; 2019:894-900.
  2. Mandell GL, Bennett JE, Dolin R. Principles and Practice of Infectious Diseases. 8th ed. Vol 2. Philadelphia, PA: Elsevier; 2015:1116-1132.
  3. Longo DL, Kasper DL. Bacterial meningitis. In: Longo DL, ed. Harrison’s Infectious Diseases. 3rd ed. New York, NY: McGraw-Hill Education; 2018:360-373.
  4. World Health Organization. Defeating meningitis by 2030. Accessed May 25, 2023. https://www.who.int/initiatives/defeating-meningitis-by-2030.
  5. GBD 2016 Meningitis Collaborators. Global, regional, and national burden of meningitis, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol. 2018 Dec;17(12):1061-1082.
  6. Parežnik A. Meningitis. October 12, 2018. Accessed May 25, 2023. https://iem-student.org/meningitis/.
  7. McGill F, Heyderman RS, Panagiotou S, Tunkel AR, Solomon T, Connor MD. Acute bacterial meningitis in adults. The Lancet. 2016;388(10063):3036-3047.
  8. Lu CH, Chang WN, Chang HW, et al. Adult bacterial meningitis in southern Taiwan: epidemiological trend and prognostic factors. J Neurol Sci. 2005;22(2):133-139.
  9. van de Beek D, de Gans J, Spanjaard L, et al. Clinical features and prognostic factors in adults with bacterial meningitis. N Engl J Med. 2004;351(18):1849-1859.
  10. Tunkel AR, Hartman BJ, Kaplan SL, et al. Practice guidelines for the management of bacterial meningitis. Clin Infect Dis. 2004;39(9):1267-1284.
  11. van de Beek D, de Gans J, Tunkel AR, et al. Community-acquired bacterial meningitis in adults. N Engl J Med. 2006;354(1):44-53.
  12. McGill F, Griffiths MJ, Solomon T. Viral meningitis: current issues in diagnosis and treatment. Curr Opin Infect Dis. 2017 Apr;30(2):248-256.
  13. Góralska K, Blaszkowska J, Dzikowiec M. Neuroinfections caused by fungi. Infection. 2018 Aug;46(4):443-459.
  14. Pana A, Vijayan V, Anilkumar AC. Amebic Meningoencephalitis. 2023 Jan 21. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan
  15. Iguchi M, Noguchi Y, Yamamoto S, Tanaka Y, Tsujimoto H. Diagnostic test accuracy of jolt accentuation for headache in acute meningitis in the emergency setting. Cochrane Database Syst Rev. 2020 Jun 11;6(6):CD012824.
  16. Roberts JR, Custalow CB, Thomsen TW. Roberts and Hedges’ Clinical Procedures in Emergency Medicine and Acute Care. Elsevier; 2018.
  17. Kumar R, Bose M, Singh SN, et al. Clinicoradiological and neurophysiological correlation in Japanese encephalitis. Ann Trop Paediatr. 1994;14(4):311-318.
  18. González-Duarte A, Cárdenas G, Torres-Narbona M, et al. Cerebrospinal fluid lactic acidosis in aspergillosis meningitis. Arch Neurol. 2007;64(9):1362-1364.
  19. Brouwer MC, Tunkel AR, van de Beek D. Epidemiology, diagnosis, and antimicrobial treatment of acute bacterial meningitis. Clin Microbiol Rev. 2010;23(3):467-492.
  20. van de Beek, D., de Gans, J., McIntyre, P., Prasad, K., & Weisfelt, M. (2004). Corticosteroids for acute bacterial meningitis. The Cochrane Database of Systematic Reviews, (1), CD004405.
  21. Thigpen MC, Whitney CG, Messonnier NE, Zell ER, Lynfield R, Hadler JL, et al. Bacterial meningitis in the United States, 1998-2007. N Engl J Med. 2011;364(21):2016-2025.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Catching Necrotizing Fasciitis Early in the ED

~ Helena Halasz, Hungary ~ Leave a comment

A well-known adage is that necrotizing fasciitis, which is colloquially abbreviated to “nec-fasc,” is a rapidly progressive and often fatal disease that proves difficult to diagnose.

Image Courtesy of DermNet NZ

Nomenclature and Background Information

Necrotizing fasciitis is a subset of a larger group of diseases known as necrotizing soft tissue infections or NSTIs. In this blog post, the term NSTI will be used in an effort to be inclusive of infection that may be affecting the muscles (myositis), deeper dermis and subcutaneous tissue (cellulitis) or fascia (fasciitis).

The first known reference to the disease process can be traced back to the 5th century; Hippocrates, who is often referred to as the father of medicine, wrote, “[m]any were attacked by the erysipelas all over the body when the exciting cause was a trivial accident…flesh, sinews, and bones fell away in large quantities…there were many deaths.” The description from over two thousand years ago still holds true today, and although NSTIs are rare, the average mortality reported has been around 20% in the past 20 years (ranging from 15% to 45%, depending on the study examined).

Classification

The types of NSTIs can be classified either by anatomical location (i.e. most commonly affects the extremities, or, if there is perineal, genital and perianal involvement, it is known as Fournier gangrene) or bacterial involvement (divided into the following types).

  • Type 1: polymicrobial (aerobic and anaerobic) – more common than type 2
    • elderly patients, comorbidities (DM, ulcers), previous surgical intervention
  • Type 2: monomicrobial (Group A streptococcus, MRSA)
    • in any age group and even patients without underlying disorders
    • 50% of cases have no clear portal entry
  • Type 3: gas gangrene (Clostridium sp.)

Risk Factors

Although NSTIs can occur in patients without significant medical disease, there are definite risk factors that increase one’s chance of developing an NSTI:

  • patient-related factors: diabetes mellitus, obesity, peripheral arterial disease, chronic alcohol abuse, immunosuppression, malignancy, end-stage renal disease
  • barrier integrity-related factors: cutaneous lesions like insect bites or penetrating trauma, injection drug use, surgical incisions (for example, neonatal circumcision), mucosal breach (such as hemorrhoids, episiotomy)

Sign and Symptoms

  • hard signs (note that only 1/3rd of patients may present with these “textbook” signs): bullae, crepitus, violaceous hue, “dishwater” discharge
  • systemic signs: low-grade fever with tachycardia (out of proportion to the fever)
    • other non-specific signs: malaise, myalgias, diarrhea, anorexia
  • edema, brownish skin discoloration, decreased sensation in affected limb, a sense of heaviness
    • PEARL: make sure to mark the borders of the erythema to track progression
  • mental status changes (delirium, irritability)

In an article titled, “Pitfalls in Diagnosing Necrotizing Fasciitis,” Table 2 outlines the evolution of physical signs from early to late disease.

Diagnosis

The gold standard for diagnosis is via surgical exploration; however, in order to get a patient to surgery in a timely fashion, there are important tests that can raise suspicion that there is an underlying NSTI.

In laboratory tests, the following findings may be suggestive of NSTI, but there is no one specific sign that would be pathognomonic. A patient may have metabolic acidosis, coagulopathy, leukocytosis with left shift, anemia, thrombocytopenia, elevated CRP/ESR, myoglobinuria, signs of renal or hepatic dysfunction, and interestingly, hyponatremia and well as hyperlactatemia.

One notable finding is that elevated serum CK or AST concentrations suggest deep infection involving muscle or fascia rather than more superficial cellulitis. Furthermore, another source considered the utility of trending procalcitonin levels as a representation of adequate infection source control.

In terms of imaging tests, radiography can be useful but is not a necessity. If suspicion for NSTI is high, patient should immediately be sent to surgery. The best imaging modality is CT, and the presence of gas is nearly pathognomonic. Other signs suggestive of NSTI may be:

  • presence of fluid collections or abscess
  • heterogeneity or absence of tissue enhancement
  • edema at or below level of fascia

LRINEC (Laboratory Risk Index) Score

While there is a score for screening NSTIs, known as the Laboratory Risk Index, it has not been externally validated as of 2017. Nevertheless, looking at the components of the score on MDCalc gives a clinician an idea of what type of parameters might be of interest in diagnosing necrotizing soft tissue infections. 

The LRINEC score determined that the laboratory findings of interest are: CRP, WBC, hemoglobin, sodium, creatinine and glucose. The score has “high specificity but low sensitivity” – what does this mean? This means that if your LRINEC score is low or normal, this does not rule out an NSTI; however, if it is 6 or higher, that raises the suspicion and further workup is recommended.

Differential diagnosis

  • cellulitis
  • dermatological rash (contact dermatitis)
  • pyoderma gangrenosum
  • pyomyositis
  • deep vein thrombosis
  • calciphylaxis (cutaneous manifestations)

Treatment

The two pillars of treatment are surgery and antibiotics.

Broad spectrum antibiotics should be given intravenously as soon as necrotizing infection is suspected, but only aftertwo sets of blood cultures have been taken. The antibiotic of choice, according to Tintinalli’s Emergency Medicine Manual (8th) edition are the following:

  • vancomycin 1 gram IV every 12 hours PLUS meropenem 500 to 1000 mg IV every 8 hours
  • alternatively: vancomycin (same regimen) PLUS piperacillin/tazobactam 4.5 gram IV every six hours
  • clindamycin can be added to the regimen (mechanism of action: inhibits toxin synthesis)

Surgical debridement is key. In severe cases, surgery will need to be radical and aggressive to ensure optimal outcomes and include fasciotomy or even amputation.

Other considerations:

  • aggressive intravenous fluid resuscitation (IV crystalloids)
  • may consider: blood transfusion (if hemolysis results in severe anemia)
  • may consider: tetanus prophylaxis (based on mechanism of injury)

Mortality

Certain clinical characteristics have been associated with higher mortality; these vary by study; the list below compiles the features that are frequently mentioned across the board:

  • advanced age
  • female sex
  • multiple comorbidities
  • sepsis upon presentation

Potential Treatment Delays

Treatment of NSTIs is unequivocally surgical debridement, but unfortunately surgery doesn’t always happen within 24 hours. There are a few factors that inhibit prompt treatment, which can be broken into three larger categories: patient delay (not seeking care early enough), physician delay (not recognizing the signs) and system delay (logistical issues within a hospital system). Issues in one or all of these categories can result in catastrophic outcomes.

Two out of these three categories are outside a physician’s control; however, with thorough training and continuing medical education, we can work to minimize the cases in which the delay is due to a “missed diagnosis” on the part of the clinician.

Tips for Recognizing NSTIs Early

Always maintain a high index of suspicion. What does that mean? It means that the threshold for considering (and ruling out) necrotizing soft tissue infections needs to be low.

Host of the Trauma ICU Rounds podcast Dr. Dennis Kim stated that for him, a patient who presents with soft tissue infection with swelling, erythema, pain out of proportion (POOP) to physical exam with systemic symptoms is enough to consider a surgical consultation.

Although knowing the classic signs and symptoms of necrotizing soft tissue infections is paramount to a timely diagnosis, it is prudent to keep in mind that not all cases will present “classically.” 

Here are some important considerations:

  • patient need not have comorbidities to develop an NSTI
  • fever may be absent; this could be due in part to use of over-the-counter NSAIDs
  • although classically associated with a break in the skin, bacteria can travel hematogenously from other sites (like Streptococcal pharyngitis)
    • in fact, patient may not have cutaneous manifestations superficially
  • infection can be acute (developing over hours) but can also be indolent (like in DM foot ulcers)
  • pain out of proportion in what appears to be a simple cellulitis should raise warning bells

References and Further Reading

  • Goh T, Goh LG. Pitfalls in diagnosing necrotizing fasciitis. Patient Safety Network. https://psnet.ahrq.gov/web-mm/pitfalls-diagnosing-necrotizing-fasciitis. Published August 21, 2014. Accessed September 1, 2021.
  • Ho, Wong Chin. MDCalc: LRINEC Score for Necrotizing Soft Tissue Infection. LINK
  • Kim, D. (Host). (2021, June 07). Necrotizing Soft Tissue Infections (No. 39) [Audio podcast episode]. In Trauma ICU Rounds. Surgery Academix Corps. LINK
  • Nawijn, F., Smeeing, D.P.J., Houwert, R.M. et al. Time is of the essence when treating necrotizing soft tissue infections: a systematic review and meta-analysis. World J Emerg Surg 15, 4 (2020). https://doi.org/10.1186/s13017-019-0286-6
  • Stevens D. Necrotizing soft tissue infections. UpToDate. https://www.uptodate.com/contents/necrotizing-soft-tissue-infections#H1. Published August 25, 2021. Accessed September 2, 2021.
  • Tintinalli, Judith E, and David Cline. Tintinalli’s Emergency Medicine Manual (8th ed.). New York: McGraw-Hill Medical, 2017.
[cite]

Question Of The Day #60

question of the day
~ Joseph Ciano, USA ~ Leave a comment
Which of the following is the most likely cause for this patient’s condition? 
  • A) Pyelonephritis
  • B) Hypovolemic shock
  • C) Distributive shock
  • D) Ureteral stone

This first-trimester pregnant patient presents with generalized weakness, nausea, and vomiting.  She is hypotensive and tachycardic with no sign of urinary infection on the urinalysis.  The many ketones in the urine indicate the patient has inadequate oral nutrition and is breaking down muscle and adipose tissue for energy.  This is likely related to the persistent vomiting the patient is experiencing.  This patient has hyperemesis, a common condition in the first trimester of pregnancy that is caused by rising levels of beta-human chorionic gonadotropin (BHCG).  Treatment for this patient should include IV hydration and antiemetics.  Admission criteria for these patients includes intractable vomiting despite antiemetic administration, over 10% maternal weight loss, persistent ketone or electrolyte abnormalities despite rehydration, or uncertainty in the diagnosis. 

The fluid losses caused by vomiting in this condition result in hypovolemic shock (Choice B).  Distributive shock (Choice C) is caused by other conditions, like sepsis, anaphylaxis, and neurogenic shock.  A ureteral stone (Choice D) is unlikely as the patient does not report any abdominal, back, or flank pain.  The urinalysis also does not show any hematuria, which is a common sign of a ureteral stone.  Pyelonephritis (Choice A) can cause vomiting and septic shock which can result in hypotension and tachycardia.  However, there is no sign of infection in the urinalysis provided, no fever, and no back or flank pain.  The best answer is choice B.  

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References

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Infectious mononucleosis

Infectious mononucleosis
~ Nadine Schottler, Great Britain ~ Leave a comment

Case Presentation

A 16-year-old boy presents to A&E with a fever, an extremely sore throat, and a recent blotchy rash on his back that has been concerning him. He complains of feeling extremely tired and lethargic for the past two weeks. He denies having recently been in contact with anyone ill and confirms that he is up-to-date with his vaccinations. He mentions a visit with his local GP last week, where his doctor prescribed a dose of amoxicillin for a suspected throat infection. He has no other significant medical history. Upon further examination, his pharynx and tonsils appear inflamed with whitewash exudate and he has swollen neck lymph nodes in both the anterior and posterior triangles of the neck.

What is/are the most appropriate next step(s) in the patient’s management?

  • A) Reassure the patient and discharge
  • B) Perform a throat swab
  • C) Arrange a full blood count and a monospot test
  • D) Arrange a rapid antigen test for group A streptococcus

The answer is c) Arrange a full blood count and a monospot test

What is Glandular Fever?

Infectious mononucleosis, also known as glandular fever, is an infection resulting most commonly (80-90%) from an Epstein-Barr virus (EBV). About 95% of adults in the world have been infected with EBV; however, it is rare for it to progress into glandular fever. Glandular fever is most commonly seen in individuals aged 15-24, but can present in all age groups. The prevalence of glandular fever is estimated to be between 5-48 cases per 1000 persons. Glandular fever is rather rate in those under 10 or older than 30 (1/1000 persons), so it may not need to be in your top differentials in those age groups! In young adults, the likelihood of developing glandular fever from a primary EBV infection is about 50%; in older adults the chances of EBV infection progressing to glandular fever is slim.

For the most part, glandular fever is not contagious. It’s mostly spread through contact with saliva; such as by kissing, sharing food, or children putting things in their mouths. It can also be spread through sexual contact. Luckily, in most occurrences, glandular fever is self-limiting and lasts two to four weeks. The most common lasting effect is fatigue, which can continue from weeks to months.

When Should You Suspect Glandular Fever?

The classic ‘triad’ of symptoms for glandular fever are: 

  • Fever
  • Lymphadenopathy
  • Pharyngitis (‘sore throat’)

Bilateral posterior cervical lymphadenopathy is typical for glandular fever. Tonsils may also be enlarged, and exudate on the tonsils is described as ‘whitewash’. 

Additional signs and symptoms that could include:

  • Prodromal symptoms: 
    • Fatigue, chills, myalgia, headache
  • Palatal petechiae
    • 1-2mm in diameter and lasting 3-4 days
  • Abdominal pains 
  • Nausea and vomiting 
  • Non-specific rash
    • In this case, the patient had a maculopapular rash which is associated with EBV infection. It can be caused by the infection directly but more commonly presents after being treat with amoxicillin; patients should not take penicillin antibiotics when they have infectious mononucleosis. 
  • Splenomegaly 

If you see, or the patient tells you, of any of the following symptoms during their visit to the emergency department, it requires hospitalization! 

  • Difficulty swallowing 
  • Difficulty breathing 
  • Severe stomach/abdominal pain

These may suggest malignancy. Difficulty swallowing and breathing are most often due to inflamed tonsils and may require steroids. Severe stomach/abdominal pain might suggest a ruptured spleen. Refer to your local guidelines for investigation and treatment if these symptoms present. 

Differential Diagnoses

Viral pharyngitis

  • This is the most common alternative diagnoses
  • Viral pharyngitis tends to be more erythematous 
  • Exudate is not common with viral pharyngitis

Bacterial tonsillitis

  • Bacterial tonsillitis is more commonly described as having ‘speckled’ exudate on tonsils, compared to the ‘whitewash’ exudate on tonsils in glandular fever
  • Lymphadenopathy is usually limited to the upper anterior cervical chain, where in glandular fever, lymphadenopathy can be commonly seen in both anterior and posterior triangles

Other differentials could include other causes of lymphadenopathy, such as inflammation/infection, lymphoma, or leukemia. Alternative viral infections should also be considered (e.g. cytomegalovirus, acute toxoplasmosis, acute viral hepatitis, inter alia). 

Investigations If Glandular Fever Is Suspected

In children younger than 12, or a person who is immunocompromised, a blood test for EBV viral serology should be arranged (if the patient has been ill for seven days). 

In individuals older than 12, a full blood count with differential white cell count and a monospot test should be arranged in their second week of illness. Glandular fever is likely if:

  • The monospot test is positive
  • The full blood count has more than 20% atypical lymphocytes 

OR

More than 10% atypical lymphocytes and the lymphocyte count is more than 50% of the total white cell count.

Treatment

The patient only needs to be hospitalized if they have stridor, difficulty swallowing, are dehydrated, or there is a chance of potentially serious complications (such as a splenic rupture). Steroids should only be used if the patient shows to have difficulty breathing, otherwise, management should be conservative. If the patient doesn’t have any of these concerning signs, it is appropriate to advise the patient of their illness and discharge them for follow-up with their GP.

Some Recommendations To Patients

Some things you can advise the patient on for self-management of glandular fever include:

  • Symptoms usually only last 2-4 weeks 
  • Fatigue may be the last symptom to resolve
  • Relieve symptoms of pain and fever with paracetamol or ibuprofen
  • Encouraging normal daily routines and that exclusion from work or school is not necessary
  • Spreading of disease can be limited by avoiding kissing and not sharing eating utensils
  • They should return to the hospital if they suspect any serious complications (such increased difficulty to breath/swallow, or severe abdominal pain)

References and Further Reading

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Sepsis – An Overview and Update

An Overview and Update
~ Kohylah Piper, Antigua & Barbuda ~ Leave a comment

What is Sepsis?

Sepsis is a composite of symptoms and clinical signs that correspond to infection within a patient. This clinically heterogeneous syndrome may be fatal due to the extensive inflammatory processes and organ dysfunction it can provoke.

The New Definition of Sepsis

In 2016, after a revision by the European Society of Intensive Care Medicine and the Society of Critical Care Medicine, sepsis was redefined as “a life-threatening organ dysfunction caused by a dysregulated host response to infection.”

This new definition of sepsis means that the patient’s body, in response to infection, reacts by causing damage to its own organ structures, and this process can progress to the point where death can be an unfortunate end result.

Along with this up-to-date definition of sepsis, up-to-date criteria for evaluating sepsis were also provided; however, let’s first consider the causes of sepsis.

What is the Aetiology of Sepsis?

Sepsis can be caused by various organisms ranging from viruses to fungi to protozoans; however, bacterial infections are the main offenders. Vincent et al. (2009) concluded in the international EPIC II study that gram-negative bacteria were the principal perpetrators, accounting for 62%, while the gram-positives followed with a frequency of 47%. Of these groups, the principle organisms include:

  • Staphylococcus aureus and Pseudomonas at 20%
  • Escherichia coli at 16%

Different risk factors may predispose persons to become infected by these organisms.

Risk Factors

  • Non-Communicable diseases (Diabetes Mellitus, Chronic Kidney Disease)
  • Hemodialysis
  • Liver disease
  • Immunodeficient conditions
  • Trauma
  • The elderly, children, infants
  • Burns
  • Corticosteroid Use
  • Cancer
  • Prolonged Hospital Stay
  • Indwelling catheters

What is the Clinical Presentation of Sepsis?

The presentation of sepsis ranges from acute to insidious. There are cases where the patient may indicate a site of infection to cases where there is none apparent. Symptoms and signs of this syndrome generally include the following:

Another early sign of sepsis includes the presence of leukopenia or leukocytosis.
Along with these parameters, there are also specific signs within each organ system that must also be taken into account when investigating the source of primary infection or exploring the secondary effects of the same.

For example, when examining the respiratory system, listen for adventitious sounds or decreased breath sounds that may point to pneumonia and other chest infections. Respiratory causes of sepsis account for 42% of cases, according to the EPIC II study.

Patients who present with abdominal pain should be evaluated to rule out infection sources in abdominal structures such as the appendix, colon, pancreas, gallbladder. Other sources of infection may include the urinary tract and the prostate gland.

Patients with a history of trauma, wounds, and recent surgeries should be evaluated for any signs of wound infection (e.g., pain, erythema, purulent discharge, weeping wound, abscess formation)

In patients who are already admitted to the hospital and have been given invasive adjuncts, such as a central line, urinary catheters, and hemodialysis access sites, evaluate for inflammatory signs around the insertion site.

Warning Signs of Severe Sepsis

Sepsis progresses through a continuum that begins with a systemic inflammatory response syndrome (SIRS) and ends with multi-organ dysfunction syndrome (MODS), where mortality is almost inevitable. Its severest form is known as Septic Shock, a subcategory of sepsis where there is a great probability of mortality due to severe metabolic and circulatory irregularities.

The New Criteria for Evaluating Sepsis

The Sequential Organ Failure Assessment score, otherwise known as the SOFA score, is the new criteria used to evaluate sepsis. It replaces the SIRS Criteria.

SOFA takes into consideration six parameters that relate to specific organ systems. These systems are aligned with clinical signs and laboratory values, which fit into a numerical score ranging from 0 to 4, where 0 corresponds to normal values, and 4 corresponds to a high level of organ failure. See the image below, adapted from Vincent et al. (1996).

Since this criteria at its base enable physicians to assess the level of dysfunction occurring in the patient’s organ systems, the higher the score given, the more probable there will be an increase in mortality.

Using the SOFA criteria,  a score equal to and greater than 2 in the presence of confirmed or suspected infection corresponds to organ dysfunction. It indicates a mortality risk of around 10%.

The abbreviated version of the SOFA score, known as quick SOFA or qSOFA, is helpful for screening patients suspected to have sepsis by quickly evaluating three parameters, mental status, systolic blood pressure, and the respiratory rate.

REBELEM Blog (2016) qSOFA Score

Laboratory and Imaging

The general laboratory, imaging, and special studies for sepsis can include various tests depending on the suspected source of the infection, for example:

  • A Chest X-ray may show signs of pneumonia or any other lung infection.
  • CT imaging may reveal abdominal abscesses, perforation of the bowels.
  • An ultrasound can rule out pelvic sources of infection, as well as in organs such as the gall bladder.
  • Cardiac tests (electrocardiogram and troponins) may reveal suspected causes such as Myocardial Infarction.
  • Routine tests such as Complete Blood Count and Chemistry studies provide a baseline analysis for infection screening and organ dysfunction (kidney and liver).
  • Procalcitonin is a sepsis biomarker and increases in the presence of systemic bacterial infection.
  • Blood, urine, and source cultures should be taken for organism identification and antibiotic sensitivities.
  • Certain clinical presentations may necessitate abscess aspiration, lumbar puncture, or paracentesis.
  • Arterial blood gas is also a beneficial test for analyzing how septic a patient may be.

It is also important to note that serum lactate has become an important test in diagnosing sepsis, especially in relation to septic shock. (Lee and An, 2016)

The image below provides a summary of test results related to sepsis, as adapted from Mahapatra and Heffner (2020):

Treatment of Sepsis

The foundational aspects of treating sepsis rest upon rapid recognition and rapid remedy.

Schmidt and Mandel (2021) explain that resuscitation must be aggressively instituted in order to reperfuse the organs; just like antibiotic therapy, fluid resuscitation should be implemented within the first hour. It is given at 30 mL/kg and should be finalized by the third hour.

Initial antibiotic therapy should aim to cover both gram-positive and gram-negative organisms, any other considerations must be fully in line with the information found in the patient’s history, and physical examination. Where the source of infection necessitates surgical intervention, this must be pursued additionally.

The patient’s response to the treatments should be continuously monitored for improvements or worsening condition, and appropriate transfers should be pre-empted, for example, if the patient needs to be transferred to the Intensive Care Unit.

Key Points

  1. Sepsis is a clinically heterogeneous syndrome, which has a progression that can lead to severe cellular, metabolic, and overall hemodynamic dysfunction.
  2. If left un-recognized or, if it is not treated aggressively, the patient outcomes may be dim.
  3. The SOFA score is a criteria that is used in-depth and in a quick overview to assess the level of organ dysfunction in suspected or confirmed sepsis.
  4. Patients should be consistently monitored while exploring for the possible primary source.
  5. Sepsis is treated with rapid infusion of intravenous fluids and by using broad-spectrum antibiotics.
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References and Further Reading

Question Of The Day #43

question of the day
~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most likely cause for this patient’s altered mental status?

  • A) Diabetic ketoacidosis
  • B) Sepsis
  • C) Intracerebral hemorrhage
  • D) Hypothyroidism

This patient presents to the Emergency Department with altered mental status and fever.  Altered mental status can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more.  The management and evaluation of a patient with altered mental status depends on the primary assessment of the patient (“ABCs”, or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination.  One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS”.  The table below outlines this mnemonic.

ALTERED MENTAL STATUS

This patient has confusion, fever, lower abdominal pain, dysuria, and no focal neurological deficits on exam.  Diabetic ketoacidosis (Choice A) is unlikely as the patient does not have marked hyperglycemia (>250mg/dL (13.8mmol/L)), polyuria, or polydipsia.  Intracranial hemorrhage (Choice C) is unlikely as the patient has no headache, history of trauma, focal neurologic deficits, or coma.  Severe hypothyroidism (Choice D), known as myxedema coma, can cause altered mental status.  This condition is marked by somnolence or coma, hypothermia, nonpitting edema on the hands and feet, dry skin, macroglossia (enlarged tongue), and hair loss.  This patient does not have symptoms consistent with severe hypothyroidism. 

Sepsis (Choice B), especially in elderly individuals, can cause altered mental status.  The patient’s fever, confusion, lower abdominal pain, and dysuria all point to a likely diagnosis of urosepsis.  Sepsis is the most likely cause of this patient’s disoriented state.  Treatment with early IV hydration and antibiotics will help remedy the patient’s altered mental status.  Correct Answer: B

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References

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Empiric Antibiotics for Sepsis in the ED Infographics

Empiric Antibiotics for Sepsis in the ED Infographics
~ Sarah Bridge, USA ~ Leave a comment
Empiric Antibiotics for Sepsis in the ED Infographics
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