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Emergency and Acute Medicine – Otologic Trauma
Otologic trauma involves injury to the external, middle, or inner ear and may result from blunt, penetrating, barotrauma, thermal, chemical, or blast mechanisms. Injuries to the pinna are particularly concerning because auricular cartilage lacks a direct blood supply and depends on the perichondrium for nutrition. Disruption of this relationship, especially from hematoma formation, can lead to ischemia, perichondritis, cartilage necrosis, and permanent deformity such as cauliflower ear. Penetrating injuries and bite wounds increase the risk of cartilage infection.
The middle ear is an air-filled cavity containing the ossicles and is vulnerable to pressure-related injuries such as blasts or diving accidents. Because it is bordered by the temporal and mastoid bones and adjacent to the cranial vault, fractures in this region may result in cerebrospinal fluid otorrhea or rhinorrhea and disruption of the vestibular system. The facial nerve traverses the middle ear, and injury can result in peripheral facial nerve paralysis. Pediatric patients with otologic trauma should always be evaluated for possible nonaccidental injury.
Patients may present with severe ear pain, bleeding, or visible deformity of the auricle. Auricular hematomas typically appear as bluish, fluctuant, or doughy swellings of the pinna and are associated with loss of normal contour. Lacerations, partial avulsions, or complete amputations may be seen. Signs of middle ear trauma include decreased hearing, tinnitus, vertigo, nystagmus, facial nerve weakness, and canal drainage. Partial hearing loss suggests tympanic membrane rupture, whereas complete hearing loss raises concern for ossicular chain or inner ear injury. Findings suggestive of basilar skull fracture include hemotympanum, Battle sign, and cerebrospinal fluid leakage from the ear or nose.
History should focus on the mechanism of injury, associated trauma, prior otologic disease, and medication use. Physical examination must include a complete head and neck evaluation with careful inspection of the pinna, external auditory canal, tympanic membrane, cranial nerves, and hearing assessment. Tuning fork tests such as Weber and Rinne are useful to differentiate conductive from sensorineural hearing loss. Concomitant injuries must always be excluded in trauma patients.
Diagnosis is primarily clinical. Wound cultures are reserved for signs of infection. Imaging with head or facial CT is indicated when intracranial injury or skull fracture is suspected, while CT of the temporal bone without contrast is recommended for significant middle ear injury or facial nerve involvement.
Initial management begins with standard trauma assessment and stabilization, including airway, breathing, and circulation. Injured ears should be covered with sterile dressings. If the auricle is amputated, it should be wrapped in moist gauze, placed in a plastic bag, and kept cool for possible reattachment. Adequate anesthesia is essential and may be achieved through auricular nerve blocks or a circumferential ring block at the base of the pinna.
Auricular hematomas require prompt drainage, ideally within 72 hours, to reapproximate the perichondrium and cartilage and prevent necrosis. Small, nonclotted hematomas may be aspirated, while larger or clotted collections are best managed with incision and drainage followed by a firm pressure dressing. Antistaphylococcal antibiotics are typically given for 7–10 days. Reaccumulation requires repeat drainage and possibly wick placement.
Lacerations should be thoroughly cleaned and debrided. Simple lacerations can be closed with nonabsorbable monofilament sutures and a pressure dressing, while exposed cartilage must be carefully covered to prevent perichondritis. Human or animal bite wounds warrant prophylactic antibiotics, most commonly amoxicillin–clavulanate. Small avulsions less than 2 cm may survive as grafts, but larger avulsions require urgent consultation with otolaryngology or plastic surgery.
Patients may be discharged if they can tolerate oral antibiotics, have no serious associated injuries, and can ensure close follow-up. Admission is indicated for patients with significant associated trauma, immunosuppression with infection, perichondritis, chondritis, or need for intravenous antibiotics. Follow-up is recommended within 24 hours for auricular hematomas to assess for reaccumulation and within five days for suture evaluation or removal.
A key clinical principle is that failure to promptly recognize and adequately treat auricular hematomas can result in permanent deformity. Early drainage, proper pressure dressing, and close follow-up are essential to prevent long-term complications.
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Emergency and Acute Medicine – Otitis Externa
Otitis externa is an inflammation or infection of the auricle, external auditory canal, or the external surface of the tympanic membrane, while sparing the middle ear. It affects approximately 4 per 1,000 individuals in the United States and is commonly referred to as “swimmer’s ear” due to its frequent association with recent swimming or water exposure, although it may also occur after routine bathing. A severe form, necrotizing (malignant) otitis externa, begins in the ear canal and can extend into periauricular tissues and the skull base. This form occurs most often in elderly patients, those with diabetes, or immunocompromised individuals, is commonly caused by Pseudomonas aeruginosa, and carries a mortality rate of up to 20%.
The condition is often precipitated by trauma or abrasion of the ear canal or by maceration of the skin from prolonged moisture or excessive dryness. Predisposing factors include prior ear surgery or tympanic membrane perforation, narrow or abnormal ear canals, humidity, allergies, eczema, trauma, and abnormal cerumen production. Common pathogens include Pseudomonas aeruginosa, Staphylococcus aureus, streptococcal species, and less commonly fungal organisms.
Patients typically present with a history of recent swimming or water exposure and may report itching of the ear canal as the earliest symptom. This is often followed over one to two days by progressive ear pain, ear drainage, decreased hearing, and a sensation of ear fullness or clogging. In patients with diabetes or immunosuppression, clinicians should specifically inquire about systemic symptoms and risk factors. On examination, pain is elicited with movement of the pinna or tragus, and the external ear canal is usually swollen, erythematous, and tender, often with visible drainage or debris. Decreased auditory acuity and preauricular swelling may be present. Necrotizing otitis externa may present with severe otalgia, headache, otorrhea, periauricular swelling, and cranial nerve palsies, most commonly involving the facial nerve.
Diagnosis is primarily clinical, based on characteristic history and physical findings. Otoscopic examination typically reveals an edematous, erythematous ear canal with purulent, cheesy white, or gray-green exudate. Laboratory studies are not routinely required unless necrotizing otitis externa is suspected, in which case evaluation may include white blood cell count, erythrocyte sedimentation rate, serum glucose, and cultures. Computed tomography or magnetic resonance imaging is indicated when there are signs of systemic toxicity, suspected bony involvement, or concern for mastoiditis. Debris removal from the ear canal using gentle curettage or irrigation is both diagnostic and therapeutic, and wick placement may be necessary to ensure medication penetration in markedly edematous canals.
The differential diagnosis includes otitis media, folliculitis, foreign bodies in the ear canal, herpes zoster oticus, parotitis, mastoiditis, dental abscess, sinusitis, temporomandibular joint disorders, and cervical adenitis. In children, an ear canal foreign body should be considered when purulent drainage is present.
Management focuses on pain control, eradication of infection, and prevention of recurrence. Treatment begins with gentle cleansing of the external auditory canal to remove debris, sometimes requiring suction or curettage. A cotton or gauze wick may be placed in cases of severe canal edema. Most cases respond well to topical therapy using antiseptic, anti-inflammatory, and antibacterial ear drops. Acetic acid solutions, combination antibiotic-steroid drops, or fluoroquinolone drops such as ofloxacin are commonly used, with ofloxacin preferred when tympanic membrane perforation is suspected. Oral antibiotics are reserved for patients with facial or neck cellulitis, severe canal edema, concurrent otitis media, or immunocompromised status. Diabetic and immunocompromised patients should be treated with oral ciprofloxacin and monitored closely for progression to necrotizing otitis externa. Intravenous antibiotics and possible surgical debridement are required for necrotizing disease or severe systemic illness.
Most patients can be safely discharged with close follow-up. Admission is indicated for necrotizing otitis externa, significant pinna involvement, or signs of systemic illness. Discharge instructions should emphasize keeping the ear dry, avoiding swimming for three to four weeks, proper use of prescribed medications, and returning promptly for worsening pain, fever, hearing loss, or neurologic symptoms. Follow-up within two to three days is recommended, particularly for wick removal or if symptoms fail to improve.
Key clinical pearls include recognizing that erythema of the tympanic membrane in otitis externa may mimic otitis media, avoiding ear canal lavage until tympanic membrane integrity is confirmed, and ensuring adequate medication penetration by clearing obstructing debris. Recurrence can often be prevented through patient education focused on minimizing moisture, trauma, and irritant exposure to the external ear canal. Necrotizing otitis externa should always be suspected in diabetics or immunocompromised patients with severe ear pain, purulent otorrhea, and granulation tissue or exposed bone in the ear canal.
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Emergency and Acute Medicine – Otitis Media
Otitis media is an inflammatory condition of the middle ear and is one of the most common infections encountered in early childhood, particularly between 6 and 36 months of age. It is characterized by a rapid onset of local and systemic symptoms and has a high recurrence rate, with more than one-third of children experiencing more than five episodes by the age of seven. Although it predominantly affects children, otitis media can also occur in adults.
The condition most often develops in association with upper respiratory tract infections, which lead to eustachian tube dysfunction and impaired drainage of the middle ear. Viral pathogens commonly implicated include parainfluenza virus, respiratory syncytial virus, influenza virus, adenovirus, and rhinovirus. Bacterial causes include Streptococcus pneumoniae, Moraxella catarrhalis, Haemophilus influenzae, Streptococcus pyogenes, and Mycoplasma pneumoniae. Predisposing factors include impaired mucociliary function, immunodeficiency, nasotracheal intubation, and certain populations such as American Indians, Eskimos, and individuals with Down syndrome, cleft palate, diabetes, vitamin A deficiency, or HIV. Additional risk factors include daycare attendance, family history, exposure to parental smoking, pacifier use, and bottle-feeding.
Diagnosis is primarily clinical and follows the American Academy of Pediatrics 2013 guidelines. Otitis media should be diagnosed when there is moderate to severe bulging of the tympanic membrane, mild bulging of the tympanic membrane accompanied by recent onset of ear pain, or new otorrhea not attributable to otitis externa. The diagnosis should not be made in the absence of middle ear effusion, which is best assessed using pneumatic otoscopy or tympanometry. Recurrent otitis media is defined as three episodes within six months or four episodes within one year, with at least one episode occurring in the preceding six months.
Patients typically present with ear pain, irritability, fever, and symptoms of an upper respiratory infection such as rhinorrhea. Younger children may exhibit poor feeding, vomiting, diarrhea, or tugging at the ear, while older children and adults may complain of a plugged-ear sensation, vertigo, tinnitus, or conjunctivitis. On physical examination, the tympanic membrane often appears erythematous, inflamed, and bulging, with decreased mobility and obscured landmarks. New-onset otorrhea in the absence of otitis externa is also a key finding.
The essential evaluation includes careful otoscopic examination with full visualization of the tympanic membrane and assessment of its mobility. Laboratory testing is generally unnecessary, and cultures are not helpful unless obtained via tympanocentesis. Imaging, such as computed tomography, is reserved for suspected complications like mastoiditis. Tympanocentesis may be indicated in cases of severe pain or toxicity, failure of antimicrobial therapy, suspected suppurative complications, illness in neonates, or immunocompromised patients.
Management depends on age, severity, and laterality of infection. Many mild cases resolve spontaneously without antibiotics. Antibiotic therapy is recommended for all infants younger than six months, children younger than two years with bilateral otitis media, children older than six months with severe symptoms (persistent otalgia for more than 48 hours or fever ≥102.2°F), and cases with tympanic membrane rupture and drainage. In otherwise healthy children aged six months or older with mild symptoms or uncertain diagnosis, a period of observation with close follow-up in two to three days is appropriate, provided caregivers are reliable. Antipyretics and analgesics are essential for symptom control, while antihistamines, decongestants, and steroids have not shown proven benefit.
First-line antibiotic therapy typically includes high-dose amoxicillin, with amoxicillin–clavulanate or alternative agents such as azithromycin or cefuroxime used based on allergy history, recent antibiotic use, or local resistance patterns. Parenteral antibiotics are reserved for toxic-appearing infants, immunocompromised patients, or those unable to tolerate oral therapy.
Most patients can be safely discharged with appropriate treatment and follow-up. Admission is indicated for febrile or toxic children younger than one year, immunocompromised patients, those with significant dehydration, inability to tolerate oral intake, suspected serious associated infection, unreliable caregivers, or concern for abuse. Follow-up is recommended within 10–14 days to ensure resolution, with earlier reassessment if symptoms fail to improve within 24–48 hours or worsen.
Important complications of otitis media include recurrent infections, tympanic membrane perforation, serous otitis media, hearing loss, facial nerve injury, mastoiditis, cholesteatoma, meningitis, and other intracranial infections. A key clinical pearl is that in otherwise healthy children aged six months or older with mild symptoms, observation without immediate antibiotics and close follow-up is often a safe and effective approach.
Otitis media is an inflammatory condition of the middle ear and is one of the most common infections encountered in early childhood, particularly between 6 and 36 months of age. It is characterized by a rapid onset of local and systemic symptoms and has a high recurrence rate, with more than one-third of children experiencing more than five episodes by the age of seven. Although it predominantly affects children, otitis media can also occur in adults.
The condition most often develops in association with upper respiratory tract infections, which lead to eustachian tube dysfunction and impaired drainage of the middle ear. Viral pathogens commonly implicated include parainfluenza virus, respiratory syncytial virus, influenza virus, adenovirus, and rhinovirus. Bacterial causes include Streptococcus pneumoniae, Moraxella catarrhalis, Haemophilus influenzae, Streptococcus pyogenes, and Mycoplasma pneumoniae. Predisposing factors include impaired mucociliary function, immunodeficiency, nasotracheal intubation, and certain populations such as American Indians, Eskimos, and individuals with Down syndrome, cleft palate, diabetes, vitamin A deficiency, or HIV. Additional risk factors include daycare attendance, family history, exposure to parental smoking, pacifier use, and bottle-feeding.
Diagnosis is primarily clinical and follows the American Academy of Pediatrics 2013 guidelines. Otitis media should be diagnosed when there is moderate to severe bulging of the tympanic membrane, mild bulging of the tympanic membrane accompanied by recent onset of ear pain, or new otorrhea not attributable to otitis externa. The diagnosis should not be made in the absence of middle ear effusion, which is best assessed using pneumatic otoscopy or tympanometry. Recurrent otitis media is defined as three episodes within six months or four episodes within one year, with at least one episode occurring in the preceding six months.
Patients typically present with ear pain, irritability, fever, and symptoms of an upper respiratory infection such as rhinorrhea. Younger children may exhibit poor feeding, vomiting, diarrhea, or tugging at the ear, while older children and adults may complain of a plugged-ear sensation, vertigo, tinnitus, or conjunctivitis. On physical examination, the tympanic membrane often appears erythematous, inflamed, and bulging, with decreased mobility and obscured landmarks. New-onset otorrhea in the absence of otitis externa is also a key finding.
The essential evaluation includes careful otoscopic examination with full visualization of the tympanic membrane and assessment of its mobility. Laboratory testing is generally unnecessary, and cultures are not helpful unless obtained via tympanocentesis. Imaging, such as computed tomography, is reserved for suspected complications like mastoiditis. Tympanocentesis may be indicated in cases of severe pain or toxicity, failure of antimicrobial therapy, suspected suppurative complications, illness in neonates, or immunocompromised patients.
Management depends on age, severity, and laterality of infection. Many mild cases resolve spontaneously without antibiotics. Antibiotic therapy is recommended for all infants younger than six months, children younger than two years with bilateral otitis media, children older than six months with severe symptoms (persistent otalgia for more than 48 hours or fever ≥102.2°F), and cases with tympanic membrane rupture and drainage. In otherwise healthy children aged six months or older with mild symptoms or uncertain diagnosis, a period of observation with close follow-up in two to three days is appropriate, provided caregivers are reliable. Antipyretics and analgesics are essential for symptom control, while antihistamines, decongestants, and steroids have not shown proven benefit.
First-line antibiotic therapy typically includes high-dose amoxicillin, with amoxicillin–clavulanate or alternative agents such as azithromycin or cefuroxime used based on allergy history, recent antibiotic use, or local resistance patterns. Parenteral antibiotics are reserved for toxic-appearing infants, immunocompromised patients, or those unable to tolerate oral therapy.
Most patients can be safely discharged with appropriate treatment and follow-up. Admission is indicated for febrile or toxic children younger than one year, immunocompromised patients, those with significant dehydration, inability to tolerate oral intake, suspected serious associated infection, unreliable caregivers, or concern for abuse. Follow-up is recommended within 10–14 days to ensure resolution, with earlier reassessment if symptoms fail to improve within 24–48 hours or worsen.
Important complications of otitis media include recurrent infections, tympanic membrane perforation, serous otitis media, hearing loss, facial nerve injury, mastoiditis, cholesteatoma, meningitis, and other intracranial infections. A key clinical pearl is that in otherwise healthy children aged six months or older with mild symptoms, observation without immediate antibiotics and close follow-up is often a safe and effective approach.
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KembaraXtra- Medicine – Atrial Flutter
Typical atrial flutter is a stable macroreentrant atrial rhythm that circulates around the tricuspid annulus in the right atrium. The critical component of this circuit is the cavotricuspid isthmus (CTI), the tissue between the inferior vena cava and the tricuspid valve, which is why typical flutter is also referred to as CTI-dependent atrial flutter. Because the circuit is anatomically and physiologically stable, atrial depolarization is regular, usually occurring at a rate of 250–350 beats per minute.
Atypical atrial flutter refers to regular macroreentrant atrial tachyarrhythmias that do not depend on the CTI. These forms often occur after cardiac surgery, in patients with congenital heart disease, or following catheter ablation procedures—particularly left atrial ablation for atrial fibrillation—although they may also occur without an identifiable cause.
Conduction through the atrioventricular (AV) node in atrial flutter often follows predictable ratios. For example, with an atrial rate of 300 beats per minute, 2:1 AV conduction produces a ventricular rate of about 150 beats per minute, while 3:1 and 4:1 conduction produce ventricular rates of approximately 100 and 75 beats per minute, respectively. When AV nodal conduction varies, the ventricular rhythm may appear irregular, although a consistent atrial cycle length is often still present.
Atrial flutter is the second most common sustained atrial tachyarrhythmia after atrial fibrillation, with an estimated 200,000 new cases each year in the United States. Its prevalence increases with age and is about 2.5 times more common in men than in women. It is frequently seen in patients with congestive heart failure, chronic obstructive pulmonary disease, pulmonary embolism, pulmonary hypertension, or in the early postoperative period following open-heart surgery. Importantly, more than half of patients with atrial flutter will develop atrial fibrillation within three years, and more than 80% within five years.
Clinically, atrial flutter may present with palpitations, dizziness, light-headedness, syncope or near syncope, chest pain, dyspnea, or worsening heart failure. Some patients develop thromboembolic complications due to intracardiac thrombus formation. Common etiologic associations include age-related atrial degeneration, rheumatic or congenital heart disease, ventricular dysfunction, mitral valve disease, thyrotoxicosis, pulmonary embolism, obesity, pericarditis, and prior cardiac surgery. Antiarrhythmic therapy for atrial fibrillation may also predispose patients to developing atrial flutter.
Diagnosis is primarily established by electrocardiography. Typical findings include absence of normal P waves and the presence of regular “sawtooth” flutter waves without an isoelectric baseline, most clearly seen in the inferior leads (II, III, and aVF). Atrioventricular conduction is usually 2:1, 3:1, or 4:1 rather than 1:1, unless pre-excitation is present. Holter or event monitoring may be useful for intermittent symptoms or to assess rate control. Echocardiography is recommended in newly diagnosed patients to evaluate for structural heart disease, and transesophageal echocardiography may be required to exclude atrial thrombus before cardioversion. Electrophysiologic studies are used for definitive diagnosis and for catheter ablation therapy.
Typical atrial flutter is a stable macroreentrant atrial rhythm that circulates around the tricuspid annulus in the right atrium. The critical component of this circuit is the cavotricuspid isthmus (CTI), the tissue between the inferior vena cava and the tricuspid valve, which is why typical flutter is also referred to as CTI-dependent atrial flutter. Because the circuit is anatomically and physiologically stable, atrial depolarization is regular, usually occurring at a rate of 250–350 beats per minute.
Atypical atrial flutter refers to regular macroreentrant atrial tachyarrhythmias that do not depend on the CTI. These forms often occur after cardiac surgery, in patients with congenital heart disease, or following catheter ablation procedures—particularly left atrial ablation for atrial fibrillation—although they may also occur without an identifiable cause.
Conduction through the atrioventricular (AV) node in atrial flutter often follows predictable ratios. For example, with an atrial rate of 300 beats per minute, 2:1 AV conduction produces a ventricular rate of about 150 beats per minute, while 3:1 and 4:1 conduction produce ventricular rates of approximately 100 and 75 beats per minute, respectively. When AV nodal conduction varies, the ventricular rhythm may appear irregular, although a consistent atrial cycle length is often still present.
Atrial flutter is the second most common sustained atrial tachyarrhythmia after atrial fibrillation, with an estimated 200,000 new cases each year in the United States. Its prevalence increases with age and is about 2.5 times more common in men than in women. It is frequently seen in patients with congestive heart failure, chronic obstructive pulmonary disease, pulmonary embolism, pulmonary hypertension, or in the early postoperative period following open-heart surgery. Importantly, more than half of patients with atrial flutter will develop atrial fibrillation within three years, and more than 80% within five years.
Clinically, atrial flutter may present with palpitations, dizziness, light-headedness, syncope or near syncope, chest pain, dyspnea, or worsening heart failure. Some patients develop thromboembolic complications due to intracardiac thrombus formation. Common etiologic associations include age-related atrial degeneration, rheumatic or congenital heart disease, ventricular dysfunction, mitral valve disease, thyrotoxicosis, pulmonary embolism, obesity, pericarditis, and prior cardiac surgery. Antiarrhythmic therapy for atrial fibrillation may also predispose patients to developing atrial flutter.
Diagnosis is primarily established by electrocardiography. Typical findings include absence of normal P waves and the presence of regular “sawtooth” flutter waves without an isoelectric baseline, most clearly seen in the inferior leads (II, III, and aVF). Atrioventricular conduction is usually 2:1, 3:1, or 4:1 rather than 1:1, unless pre-excitation is present. Holter or event monitoring may be useful for intermittent symptoms or to assess rate control. Echocardiography is recommended in newly diagnosed patients to evaluate for structural heart disease, and transesophageal echocardiography may be required to exclude atrial thrombus before cardioversion. Electrophysiologic studies are used for definitive diagnosis and for catheter ablation therapy.
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KembaraXtra-Medicine – Atrial Myxoma
Atrial myxoma is a benign neoplasm of mesenchymal origin and represents the most common primary tumor of the heart. Although histologically benign, atrial myxomas are clinically significant because their size, mobility, and intracardiac location can lead to serious and sometimes life-threatening complications. They are most commonly referred to as cardiac myxomas.
Primary cardiac tumors are extremely rare, with an autopsy prevalence ranging from 0.001% to 0.3%, and metastatic tumors occur far more frequently than primary tumors. Among primary cardiac tumors, myxomas account for 30% to 50% of benign cases. Approximately 65% occur in females. Most cases are sporadic, but 4.5% to 10% are familial, commonly associated with Carney complex. The median age of presentation is about 56 years, although familial cases tend to occur earlier, with an average age of 25 years. Most myxomas arise in the left atrium (about 75%), followed by the right atrium, right ventricle, and left ventricle. They are typically pedunculated and attached to the interatrial septum.
Histopathologically, atrial myxomas are characterized by abundant loose myxoid stroma containing scattered round, polygonal, or stellate cells with dense, irregular nuclei derived from multipotent mesenchymal cells. While benign in classification, myxomas can secrete cytokines and growth factors, contributing to systemic and constitutional symptoms in addition to mechanical complications.
Clinically, patients with atrial myxomas usually present in one of three ways: atrioventricular valve obstruction, systemic embolization, or constitutional symptoms. Obstructive symptoms may mimic mitral or tricuspid valve disease and include dyspnea, orthopnea, paroxysmal nocturnal dyspnea, syncope, dizziness, edema, atrial fibrillation, or rarely sudden death. Symptoms that vary with body position, particularly improvement when recumbent, are suggestive. Systemic embolization occurs in nearly one third of patients and may manifest as stroke, pulmonary embolism, paradoxical embolism, or acute coronary syndrome. Constitutional features such as fever, weight loss, arthralgia, and Raynaud phenomenon are also common, while rare presentations include peripheral neuropathy, vasculitis, or paraneoplastic syndromes. On examination, findings may include murmurs, signs of pulmonary hypertension, a widely split first heart sound, or a characteristic early diastolic “tumor plop.”
Most atrial myxomas are sporadic, but familial cases are commonly associated with Carney complex, an autosomal dominant condition characterized by cardiac and extracardiac myxomas, pigmented skin lesions, endocrine hyperactivity, and other tumors such as schwannomas. Multiple genetic loci and mutations have been identified in this syndrome.
Diagnosis requires a high index of suspicion due to nonspecific symptoms that overlap with many cardiovascular and pulmonary conditions. Laboratory tests may show anemia, thrombocytopenia, elevated inflammatory markers, increased immunoglobulins, or elevated cardiac biomarkers, though these findings are nonspecific. Electrocardiography may reveal atrial enlargement, arrhythmias, or conduction abnormalities. Transthoracic echocardiography is the initial diagnostic test of choice, with approximately 95% sensitivity, while transesophageal echocardiography approaches 100% sensitivity and better defines tumor attachment and mobility. CT and MRI are valuable for delineating tumor size, extension, vascularity, and for distinguishing myxoma from atrial thrombus. Cardiac catheterization may demonstrate neovascularization and is sometimes used to assess for concomitant coronary artery disease before surgery.
The definitive treatment for atrial myxoma is prompt surgical excision, which should not be delayed due to the risk of embolization or sudden death. Postoperatively, arrhythmias or conduction disturbances may occur and are managed accordingly. In rare cases, particularly with recurrent tumors associated with Carney complex, advanced surgical approaches such as cardiac autotransplantation or transplantation may be required.
Prognosis after surgical excision is excellent, with reported survival rates of approximately 95% at three years. However, recurrence can occur in up to 5% of sporadic cases and up to 20% of familial cases, particularly within the first six years. Risk factors for recurrence include familial disease, atypical tumor location, and multicentric tumors. Malignant transformation into atrial myxofibrosarcoma, although rare, should be considered in cases of early recurrence. Untreated atrial myxomas carry a significant risk of sudden death, estimated at up to 15%.
Referral to a cardiologist is recommended for diagnosis and management, and once identified, early consultation with a cardiovascular surgeon is essential. Long-term follow-up with periodic echocardiography is advised to monitor for recurrence, especially in patients with familial disease or Carney complex.
Atrial myxoma is a benign neoplasm of mesenchymal origin and represents the most common primary tumor of the heart. Although histologically benign, atrial myxomas are clinically significant because their size, mobility, and intracardiac location can lead to serious and sometimes life-threatening complications. They are most commonly referred to as cardiac myxomas.
Primary cardiac tumors are extremely rare, with an autopsy prevalence ranging from 0.001% to 0.3%, and metastatic tumors occur far more frequently than primary tumors. Among primary cardiac tumors, myxomas account for 30% to 50% of benign cases. Approximately 65% occur in females. Most cases are sporadic, but 4.5% to 10% are familial, commonly associated with Carney complex. The median age of presentation is about 56 years, although familial cases tend to occur earlier, with an average age of 25 years. Most myxomas arise in the left atrium (about 75%), followed by the right atrium, right ventricle, and left ventricle. They are typically pedunculated and attached to the interatrial septum.
Histopathologically, atrial myxomas are characterized by abundant loose myxoid stroma containing scattered round, polygonal, or stellate cells with dense, irregular nuclei derived from multipotent mesenchymal cells. While benign in classification, myxomas can secrete cytokines and growth factors, contributing to systemic and constitutional symptoms in addition to mechanical complications.
Clinically, patients with atrial myxomas usually present in one of three ways: atrioventricular valve obstruction, systemic embolization, or constitutional symptoms. Obstructive symptoms may mimic mitral or tricuspid valve disease and include dyspnea, orthopnea, paroxysmal nocturnal dyspnea, syncope, dizziness, edema, atrial fibrillation, or rarely sudden death. Symptoms that vary with body position, particularly improvement when recumbent, are suggestive. Systemic embolization occurs in nearly one third of patients and may manifest as stroke, pulmonary embolism, paradoxical embolism, or acute coronary syndrome. Constitutional features such as fever, weight loss, arthralgia, and Raynaud phenomenon are also common, while rare presentations include peripheral neuropathy, vasculitis, or paraneoplastic syndromes. On examination, findings may include murmurs, signs of pulmonary hypertension, a widely split first heart sound, or a characteristic early diastolic “tumor plop.”
Most atrial myxomas are sporadic, but familial cases are commonly associated with Carney complex, an autosomal dominant condition characterized by cardiac and extracardiac myxomas, pigmented skin lesions, endocrine hyperactivity, and other tumors such as schwannomas. Multiple genetic loci and mutations have been identified in this syndrome.
Diagnosis requires a high index of suspicion due to nonspecific symptoms that overlap with many cardiovascular and pulmonary conditions. Laboratory tests may show anemia, thrombocytopenia, elevated inflammatory markers, increased immunoglobulins, or elevated cardiac biomarkers, though these findings are nonspecific. Electrocardiography may reveal atrial enlargement, arrhythmias, or conduction abnormalities. Transthoracic echocardiography is the initial diagnostic test of choice, with approximately 95% sensitivity, while transesophageal echocardiography approaches 100% sensitivity and better defines tumor attachment and mobility. CT and MRI are valuable for delineating tumor size, extension, vascularity, and for distinguishing myxoma from atrial thrombus. Cardiac catheterization may demonstrate neovascularization and is sometimes used to assess for concomitant coronary artery disease before surgery.
The definitive treatment for atrial myxoma is prompt surgical excision, which should not be delayed due to the risk of embolization or sudden death. Postoperatively, arrhythmias or conduction disturbances may occur and are managed accordingly. In rare cases, particularly with recurrent tumors associated with Carney complex, advanced surgical approaches such as cardiac autotransplantation or transplantation may be required.
Prognosis after surgical excision is excellent, with reported survival rates of approximately 95% at three years. However, recurrence can occur in up to 5% of sporadic cases and up to 20% of familial cases, particularly within the first six years. Risk factors for recurrence include familial disease, atypical tumor location, and multicentric tumors. Malignant transformation into atrial myxofibrosarcoma, although rare, should be considered in cases of early recurrence. Untreated atrial myxomas carry a significant risk of sudden death, estimated at up to 15%.
Referral to a cardiologist is recommended for diagnosis and management, and once identified, early consultation with a cardiovascular surgeon is essential. Long-term follow-up with periodic echocardiography is advised to monitor for recurrence, especially in patients with familial disease or Carney complex.
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Emergency and Acute Medicine – Mallory–Weiss Syndrome
Basics description
Mallory–Weiss syndrome is a partial-thickness, longitudinal mucosal tear of the distal esophagus or proximal stomach. It results from a sudden increase in intra-abdominal or transgastric pressure, leading to mild to moderate submucosal arterial or venous bleeding. Endoscopic observations suggest that transient “mushrooming” of the stomach into the esophagus during forceful retching contributes to tear formation. It accounts for approximately 5% of all cases of upper gastrointestinal bleeding.
Etiology and risk factors
The condition is most commonly associated with forceful vomiting or retching but may also occur with coughing, laughing, lifting, straining, blunt abdominal trauma, seizures, childbirth, or cardiopulmonary resuscitation. Alcohol use, particularly following binge drinking, and the presence of a hiatal hernia are significant risk factors. More severe bleeding is seen in patients with portal hypertension, esophageal varices, or underlying coagulopathy.
Diagnosis signs and symptoms
Patients typically report multiple episodes of nonbloody vomiting or retching followed by hematemesis. Most bleeding is self-limited, though severe or life-threatening hemorrhage can occur. Associated symptoms include epigastric or back pain and signs of volume depletion such as dizziness, light-headedness, or syncope. Physical examination may reveal hematemesis, melena, postural hypotension, or shock in severe cases.
Essential workup and diagnostic testing
Initial evaluation includes a complete blood count and rectal examination for occult blood. Additional laboratory studies include coagulation parameters, electrolytes, renal function tests, liver function tests, and type and cross-match if bleeding is significant. Upright chest radiography may be obtained to exclude esophageal or gastric perforation. Upper endoscopy is the diagnostic and therapeutic modality of choice, allowing direct visualization and management of the bleeding source.
Differential diagnosis
Conditions to consider include nasopharyngeal bleeding, hemoptysis, esophageal rupture (Boerhaave syndrome), esophagitis, gastritis, peptic ulcer disease, variceal bleeding, malignancy, and vascular-enteric fistula.
Treatment and emergency management
Initial management focuses on airway protection, oxygenation, and hemodynamic stabilization with large-bore intravenous access and fluid resuscitation. Blood transfusion is indicated for ongoing bleeding or hemodynamic instability. Most cases resolve with conservative therapy. Persistent or active bleeding requires urgent endoscopic intervention, which may include injection therapy, thermal coagulation, clipping, or band ligation. Proton pump inhibitors and antiemetics are used adjunctively. Surgical or angiographic intervention is reserved for refractory cases.
Disposition and follow-up
Patients with ongoing or massive hemorrhage, hemodynamic instability, significant comorbidities, or advanced age require ICU admission. Stable patients with minimal bleeding that has resolved and stable hematocrit may be admitted for observation or, in select cases, discharged with close follow-up and outpatient endoscopy.
Key points and cautions
Early placement of large-bore intravenous access and prompt resuscitation are critical in upper gastrointestinal bleeding. Early gastroenterology consultation is essential when bleeding is significant. Rebleeding most often occurs within the first 24 hours and is more likely in patients with coagulopathy or portal hypertension.
Basics description
Mallory–Weiss syndrome is a partial-thickness, longitudinal mucosal tear of the distal esophagus or proximal stomach. It results from a sudden increase in intra-abdominal or transgastric pressure, leading to mild to moderate submucosal arterial or venous bleeding. Endoscopic observations suggest that transient “mushrooming” of the stomach into the esophagus during forceful retching contributes to tear formation. It accounts for approximately 5% of all cases of upper gastrointestinal bleeding.
Etiology and risk factors
The condition is most commonly associated with forceful vomiting or retching but may also occur with coughing, laughing, lifting, straining, blunt abdominal trauma, seizures, childbirth, or cardiopulmonary resuscitation. Alcohol use, particularly following binge drinking, and the presence of a hiatal hernia are significant risk factors. More severe bleeding is seen in patients with portal hypertension, esophageal varices, or underlying coagulopathy.
Diagnosis signs and symptoms
Patients typically report multiple episodes of nonbloody vomiting or retching followed by hematemesis. Most bleeding is self-limited, though severe or life-threatening hemorrhage can occur. Associated symptoms include epigastric or back pain and signs of volume depletion such as dizziness, light-headedness, or syncope. Physical examination may reveal hematemesis, melena, postural hypotension, or shock in severe cases.
Essential workup and diagnostic testing
Initial evaluation includes a complete blood count and rectal examination for occult blood. Additional laboratory studies include coagulation parameters, electrolytes, renal function tests, liver function tests, and type and cross-match if bleeding is significant. Upright chest radiography may be obtained to exclude esophageal or gastric perforation. Upper endoscopy is the diagnostic and therapeutic modality of choice, allowing direct visualization and management of the bleeding source.
Differential diagnosis
Conditions to consider include nasopharyngeal bleeding, hemoptysis, esophageal rupture (Boerhaave syndrome), esophagitis, gastritis, peptic ulcer disease, variceal bleeding, malignancy, and vascular-enteric fistula.
Treatment and emergency management
Initial management focuses on airway protection, oxygenation, and hemodynamic stabilization with large-bore intravenous access and fluid resuscitation. Blood transfusion is indicated for ongoing bleeding or hemodynamic instability. Most cases resolve with conservative therapy. Persistent or active bleeding requires urgent endoscopic intervention, which may include injection therapy, thermal coagulation, clipping, or band ligation. Proton pump inhibitors and antiemetics are used adjunctively. Surgical or angiographic intervention is reserved for refractory cases.
Disposition and follow-up
Patients with ongoing or massive hemorrhage, hemodynamic instability, significant comorbidities, or advanced age require ICU admission. Stable patients with minimal bleeding that has resolved and stable hematocrit may be admitted for observation or, in select cases, discharged with close follow-up and outpatient endoscopy.
Key points and cautions
Early placement of large-bore intravenous access and prompt resuscitation are critical in upper gastrointestinal bleeding. Early gastroenterology consultation is essential when bleeding is significant. Rebleeding most often occurs within the first 24 hours and is more likely in patients with coagulopathy or portal hypertension.
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Emergency and Acute Medicine – Lymphadenitis
Basics description
Lymphadenitis refers to inflammation and enlargement of lymph nodes, most commonly as part of a systemic response to infection. Nodes become engorged with lymphocytes and macrophages and may be secondarily involved from infection in a distal extremity, producing painful, tender adenopathy proximally. Acute suppurative lymphadenitis may follow pharyngeal or skin infections and can progress to abscess formation.
Etiology
Lymphadenitis is most frequently caused by bacterial infection. The most common organisms in pyogenic lymphadenitis are Staphylococcus aureus, including community-associated methicillin-resistant S. aureus (CA-MRSA), and group A β-hemolytic Streptococcus. CA-MRSA risk factors include prior MRSA infection, household exposure, military service, incarceration, contact sports, injection drug use, and men who have sex with men. Cervical lymphadenitis usually originates from pharyngeal or periodontal infections and commonly involves streptococci and anaerobes. Axillary lymphadenitis is often caused by group A streptococcus. Nosocomial MRSA should be suspected in patients with recent hospitalization, surgery, dialysis, vascular catheters, recent antibiotic use, or unresponsive infection. In children, acute unilateral cervical suppurative lymphadenitis is most common in those younger than six years and is typically caused by S. aureus, group A streptococcus, or anaerobes.
Diagnosis signs and symptoms
Patients typically present with painful swelling and inflammation of affected lymph nodes, often in association with cellulitis or abscess if the cause is pyogenic. Axillary lymphadenitis may present with fever, axillary pain, and acute lymphedema of the arm or chest and may be associated with ipsilateral pleural effusion. History should include duration of lymphadenopathy, pain, fever, night sweats, weight loss, fatigue, sore throat, cough, occupational and animal exposures, sexual history, drug use, and travel. Physical examination should assess whether lymphadenopathy is localized or generalized, node size, tenderness, overlying skin changes, presence of skin lesions, splenomegaly, and involvement of supraclavicular or scalene nodes, which is always abnormal.
Essential workup
Acute regional lymphadenitis is usually a clinical diagnosis and often part of a broader infectious syndrome such as cellulitis. History and physical examination should focus on identifying an infectious source.
Diagnosis tests and interpretation
Laboratory testing is not always required. A CBC may show leukocytosis with left shift or be normal. Serologic testing for EBV, CMV, HIV, or other pathogens should be guided by clinical suspicion. Ultrasound or CT imaging is indicated when patients fail to improve with therapy or when suppuration is suspected. Percutaneous needle aspiration or surgical drainage should be considered if abscess formation occurs or if there is poor clinical response.
Differential diagnosis
The differential diagnosis includes common infections such as adenovirus, scarlet fever, cat scratch disease, fungal infections, and herpes zoster, as well as unusual infections including sporotrichosis, diphtheria, plague, anthrax, typhoid, rubella, and West Nile virus. Sexually transmitted infections, systemic infections such as HIV, infectious mononucleosis, toxoplasmosis, tuberculosis, hepatitis, and dengue should be considered. Noninfectious causes include drug reactions, malignancy, rheumatologic disorders, and pediatric-specific conditions such as Kawasaki disease and PFAPA syndrome.
Treatment
Initial management includes ensuring airway, breathing, and circulation stability. Treatment is directed at the underlying cause and should account for local resistance patterns, including CA-MRSA prevalence. Outpatient therapy typically lasts 7–10 days and includes limb elevation, moist heat, analgesics, and antibiotics. Abscesses require drainage with culture when possible. Skin-source infections are commonly treated with oral cephalexin plus trimethoprim–sulfamethoxazole or alternatives such as clindamycin or doxycycline. Pharyngeal or periodontal sources are treated with penicillin VK or alternatives such as clindamycin or amoxicillin–clavulanate. Inpatient therapy may require IV penicillin-based regimens with MRSA coverage using vancomycin or clindamycin when indicated.
Disposition and follow-up
Admission is indicated for toxic-appearing patients, those with immunosuppression or significant comorbidities, inability to tolerate oral therapy, or unreliable follow-up. Patients with mild infection who are nontoxic, can take oral antibiotics, and have reliable follow-up within 24–48 hours may be discharged. Failure to resolve promptly with antibiotics should prompt evaluation for malignancy or other serious causes, and lymph node biopsy may be indicated for persistent, large, or supraclavicular nodes.
Pearls and pitfalls
Staphylococcus species are the most common cause of acute regional pyogenic lymphadenitis. Empiric antibiotic therapy should include coverage for CA-MRSA in addition to streptococci, particularly in unresponsive or high-risk infections.
Basics description
Lymphadenitis refers to inflammation and enlargement of lymph nodes, most commonly as part of a systemic response to infection. Nodes become engorged with lymphocytes and macrophages and may be secondarily involved from infection in a distal extremity, producing painful, tender adenopathy proximally. Acute suppurative lymphadenitis may follow pharyngeal or skin infections and can progress to abscess formation.
Etiology
Lymphadenitis is most frequently caused by bacterial infection. The most common organisms in pyogenic lymphadenitis are Staphylococcus aureus, including community-associated methicillin-resistant S. aureus (CA-MRSA), and group A β-hemolytic Streptococcus. CA-MRSA risk factors include prior MRSA infection, household exposure, military service, incarceration, contact sports, injection drug use, and men who have sex with men. Cervical lymphadenitis usually originates from pharyngeal or periodontal infections and commonly involves streptococci and anaerobes. Axillary lymphadenitis is often caused by group A streptococcus. Nosocomial MRSA should be suspected in patients with recent hospitalization, surgery, dialysis, vascular catheters, recent antibiotic use, or unresponsive infection. In children, acute unilateral cervical suppurative lymphadenitis is most common in those younger than six years and is typically caused by S. aureus, group A streptococcus, or anaerobes.
Diagnosis signs and symptoms
Patients typically present with painful swelling and inflammation of affected lymph nodes, often in association with cellulitis or abscess if the cause is pyogenic. Axillary lymphadenitis may present with fever, axillary pain, and acute lymphedema of the arm or chest and may be associated with ipsilateral pleural effusion. History should include duration of lymphadenopathy, pain, fever, night sweats, weight loss, fatigue, sore throat, cough, occupational and animal exposures, sexual history, drug use, and travel. Physical examination should assess whether lymphadenopathy is localized or generalized, node size, tenderness, overlying skin changes, presence of skin lesions, splenomegaly, and involvement of supraclavicular or scalene nodes, which is always abnormal.
Essential workup
Acute regional lymphadenitis is usually a clinical diagnosis and often part of a broader infectious syndrome such as cellulitis. History and physical examination should focus on identifying an infectious source.
Diagnosis tests and interpretation
Laboratory testing is not always required. A CBC may show leukocytosis with left shift or be normal. Serologic testing for EBV, CMV, HIV, or other pathogens should be guided by clinical suspicion. Ultrasound or CT imaging is indicated when patients fail to improve with therapy or when suppuration is suspected. Percutaneous needle aspiration or surgical drainage should be considered if abscess formation occurs or if there is poor clinical response.
Differential diagnosis
The differential diagnosis includes common infections such as adenovirus, scarlet fever, cat scratch disease, fungal infections, and herpes zoster, as well as unusual infections including sporotrichosis, diphtheria, plague, anthrax, typhoid, rubella, and West Nile virus. Sexually transmitted infections, systemic infections such as HIV, infectious mononucleosis, toxoplasmosis, tuberculosis, hepatitis, and dengue should be considered. Noninfectious causes include drug reactions, malignancy, rheumatologic disorders, and pediatric-specific conditions such as Kawasaki disease and PFAPA syndrome.
Treatment
Initial management includes ensuring airway, breathing, and circulation stability. Treatment is directed at the underlying cause and should account for local resistance patterns, including CA-MRSA prevalence. Outpatient therapy typically lasts 7–10 days and includes limb elevation, moist heat, analgesics, and antibiotics. Abscesses require drainage with culture when possible. Skin-source infections are commonly treated with oral cephalexin plus trimethoprim–sulfamethoxazole or alternatives such as clindamycin or doxycycline. Pharyngeal or periodontal sources are treated with penicillin VK or alternatives such as clindamycin or amoxicillin–clavulanate. Inpatient therapy may require IV penicillin-based regimens with MRSA coverage using vancomycin or clindamycin when indicated.
Disposition and follow-up
Admission is indicated for toxic-appearing patients, those with immunosuppression or significant comorbidities, inability to tolerate oral therapy, or unreliable follow-up. Patients with mild infection who are nontoxic, can take oral antibiotics, and have reliable follow-up within 24–48 hours may be discharged. Failure to resolve promptly with antibiotics should prompt evaluation for malignancy or other serious causes, and lymph node biopsy may be indicated for persistent, large, or supraclavicular nodes.
Pearls and pitfalls
Staphylococcus species are the most common cause of acute regional pyogenic lymphadenitis. Empiric antibiotic therapy should include coverage for CA-MRSA in addition to streptococci, particularly in unresponsive or high-risk infections.
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Emergency and Acute Medicine – Lyme Disease
Basics description
Lyme disease is the most common tick-borne illness in North America. It is endemic in the northeastern United States, the upper Midwest, and parts of northwestern California. The disease follows a multisystem course and may present with dermatologic, neurologic, cardiac, and musculoskeletal manifestations.
Etiology and pathophysiology
Lyme disease is caused by the spirochete Borrelia burgdorferi, which is transmitted through the bite of an Ixodes tick, most commonly Ixodes dammini (the deer tick). Transmission occurs primarily between April and November, with 80–90% of cases in the summer months. Fewer than half of patients recall a tick bite. Disease pathogenesis involves organism-induced local inflammation, cytokine release, and autoimmune mechanisms. There is no person-to-person transmission. A related spirochete, Borrelia miyamotoi, has also been identified as a cause of a Lyme-like illness.
Clinical presentation and stages
Lyme disease progresses through three clinical stages, although not all patients experience every stage.
Stage I, or early localized disease, begins days to weeks after a tick bite. The hallmark finding is erythema chronicum migrans, a pathognomonic expanding annular rash greater than 5 cm in diameter, often with central clearing and a red outer border (“bull’s-eye” rash). Associated symptoms include regional lymphadenopathy, low-grade fever, headache, myalgias, arthralgias, fatigue, and malaise.
Stage II, or early disseminated disease, occurs days to weeks after infection and is characterized by intermittent, fluctuating symptoms. Neurologic involvement includes the triad of aseptic meningitis, cranial neuritis, and radiculoneuritis, with facial (Bell) palsy being the most common cranial nerve deficit. Cardiac manifestations may include tachycardia, bradycardia, atrioventricular block, and myopericarditis. Rash may be absent at this stage. Prognosis is generally good with appropriate treatment.
Stage III, or late disease, develops months to years after initial infection. Musculoskeletal involvement is most common, typically presenting as recurrent monoarticular or oligoarticular arthritis, most often affecting the knee. Dermatologic findings may include acrodermatitis chronica atrophicans on the extensor surfaces of the extremities. Less commonly, late neurologic complications such as chronic polyneuropathy or encephalopathy may occur. A Jarisch–Herxheimer reaction, consisting of transient symptom worsening shortly after treatment initiation, may be seen.
Special populations
Children are more likely than adults to present with fever and may lack a history of erythema migrans. Facial palsy in pediatric patients is frequently associated with aseptic meningitis. Cardiac involvement may be asymptomatic but detectable on ECG. With appropriate treatment, children generally have excellent long-term outcomes. There is no clear evidence that Lyme disease during pregnancy causes fetal harm.
Diagnosis and evaluation
Lyme disease is primarily a clinical diagnosis. The presence of erythema migrans eliminates the need for serologic testing. In patients without the classic rash, serologic testing with ELISA followed by confirmatory Western blot is indicated. Lumbar puncture is reserved for patients with meningeal signs, arthrocentesis for acute arthritis, and ECG for suspected cardiac involvement.
Laboratory findings are nonspecific and may include elevated erythrocyte sedimentation rate, mild cytopenias, or elevated liver enzymes. Cerebrospinal fluid analysis may show pleocytosis and elevated protein in neuroborreliosis.
Differential diagnosis
The differential diagnosis includes other tick-borne illnesses, viral meningitis, septic arthritis, rheumatic fever, syphilis, parvovirus B19 infection, infectious endocarditis, juvenile idiopathic arthritis, fibromyalgia, and chronic fatigue syndrome.
Treatment
Initial stabilization focuses on hydration, IV access for neurologic or cardiac involvement, and cardiac monitoring when indicated. Tick removal should be performed promptly using blunt forceps applied close to the skin.
Antibiotic therapy depends on disease stage and severity. Early localized disease is treated with oral antibiotics such as amoxicillin, doxycycline (for patients ≥8 years old and nonpregnant), or cefuroxime. Disseminated disease with mild neurologic involvement may be treated orally, while meningitis, significant carditis, or severe arthritis requires parenteral therapy, typically with ceftriaxone, cefotaxime, or penicillin G. Late disease usually requires prolonged parenteral therapy. NSAIDs are used for arthralgias and arthritis, and aspirin may be used adjunctively in cardiac involvement.
Disposition and follow-up
Hospital admission is required for patients with meningoencephalitis or significant cardiac involvement requiring telemetry or ICU monitoring. Patients with uncomplicated disease treated with oral antibiotics may be discharged with close outpatient follow-up.
Key points
Early recognition and treatment of Lyme disease prevent late complications. The presence of erythema migrans is diagnostic and should prompt immediate treatment without waiting for serology. Clinicians should remain vigilant for coinfections such as anaplasmosis and babesiosis in endemic regions, and prolonged treatment is required for later-stage organ involvement.
Basics description
Lyme disease is the most common tick-borne illness in North America. It is endemic in the northeastern United States, the upper Midwest, and parts of northwestern California. The disease follows a multisystem course and may present with dermatologic, neurologic, cardiac, and musculoskeletal manifestations.
Etiology and pathophysiology
Lyme disease is caused by the spirochete Borrelia burgdorferi, which is transmitted through the bite of an Ixodes tick, most commonly Ixodes dammini (the deer tick). Transmission occurs primarily between April and November, with 80–90% of cases in the summer months. Fewer than half of patients recall a tick bite. Disease pathogenesis involves organism-induced local inflammation, cytokine release, and autoimmune mechanisms. There is no person-to-person transmission. A related spirochete, Borrelia miyamotoi, has also been identified as a cause of a Lyme-like illness.
Clinical presentation and stages
Lyme disease progresses through three clinical stages, although not all patients experience every stage.
Stage I, or early localized disease, begins days to weeks after a tick bite. The hallmark finding is erythema chronicum migrans, a pathognomonic expanding annular rash greater than 5 cm in diameter, often with central clearing and a red outer border (“bull’s-eye” rash). Associated symptoms include regional lymphadenopathy, low-grade fever, headache, myalgias, arthralgias, fatigue, and malaise.
Stage II, or early disseminated disease, occurs days to weeks after infection and is characterized by intermittent, fluctuating symptoms. Neurologic involvement includes the triad of aseptic meningitis, cranial neuritis, and radiculoneuritis, with facial (Bell) palsy being the most common cranial nerve deficit. Cardiac manifestations may include tachycardia, bradycardia, atrioventricular block, and myopericarditis. Rash may be absent at this stage. Prognosis is generally good with appropriate treatment.
Stage III, or late disease, develops months to years after initial infection. Musculoskeletal involvement is most common, typically presenting as recurrent monoarticular or oligoarticular arthritis, most often affecting the knee. Dermatologic findings may include acrodermatitis chronica atrophicans on the extensor surfaces of the extremities. Less commonly, late neurologic complications such as chronic polyneuropathy or encephalopathy may occur. A Jarisch–Herxheimer reaction, consisting of transient symptom worsening shortly after treatment initiation, may be seen.
Special populations
Children are more likely than adults to present with fever and may lack a history of erythema migrans. Facial palsy in pediatric patients is frequently associated with aseptic meningitis. Cardiac involvement may be asymptomatic but detectable on ECG. With appropriate treatment, children generally have excellent long-term outcomes. There is no clear evidence that Lyme disease during pregnancy causes fetal harm.
Diagnosis and evaluation
Lyme disease is primarily a clinical diagnosis. The presence of erythema migrans eliminates the need for serologic testing. In patients without the classic rash, serologic testing with ELISA followed by confirmatory Western blot is indicated. Lumbar puncture is reserved for patients with meningeal signs, arthrocentesis for acute arthritis, and ECG for suspected cardiac involvement.
Laboratory findings are nonspecific and may include elevated erythrocyte sedimentation rate, mild cytopenias, or elevated liver enzymes. Cerebrospinal fluid analysis may show pleocytosis and elevated protein in neuroborreliosis.
Differential diagnosis
The differential diagnosis includes other tick-borne illnesses, viral meningitis, septic arthritis, rheumatic fever, syphilis, parvovirus B19 infection, infectious endocarditis, juvenile idiopathic arthritis, fibromyalgia, and chronic fatigue syndrome.
Treatment
Initial stabilization focuses on hydration, IV access for neurologic or cardiac involvement, and cardiac monitoring when indicated. Tick removal should be performed promptly using blunt forceps applied close to the skin.
Antibiotic therapy depends on disease stage and severity. Early localized disease is treated with oral antibiotics such as amoxicillin, doxycycline (for patients ≥8 years old and nonpregnant), or cefuroxime. Disseminated disease with mild neurologic involvement may be treated orally, while meningitis, significant carditis, or severe arthritis requires parenteral therapy, typically with ceftriaxone, cefotaxime, or penicillin G. Late disease usually requires prolonged parenteral therapy. NSAIDs are used for arthralgias and arthritis, and aspirin may be used adjunctively in cardiac involvement.
Disposition and follow-up
Hospital admission is required for patients with meningoencephalitis or significant cardiac involvement requiring telemetry or ICU monitoring. Patients with uncomplicated disease treated with oral antibiotics may be discharged with close outpatient follow-up.
Key points
Early recognition and treatment of Lyme disease prevent late complications. The presence of erythema migrans is diagnostic and should prompt immediate treatment without waiting for serology. Clinicians should remain vigilant for coinfections such as anaplasmosis and babesiosis in endemic regions, and prolonged treatment is required for later-stage organ involvement.
- Published on
Emergency and Acute Medicine – Lymphadenitis
Basics description
Lymphadenitis refers to inflammation and enlargement of lymph nodes, most commonly as part of a systemic response to infection. Nodes become engorged with lymphocytes and macrophages and may be secondarily involved from infection in a distal extremity, producing painful, tender adenopathy proximally. Acute suppurative lymphadenitis may follow pharyngeal or skin infections and can progress to abscess formation.
Etiology
Lymphadenitis is most frequently caused by bacterial infection. The most common organisms in pyogenic lymphadenitis are Staphylococcus aureus, including community-associated methicillin-resistant S. aureus (CA-MRSA), and group A β-hemolytic Streptococcus. CA-MRSA risk factors include prior MRSA infection, household exposure, military service, incarceration, contact sports, injection drug use, and men who have sex with men. Cervical lymphadenitis usually originates from pharyngeal or periodontal infections and commonly involves streptococci and anaerobes. Axillary lymphadenitis is often caused by group A streptococcus. Nosocomial MRSA should be suspected in patients with recent hospitalization, surgery, dialysis, vascular catheters, recent antibiotic use, or unresponsive infection. In children, acute unilateral cervical suppurative lymphadenitis is most common in those younger than six years and is typically caused by S. aureus, group A streptococcus, or anaerobes.
Diagnosis signs and symptoms
Patients typically present with painful swelling and inflammation of affected lymph nodes, often in association with cellulitis or abscess if the cause is pyogenic. Axillary lymphadenitis may present with fever, axillary pain, and acute lymphedema of the arm or chest and may be associated with ipsilateral pleural effusion. History should include duration of lymphadenopathy, pain, fever, night sweats, weight loss, fatigue, sore throat, cough, occupational and animal exposures, sexual history, drug use, and travel. Physical examination should assess whether lymphadenopathy is localized or generalized, node size, tenderness, overlying skin changes, presence of skin lesions, splenomegaly, and involvement of supraclavicular or scalene nodes, which is always abnormal.
Essential workup
Acute regional lymphadenitis is usually a clinical diagnosis and often part of a broader infectious syndrome such as cellulitis. History and physical examination should focus on identifying an infectious source.
Diagnosis tests and interpretation
Laboratory testing is not always required. A CBC may show leukocytosis with left shift or be normal. Serologic testing for EBV, CMV, HIV, or other pathogens should be guided by clinical suspicion. Ultrasound or CT imaging is indicated when patients fail to improve with therapy or when suppuration is suspected. Percutaneous needle aspiration or surgical drainage should be considered if abscess formation occurs or if there is poor clinical response.
Differential diagnosis
The differential diagnosis includes common infections such as adenovirus, scarlet fever, cat scratch disease, fungal infections, and herpes zoster, as well as unusual infections including sporotrichosis, diphtheria, plague, anthrax, typhoid, rubella, and West Nile virus. Sexually transmitted infections, systemic infections such as HIV, infectious mononucleosis, toxoplasmosis, tuberculosis, hepatitis, and dengue should be considered. Noninfectious causes include drug reactions, malignancy, rheumatologic disorders, and pediatric-specific conditions such as Kawasaki disease and PFAPA syndrome.
Treatment
Initial management includes ensuring airway, breathing, and circulation stability. Treatment is directed at the underlying cause and should account for local resistance patterns, including CA-MRSA prevalence. Outpatient therapy typically lasts 7–10 days and includes limb elevation, moist heat, analgesics, and antibiotics. Abscesses require drainage with culture when possible. Skin-source infections are commonly treated with oral cephalexin plus trimethoprim–sulfamethoxazole or alternatives such as clindamycin or doxycycline. Pharyngeal or periodontal sources are treated with penicillin VK or alternatives such as clindamycin or amoxicillin–clavulanate. Inpatient therapy may require IV penicillin-based regimens with MRSA coverage using vancomycin or clindamycin when indicated.
Disposition and follow-up
Admission is indicated for toxic-appearing patients, those with immunosuppression or significant comorbidities, inability to tolerate oral therapy, or unreliable follow-up. Patients with mild infection who are nontoxic, can take oral antibiotics, and have reliable follow-up within 24–48 hours may be discharged. Failure to resolve promptly with antibiotics should prompt evaluation for malignancy or other serious causes, and lymph node biopsy may be indicated for persistent, large, or supraclavicular nodes.
Pearls and pitfalls
Staphylococcus species are the most common cause of acute regional pyogenic lymphadenitis. Empiric antibiotic therapy should include coverage for CA-MRSA in addition to streptococci, particularly in unresponsive or high-risk infections.
Basics description
Lymphadenitis refers to inflammation and enlargement of lymph nodes, most commonly as part of a systemic response to infection. Nodes become engorged with lymphocytes and macrophages and may be secondarily involved from infection in a distal extremity, producing painful, tender adenopathy proximally. Acute suppurative lymphadenitis may follow pharyngeal or skin infections and can progress to abscess formation.
Etiology
Lymphadenitis is most frequently caused by bacterial infection. The most common organisms in pyogenic lymphadenitis are Staphylococcus aureus, including community-associated methicillin-resistant S. aureus (CA-MRSA), and group A β-hemolytic Streptococcus. CA-MRSA risk factors include prior MRSA infection, household exposure, military service, incarceration, contact sports, injection drug use, and men who have sex with men. Cervical lymphadenitis usually originates from pharyngeal or periodontal infections and commonly involves streptococci and anaerobes. Axillary lymphadenitis is often caused by group A streptococcus. Nosocomial MRSA should be suspected in patients with recent hospitalization, surgery, dialysis, vascular catheters, recent antibiotic use, or unresponsive infection. In children, acute unilateral cervical suppurative lymphadenitis is most common in those younger than six years and is typically caused by S. aureus, group A streptococcus, or anaerobes.
Diagnosis signs and symptoms
Patients typically present with painful swelling and inflammation of affected lymph nodes, often in association with cellulitis or abscess if the cause is pyogenic. Axillary lymphadenitis may present with fever, axillary pain, and acute lymphedema of the arm or chest and may be associated with ipsilateral pleural effusion. History should include duration of lymphadenopathy, pain, fever, night sweats, weight loss, fatigue, sore throat, cough, occupational and animal exposures, sexual history, drug use, and travel. Physical examination should assess whether lymphadenopathy is localized or generalized, node size, tenderness, overlying skin changes, presence of skin lesions, splenomegaly, and involvement of supraclavicular or scalene nodes, which is always abnormal.
Essential workup
Acute regional lymphadenitis is usually a clinical diagnosis and often part of a broader infectious syndrome such as cellulitis. History and physical examination should focus on identifying an infectious source.
Diagnosis tests and interpretation
Laboratory testing is not always required. A CBC may show leukocytosis with left shift or be normal. Serologic testing for EBV, CMV, HIV, or other pathogens should be guided by clinical suspicion. Ultrasound or CT imaging is indicated when patients fail to improve with therapy or when suppuration is suspected. Percutaneous needle aspiration or surgical drainage should be considered if abscess formation occurs or if there is poor clinical response.
Differential diagnosis
The differential diagnosis includes common infections such as adenovirus, scarlet fever, cat scratch disease, fungal infections, and herpes zoster, as well as unusual infections including sporotrichosis, diphtheria, plague, anthrax, typhoid, rubella, and West Nile virus. Sexually transmitted infections, systemic infections such as HIV, infectious mononucleosis, toxoplasmosis, tuberculosis, hepatitis, and dengue should be considered. Noninfectious causes include drug reactions, malignancy, rheumatologic disorders, and pediatric-specific conditions such as Kawasaki disease and PFAPA syndrome.
Treatment
Initial management includes ensuring airway, breathing, and circulation stability. Treatment is directed at the underlying cause and should account for local resistance patterns, including CA-MRSA prevalence. Outpatient therapy typically lasts 7–10 days and includes limb elevation, moist heat, analgesics, and antibiotics. Abscesses require drainage with culture when possible. Skin-source infections are commonly treated with oral cephalexin plus trimethoprim–sulfamethoxazole or alternatives such as clindamycin or doxycycline. Pharyngeal or periodontal sources are treated with penicillin VK or alternatives such as clindamycin or amoxicillin–clavulanate. Inpatient therapy may require IV penicillin-based regimens with MRSA coverage using vancomycin or clindamycin when indicated.
Disposition and follow-up
Admission is indicated for toxic-appearing patients, those with immunosuppression or significant comorbidities, inability to tolerate oral therapy, or unreliable follow-up. Patients with mild infection who are nontoxic, can take oral antibiotics, and have reliable follow-up within 24–48 hours may be discharged. Failure to resolve promptly with antibiotics should prompt evaluation for malignancy or other serious causes, and lymph node biopsy may be indicated for persistent, large, or supraclavicular nodes.
Pearls and pitfalls
Staphylococcus species are the most common cause of acute regional pyogenic lymphadenitis. Empiric antibiotic therapy should include coverage for CA-MRSA in addition to streptococci, particularly in unresponsive or high-risk infections.
- Published on
Emergency and Acute Medicine – Lymphogranuloma Venereum
Basics description
Lymphogranuloma venereum (LGV) is a sexually transmitted infection characterized by an initial painless genital lesion followed by regional lymphatic spread. The disease progresses through primary, secondary, and tertiary stages and is responsive to appropriate antibacterial therapy in early phases. LGV is endemic in Southeast Asia, Latin America, parts of Africa, and the Caribbean, with increasing incidence among men who have sex with men. It is also known as struma, tropical bubo, or Nicolas–Favre–Durand disease.
Etiology
LGV is caused by Chlamydia trachomatis serotypes L1, L2, and L3.
Diagnosis signs and symptoms
The primary stage occurs after an incubation period of 3–30 days and presents as a painless papule, pustule, vesicle, or ulcer in the anogenital region. These lesions are transient, often last only a few days, and are frequently unnoticed. The secondary stage develops 1–3 weeks later with systemic symptoms such as fever, malaise, and myalgias, along with tender inguinal lymphadenopathy that may be unilateral or bilateral. Large, fluctuant lymph nodes (buboes) can ulcerate and drain purulent material. Proctitis is common in anal-receptive patients and may cause rectal bleeding, tenesmus, and constipation. The tertiary stage occurs in untreated disease and results in chronic inflammatory changes including proctocolitis, strictures, fistulae, and elephantiasis of the genitalia or lower extremities, mimicking inflammatory bowel disease.
Physical examination
Findings in the primary stage include a painless anogenital lesion. During the secondary stage, tender inguinal or femoral lymphadenopathy is typical, with buboes forming in up to two-thirds of cases. The “groove sign,” caused by lymph node enlargement above and below the inguinal ligament, may be seen. Anal-receptive patients may demonstrate signs of hemorrhagic proctocolitis. Advanced tertiary disease shows chronic inflammatory damage with strictures, fistulae, and elephantiasis.
Diagnosis tests and interpretation
Routine chlamydia nucleic acid amplification tests do not differentiate LGV strains. Diagnosis is based on clinical suspicion, epidemiologic context, and serologic testing. Complement fixation titers greater than 1:64 support the diagnosis. False-positive VDRL tests may occur. Bubo aspiration is specific but rarely practical and is not routinely required.
Differential diagnosis
Conditions to consider include genital herpes, syphilis, chancroid, and granuloma inguinale. Compared with LGV, syphilis typically causes nontender lymphadenopathy with a longer incubation period, while chancroid presents with painful ulcers and granuloma inguinale causes painless, friable lesions that bleed easily.
Treatment
No prehospital or emergency stabilization is typically required. Large, fluctuant buboes may require aspiration or drainage to reduce pain and scarring. First-line therapy is doxycycline 100 mg orally twice daily for 21 days. Alternative regimens include azithromycin 1 g orally weekly for 3 weeks or erythromycin 500 mg orally four times daily for 3 weeks. In pregnancy or during lactation, erythromycin is the recommended treatment.
Disposition and follow-up
Hospitalization is rarely necessary and is reserved for patients with severe systemic illness or complications. Most immunocompetent patients without systemic involvement can be discharged with outpatient management. Sexual partners within the previous 60 days should be tested and treated with appropriate antichlamydial therapy. Follow-up is essential to confirm cure, particularly in cases of rectal involvement, which may require retreatment.
Pearls and pitfalls
LGV should be suspected in at-risk populations, particularly men who have sex with men presenting with inguinal lymphadenopathy or proctitis. Early recognition and treatment are critical to prevent progression to tertiary disease, which may cause irreversible tissue damage and is less responsive to antibiotics alone.
Basics description
Lymphogranuloma venereum (LGV) is a sexually transmitted infection characterized by an initial painless genital lesion followed by regional lymphatic spread. The disease progresses through primary, secondary, and tertiary stages and is responsive to appropriate antibacterial therapy in early phases. LGV is endemic in Southeast Asia, Latin America, parts of Africa, and the Caribbean, with increasing incidence among men who have sex with men. It is also known as struma, tropical bubo, or Nicolas–Favre–Durand disease.
Etiology
LGV is caused by Chlamydia trachomatis serotypes L1, L2, and L3.
Diagnosis signs and symptoms
The primary stage occurs after an incubation period of 3–30 days and presents as a painless papule, pustule, vesicle, or ulcer in the anogenital region. These lesions are transient, often last only a few days, and are frequently unnoticed. The secondary stage develops 1–3 weeks later with systemic symptoms such as fever, malaise, and myalgias, along with tender inguinal lymphadenopathy that may be unilateral or bilateral. Large, fluctuant lymph nodes (buboes) can ulcerate and drain purulent material. Proctitis is common in anal-receptive patients and may cause rectal bleeding, tenesmus, and constipation. The tertiary stage occurs in untreated disease and results in chronic inflammatory changes including proctocolitis, strictures, fistulae, and elephantiasis of the genitalia or lower extremities, mimicking inflammatory bowel disease.
Physical examination
Findings in the primary stage include a painless anogenital lesion. During the secondary stage, tender inguinal or femoral lymphadenopathy is typical, with buboes forming in up to two-thirds of cases. The “groove sign,” caused by lymph node enlargement above and below the inguinal ligament, may be seen. Anal-receptive patients may demonstrate signs of hemorrhagic proctocolitis. Advanced tertiary disease shows chronic inflammatory damage with strictures, fistulae, and elephantiasis.
Diagnosis tests and interpretation
Routine chlamydia nucleic acid amplification tests do not differentiate LGV strains. Diagnosis is based on clinical suspicion, epidemiologic context, and serologic testing. Complement fixation titers greater than 1:64 support the diagnosis. False-positive VDRL tests may occur. Bubo aspiration is specific but rarely practical and is not routinely required.
Differential diagnosis
Conditions to consider include genital herpes, syphilis, chancroid, and granuloma inguinale. Compared with LGV, syphilis typically causes nontender lymphadenopathy with a longer incubation period, while chancroid presents with painful ulcers and granuloma inguinale causes painless, friable lesions that bleed easily.
Treatment
No prehospital or emergency stabilization is typically required. Large, fluctuant buboes may require aspiration or drainage to reduce pain and scarring. First-line therapy is doxycycline 100 mg orally twice daily for 21 days. Alternative regimens include azithromycin 1 g orally weekly for 3 weeks or erythromycin 500 mg orally four times daily for 3 weeks. In pregnancy or during lactation, erythromycin is the recommended treatment.
Disposition and follow-up
Hospitalization is rarely necessary and is reserved for patients with severe systemic illness or complications. Most immunocompetent patients without systemic involvement can be discharged with outpatient management. Sexual partners within the previous 60 days should be tested and treated with appropriate antichlamydial therapy. Follow-up is essential to confirm cure, particularly in cases of rectal involvement, which may require retreatment.
Pearls and pitfalls
LGV should be suspected in at-risk populations, particularly men who have sex with men presenting with inguinal lymphadenopathy or proctitis. Early recognition and treatment are critical to prevent progression to tertiary disease, which may cause irreversible tissue damage and is less responsive to antibiotics alone.
