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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.
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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 – 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.
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KembaraXtra-Medicine – Autoimmune Hemolytic Anemia
Autoimmune hemolytic anemia (AIHA) is a condition in which autoantibodies and/or complement bind to red blood cells (RBCs), leading to their premature destruction. About half of cases are primary (idiopathic), while the rest are secondary to underlying diseases or drugs. AIHA is commonly categorized into warm antibody–mediated disease (usually IgG, reacting best at 37°C), cold antibody–mediated disease (typically IgM with complement), and drug-induced immune hemolysis.
AIHA is uncommon, with an annual incidence of about 1 to 3 cases per 100,000 people and an estimated mortality around 10%. It is reported more often in women younger than 50 years. Patients most commonly present with fatigue and dyspnea. Pallor and jaundice may be present, and tachycardia with a flow murmur can occur when anemia is significant. Intravascular hemolysis may cause dark urine and back pain. Hepatomegaly or lymphadenopathy suggests a lymphoproliferative disorder or malignancy, while splenomegaly may suggest hypersplenism. The course is often chronic with relapses.
Warm AIHA is usually mediated by IgG antibodies and may be idiopathic or associated with leukemia/lymphoma, thymoma, myeloma, viral infections, babesiosis, and collagen-vascular diseases. Cold AIHA is commonly IgM- and complement-mediated and may be idiopathic or linked to infections, lymphoma, or cold agglutinin disease. Drug-induced AIHA can occur through different immune mechanisms, including antibodies directed against RBC antigens (e.g., methyldopa), antibodies against an RBC–drug complex (hapten type, e.g., penicillin), or immune complex mechanisms (e.g., quinidine).
The differential diagnosis includes non-immune causes of hemolysis such as microangiopathic hemolytic anemia (e.g., TTP/HUS), hypersplenism, prosthetic valve hemolysis, infections, toxins, and inherited causes such as membrane disorders (e.g., hereditary spherocytosis), hemoglobinopathies, and enzyme deficiencies (e.g., G6PD). Chronic lymphocytic leukemia (CLL) can cause a positive direct antiglobulin test (DAT) without true AIHA, so labs and clinical evidence of hemolysis are important.
Evaluation focuses on confirming hemolysis and establishing immune causation. Typical hemolysis findings include reticulocytosis (or reticulocytopenia if marrow suppression is present), low haptoglobin, elevated indirect bilirubin, and elevated LDH. Initial tests include CBC, reticulocyte count, bilirubin/LDH, and a peripheral smear (spherocytes are typical in warm AIHA). The key diagnostic test is the direct antiglobulin test (DAT/Coombs), performed initially with a polyspecific reagent to detect IgG and/or complement on RBCs. A positive DAT supports AIHA: IgG ± C3d suggests warm AIHA, while C3d alone suggests cold AIHA. Additional evaluation may include hepatitis serologies, HIV testing, ANA, urine testing for hemoglobinuria/hemosiderinuria, and imaging (such as CT chest/abdomen/pelvis) if an underlying lymphoproliferative disorder is suspected.
Management includes stopping any offending drug when drug-induced disease is possible. Severe, life-threatening cases may rarely require plasmapheresis or exchange transfusion. Patients with cold antibody AIHA should avoid cold exposure. Warm AIHA is typically treated first with prednisone 1 to 2 mg/kg/day, with tapering after response. Some evidence supports upfront combination therapy with steroids plus rituximab to improve outcomes and durability of response. For relapse or steroid-refractory disease, rituximab is commonly used and has high response rates, with a substantial portion maintaining remission years later. Splenectomy is now usually reserved for cases refractory to both steroids and rituximab, and further options include immunosuppressive agents such as mycophenolate, cyclosporine, cyclophosphamide, IVIG, and sometimes danazol as an adjunct.
Cold AIHA generally responds poorly to corticosteroids, and treating underlying infection or lymphoproliferative disease is important. In primary cold agglutinin disease, rituximab-based regimens (often with bendamustine in fit patients) are commonly used, while rituximab alone may be used in older or frailer patients. IVIG or plasmapheresis can be used temporarily in severe cases while waiting for a durable therapy to work. Complement-directed therapies may be considered in severe disease; sutimlimab (targeting C1s) has been shown to rapidly reduce hemolysis and improve hemoglobin and fatigue in cold agglutinin disease. Splenectomy is generally ineffective in cold AIHA because clearance occurs mainly in the liver.
Prognosis is generally good unless AIHA is driven by a serious underlying condition such as leukemia or myeloma. Hematology referral is recommended for all AIHA cases, and surgical referral may be needed if splenectomy is being considered for refractory warm AIHA.
Autoimmune hemolytic anemia (AIHA) is a condition in which autoantibodies and/or complement bind to red blood cells (RBCs), leading to their premature destruction. About half of cases are primary (idiopathic), while the rest are secondary to underlying diseases or drugs. AIHA is commonly categorized into warm antibody–mediated disease (usually IgG, reacting best at 37°C), cold antibody–mediated disease (typically IgM with complement), and drug-induced immune hemolysis.
AIHA is uncommon, with an annual incidence of about 1 to 3 cases per 100,000 people and an estimated mortality around 10%. It is reported more often in women younger than 50 years. Patients most commonly present with fatigue and dyspnea. Pallor and jaundice may be present, and tachycardia with a flow murmur can occur when anemia is significant. Intravascular hemolysis may cause dark urine and back pain. Hepatomegaly or lymphadenopathy suggests a lymphoproliferative disorder or malignancy, while splenomegaly may suggest hypersplenism. The course is often chronic with relapses.
Warm AIHA is usually mediated by IgG antibodies and may be idiopathic or associated with leukemia/lymphoma, thymoma, myeloma, viral infections, babesiosis, and collagen-vascular diseases. Cold AIHA is commonly IgM- and complement-mediated and may be idiopathic or linked to infections, lymphoma, or cold agglutinin disease. Drug-induced AIHA can occur through different immune mechanisms, including antibodies directed against RBC antigens (e.g., methyldopa), antibodies against an RBC–drug complex (hapten type, e.g., penicillin), or immune complex mechanisms (e.g., quinidine).
The differential diagnosis includes non-immune causes of hemolysis such as microangiopathic hemolytic anemia (e.g., TTP/HUS), hypersplenism, prosthetic valve hemolysis, infections, toxins, and inherited causes such as membrane disorders (e.g., hereditary spherocytosis), hemoglobinopathies, and enzyme deficiencies (e.g., G6PD). Chronic lymphocytic leukemia (CLL) can cause a positive direct antiglobulin test (DAT) without true AIHA, so labs and clinical evidence of hemolysis are important.
Evaluation focuses on confirming hemolysis and establishing immune causation. Typical hemolysis findings include reticulocytosis (or reticulocytopenia if marrow suppression is present), low haptoglobin, elevated indirect bilirubin, and elevated LDH. Initial tests include CBC, reticulocyte count, bilirubin/LDH, and a peripheral smear (spherocytes are typical in warm AIHA). The key diagnostic test is the direct antiglobulin test (DAT/Coombs), performed initially with a polyspecific reagent to detect IgG and/or complement on RBCs. A positive DAT supports AIHA: IgG ± C3d suggests warm AIHA, while C3d alone suggests cold AIHA. Additional evaluation may include hepatitis serologies, HIV testing, ANA, urine testing for hemoglobinuria/hemosiderinuria, and imaging (such as CT chest/abdomen/pelvis) if an underlying lymphoproliferative disorder is suspected.
Management includes stopping any offending drug when drug-induced disease is possible. Severe, life-threatening cases may rarely require plasmapheresis or exchange transfusion. Patients with cold antibody AIHA should avoid cold exposure. Warm AIHA is typically treated first with prednisone 1 to 2 mg/kg/day, with tapering after response. Some evidence supports upfront combination therapy with steroids plus rituximab to improve outcomes and durability of response. For relapse or steroid-refractory disease, rituximab is commonly used and has high response rates, with a substantial portion maintaining remission years later. Splenectomy is now usually reserved for cases refractory to both steroids and rituximab, and further options include immunosuppressive agents such as mycophenolate, cyclosporine, cyclophosphamide, IVIG, and sometimes danazol as an adjunct.
Cold AIHA generally responds poorly to corticosteroids, and treating underlying infection or lymphoproliferative disease is important. In primary cold agglutinin disease, rituximab-based regimens (often with bendamustine in fit patients) are commonly used, while rituximab alone may be used in older or frailer patients. IVIG or plasmapheresis can be used temporarily in severe cases while waiting for a durable therapy to work. Complement-directed therapies may be considered in severe disease; sutimlimab (targeting C1s) has been shown to rapidly reduce hemolysis and improve hemoglobin and fatigue in cold agglutinin disease. Splenectomy is generally ineffective in cold AIHA because clearance occurs mainly in the liver.
Prognosis is generally good unless AIHA is driven by a serious underlying condition such as leukemia or myeloma. Hematology referral is recommended for all AIHA cases, and surgical referral may be needed if splenectomy is being considered for refractory warm AIHA.
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Emergency and Acute Medicine – Lymphangitis
Basics description
Lymphangitis is an infection of the lymphatic vessels that drain an area of inflammation or infection. Histologically, lymphatic channels become dilated and filled with lymphocytes and histiocytes. Inflammation often extends into surrounding perilymphatic tissues and may progress to cellulitis or abscess formation if untreated.
Etiology
Acute lymphangitis is most commonly caused by bacterial infection, particularly group A β-hemolytic Streptococcus. Less common causes include other streptococcal species and Staphylococcus aureus, including community-associated methicillin-resistant S. aureus (CA-MRSA). CA-MRSA risk factors include prior MRSA infection, close household contact, military service, incarceration, contact sports, injection drug use, and men who have sex with men. CA-MRSA is now prevalent enough to warrant empiric coverage in many settings, especially in unresponsive or recurrent infections. Other causes include Pasteurella multocida from animal bites, Spirillum minus in rat-bite fever, and Wuchereria bancrofti in filariasis, particularly in immigrants from endemic regions. Chronic lymphangitis is usually due to fungal, mycobacterial, or parasitic infections, most commonly Sporothrix schenckii, acquired through gardening or farming injuries, and Mycobacterium marinum, associated with fish tanks and swimming pools.
Diagnosis signs and symptoms
Acute lymphangitis presents with warm, tender, erythematous streaks extending proximally from a primary site of infection toward regional lymph nodes. Associated findings include painful lymphadenopathy, peripheral edema of the involved extremity, and systemic symptoms such as fever, rigors, tachycardia, and headache. Chronic nodular lymphangitis typically presents with painless erythematous nodules, chancriform ulcers, or wart-like lesions at the inoculation site, with possible progression along lymphatic channels and minimal systemic symptoms.
Essential workup
Lymphangitis is primarily a clinical diagnosis based on history and physical examination, with attention directed toward identifying the source of infection.
Diagnosis tests and interpretation
Laboratory testing is often unnecessary, though leukocytosis may be present. Gram stain and culture of aspirate or biopsy from the most inflamed area are recommended in cases of treatment failure or when resistant organisms such as MRSA are suspected. Culture confirmation is essential when sporotrichosis or M. marinum infection is considered. Blood cultures may be positive in severe cases. Imaging is rarely required but plain radiographs may help identify abscesses, subcutaneous gas, or foreign bodies, and Doppler ultrasound may be useful to exclude deep venous thrombosis.
Differential diagnosis
The differential diagnosis includes superficial or deep thrombophlebitis, which typically lacks an initial infectious focus or regional lymphadenopathy, IV line infiltration, vaccine-related reactions, and phytophotodermatitis, which can cause linear inflammatory skin changes mimicking lymphangitis.
Treatment
Initial management focuses on stabilizing septic patients with airway support and resuscitation as needed. Antimicrobial therapy should be initiated promptly, with the first dose given in the emergency department. Treatment typically lasts 7–10 days and includes limb elevation, moist heat, and antibiotics guided by local resistance patterns. Empiric outpatient therapy often includes oral cephalexin plus trimethoprim–sulfamethoxazole to cover CA-MRSA, with alternatives such as clindamycin or doxycycline. Inpatient therapy may require IV nafcillin or equivalent agents. Animal bite–associated lymphangitis is treated with IV ampicillin–sulbactam. Chronic infections require organism-specific therapy, such as itraconazole or potassium iodide for sporotrichosis and combination antimycobacterial therapy for M. marinum.
Disposition and follow-up
Admission is indicated for toxic-appearing patients, those with immunosuppression, significant comorbidities, inability to tolerate oral therapy, or unreliable follow-up. Patients with mild disease who are clinically stable and able to take oral antibiotics may be discharged with close follow-up within 24–48 hours. Marking the borders of erythema before discharge helps assess treatment response.
Pearls and pitfalls
Empiric antibiotic therapy should include coverage for CA-MRSA in addition to streptococcal species. Failure to recognize resistant organisms or chronic infectious causes can lead to treatment failure and progression of disease.
Basics description
Lymphangitis is an infection of the lymphatic vessels that drain an area of inflammation or infection. Histologically, lymphatic channels become dilated and filled with lymphocytes and histiocytes. Inflammation often extends into surrounding perilymphatic tissues and may progress to cellulitis or abscess formation if untreated.
Etiology
Acute lymphangitis is most commonly caused by bacterial infection, particularly group A β-hemolytic Streptococcus. Less common causes include other streptococcal species and Staphylococcus aureus, including community-associated methicillin-resistant S. aureus (CA-MRSA). CA-MRSA risk factors include prior MRSA infection, close household contact, military service, incarceration, contact sports, injection drug use, and men who have sex with men. CA-MRSA is now prevalent enough to warrant empiric coverage in many settings, especially in unresponsive or recurrent infections. Other causes include Pasteurella multocida from animal bites, Spirillum minus in rat-bite fever, and Wuchereria bancrofti in filariasis, particularly in immigrants from endemic regions. Chronic lymphangitis is usually due to fungal, mycobacterial, or parasitic infections, most commonly Sporothrix schenckii, acquired through gardening or farming injuries, and Mycobacterium marinum, associated with fish tanks and swimming pools.
Diagnosis signs and symptoms
Acute lymphangitis presents with warm, tender, erythematous streaks extending proximally from a primary site of infection toward regional lymph nodes. Associated findings include painful lymphadenopathy, peripheral edema of the involved extremity, and systemic symptoms such as fever, rigors, tachycardia, and headache. Chronic nodular lymphangitis typically presents with painless erythematous nodules, chancriform ulcers, or wart-like lesions at the inoculation site, with possible progression along lymphatic channels and minimal systemic symptoms.
Essential workup
Lymphangitis is primarily a clinical diagnosis based on history and physical examination, with attention directed toward identifying the source of infection.
Diagnosis tests and interpretation
Laboratory testing is often unnecessary, though leukocytosis may be present. Gram stain and culture of aspirate or biopsy from the most inflamed area are recommended in cases of treatment failure or when resistant organisms such as MRSA are suspected. Culture confirmation is essential when sporotrichosis or M. marinum infection is considered. Blood cultures may be positive in severe cases. Imaging is rarely required but plain radiographs may help identify abscesses, subcutaneous gas, or foreign bodies, and Doppler ultrasound may be useful to exclude deep venous thrombosis.
Differential diagnosis
The differential diagnosis includes superficial or deep thrombophlebitis, which typically lacks an initial infectious focus or regional lymphadenopathy, IV line infiltration, vaccine-related reactions, and phytophotodermatitis, which can cause linear inflammatory skin changes mimicking lymphangitis.
Treatment
Initial management focuses on stabilizing septic patients with airway support and resuscitation as needed. Antimicrobial therapy should be initiated promptly, with the first dose given in the emergency department. Treatment typically lasts 7–10 days and includes limb elevation, moist heat, and antibiotics guided by local resistance patterns. Empiric outpatient therapy often includes oral cephalexin plus trimethoprim–sulfamethoxazole to cover CA-MRSA, with alternatives such as clindamycin or doxycycline. Inpatient therapy may require IV nafcillin or equivalent agents. Animal bite–associated lymphangitis is treated with IV ampicillin–sulbactam. Chronic infections require organism-specific therapy, such as itraconazole or potassium iodide for sporotrichosis and combination antimycobacterial therapy for M. marinum.
Disposition and follow-up
Admission is indicated for toxic-appearing patients, those with immunosuppression, significant comorbidities, inability to tolerate oral therapy, or unreliable follow-up. Patients with mild disease who are clinically stable and able to take oral antibiotics may be discharged with close follow-up within 24–48 hours. Marking the borders of erythema before discharge helps assess treatment response.
Pearls and pitfalls
Empiric antibiotic therapy should include coverage for CA-MRSA in addition to streptococcal species. Failure to recognize resistant organisms or chronic infectious causes can lead to treatment failure and progression of disease.
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Emergency and Acute Medicine – Malaria
Basics description
Malaria is a protozoan infection transmitted through the bite of an infected female Anopheles mosquito. The incubation period is typically 8–16 days, although symptoms may be delayed for months depending on the species. The periodic nature of malaria symptoms reflects the parasite life cycle, which includes an exoerythrocytic phase in the liver followed by an erythrocytic phase in red blood cells. Fever corresponds to synchronous red blood cell lysis and release of merozoites into the circulation.
Pathophysiology and species differences
In the exoerythrocytic phase, sporozoites migrate to the liver and multiply into merozoites. These then enter the bloodstream and invade red blood cells, where replication leads to cell rupture every 48–72 hours. Plasmodium falciparum causes most severe disease and nearly all malaria-related deaths. It infects red blood cells of all ages, leading to profound hemolysis, anemia, and capillary obstruction with resultant end-organ hypoxia. Plasmodium vivax and Plasmodium ovale may cause relapsing disease due to dormant liver forms (hypnozoites), while Plasmodium malariae can persist at low levels in the bloodstream for decades.
Etiology and transmission
Transmission usually occurs via mosquito bite but may also result from blood transfusions or shared needles. Rare autochthonous transmission has been reported in North America due to the presence of Anopheles mosquitoes. Post-traumatic immunosuppression may precipitate relapse in individuals previously exposed in endemic regions. Children with sickle cell trait have partial protection, while pregnant patients—especially primigravidas—are at higher risk for severe disease.
Diagnosis signs and symptoms
Most patients become symptomatic within one year of exposure. Common symptoms include malaise, chills, fever greater than 38°C, myalgias, arthralgias, and orthostatic hypotension. The classic malaria paroxysm consists of chills followed by high fever and subsequent diaphoresis, although this pattern is uncommon in clinical practice. Hemolysis may lead to jaundice, dark urine (blackwater fever), anemia, and splenomegaly. Severe manifestations include cerebral malaria with headache, altered mental status, seizures, or coma; pulmonary edema; renal failure; abnormal bleeding; and circulatory collapse.
Essential workup and diagnostic testing
Diagnosis relies on oil immersion light microscopy of thick and thin Giemsa-stained blood smears, which demonstrate intraerythrocytic parasites. At least three negative smears over 48 hours are required to exclude malaria. Laboratory findings commonly include anemia, thrombocytopenia, leukocytopenia, elevated bilirubin and lactate dehydrogenase, electrolyte abnormalities, and evidence of renal or hepatic dysfunction. Chest radiography may reveal pulmonary edema. Advanced testing such as antigen detection assays or PCR can identify Plasmodium species and mixed infections. Lumbar puncture may be necessary to distinguish cerebral malaria from meningitis.
Differential diagnosis
The differential includes meningitis, encephalitis, sepsis, acute renal failure, viral hepatitis, acute hemolytic anemia, hypoglycemic coma, and heat stroke. In travelers or immigrants from endemic areas, malaria must be considered in any febrile illness.
Treatment and emergency management
Initial stabilization includes airway, breathing, and circulation management, isotonic fluid resuscitation for hypotension, active cooling for hyperthermia, and treatment of hypoglycemia or seizures as indicated. Antimalarial therapy depends on species, severity, and geographic resistance patterns, with artemisinin-based combination therapies recommended as first-line treatment worldwide. Severe P. falciparum infection requires intravenous artesunate. Supportive care for complications such as anemia, renal failure, and cerebral edema is critical.
Disposition and follow-up
ICU admission is indicated for severe P. falciparum malaria, high parasitemia, neurologic involvement, or inability to tolerate oral therapy. Patients with non–P. falciparum malaria who are clinically stable and able to take oral medications may be treated as outpatients with close follow-up.
Pearls and pitfalls
Malaria should always be considered in patients with fever and compatible exposure history, even months after travel. Fever patterns are unreliable, and early recognition is essential, as delays in treatment—especially with P. falciparum—are associated with high mortality.
Basics description
Malaria is a protozoan infection transmitted through the bite of an infected female Anopheles mosquito. The incubation period is typically 8–16 days, although symptoms may be delayed for months depending on the species. The periodic nature of malaria symptoms reflects the parasite life cycle, which includes an exoerythrocytic phase in the liver followed by an erythrocytic phase in red blood cells. Fever corresponds to synchronous red blood cell lysis and release of merozoites into the circulation.
Pathophysiology and species differences
In the exoerythrocytic phase, sporozoites migrate to the liver and multiply into merozoites. These then enter the bloodstream and invade red blood cells, where replication leads to cell rupture every 48–72 hours. Plasmodium falciparum causes most severe disease and nearly all malaria-related deaths. It infects red blood cells of all ages, leading to profound hemolysis, anemia, and capillary obstruction with resultant end-organ hypoxia. Plasmodium vivax and Plasmodium ovale may cause relapsing disease due to dormant liver forms (hypnozoites), while Plasmodium malariae can persist at low levels in the bloodstream for decades.
Etiology and transmission
Transmission usually occurs via mosquito bite but may also result from blood transfusions or shared needles. Rare autochthonous transmission has been reported in North America due to the presence of Anopheles mosquitoes. Post-traumatic immunosuppression may precipitate relapse in individuals previously exposed in endemic regions. Children with sickle cell trait have partial protection, while pregnant patients—especially primigravidas—are at higher risk for severe disease.
Diagnosis signs and symptoms
Most patients become symptomatic within one year of exposure. Common symptoms include malaise, chills, fever greater than 38°C, myalgias, arthralgias, and orthostatic hypotension. The classic malaria paroxysm consists of chills followed by high fever and subsequent diaphoresis, although this pattern is uncommon in clinical practice. Hemolysis may lead to jaundice, dark urine (blackwater fever), anemia, and splenomegaly. Severe manifestations include cerebral malaria with headache, altered mental status, seizures, or coma; pulmonary edema; renal failure; abnormal bleeding; and circulatory collapse.
Essential workup and diagnostic testing
Diagnosis relies on oil immersion light microscopy of thick and thin Giemsa-stained blood smears, which demonstrate intraerythrocytic parasites. At least three negative smears over 48 hours are required to exclude malaria. Laboratory findings commonly include anemia, thrombocytopenia, leukocytopenia, elevated bilirubin and lactate dehydrogenase, electrolyte abnormalities, and evidence of renal or hepatic dysfunction. Chest radiography may reveal pulmonary edema. Advanced testing such as antigen detection assays or PCR can identify Plasmodium species and mixed infections. Lumbar puncture may be necessary to distinguish cerebral malaria from meningitis.
Differential diagnosis
The differential includes meningitis, encephalitis, sepsis, acute renal failure, viral hepatitis, acute hemolytic anemia, hypoglycemic coma, and heat stroke. In travelers or immigrants from endemic areas, malaria must be considered in any febrile illness.
Treatment and emergency management
Initial stabilization includes airway, breathing, and circulation management, isotonic fluid resuscitation for hypotension, active cooling for hyperthermia, and treatment of hypoglycemia or seizures as indicated. Antimalarial therapy depends on species, severity, and geographic resistance patterns, with artemisinin-based combination therapies recommended as first-line treatment worldwide. Severe P. falciparum infection requires intravenous artesunate. Supportive care for complications such as anemia, renal failure, and cerebral edema is critical.
Disposition and follow-up
ICU admission is indicated for severe P. falciparum malaria, high parasitemia, neurologic involvement, or inability to tolerate oral therapy. Patients with non–P. falciparum malaria who are clinically stable and able to take oral medications may be treated as outpatients with close follow-up.
Pearls and pitfalls
Malaria should always be considered in patients with fever and compatible exposure history, even months after travel. Fever patterns are unreliable, and early recognition is essential, as delays in treatment—especially with P. falciparum—are associated with high mortality.
