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Emergency and Acute Medicine – Periodontal Abscess
A periodontal abscess is a localized collection of pus within the supporting structures of the teeth, including the periodontal ligament and alveolar bone. It typically develops as a complication of progressive periodontal disease, where bone loss leads to the formation of periodontal pockets. Food particles and debris accumulate within these pockets. Coronal epithelial tissues may reattach to the tooth surface while bacteria and debris remain trapped, impairing drainage. This environment promotes secondary infection and abscess formation.
Although primarily localized, periodontal abscesses can lead to serious complications if untreated. These include osteomyelitis, dentocutaneous fistula, cavernous sinus thrombosis, Ludwig angina, maxillary sinusitis, mediastinitis, tooth loss, and sepsis. In children, periodontal abscesses are rare; periapical abscesses are more common and typically originate in the pulp, often associated with dental caries.
The infection is usually polymicrobial. Common pathogens include anaerobic gram-negative rods, Peptostreptococci, viridans group streptococci, and Neisseria species.
Diagnosis is clinical. Patients typically present with localized dental pain, facial swelling, malaise, and sometimes fever. On examination, there may be focal gingival swelling or fluctuance, tenderness to palpation, increased tooth mobility, and possible lymphadenopathy. A parulis—a pimple-like lesion on the gingiva—may be present in chronic abscesses, representing the end of a draining sinus tract. Pus may be expressed from the sinus tract. Heat sensitivity may occur. Trismus is generally absent unless infection has spread to the muscles of mastication.
Imaging and laboratory studies are not routinely required for diagnosis. However, panoramic, periapical, or occlusal radiographs may help confirm the diagnosis and determine the extent of disease. Bedside ultrasound can assist in identifying fluid collections. CT imaging may be indicated if there is concern for extension into adjacent structures. Anaerobic cultures may be considered in complicated cases or in immunocompromised patients. Electric pulp testing, performed by a dental specialist during follow-up, helps assess tooth viability.
The differential diagnosis includes periapical abscess, maxillary sinusitis, aphthous ulcers, oral herpes, salivary gland tumors, mumps, sialadenitis, localized adenopathy, facial cellulitis, acute otitis media, and peritonsillar abscess. In children, periapical abscess is more likely. For asymptomatic parulis, fibroma, pyogenic granuloma, peripheral ossifying granuloma, or Kaposi sarcoma should be considered.
Prehospital management rarely involves airway emergencies. However, if signs of airway compromise are present, airway equipment should be available, the patient transported upright, and supplemental oxygen provided. Initial stabilization in the emergency setting includes assessment of airway patency and securing the airway if there is respiratory distress, inability to manage secretions, or significant oropharyngeal swelling.
Emergency department management focuses on analgesia and drainage. NSAIDs or opioids may be used for pain control. Incision and drainage are performed under local anesthesia, typically using 2% lidocaine with epinephrine. A small stab incision is made toward the alveolar bone, followed by blunt dissection and irrigation with saline. If the cavity is large, a small iodoform gauze or Penrose drain may be placed for 24–48 hours and secured to prevent aspiration.
Antibiotics are indicated when the abscess is extensive or when systemic signs are present. Penicillin VK is considered first-line therapy. For penicillin-allergic patients, azithromycin, erythromycin, or clindamycin may be used. Clindamycin is also appropriate for patients who fail penicillin therapy. Ampicillin/sulbactam may be required for severe infections. Warm salt water rinses are recommended hourly while awake for 24–48 hours.
Admission is required for severe infections, complications such as cavernous sinus thrombosis or osteomyelitis, airway compromise, Ludwig angina, systemic toxicity, immunocompromised patients, treatment failure, or inability to manage the condition at home. Uncomplicated cases may be discharged with close dental follow-up within 24–48 hours.
Dental follow-up is essential for definitive care, including assessment of tooth viability, possible extraction, root canal therapy, and removal of drains. Without proper dental evaluation, symptoms may recur and long-term tooth preservation may be compromised. Maxillary sinusitis may be misdiagnosed if a thorough oral examination is not performed, underscoring the importance of careful assessment and timely referral.
A periodontal abscess is a localized collection of pus within the supporting structures of the teeth, including the periodontal ligament and alveolar bone. It typically develops as a complication of progressive periodontal disease, where bone loss leads to the formation of periodontal pockets. Food particles and debris accumulate within these pockets. Coronal epithelial tissues may reattach to the tooth surface while bacteria and debris remain trapped, impairing drainage. This environment promotes secondary infection and abscess formation.
Although primarily localized, periodontal abscesses can lead to serious complications if untreated. These include osteomyelitis, dentocutaneous fistula, cavernous sinus thrombosis, Ludwig angina, maxillary sinusitis, mediastinitis, tooth loss, and sepsis. In children, periodontal abscesses are rare; periapical abscesses are more common and typically originate in the pulp, often associated with dental caries.
The infection is usually polymicrobial. Common pathogens include anaerobic gram-negative rods, Peptostreptococci, viridans group streptococci, and Neisseria species.
Diagnosis is clinical. Patients typically present with localized dental pain, facial swelling, malaise, and sometimes fever. On examination, there may be focal gingival swelling or fluctuance, tenderness to palpation, increased tooth mobility, and possible lymphadenopathy. A parulis—a pimple-like lesion on the gingiva—may be present in chronic abscesses, representing the end of a draining sinus tract. Pus may be expressed from the sinus tract. Heat sensitivity may occur. Trismus is generally absent unless infection has spread to the muscles of mastication.
Imaging and laboratory studies are not routinely required for diagnosis. However, panoramic, periapical, or occlusal radiographs may help confirm the diagnosis and determine the extent of disease. Bedside ultrasound can assist in identifying fluid collections. CT imaging may be indicated if there is concern for extension into adjacent structures. Anaerobic cultures may be considered in complicated cases or in immunocompromised patients. Electric pulp testing, performed by a dental specialist during follow-up, helps assess tooth viability.
The differential diagnosis includes periapical abscess, maxillary sinusitis, aphthous ulcers, oral herpes, salivary gland tumors, mumps, sialadenitis, localized adenopathy, facial cellulitis, acute otitis media, and peritonsillar abscess. In children, periapical abscess is more likely. For asymptomatic parulis, fibroma, pyogenic granuloma, peripheral ossifying granuloma, or Kaposi sarcoma should be considered.
Prehospital management rarely involves airway emergencies. However, if signs of airway compromise are present, airway equipment should be available, the patient transported upright, and supplemental oxygen provided. Initial stabilization in the emergency setting includes assessment of airway patency and securing the airway if there is respiratory distress, inability to manage secretions, or significant oropharyngeal swelling.
Emergency department management focuses on analgesia and drainage. NSAIDs or opioids may be used for pain control. Incision and drainage are performed under local anesthesia, typically using 2% lidocaine with epinephrine. A small stab incision is made toward the alveolar bone, followed by blunt dissection and irrigation with saline. If the cavity is large, a small iodoform gauze or Penrose drain may be placed for 24–48 hours and secured to prevent aspiration.
Antibiotics are indicated when the abscess is extensive or when systemic signs are present. Penicillin VK is considered first-line therapy. For penicillin-allergic patients, azithromycin, erythromycin, or clindamycin may be used. Clindamycin is also appropriate for patients who fail penicillin therapy. Ampicillin/sulbactam may be required for severe infections. Warm salt water rinses are recommended hourly while awake for 24–48 hours.
Admission is required for severe infections, complications such as cavernous sinus thrombosis or osteomyelitis, airway compromise, Ludwig angina, systemic toxicity, immunocompromised patients, treatment failure, or inability to manage the condition at home. Uncomplicated cases may be discharged with close dental follow-up within 24–48 hours.
Dental follow-up is essential for definitive care, including assessment of tooth viability, possible extraction, root canal therapy, and removal of drains. Without proper dental evaluation, symptoms may recur and long-term tooth preservation may be compromised. Maxillary sinusitis may be misdiagnosed if a thorough oral examination is not performed, underscoring the importance of careful assessment and timely referral.
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KembaraXtra -Medicine- Emergency and Acute Medicine – Peripheral Neuropathy
Peripheral neuropathy is a broad term describing disorders of peripheral nerves that may involve motor, sensory, or autonomic fibers. Patients commonly present with muscle weakness, atrophy, pain, numbness, or a combination of these symptoms. The condition may be acute or chronic, symmetric or asymmetric, and distal or proximal in distribution.
Etiology varies widely and depends on the clinical presentation. Causes include metabolic disorders, endocrine disease, nutritional deficiencies, toxins, medications, autoimmune conditions, infections, hereditary disorders, trauma, and neoplastic processes. Diabetes mellitus is the most common cause of symmetric peripheral neuropathy. Acute demyelinating processes such as Guillain–Barré syndrome must be considered in rapidly progressive cases.
Sensory nerve dysfunction presents with numbness, tingling, paresthesias, dysesthesias, or burning pain. Large-fiber neuropathy leads to decreased vibration and position sense, whereas small-fiber neuropathy affects pain and temperature sensation. Deep tendon reflexes are often reduced due to impairment of the sensory afferent limb. Symptoms typically follow a stocking-glove distribution in symmetric polyneuropathy.
Motor nerve involvement causes weakness, usually distal greater than proximal. Fasciculations may occur, and chronic disease can lead to muscle atrophy and diminished tone. Reflexes may be reduced or absent due to impaired motor efferent conduction.
Autonomic dysfunction may manifest as orthostatic hypotension, constipation, urinary retention, erectile dysfunction, or other signs of impaired autonomic regulation.
History should focus on duration of symptoms, pattern of involvement (symmetric versus asymmetric), distribution (distal versus proximal), and whether symptoms are sensory, motor, or mixed. Medication exposure, toxin exposure, systemic disease, recent infections, and family history should be reviewed.
Physical examination requires a thorough neurologic assessment, including strength testing, reflex evaluation, and detailed sensory examination. Sensory loss in a stocking-glove pattern supports a length-dependent polyneuropathy. Early absence of reflexes, particularly in an acute presentation, should raise concern for demyelinating neuropathy such as Guillain–Barré syndrome, which can progress to respiratory failure.
Essential evaluation depends on acuity and severity. In acute or rapidly progressive weakness, early neurology consultation is critical. Laboratory studies may include a basic metabolic panel, complete blood count, liver function tests, urinalysis, thyroid-stimulating hormone, and targeted testing such as HIV or vitamin B12 levels based on clinical suspicion. Electrocardiogram and imaging such as chest radiograph or head CT may be obtained when indicated by associated symptoms.
Electromyography and nerve conduction studies are typically arranged by neurology to characterize axonal versus demyelinating patterns. Lumbar puncture may be required when Guillain–Barré syndrome is suspected.
Differential diagnosis depends on distribution. Focal neuropathies are often due to entrapment syndromes such as carpal tunnel, ulnar tunnel, tarsal tunnel, or peroneal nerve compression. Multifocal neuropathy (mononeuropathy multiplex) may result from diabetes, vasculitis, connective tissue disease, sarcoidosis, leprosy, malignancy, or HIV infection. Symmetric polyneuropathy commonly results from diabetes, hypothyroidism, nutritional deficiency, alcohol use, medication toxicity, critical illness, electrolyte disturbances, toxins, or Guillain–Barré syndrome. Myelopathy may mimic peripheral neuropathy and should be suspected in patients with back pain, saddle anesthesia, or lower extremity weakness.
Initial management in the emergency setting focuses on airway protection in severe cases, especially when Guillain–Barré syndrome is suspected. Monitoring for respiratory compromise is essential. Offending toxins or medications should be discontinued, and underlying systemic conditions should be treated.
Pain control may include opioids when necessary. Neuropathic pain can be managed with agents such as gabapentin, titrated gradually to effect. Carbamazepine may be used for specific neuropathic syndromes such as trigeminal neuralgia. Intravenous immunoglobulin is indicated for Guillain–Barré syndrome.
Admission is required for patients with respiratory distress, acute gait disturbance, rapidly progressive weakness, or intractable pain. Stable patients without respiratory compromise or significant functional impairment may be discharged with appropriate outpatient follow-up.
Failure to recognize Guillain–Barré syndrome is a critical pitfall, as delayed diagnosis can lead to respiratory failure and significant morbidity. Early identification and appropriate monitoring are essential in patients with acute, progressive peripheral neuropathy.
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Infectious Diseases and Microbiology: Postoperative Fever
Basics
Description
Postoperative fever is defined as a body temperature above 38°C (100.4°F) occurring after an invasive procedure. It is classified by timing: immediate (during surgery or within hours), acute (within the first postoperative week), subacute (1–4 weeks after surgery), and delayed (more than one month postoperatively). Most cases result from the inflammatory response to surgery and resolve spontaneously, but fever may signal a serious complication. Evaluation requires careful history, physical examination, and appropriate laboratory and imaging studies, including cultures and Gram stains when indicated. Early postoperative fever is frequently noninfectious; however, fever persisting beyond 96 hours is more likely infectious. Consider that patients may have been incubating community-acquired infection preoperatively. New or persistent fever beyond four days strongly suggests ongoing pathology or a new complication. Surgical wounds, catheter insertion sites, and all dressings must be inspected, and recent interventions such as blood transfusions reviewed.
Epidemiology
Drug fever is the most common noninfectious cause of postoperative fever, most often linked to antimicrobials and heparin. Pneumonia is a common cause after cardiac surgery and occurs in more than 5% of such patients. Sternal wound infections after cardiothoracic surgery occur in up to 5%, typically around postoperative day seven. Postoperative aspergillosis after cardiothoracic procedures carries very high mortality. Fever alone is a poor predictor of infection, with low sensitivity. Postsurgical mediastinitis has high mortality. In obstetrics and gynecology, bacterial vaginosis may increase postoperative infection risk.
General Prevention
Aggressive pulmonary hygiene, including incentive spirometry and mobilization, reduces pulmonary complications such as atelectasis.
Etiology
Common infectious causes include urinary tract infection, pneumonia, sinusitis, suppurative thrombophlebitis, catheter-related infections, and Clostridioides difficile–associated diarrhea. Noninfectious causes include deep venous thrombosis, pulmonary embolism, subarachnoid hemorrhage, gout, and fat embolism. Surgical site infections are uncommon within the first 1–3 days except for aggressive pathogens such as group A streptococci or clostridia, which can present early. Atelectasis is frequently blamed but likely coincidental rather than causal. Other serious causes include transplant rejection. Drug-induced fever is most often associated with beta-lactams, antiepileptics, and heparin. Inflammatory states such as acute myocardial infarction, pancreatitis, or acute respiratory distress syndrome may produce fever without infection. Endocrine emergencies such as adrenal insufficiency or thyrotoxicosis may also present with fever.
Diagnosis
Physical Examination
Drug fever lacks specific features and usually develops days after medication exposure; rash and eosinophilia are uncommon. Malignant hyperthermia typically occurs intraoperatively but may be delayed up to 24 hours and is associated with agents such as succinylcholine or volatile anesthetics. Neuroleptic malignant syndrome is associated with antipsychotics, particularly haloperidol. Withdrawal syndromes from alcohol, opioids, barbiturates, or benzodiazepines may cause fever hours to days after admission, and prior substance use history may not be readily available.
Diagnostic Tests and Interpretation
Laboratory Studies
Urinalysis and urine culture are recommended in patients with indwelling catheters longer than 72 hours. Procalcitonin has uncertain value in distinguishing bacterial causes of postoperative fever.
Imaging
Duplex ultrasonography with Doppler should be considered for new extremity swelling suggestive of deep venous thrombosis. Routine chest radiography is not required within the first 72 postoperative hours if fever is the only indication.
Diagnostic Procedures/Other
Wound swab cultures are rarely useful unless there is clear clinical evidence of infection. Suspected deep intraabdominal abscess may require imaging and, if inconclusive, surgical exploration.
Treatment
Medications
Antibiotics are generally not indicated for early postoperative fever without evidence of infection. Critically ill patients or those with hemodynamic instability should receive empiric broad-spectrum antibiotics after thorough evaluation, but therapy should be discontinued after 48 hours if no infectious source is identified. Atelectasis management includes coughing exercises, incentive spirometry, chest physiotherapy, beta-2 agonists, intermittent positive-pressure breathing, and nebulization. Empiric antifungal therapy is not recommended initially.
Ongoing Care and Follow-Up
Drug fever is diagnosed by exclusion when other causes are ruled out. Surgical wounds and invasive device sites must be repeatedly examined for signs of infection.
Complications
Postoperative infections increase morbidity and mortality, may lead to sepsis, impair wound healing, and cause respiratory failure and other serious outcomes.
Basics
Description
Postoperative fever is defined as a body temperature above 38°C (100.4°F) occurring after an invasive procedure. It is classified by timing: immediate (during surgery or within hours), acute (within the first postoperative week), subacute (1–4 weeks after surgery), and delayed (more than one month postoperatively). Most cases result from the inflammatory response to surgery and resolve spontaneously, but fever may signal a serious complication. Evaluation requires careful history, physical examination, and appropriate laboratory and imaging studies, including cultures and Gram stains when indicated. Early postoperative fever is frequently noninfectious; however, fever persisting beyond 96 hours is more likely infectious. Consider that patients may have been incubating community-acquired infection preoperatively. New or persistent fever beyond four days strongly suggests ongoing pathology or a new complication. Surgical wounds, catheter insertion sites, and all dressings must be inspected, and recent interventions such as blood transfusions reviewed.
Epidemiology
Drug fever is the most common noninfectious cause of postoperative fever, most often linked to antimicrobials and heparin. Pneumonia is a common cause after cardiac surgery and occurs in more than 5% of such patients. Sternal wound infections after cardiothoracic surgery occur in up to 5%, typically around postoperative day seven. Postoperative aspergillosis after cardiothoracic procedures carries very high mortality. Fever alone is a poor predictor of infection, with low sensitivity. Postsurgical mediastinitis has high mortality. In obstetrics and gynecology, bacterial vaginosis may increase postoperative infection risk.
General Prevention
Aggressive pulmonary hygiene, including incentive spirometry and mobilization, reduces pulmonary complications such as atelectasis.
Etiology
Common infectious causes include urinary tract infection, pneumonia, sinusitis, suppurative thrombophlebitis, catheter-related infections, and Clostridioides difficile–associated diarrhea. Noninfectious causes include deep venous thrombosis, pulmonary embolism, subarachnoid hemorrhage, gout, and fat embolism. Surgical site infections are uncommon within the first 1–3 days except for aggressive pathogens such as group A streptococci or clostridia, which can present early. Atelectasis is frequently blamed but likely coincidental rather than causal. Other serious causes include transplant rejection. Drug-induced fever is most often associated with beta-lactams, antiepileptics, and heparin. Inflammatory states such as acute myocardial infarction, pancreatitis, or acute respiratory distress syndrome may produce fever without infection. Endocrine emergencies such as adrenal insufficiency or thyrotoxicosis may also present with fever.
Diagnosis
Physical Examination
Drug fever lacks specific features and usually develops days after medication exposure; rash and eosinophilia are uncommon. Malignant hyperthermia typically occurs intraoperatively but may be delayed up to 24 hours and is associated with agents such as succinylcholine or volatile anesthetics. Neuroleptic malignant syndrome is associated with antipsychotics, particularly haloperidol. Withdrawal syndromes from alcohol, opioids, barbiturates, or benzodiazepines may cause fever hours to days after admission, and prior substance use history may not be readily available.
Diagnostic Tests and Interpretation
Laboratory Studies
Urinalysis and urine culture are recommended in patients with indwelling catheters longer than 72 hours. Procalcitonin has uncertain value in distinguishing bacterial causes of postoperative fever.
Imaging
Duplex ultrasonography with Doppler should be considered for new extremity swelling suggestive of deep venous thrombosis. Routine chest radiography is not required within the first 72 postoperative hours if fever is the only indication.
Diagnostic Procedures/Other
Wound swab cultures are rarely useful unless there is clear clinical evidence of infection. Suspected deep intraabdominal abscess may require imaging and, if inconclusive, surgical exploration.
Treatment
Medications
Antibiotics are generally not indicated for early postoperative fever without evidence of infection. Critically ill patients or those with hemodynamic instability should receive empiric broad-spectrum antibiotics after thorough evaluation, but therapy should be discontinued after 48 hours if no infectious source is identified. Atelectasis management includes coughing exercises, incentive spirometry, chest physiotherapy, beta-2 agonists, intermittent positive-pressure breathing, and nebulization. Empiric antifungal therapy is not recommended initially.
Ongoing Care and Follow-Up
Drug fever is diagnosed by exclusion when other causes are ruled out. Surgical wounds and invasive device sites must be repeatedly examined for signs of infection.
Complications
Postoperative infections increase morbidity and mortality, may lead to sepsis, impair wound healing, and cause respiratory failure and other serious outcomes.
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KembaraXtra – Emergency & Acute Medicine – Peripheral Vascular Disease
Peripheral vascular disease (PVD), also known as peripheral artery disease (PAD), refers to obstruction of one or more peripheral arteries due to atherosclerosis, thrombosis, or embolism. Many patients also have coexisting coronary artery disease and cerebrovascular disease. Major risk factors include age, smoking, diabetes mellitus, hyperlipidemia, and hypertension. PVD is associated with significant morbidity and mortality related to systemic atherosclerosis. Complications include aneurysm formation, thrombosis, ulceration, limb loss, and progression to critical limb ischemia.
Chronic arterial insufficiency (CAI) results from progressive atherosclerotic narrowing that produces subacute ischemia and claudication. About 10% of patients progress to critical limb ischemia. Acute arterial insufficiency (AAI) is caused by arterial thrombosis (approximately 50%) or embolism and produces acute limb ischemia characterized by the “6 Ps.” Atheroembolism occurs when rupture or disruption of an atherosclerotic plaque in the aorta, iliac, or femoral arteries releases cholesterol emboli that obstruct small vessels. It is often precipitated by invasive arterial procedures such as cardiac catheterization.
Etiologies include atherosclerotic plaque obstruction, arterial thrombosis, cardiac emboli (commonly from atrial fibrillation, valvular disease, or cardiomyopathy), aneurysm, infection, tumor, vasculitis, foreign body, thrombosis superimposed on chronic disease, and atheroembolism.
Patients with CAI typically report claudication—aching calf pain in femoropopliteal disease or buttock and thigh pain in aortoiliac disease—brought on by exertion and relieved with rest or dependent positioning. Severe disease presents with rest pain, usually beginning in the foot, or rapidly progressive claudication and ulceration. Acute arterial insufficiency presents with sudden extremity pain that increases in severity, often beginning distally and progressing proximally. Pain may decrease once sensory loss occurs. Atheroembolism presents with cold, painful digits and may involve multiple organs including kidneys, mesentery, and skin, especially following recent vascular procedures.
On examination, sudden onset of pain and pallor in an extremity is limb- and life-threatening. In CAI, findings include diminished or absent peripheral pulses, delayed capillary refill, cool skin, prolonged venous filling time, bruits, pallor with elevation and dependent rubor, muscle and skin atrophy, thickened nails, hair loss, and toe or heel ulcerations. Acute arterial insufficiency presents with the 6 Ps: pain, pallor, pulselessness, poikilothermia, paresthesias, and paralysis. Identifying a potential embolic source such as atrial fibrillation is essential. Atheroembolism may show painful ischemic digits, “blue toe syndrome,” and livedo reticularis.
The ankle–brachial index (ABI) is an important bedside test in chronic disease. An ABI <0.9 is abnormal and <0.4-0.5 indicates severe disease. in patients with diabetes, calcified vessels may produce falsely elevated values (>1.3). Acute arterial insufficiency is primarily a clinical diagnosis based on the 6 Ps. Patients with acute-on-chronic disease may tolerate ischemia better due to collateral circulation. Atheroembolism is diagnosed clinically, with further evaluation to identify the embolic source.
Laboratory evaluation includes CBC, platelets, electrolytes, renal function, glucose, coagulation studies, and creatine phosphokinase to assess muscle ischemia. Additional studies may include inflammatory markers for vasculitis, blood cultures for suspected endocarditis, and hypercoagulable testing when indicated.
Doppler ultrasound is commonly used to identify the level of arterial occlusion and detect thrombosis or aneurysm. CT angiography is widely used as a first-line diagnostic tool and guides decisions for operative or endovascular intervention. Angiography allows simultaneous diagnosis and treatment with angioplasty, atherectomy, or thrombolysis. MRI is sensitive but less practical in emergency settings.
Differential diagnoses include acute thrombosis or embolism, arterial dissection, deep venous thrombosis, venous insufficiency, compartment syndrome, Buerger disease, spinal stenosis, neuropathy, bursitis, arthritis, and reflex sympathetic dystrophy.
Prehospital care includes maintaining hemodynamic stability, placing the limb at rest in a dependent position, providing oxygen when needed, and cardiac monitoring. In the emergency department, management includes IV fluids for hypotension, cardiac monitoring, supplemental oxygen, adequate analgesia, and avoidance of temperature extremes.
Management of chronic arterial insufficiency includes antiplatelet therapy with aspirin (75–325 mg daily) or clopidogrel (75 mg daily). Cilostazol, pentoxifylline, or dipyridamole may be used in selected patients. Risk-factor modification is essential and includes smoking cessation, lipid and blood pressure control, diabetes management, and structured exercise therapy. Revascularization options include balloon angioplasty, atherectomy, or bypass grafting depending on anatomy and severity.
Acute arterial insufficiency requires immediate IV heparin (80 U/kg bolus followed by infusion at 18 U/kg/hr), unless aortic dissection or aneurysm is suspected. Emergent consultation with vascular surgery or interventional radiology is mandatory. Revascularization must occur within 4–6 hours of symptom onset to prevent irreversible ischemia. Treatment options include thrombectomy, embolectomy, angioplasty, thrombolysis, or bypass grafting. Complications include compartment syndrome, irreversible limb ischemia requiring amputation, rhabdomyolysis, renal failure, and electrolyte disturbances.
Atheroembolism is managed conservatively when tissue involvement is limited and renal function preserved. Treatment is supportive with wound care and analgesia. Vascular surgery referral within 12–24 hours is recommended, and evaluation to prevent further embolic events is essential. Amputation may be required for irreversibly necrotic tissue.
All patients with acute arterial insufficiency require hospital admission for evaluation and revascularization. Patients with chronic disease should be admitted if they develop rapidly progressive claudication or ischemic rest pain. Atheroembolism warrants admission if there is significant tissue involvement, infection, pain, or renal compromise. Stable patients with mild chronic disease or limited atheroembolism may be discharged with close follow-up.
Early recognition of acute limb ischemia is critical, as time to reperfusion determines limb salvage and survival.
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Emergency And Acute Medicine – Pertussis
Pertussis is an acute respiratory tract infection transmitted by small respiratory droplets. The organism attaches to respiratory epithelial cells via fimbriae and produces toxins that cause ciliary dysfunction, accumulation of debris, increased mucus production, and inflammatory infiltration. Bronchiolar congestion, obstruction, and necrosis may develop. Airway obstruction from mucus plugging can lead to hypoxia, hypoventilation, and increased intrathoracic or intracranial pressure. Secondary bacterial pneumonia may worsen respiratory failure. Central nervous system injury may result from encephalitis, hypoxia, or elevated intracranial pressure. Uncomplicated illness typically lasts 6–10 weeks, although about half resolve in under 6 weeks. Mortality is highest in infants under 1 year, especially those younger than 1 month. Most deaths are due to secondary bacterial pneumonia. The incubation period is usually 7–10 days. Disease is most common in young children, but incidence is increasing among adolescents. Adults serve as the primary reservoir. Peak incidence occurs in late summer and fall. Vaccination with Tdap provides prevention. The causative organism is Bordetella pertussis, a fastidious gram-negative pleomorphic bacillus.
The illness classically progresses through three phases, although infants may not follow distinct stages. The catarrhal stage lasts 1–2 weeks and resembles a mild upper respiratory infection with rhinorrhea, low-grade fever, malaise, sore throat, lacrimation, and mild cough. The paroxysmal stage lasts 1–6 weeks and is characterized by severe coughing spells that end with a sudden inspiratory “whoop.” Paroxysms may be associated with cyanosis, apnea (especially in infants under 6 months), post-tussive emesis, and altered mental status due to hypoxia. The convalescent stage lasts 2–12 weeks with gradual improvement and decreasing frequency of cough. Adults and partially immunized children often have milder or atypical presentations, sometimes limited to persistent cough without a classic whoop.
Diagnosis in the emergency setting is primarily clinical, especially when a characteristic paroxysmal cough is observed or there is a known exposure. Laboratory confirmation may support the diagnosis. PCR testing from a posterior nasopharyngeal swab or aspirate has high sensitivity and specificity but may produce false positives and false negatives depending on timing and prior antibiotic use. Culture on Bordet–Gengou medium remains the gold standard due to high specificity but has low sensitivity and requires 7–12 days for results. Serology is useful later in the course. Leukocytosis with marked lymphocytosis is common and correlates with disease severity. Chest radiographs are often normal but may show perihilar infiltrates, atelectasis, or secondary pneumonia.
Differential diagnoses include other causes of prolonged or paroxysmal cough such as infections with Bordetella parapertussis, Chlamydia species, adenovirus, pneumonia, bronchiolitis, influenza, reactive airway disease, foreign body aspiration, and cystic fibrosis.
Initial management focuses on airway and respiratory support. Oxygen supplementation and suctioning of mucus plugs are important, particularly in infants. Droplet precautions are required for 5 days after initiation of effective antimicrobial therapy. Adequate hydration must be maintained. Continuous monitoring is recommended during severe paroxysms, especially in infants. Antibiotics are most effective during the catarrhal phase but are still indicated during the paroxysmal phase to reduce transmission. Azithromycin is the first-line agent. Alternatives include clarithromycin, erythromycin, or trimethoprim–sulfamethoxazole, although erythromycin carries a risk of pyloric stenosis in neonates. Bronchodilators and corticosteroids are generally not recommended. Tdap vaccination should be offered when appropriate, including during each pregnancy between 27 and 36 weeks gestation to protect newborns.
Admission is indicated for patients under 1 year of age, those with apnea, cyanosis, pneumonia, encephalitis, or significant respiratory distress. Children without respiratory compromise may be discharged with close follow-up, hydration guidance, and avoidance of cough triggers such as smoke and pollutants. Postexposure prophylaxis with antibiotics is recommended for all close contacts regardless of age or immunization status. Patients may return to school or work after 5 days of appropriate antibiotic therapy.
Complications include epistaxis, subconjunctival hemorrhage, pneumonia, pneumothorax, subcutaneous or mediastinal emphysema, bronchiectasis, hernias, rectal prolapse, seizures, encephalitis, intracranial hemorrhage, and spinal epidural hemorrhage. Infants require particular vigilance due to high risk of apnea and severe respiratory compromise. Cases must be reported to public health authorities, and strict droplet precautions are essential to prevent spread.
Pertussis is an acute respiratory tract infection transmitted by small respiratory droplets. The organism attaches to respiratory epithelial cells via fimbriae and produces toxins that cause ciliary dysfunction, accumulation of debris, increased mucus production, and inflammatory infiltration. Bronchiolar congestion, obstruction, and necrosis may develop. Airway obstruction from mucus plugging can lead to hypoxia, hypoventilation, and increased intrathoracic or intracranial pressure. Secondary bacterial pneumonia may worsen respiratory failure. Central nervous system injury may result from encephalitis, hypoxia, or elevated intracranial pressure. Uncomplicated illness typically lasts 6–10 weeks, although about half resolve in under 6 weeks. Mortality is highest in infants under 1 year, especially those younger than 1 month. Most deaths are due to secondary bacterial pneumonia. The incubation period is usually 7–10 days. Disease is most common in young children, but incidence is increasing among adolescents. Adults serve as the primary reservoir. Peak incidence occurs in late summer and fall. Vaccination with Tdap provides prevention. The causative organism is Bordetella pertussis, a fastidious gram-negative pleomorphic bacillus.
The illness classically progresses through three phases, although infants may not follow distinct stages. The catarrhal stage lasts 1–2 weeks and resembles a mild upper respiratory infection with rhinorrhea, low-grade fever, malaise, sore throat, lacrimation, and mild cough. The paroxysmal stage lasts 1–6 weeks and is characterized by severe coughing spells that end with a sudden inspiratory “whoop.” Paroxysms may be associated with cyanosis, apnea (especially in infants under 6 months), post-tussive emesis, and altered mental status due to hypoxia. The convalescent stage lasts 2–12 weeks with gradual improvement and decreasing frequency of cough. Adults and partially immunized children often have milder or atypical presentations, sometimes limited to persistent cough without a classic whoop.
Diagnosis in the emergency setting is primarily clinical, especially when a characteristic paroxysmal cough is observed or there is a known exposure. Laboratory confirmation may support the diagnosis. PCR testing from a posterior nasopharyngeal swab or aspirate has high sensitivity and specificity but may produce false positives and false negatives depending on timing and prior antibiotic use. Culture on Bordet–Gengou medium remains the gold standard due to high specificity but has low sensitivity and requires 7–12 days for results. Serology is useful later in the course. Leukocytosis with marked lymphocytosis is common and correlates with disease severity. Chest radiographs are often normal but may show perihilar infiltrates, atelectasis, or secondary pneumonia.
Differential diagnoses include other causes of prolonged or paroxysmal cough such as infections with Bordetella parapertussis, Chlamydia species, adenovirus, pneumonia, bronchiolitis, influenza, reactive airway disease, foreign body aspiration, and cystic fibrosis.
Initial management focuses on airway and respiratory support. Oxygen supplementation and suctioning of mucus plugs are important, particularly in infants. Droplet precautions are required for 5 days after initiation of effective antimicrobial therapy. Adequate hydration must be maintained. Continuous monitoring is recommended during severe paroxysms, especially in infants. Antibiotics are most effective during the catarrhal phase but are still indicated during the paroxysmal phase to reduce transmission. Azithromycin is the first-line agent. Alternatives include clarithromycin, erythromycin, or trimethoprim–sulfamethoxazole, although erythromycin carries a risk of pyloric stenosis in neonates. Bronchodilators and corticosteroids are generally not recommended. Tdap vaccination should be offered when appropriate, including during each pregnancy between 27 and 36 weeks gestation to protect newborns.
Admission is indicated for patients under 1 year of age, those with apnea, cyanosis, pneumonia, encephalitis, or significant respiratory distress. Children without respiratory compromise may be discharged with close follow-up, hydration guidance, and avoidance of cough triggers such as smoke and pollutants. Postexposure prophylaxis with antibiotics is recommended for all close contacts regardless of age or immunization status. Patients may return to school or work after 5 days of appropriate antibiotic therapy.
Complications include epistaxis, subconjunctival hemorrhage, pneumonia, pneumothorax, subcutaneous or mediastinal emphysema, bronchiectasis, hernias, rectal prolapse, seizures, encephalitis, intracranial hemorrhage, and spinal epidural hemorrhage. Infants require particular vigilance due to high risk of apnea and severe respiratory compromise. Cases must be reported to public health authorities, and strict droplet precautions are essential to prevent spread.
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KembaraXtra – Emergency & Acute Medicine – Perirectal Abscess
Perirectal abscess is a localized infection with accumulation of purulent material adjacent to the anus or rectum. It most commonly results from infection of the anal crypt glands with spread into adjacent potential spaces separated by muscle and fascia. Perianal abscesses are the most common and typically present with a visible, tender red bulge near the anus. Ischiorectal abscesses occur in a large potential space and may grow significantly before diagnosis; they can communicate posteriorly to form a horseshoe abscess. Intersphincteric abscesses remain confined between the internal and external sphincters. Supralevator abscesses are deep, located above the levator ani, often present with systemic symptoms, and usually require operative drainage under general anesthesia. Infections are typically polymicrobial with mixed enteric organisms. Associated conditions include diabetes, inflammatory bowel disease, malignancy, and immunocompromised states.
Patients commonly present with constant perianal, rectal, or pelvic pain. Pain is often worsened by defecation, sitting, or coughing. Deeper abscesses such as ischiorectal or supralevator may produce dull pelvic or rectal pain and may be less painful if located above the dentate line. Fever, chills, constipation, and drainage may occur. On examination, findings include perianal swelling, erythema, induration, fluctuance, and marked tenderness. An abscess in the inner buttock cleft is a red flag, as rectal abscesses can track outward. Digital rectal examination is essential and may reveal rectal wall swelling or focal tenderness. A fistulous tract may be palpable as a cord-like structure or identified with gentle probing.
Diagnosis is primarily clinical and based on careful history and thorough rectal examination. A high index of suspicion is required in patients with persistent perirectal pain. Routine laboratory testing and imaging are not required for simple perianal abscesses. Leukocytosis with left shift may be present. Blood cultures are reserved for patients with signs of sepsis. CT scan with IV contrast or MRI is helpful when a deeper abscess is suspected or when the diagnosis is unclear. MRI is particularly useful for identifying fistulous tracts. Endoanal ultrasound may also assist in selected cases.
The differential diagnosis includes anal fissure, thrombosed or inflamed hemorrhoids, sentinel pile, anal ulcer, proctitis, and anorectal carcinoma.
Prompt incision and drainage are the definitive treatments. Delay in drainage may worsen outcomes. Bedside drainage is appropriate only for localized perianal abscesses. A radial incision should be made close to the anal verge, the cavity explored to break loculations, and copious irrigation performed. Loose packing may be placed and removed after 48 hours. Operative drainage under general anesthesia is indicated for deeper abscesses or when adequate drainage cannot be achieved with local anesthesia.
Antibiotics are not routinely required after adequate drainage but are indicated in patients with extensive cellulitis, systemic infection, immunosuppression, valvular heart disease, prosthetic devices, or diabetes. Oral options include amoxicillin-clavulanate or a fluoroquinolone with consideration for MRSA coverage when indicated. Intravenous regimens may include cefoxitin, ampicillin-sulbactam, or combination therapy with ampicillin, gentamicin, and either clindamycin or metronidazole.
Postprocedural care includes sitz baths three times daily beginning 24 hours after drainage, high-fiber diet or bulking agents, and adequate analgesia.
Patients requiring operative drainage or those with systemic toxicity or sepsis should be admitted. Patients with adequate bedside drainage and no systemic illness may be discharged with close follow-up. All patients should be referred to a surgeon within 24–48 hours to evaluate for fistula formation, which occurs in approximately 25–50% of anorectal abscesses.
Careful assessment of the extent of infection is critical. Thorough rectal examination and probing are mandatory, and imaging should be obtained when deeper extension is suspected. Deep abscesses above the dentate line may present with minimal pain and isolated fever, increasing the risk of delayed diagnosis.
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Emergency and Acute Medicine – Peritonsillar Abscess
Peritonsillar abscess is a suppurative complication of tonsillitis in which infection spreads beyond the tonsillar capsule into the space between the palatine tonsil and the pharyngeal muscles. It is the most common deep infection of the head and neck, with an incidence of approximately 30 per 100,000 people per year and about 45,000 cases annually in the United States. It occurs at any age but is most common in young adults between 20 and 40 years. Incidence peaks during November to December and April to May, corresponding with higher rates of streptococcal pharyngitis. Although uncommon, complications can include airway compromise, sepsis, recurrence in 12–15% of patients, spread to the lateral neck or mediastinum, spontaneous rupture with aspiration pneumonitis, internal jugular vein thrombosis (Lemierre syndrome), poststreptococcal glomerulonephritis or rheumatic fever, carotid sheath erosion with hemorrhage, severe dehydration, and intracranial extension such as meningitis, cavernous sinus thrombosis, cerebral abscess, or dural sinus thrombosis.
Two primary mechanisms are proposed for its development. One theory involves direct bacterial invasion into deeper tissues during acute pharyngitis. The other suggests obstruction and infection of the Weber glands located in the superior tonsillar pole. Smoking may increase risk. Infection is typically polymicrobial. Common pathogens include Group A Streptococcus, Staphylococcus species including MRSA, and anaerobes such as Prevotella, Peptostreptococcus, and Fusobacterium.
Patients commonly present with unilateral sore throat, fever, voice change, odynophagia, drooling, headache, referred ear pain, decreased oral intake, and malaise. Physical examination often reveals fever, trismus, a muffled “hot potato” voice, erythematous tonsils and soft palate, medial and inferior displacement of the superior pole of the affected tonsil, uvular deviation away from the affected side, halitosis, cervical lymphadenitis, and tenderness along the ipsilateral angle of the jaw. Airway assessment is critical, with attention to stridor, tripod positioning, or inability to handle secretions. Clinicians must also consider possible extension into deeper neck spaces when systemic toxicity or atypical findings are present.
Diagnosis is usually clinical based on careful oropharyngeal examination, although severe trismus may limit visualization. Throat culture and monospot testing may be considered, as infectious mononucleosis is present in up to 20% of cases. A complete blood count and abscess culture may be useful in selected patients. A basic metabolic panel may help assess dehydration. Bedside intraoral ultrasound can assist in identifying and localizing the abscess, particularly in cooperative patients, while transcutaneous ultrasound may be useful if trismus prevents intraoral imaging. CT of the neck with contrast is indicated when deep neck infection is suspected, after failed needle aspiration, or when examination is limited. MRI may help detect complications such as internal jugular vein thrombosis or carotid sheath involvement. Needle aspiration is both diagnostic and frequently therapeutic, and incision and drainage is also effective.
Management begins with airway evaluation and stabilization, IV access, cardiac and pulse oximetry monitoring, and supplemental oxygen as needed. Children account for 25–30% of cases and may require sedation or general anesthesia for drainage procedures. In young children with signs of upper airway obstruction, a lateral neck radiograph may be obtained before oral examination. Antibiotics should be started promptly, along with IV fluids for dehydration and appropriate analgesia. A single dose of corticosteroid such as dexamethasone may improve symptoms. Adequate local anesthesia using benzocaine spray and lidocaine with epinephrine is essential before drainage. Needle aspiration has a success rate of 87–94% and should be performed by clinicians experienced in airway management. The internal carotid artery lies approximately 2.5 cm posterolateral to the tonsil, so limiting needle depth to less than 0.5 cm is recommended. The superior pole is the most common site of maximal fluctuance. Incision and drainage has a success rate of 90–92% and should be performed using a guarded blade with no more than 1 cm exposed, avoiding incisions deeper than 0.5 cm. Packing is generally not required. Tonsillectomy may be indicated in cases of airway obstruction, recurrent severe pharyngitis, recurrent abscess, or failure of drainage.
Antibiotic therapy should continue for 14 days, as shorter courses may increase recurrence risk. Intravenous options include ampicillin/sulbactam or penicillin G combined with metronidazole. Clindamycin is appropriate for penicillin-allergic patients. Oral regimens include amoxicillin/clavulanate, penicillin VK with metronidazole, or clindamycin. A single dose of dexamethasone 10 mg (0.6 mg/kg in children, maximum 10 mg) may be administered.
Admission is indicated for airway compromise, sepsis, altered mental status, significant dehydration, or extension beyond the peritonsillar space. Most patients can be discharged after successful drainage if they tolerate oral intake and medications. Referral to otolaryngology is recommended, and interval tonsillectomy is often considered 6–8 weeks after resolution. Close follow-up within 24–48 hours is essential because treatment failure and recurrence are relatively common.
Peritonsillar abscess is a suppurative complication of tonsillitis in which infection spreads beyond the tonsillar capsule into the space between the palatine tonsil and the pharyngeal muscles. It is the most common deep infection of the head and neck, with an incidence of approximately 30 per 100,000 people per year and about 45,000 cases annually in the United States. It occurs at any age but is most common in young adults between 20 and 40 years. Incidence peaks during November to December and April to May, corresponding with higher rates of streptococcal pharyngitis. Although uncommon, complications can include airway compromise, sepsis, recurrence in 12–15% of patients, spread to the lateral neck or mediastinum, spontaneous rupture with aspiration pneumonitis, internal jugular vein thrombosis (Lemierre syndrome), poststreptococcal glomerulonephritis or rheumatic fever, carotid sheath erosion with hemorrhage, severe dehydration, and intracranial extension such as meningitis, cavernous sinus thrombosis, cerebral abscess, or dural sinus thrombosis.
Two primary mechanisms are proposed for its development. One theory involves direct bacterial invasion into deeper tissues during acute pharyngitis. The other suggests obstruction and infection of the Weber glands located in the superior tonsillar pole. Smoking may increase risk. Infection is typically polymicrobial. Common pathogens include Group A Streptococcus, Staphylococcus species including MRSA, and anaerobes such as Prevotella, Peptostreptococcus, and Fusobacterium.
Patients commonly present with unilateral sore throat, fever, voice change, odynophagia, drooling, headache, referred ear pain, decreased oral intake, and malaise. Physical examination often reveals fever, trismus, a muffled “hot potato” voice, erythematous tonsils and soft palate, medial and inferior displacement of the superior pole of the affected tonsil, uvular deviation away from the affected side, halitosis, cervical lymphadenitis, and tenderness along the ipsilateral angle of the jaw. Airway assessment is critical, with attention to stridor, tripod positioning, or inability to handle secretions. Clinicians must also consider possible extension into deeper neck spaces when systemic toxicity or atypical findings are present.
Diagnosis is usually clinical based on careful oropharyngeal examination, although severe trismus may limit visualization. Throat culture and monospot testing may be considered, as infectious mononucleosis is present in up to 20% of cases. A complete blood count and abscess culture may be useful in selected patients. A basic metabolic panel may help assess dehydration. Bedside intraoral ultrasound can assist in identifying and localizing the abscess, particularly in cooperative patients, while transcutaneous ultrasound may be useful if trismus prevents intraoral imaging. CT of the neck with contrast is indicated when deep neck infection is suspected, after failed needle aspiration, or when examination is limited. MRI may help detect complications such as internal jugular vein thrombosis or carotid sheath involvement. Needle aspiration is both diagnostic and frequently therapeutic, and incision and drainage is also effective.
Management begins with airway evaluation and stabilization, IV access, cardiac and pulse oximetry monitoring, and supplemental oxygen as needed. Children account for 25–30% of cases and may require sedation or general anesthesia for drainage procedures. In young children with signs of upper airway obstruction, a lateral neck radiograph may be obtained before oral examination. Antibiotics should be started promptly, along with IV fluids for dehydration and appropriate analgesia. A single dose of corticosteroid such as dexamethasone may improve symptoms. Adequate local anesthesia using benzocaine spray and lidocaine with epinephrine is essential before drainage. Needle aspiration has a success rate of 87–94% and should be performed by clinicians experienced in airway management. The internal carotid artery lies approximately 2.5 cm posterolateral to the tonsil, so limiting needle depth to less than 0.5 cm is recommended. The superior pole is the most common site of maximal fluctuance. Incision and drainage has a success rate of 90–92% and should be performed using a guarded blade with no more than 1 cm exposed, avoiding incisions deeper than 0.5 cm. Packing is generally not required. Tonsillectomy may be indicated in cases of airway obstruction, recurrent severe pharyngitis, recurrent abscess, or failure of drainage.
Antibiotic therapy should continue for 14 days, as shorter courses may increase recurrence risk. Intravenous options include ampicillin/sulbactam or penicillin G combined with metronidazole. Clindamycin is appropriate for penicillin-allergic patients. Oral regimens include amoxicillin/clavulanate, penicillin VK with metronidazole, or clindamycin. A single dose of dexamethasone 10 mg (0.6 mg/kg in children, maximum 10 mg) may be administered.
Admission is indicated for airway compromise, sepsis, altered mental status, significant dehydration, or extension beyond the peritonsillar space. Most patients can be discharged after successful drainage if they tolerate oral intake and medications. Referral to otolaryngology is recommended, and interval tonsillectomy is often considered 6–8 weeks after resolution. Close follow-up within 24–48 hours is essential because treatment failure and recurrence are relatively common.
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Infectious Diseases and Microbiology: Sore Throat
Basics
Description
Sore throat refers to painful inflammation of the pharynx, typically worse with swallowing. Common infectious causes are covered elsewhere; the emphasis here is recognizing distinguishing clinical features and considering noninfectious etiologies.
Approach to the Patient
First assess for airway compromise and decide whether the illness is localized or part of a systemic process, most often viral. Clarify symptom type and duration and ask about hoarseness and fever. History should include sick contacts, oral–genital sexual exposure, recent weight loss, and other features suggesting noninfectious causes such as neoplasms. Findings that strongly support streptococcal pharyngitis include fever, marked tonsillar exudate and enlargement, tender anterior cervical nodes, myalgias, and supportive epidemiology such as age, season, and community colonization prevalence. Conjunctivitis points toward viral illness. When clinical and epidemiologic clues suggest gonococcal pharyngitis or diphtheria, use specific microbiologic techniques and begin appropriate therapy promptly. Differentiate laryngitis, croup, and other hoarseness syndromes from epiglottitis. The main practical distinction is group A streptococcal versus nonstreptococcal pharyngitis, confirmed by throat culture or rapid antigen testing.
Epidemiology
Most pharyngitis is viral, accounting for roughly 90% of adult cases and 70% of pediatric cases. Group A beta-hemolytic Streptococcus is more common in children than adults. Antibiotic prescribing is frequent in adults with pharyngitis. In outbreaks involving rheumatogenic strains, untreated group A streptococcal infection can be followed by acute rheumatic fever in a small but meaningful percentage. Lancefield groups C and G streptococci can cause syndromes similar to group A disease and are often opportunistic or healthcare-associated. Arcanobacterium hemolyticum is seen particularly in adolescents and young adults. Parainfluenza infection is most common in children.
General Prevention
Advise patients with streptococcal pharyngitis to avoid close contact with others, and counsel on safer sex practices to reduce sexually transmitted causes.
Etiology
Acute pharyngitis is most often viral, including rhinovirus, coronavirus, influenza A/B, and parainfluenza, and may involve broader respiratory tract symptoms. Acute laryngitis is usually viral and can be caused by rhinovirus, influenza, parainfluenza, coxsackievirus, adenovirus, or respiratory syncytial virus. Some viruses produce characteristic patterns, including herpangina from coxsackie A, infectious mononucleosis from Epstein–Barr virus or cytomegalovirus, HSV gingivostomatitis, and adenoviral pharyngoconjunctival fever. Primary HSV-1 can cause acute pharyngitis, and HSV-2 can cause similar illness after oral–genital exposure. Acute pharyngitis can occur during primary HIV infection. The key bacterial cause is group A Streptococcus, with additional causes including groups C and G streptococci, Arcanobacterium hemolyticum, Neisseria gonorrhoeae, Corynebacterium diphtheriae, Mycoplasma pneumoniae, and Chlamydophila pneumoniae. Sore throat can also occur with systemic infections such as toxoplasmosis, plague, brucellosis, leptospirosis, secondary syphilis, Yersinia infections, and tularemia. Histoplasma and Blastomyces can cause laryngeal nodules with or without ulceration. Candida can cause sore throat with thrush in immunosuppressed patients or those with mucocutaneous candidiasis. West Nile virus can present as a febrile illness with malaise, headache, myalgias, rash, and occasional pharyngitis. Lemierre syndrome can present with sore throat. Deep neck infections include parapharyngeal abscess from spread of tonsillitis, pharyngitis with adenoid involvement, parotitis, mastoiditis, or periodontal infection, and retropharyngeal abscess from spread, lymphatic seeding, trauma, or cervical osteomyelitis extension. Acute necrotizing pharyngeal infections can cause foul breath, fever, and choking sensation, often associated with ulcerative gingivitis. Ludwig angina arises from dental infection near the third molar and causes rapidly spreading bilateral submandibular and sublingual cellulitis with swelling, pain, trismus, drooling, tongue displacement, and progressive dysphagia and sore throat that can lead to airway obstruction. PFAPA syndrome affects young children and causes periodic high fevers lasting several days with aphthous stomatitis, pharyngitis, and cervical adenitis, recurring at regular short intervals without other symptoms.
Diagnosis
Parapharyngeal space infection typically causes toxic appearance, fever, sore throat, dysphagia, and leukocytosis, with possible neck rigidity or contralateral torticollis; advanced disease can produce dyspnea and stridor. Acute necrotizing pharyngeal infection presents with swollen erythematous ulcerated tonsillar pillars covered by a gray membrane that peels easily and is often accompanied by lymphadenopathy. In infectious mononucleosis, pharyngitis is most prominent in the first two weeks. Herpangina presents with fever, sore throat, myalgias, and vesicles on the soft palate between the uvula and tonsils. Tuberculous laryngitis can cause mucosal hyperemia, thickening, nodules, and ulcerations.
Diagnostic Tests and Interpretation
Laboratory Studies
Throat culture is the reference standard for streptococcal diagnosis but takes 24–72 hours. Rapid antigen tests are highly specific but have variable sensitivity.
Imaging
Retropharyngeal infection may be suggested by lateral neck soft-tissue radiography, while CT or MRI best defines source and extent.
Diagnostic Procedures/Other
In suspected tuberculous laryngitis, biopsy may show granulomas with acid-fast bacilli, with cultures needed for confirmation and susceptibility testing.
Differential Diagnosis
Viral pharyngitis commonly includes sore throat with coryza and cough, an inflamed edematous pharynx, and usually no exudate, though adenovirus and mononucleosis can be exudative. Fever, tender anterior cervical nodes, erythematous pharynx with or without tonsillar enlargement or exudate, and absence of cough support streptococcal pharyngitis in children and adults. Mycoplasma-related sore throat typically occurs in young healthy patients with mild pharyngitis and prominent tracheobronchitis symptoms.
Treatment
Medications
Patients at high risk of complications from streptococcal infection, such as those with prior rheumatic carditis or valvular disease, should receive immediate antibiotics while awaiting culture confirmation. Parapharyngeal space infection management includes airway protection, operative drainage, and intravenous antibiotics targeting streptococci and oral anaerobes, using regimens such as penicillin plus metronidazole, cefoxitin, or ampicillin-sulbactam. For streptococcal pharyngitis, a single intramuscular dose of benzathine penicillin may be slightly more effective than oral penicillin VK and ensures adherence.
Ongoing Care and Follow-Up
Post-viral chronic fatigue syndrome can include fatigue, fever, sore throat, painful lymph nodes, myalgias, arthralgias, sleep disturbance, and headache. Appropriate treatment and monitoring of group A streptococcal infection aims to prevent nonsuppurative complications such as acute rheumatic fever and glomerulonephritis, reduce toxic complications and local suppurative spread, limit transmission, and shorten illness duration. Sore throat can also precede broader constitutional symptoms that culminate in viral encephalitis.
Complications
Peritonsillar abscess can follow untreated streptococcal pharyngitis and presents with unilateral swelling and erythema and uvular deviation. Parapharyngeal infections can lead to airway obstruction, aspiration after intraoral rupture, jugular vein thrombophlebitis with pulmonary emboli, carotid artery erosion, and mediastinitis.
Basics
Description
Sore throat refers to painful inflammation of the pharynx, typically worse with swallowing. Common infectious causes are covered elsewhere; the emphasis here is recognizing distinguishing clinical features and considering noninfectious etiologies.
Approach to the Patient
First assess for airway compromise and decide whether the illness is localized or part of a systemic process, most often viral. Clarify symptom type and duration and ask about hoarseness and fever. History should include sick contacts, oral–genital sexual exposure, recent weight loss, and other features suggesting noninfectious causes such as neoplasms. Findings that strongly support streptococcal pharyngitis include fever, marked tonsillar exudate and enlargement, tender anterior cervical nodes, myalgias, and supportive epidemiology such as age, season, and community colonization prevalence. Conjunctivitis points toward viral illness. When clinical and epidemiologic clues suggest gonococcal pharyngitis or diphtheria, use specific microbiologic techniques and begin appropriate therapy promptly. Differentiate laryngitis, croup, and other hoarseness syndromes from epiglottitis. The main practical distinction is group A streptococcal versus nonstreptococcal pharyngitis, confirmed by throat culture or rapid antigen testing.
Epidemiology
Most pharyngitis is viral, accounting for roughly 90% of adult cases and 70% of pediatric cases. Group A beta-hemolytic Streptococcus is more common in children than adults. Antibiotic prescribing is frequent in adults with pharyngitis. In outbreaks involving rheumatogenic strains, untreated group A streptococcal infection can be followed by acute rheumatic fever in a small but meaningful percentage. Lancefield groups C and G streptococci can cause syndromes similar to group A disease and are often opportunistic or healthcare-associated. Arcanobacterium hemolyticum is seen particularly in adolescents and young adults. Parainfluenza infection is most common in children.
General Prevention
Advise patients with streptococcal pharyngitis to avoid close contact with others, and counsel on safer sex practices to reduce sexually transmitted causes.
Etiology
Acute pharyngitis is most often viral, including rhinovirus, coronavirus, influenza A/B, and parainfluenza, and may involve broader respiratory tract symptoms. Acute laryngitis is usually viral and can be caused by rhinovirus, influenza, parainfluenza, coxsackievirus, adenovirus, or respiratory syncytial virus. Some viruses produce characteristic patterns, including herpangina from coxsackie A, infectious mononucleosis from Epstein–Barr virus or cytomegalovirus, HSV gingivostomatitis, and adenoviral pharyngoconjunctival fever. Primary HSV-1 can cause acute pharyngitis, and HSV-2 can cause similar illness after oral–genital exposure. Acute pharyngitis can occur during primary HIV infection. The key bacterial cause is group A Streptococcus, with additional causes including groups C and G streptococci, Arcanobacterium hemolyticum, Neisseria gonorrhoeae, Corynebacterium diphtheriae, Mycoplasma pneumoniae, and Chlamydophila pneumoniae. Sore throat can also occur with systemic infections such as toxoplasmosis, plague, brucellosis, leptospirosis, secondary syphilis, Yersinia infections, and tularemia. Histoplasma and Blastomyces can cause laryngeal nodules with or without ulceration. Candida can cause sore throat with thrush in immunosuppressed patients or those with mucocutaneous candidiasis. West Nile virus can present as a febrile illness with malaise, headache, myalgias, rash, and occasional pharyngitis. Lemierre syndrome can present with sore throat. Deep neck infections include parapharyngeal abscess from spread of tonsillitis, pharyngitis with adenoid involvement, parotitis, mastoiditis, or periodontal infection, and retropharyngeal abscess from spread, lymphatic seeding, trauma, or cervical osteomyelitis extension. Acute necrotizing pharyngeal infections can cause foul breath, fever, and choking sensation, often associated with ulcerative gingivitis. Ludwig angina arises from dental infection near the third molar and causes rapidly spreading bilateral submandibular and sublingual cellulitis with swelling, pain, trismus, drooling, tongue displacement, and progressive dysphagia and sore throat that can lead to airway obstruction. PFAPA syndrome affects young children and causes periodic high fevers lasting several days with aphthous stomatitis, pharyngitis, and cervical adenitis, recurring at regular short intervals without other symptoms.
Diagnosis
Parapharyngeal space infection typically causes toxic appearance, fever, sore throat, dysphagia, and leukocytosis, with possible neck rigidity or contralateral torticollis; advanced disease can produce dyspnea and stridor. Acute necrotizing pharyngeal infection presents with swollen erythematous ulcerated tonsillar pillars covered by a gray membrane that peels easily and is often accompanied by lymphadenopathy. In infectious mononucleosis, pharyngitis is most prominent in the first two weeks. Herpangina presents with fever, sore throat, myalgias, and vesicles on the soft palate between the uvula and tonsils. Tuberculous laryngitis can cause mucosal hyperemia, thickening, nodules, and ulcerations.
Diagnostic Tests and Interpretation
Laboratory Studies
Throat culture is the reference standard for streptococcal diagnosis but takes 24–72 hours. Rapid antigen tests are highly specific but have variable sensitivity.
Imaging
Retropharyngeal infection may be suggested by lateral neck soft-tissue radiography, while CT or MRI best defines source and extent.
Diagnostic Procedures/Other
In suspected tuberculous laryngitis, biopsy may show granulomas with acid-fast bacilli, with cultures needed for confirmation and susceptibility testing.
Differential Diagnosis
Viral pharyngitis commonly includes sore throat with coryza and cough, an inflamed edematous pharynx, and usually no exudate, though adenovirus and mononucleosis can be exudative. Fever, tender anterior cervical nodes, erythematous pharynx with or without tonsillar enlargement or exudate, and absence of cough support streptococcal pharyngitis in children and adults. Mycoplasma-related sore throat typically occurs in young healthy patients with mild pharyngitis and prominent tracheobronchitis symptoms.
Treatment
Medications
Patients at high risk of complications from streptococcal infection, such as those with prior rheumatic carditis or valvular disease, should receive immediate antibiotics while awaiting culture confirmation. Parapharyngeal space infection management includes airway protection, operative drainage, and intravenous antibiotics targeting streptococci and oral anaerobes, using regimens such as penicillin plus metronidazole, cefoxitin, or ampicillin-sulbactam. For streptococcal pharyngitis, a single intramuscular dose of benzathine penicillin may be slightly more effective than oral penicillin VK and ensures adherence.
Ongoing Care and Follow-Up
Post-viral chronic fatigue syndrome can include fatigue, fever, sore throat, painful lymph nodes, myalgias, arthralgias, sleep disturbance, and headache. Appropriate treatment and monitoring of group A streptococcal infection aims to prevent nonsuppurative complications such as acute rheumatic fever and glomerulonephritis, reduce toxic complications and local suppurative spread, limit transmission, and shorten illness duration. Sore throat can also precede broader constitutional symptoms that culminate in viral encephalitis.
Complications
Peritonsillar abscess can follow untreated streptococcal pharyngitis and presents with unilateral swelling and erythema and uvular deviation. Parapharyngeal infections can lead to airway obstruction, aspiration after intraoral rupture, jugular vein thrombophlebitis with pulmonary emboli, carotid artery erosion, and mediastinitis.
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Infectious Diseases and Microbiology: Red Eye
Basics
Description
Red eye may result from sight-threatening conditions such as uveitis, endophthalmitis, acute angle-closure glaucoma, or scleritis, which typically produce ciliary injection. More commonly, redness is due to conjunctival hyperemia associated with conjunctivitis, keratitis, dry eye disease, foreign body irritation (including contact lenses), blepharitis, or environmental irritants. Ocular trauma may cause subconjunctival hemorrhage. Not all causes are infectious. Uveitis involves intraocular inflammation and may be anterior, posterior, or pan-uveitis. Endophthalmitis is a severe intraocular infection involving the vitreous cavity. Acute angle-closure glaucoma is an ophthalmic emergency caused by obstruction of aqueous outflow and elevated intraocular pressure. Episcleritis affects superficial scleral tissues, while scleritis is a deeper, more severe inflammatory process that may occur with keratitis or uveitis. Conjunctivitis is the most common cause of red eye and usually includes discharge. Keratitis primarily affects the cornea.
Epidemiology
Primary acute angle closure occurs more frequently in Asian populations than in Caucasians. Incidence rates for conjunctivitis, keratitis, and uveitis vary and are addressed in their respective discussions.
Risk Factors
Risk factors for angle-closure glaucoma include advanced age, hyperopia, cataract, female sex, prior angle closure in the fellow eye, and Asian ethnicity; prophylactic laser iridotomy is often performed in the unaffected eye. Contact lens use increases the risk of bacterial keratitis. Subconjunctival hemorrhage may occur spontaneously or with bleeding disorders, minor trauma, or increased venous pressure from coughing or sneezing. Autoimmune connective tissue disorders are associated with ocular inflammation, and uveitis may be an initial manifestation.
General Prevention
Proper contact lens hygiene reduces infectious and inflammatory complications. Screening with gonioscopy and preventive laser iridotomy can prevent acute angle closure in high-risk individuals.
Pathophysiology
Ciliary injection involves deeper vascular branches and indicates inflammation of the cornea, iris, ciliary body, or sclera. Conjunctival injection is superficial, mobile with the conjunctiva, and improves with topical vasoconstrictors. Acute angle closure usually results from pupillary block, causing pressure differential between the posterior and anterior chambers, forward bowing of the iris, and obstruction of aqueous outflow through the trabecular meshwork.
Etiology
Conjunctivitis, keratitis, uveitis, and endophthalmitis have infectious and noninfectious causes. Acute angle-closure glaucoma and subconjunctival hemorrhage are noninfectious. Episcleritis is usually idiopathic, though immunologic reactions to herpes simplex or varicella zoster may occur. Scleritis is rarely infectious but may result from systemic infections or extension from keratitis; reported pathogens include fungi (Aspergillus, Fusarium), herpes viruses, mycobacteria, Nocardia, Pseudomonas, Proteus (after scleral buckle procedures), syphilis, leprosy, Lyme disease, and tuberculosis.
Commonly Associated Conditions
Endophthalmitis most commonly follows intraocular surgery. Contact lens wear strongly predisposes to bacterial keratitis.
Diagnosis
History
Subconjunctival hemorrhage is unilateral, painless, and vision is unaffected. Conjunctivitis often begins in one eye but is commonly bilateral and features discharge with minimal visual change. Keratitis is usually unilateral and associated with redness, foreign body sensation, tearing, and decreased vision. Uveitis presents with reduced vision, photophobia, and ocular pain. Acute angle-closure glaucoma presents with severe unilateral pain, decreased vision, nausea, and vomiting. Anterior scleritis causes severe pain and tenderness; posterior scleritis may cause significant visual impairment with less obvious redness. Episcleritis resembles conjunctivitis but has mild discomfort and no discharge. Endophthalmitis presents with pain and significant vision loss.
Physical Examination
Slit-lamp examination is essential. Subconjunctival hemorrhage appears as a sharply demarcated red patch under the conjunctiva. Conjunctivitis shows hyperemia, discharge, membranes or pseudomembranes, papillary or follicular reaction, and possibly preauricular lymphadenopathy. Keratitis reveals epithelial defects, stromal opacities, discharge, and anterior chamber inflammation. Anterior uveitis is diagnosed by inflammatory cells in the anterior chamber and keratic precipitates. Acute angle closure presents with a mid-dilated poorly reactive pupil, corneal edema, and elevated intraocular pressure.
Diagnostic Tests and Interpretation
Laboratory Studies
Routine cultures are unnecessary in typical conjunctivitis except in hyperacute cases suggestive of Neisseria gonorrhoeae. Keratitis lesions are sampled for Gram stain and culture.
Imaging
Confocal microscopy assists in diagnosing Acanthamoeba keratitis. Neuroimaging may identify vascular abnormalities such as carotid-cavernous fistulas or arteriovenous malformations associated with red eye.
Diagnostic Procedures/Other
Corneal biopsy may be needed for refractory keratitis. Vitreous sampling during vitrectomy can assist in diagnosing uveitis or endophthalmitis via cytology, culture, and PCR.
Differential Diagnosis
Key distinguishing features include:
Visual acuity is typically preserved in conjunctivitis and subconjunctival hemorrhage but reduced in uveitis, keratitis, and acute angle closure. Discharge is common in conjunctivitis and keratitis but absent in subconjunctival hemorrhage, uveitis, and acute angle closure. Pain is absent in conjunctivitis and subconjunctival hemorrhage but present in uveitis, keratitis, and acute angle closure. Photophobia is typical of uveitis and sometimes keratitis. Pruritus suggests allergic conjunctivitis.
Treatment
Medications
Viral conjunctivitis is managed supportively with artificial tears and cold compresses; topical steroids are rarely required. Mild bacterial conjunctivitis is treated with topical antibiotics such as trimethoprim-polymyxin B or a fluoroquinolone for several days. Bacterial keratitis requires intensive fortified topical antibiotics administered hourly. Acute bacterial endophthalmitis is treated with intravitreal antibiotics targeting gram-positive and gram-negative organisms. Anterior uveitis is treated with topical corticosteroids and cycloplegic agents; infectious causes require specific antimicrobial therapy. Acute angle-closure glaucoma requires urgent reduction of intraocular pressure with systemic acetazolamide, intravenous mannitol, topical beta-blockers, and pilocarpine, followed by laser iridotomy. Episcleritis is treated with artificial tears, topical steroids, and oral NSAIDs. Scleritis often requires systemic corticosteroids and may necessitate immunomodulatory therapy depending on associated systemic disease.
Additional Treatment / Surgery
Laser iridotomy is definitive for angle closure after stabilization. Severe infectious keratitis or scleritis causing tissue thinning may require surgical grafting.
Prognosis
Outcome depends on etiology, ranging from benign in subconjunctival hemorrhage to guarded in endophthalmitis.
Complications
Chronic inflammation may lead to cataract formation, secondary glaucoma, and cystoid macular edema.
Basics
Description
Red eye may result from sight-threatening conditions such as uveitis, endophthalmitis, acute angle-closure glaucoma, or scleritis, which typically produce ciliary injection. More commonly, redness is due to conjunctival hyperemia associated with conjunctivitis, keratitis, dry eye disease, foreign body irritation (including contact lenses), blepharitis, or environmental irritants. Ocular trauma may cause subconjunctival hemorrhage. Not all causes are infectious. Uveitis involves intraocular inflammation and may be anterior, posterior, or pan-uveitis. Endophthalmitis is a severe intraocular infection involving the vitreous cavity. Acute angle-closure glaucoma is an ophthalmic emergency caused by obstruction of aqueous outflow and elevated intraocular pressure. Episcleritis affects superficial scleral tissues, while scleritis is a deeper, more severe inflammatory process that may occur with keratitis or uveitis. Conjunctivitis is the most common cause of red eye and usually includes discharge. Keratitis primarily affects the cornea.
Epidemiology
Primary acute angle closure occurs more frequently in Asian populations than in Caucasians. Incidence rates for conjunctivitis, keratitis, and uveitis vary and are addressed in their respective discussions.
Risk Factors
Risk factors for angle-closure glaucoma include advanced age, hyperopia, cataract, female sex, prior angle closure in the fellow eye, and Asian ethnicity; prophylactic laser iridotomy is often performed in the unaffected eye. Contact lens use increases the risk of bacterial keratitis. Subconjunctival hemorrhage may occur spontaneously or with bleeding disorders, minor trauma, or increased venous pressure from coughing or sneezing. Autoimmune connective tissue disorders are associated with ocular inflammation, and uveitis may be an initial manifestation.
General Prevention
Proper contact lens hygiene reduces infectious and inflammatory complications. Screening with gonioscopy and preventive laser iridotomy can prevent acute angle closure in high-risk individuals.
Pathophysiology
Ciliary injection involves deeper vascular branches and indicates inflammation of the cornea, iris, ciliary body, or sclera. Conjunctival injection is superficial, mobile with the conjunctiva, and improves with topical vasoconstrictors. Acute angle closure usually results from pupillary block, causing pressure differential between the posterior and anterior chambers, forward bowing of the iris, and obstruction of aqueous outflow through the trabecular meshwork.
Etiology
Conjunctivitis, keratitis, uveitis, and endophthalmitis have infectious and noninfectious causes. Acute angle-closure glaucoma and subconjunctival hemorrhage are noninfectious. Episcleritis is usually idiopathic, though immunologic reactions to herpes simplex or varicella zoster may occur. Scleritis is rarely infectious but may result from systemic infections or extension from keratitis; reported pathogens include fungi (Aspergillus, Fusarium), herpes viruses, mycobacteria, Nocardia, Pseudomonas, Proteus (after scleral buckle procedures), syphilis, leprosy, Lyme disease, and tuberculosis.
Commonly Associated Conditions
Endophthalmitis most commonly follows intraocular surgery. Contact lens wear strongly predisposes to bacterial keratitis.
Diagnosis
History
Subconjunctival hemorrhage is unilateral, painless, and vision is unaffected. Conjunctivitis often begins in one eye but is commonly bilateral and features discharge with minimal visual change. Keratitis is usually unilateral and associated with redness, foreign body sensation, tearing, and decreased vision. Uveitis presents with reduced vision, photophobia, and ocular pain. Acute angle-closure glaucoma presents with severe unilateral pain, decreased vision, nausea, and vomiting. Anterior scleritis causes severe pain and tenderness; posterior scleritis may cause significant visual impairment with less obvious redness. Episcleritis resembles conjunctivitis but has mild discomfort and no discharge. Endophthalmitis presents with pain and significant vision loss.
Physical Examination
Slit-lamp examination is essential. Subconjunctival hemorrhage appears as a sharply demarcated red patch under the conjunctiva. Conjunctivitis shows hyperemia, discharge, membranes or pseudomembranes, papillary or follicular reaction, and possibly preauricular lymphadenopathy. Keratitis reveals epithelial defects, stromal opacities, discharge, and anterior chamber inflammation. Anterior uveitis is diagnosed by inflammatory cells in the anterior chamber and keratic precipitates. Acute angle closure presents with a mid-dilated poorly reactive pupil, corneal edema, and elevated intraocular pressure.
Diagnostic Tests and Interpretation
Laboratory Studies
Routine cultures are unnecessary in typical conjunctivitis except in hyperacute cases suggestive of Neisseria gonorrhoeae. Keratitis lesions are sampled for Gram stain and culture.
Imaging
Confocal microscopy assists in diagnosing Acanthamoeba keratitis. Neuroimaging may identify vascular abnormalities such as carotid-cavernous fistulas or arteriovenous malformations associated with red eye.
Diagnostic Procedures/Other
Corneal biopsy may be needed for refractory keratitis. Vitreous sampling during vitrectomy can assist in diagnosing uveitis or endophthalmitis via cytology, culture, and PCR.
Differential Diagnosis
Key distinguishing features include:
Visual acuity is typically preserved in conjunctivitis and subconjunctival hemorrhage but reduced in uveitis, keratitis, and acute angle closure. Discharge is common in conjunctivitis and keratitis but absent in subconjunctival hemorrhage, uveitis, and acute angle closure. Pain is absent in conjunctivitis and subconjunctival hemorrhage but present in uveitis, keratitis, and acute angle closure. Photophobia is typical of uveitis and sometimes keratitis. Pruritus suggests allergic conjunctivitis.
Treatment
Medications
Viral conjunctivitis is managed supportively with artificial tears and cold compresses; topical steroids are rarely required. Mild bacterial conjunctivitis is treated with topical antibiotics such as trimethoprim-polymyxin B or a fluoroquinolone for several days. Bacterial keratitis requires intensive fortified topical antibiotics administered hourly. Acute bacterial endophthalmitis is treated with intravitreal antibiotics targeting gram-positive and gram-negative organisms. Anterior uveitis is treated with topical corticosteroids and cycloplegic agents; infectious causes require specific antimicrobial therapy. Acute angle-closure glaucoma requires urgent reduction of intraocular pressure with systemic acetazolamide, intravenous mannitol, topical beta-blockers, and pilocarpine, followed by laser iridotomy. Episcleritis is treated with artificial tears, topical steroids, and oral NSAIDs. Scleritis often requires systemic corticosteroids and may necessitate immunomodulatory therapy depending on associated systemic disease.
Additional Treatment / Surgery
Laser iridotomy is definitive for angle closure after stabilization. Severe infectious keratitis or scleritis causing tissue thinning may require surgical grafting.
Prognosis
Outcome depends on etiology, ranging from benign in subconjunctival hemorrhage to guarded in endophthalmitis.
Complications
Chronic inflammation may lead to cataract formation, secondary glaucoma, and cystoid macular edema.
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Infectious Diseases and Microbiology: Rash and Fever
Basics
Description
Rash refers to temporary skin eruptions that accompany localized or generalized infectious diseases. This topic emphasizes the differential diagnosis and early recognition of potentially life-threatening generalized eruptions.
Approach to the Patient
A detailed history should assess immune status, full medication list, travel history, immunization record, exposure to pets or animals, arthropod bites, cardiac abnormalities, prosthetic material, recent contact with ill persons, and possible sexually transmitted infections. Clarify the initial site of rash, pruritus or pain, and speed and direction of spread. Document associated symptoms including prodrome, fever, and itching. Physical examination should define lesion morphology (macules, papules, vesicles, plaques, nodules), configuration (annular, target), arrangement, and distribution (central versus peripheral).
Epidemiology
Infectious mononucleosis may present with generalized maculopapular, petechial, or urticarial rash, often after antibiotic exposure. Approximately one-fifth of erythema infectiosum cases occur in adults, though rash may resemble rubella. Up to half of patients with primary HIV infection develop a maculopapular rash within days of fever onset, typically involving the upper trunk and face. Rubella has been declared eliminated in the United States. Cutaneous leishmaniasis affects up to 1.5 million individuals annually worldwide. Rash occurs in about half of dengue cases. In early Lyme disease, erythema migrans develops at the tick bite site in most patients.
General Prevention
Women of reproductive age should be immunized against rubella. Pregnant women diagnosed with early rubella infection should receive counseling regarding fetal risks and management options.
Etiology
Common adult rash patterns include centrally distributed maculopapular eruptions (such as dengue, infectious mononucleosis, leptospirosis, Lyme disease, primary HIV infection, rubella, measles, typhoid fever, systemic lupus erythematosus, and various rickettsial infections), peripheral eruptions (including bacterial endocarditis, chronic meningococcemia, disseminated gonococcal infection, erythema multiforme, Rocky Mountain spotted fever, and secondary syphilis), confluent desquamative erythemas (graft-versus-host disease, Kawasaki disease, scarlet fever, staphylococcal and streptococcal toxic shock syndromes), vesiculobullous eruptions (disseminated Vibrio vulnificus infection, ecthyma gangrenosum, rickettsialpox), nodular eruptions (disseminated fungal or mycobacterial infections, erythema nodosum, Sweet syndrome), and purpuric eruptions (acute or chronic meningococcemia, disseminated gonococcal infection, enteroviral petechiae, Rocky Mountain spotted fever, thrombotic thrombocytopenic purpura).
Diagnosis
Rocky Mountain spotted fever (RMSF) typically presents with rash around day four of illness, beginning as blanching macules that may progress to purpura and necrosis; genital involvement may be suggestive. Rash may be absent in some cases and is associated with worse prognosis. Meningococcal disease often produces petechiae that evolve into palpable purpura, though other lesion types can occur. Fulminant meningococcemia with disseminated intravascular coagulation constitutes Waterhouse–Friderichsen syndrome. Cutaneous findings in infective endocarditis include vascular phenomena such as petechiae, splinter hemorrhages, and Janeway lesions, and immunologic signs such as Osler nodes and Roth spots. Lyme disease progresses from erythema migrans to neurologic or cardiac involvement and later arthritis or chronic skin changes. Ehrlichiosis often features headache and high fever, with variable rash. Staphylococcal toxic shock syndrome presents with diffuse erythematous rash resembling sunburn, followed by desquamation within two weeks, along with conjunctival injection, mucosal hyperemia, and strawberry tongue. Streptococcal toxic shock syndrome often arises from invasive soft-tissue infection. Dengue rash is typically maculopapular and appears within several days of illness onset.
Diagnostic Tests and Interpretation
Laboratory Studies
Gram stain and culture of pustular or bullous lesions should be performed when infection is suspected. Antibodies to Rickettsia rickettsii become detectable after the first week of RMSF. Meningococcal disease is confirmed by Gram stain and culture of blood or cerebrospinal fluid; skin biopsy may assist. Streptococcal toxic shock syndrome more commonly involves bacteremia than staphylococcal toxic shock syndrome.
Diagnostic Procedures/Other
Skin biopsy with culture and histopathologic examination may establish diagnosis in unclear cases.
Differential Diagnosis
Desquamating erythroderma is more common in staphylococcal than streptococcal toxic shock syndrome. Gonococcemia frequently causes a pustular hemorrhagic rash but may present with diverse lesion types.
Treatment
Management depends on the underlying etiology and may require urgent antimicrobial or supportive therapy.
Ongoing Care and Follow-Up
Serial documentation of rash progression with photography or ink demarcation can assist monitoring.
Complications
Untreated Rocky Mountain spotted fever carries high mortality, underscoring the importance of early recognition and treatment.
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Basics
Description
Rash refers to temporary skin eruptions that accompany localized or generalized infectious diseases. This topic emphasizes the differential diagnosis and early recognition of potentially life-threatening generalized eruptions.
Approach to the Patient
A detailed history should assess immune status, full medication list, travel history, immunization record, exposure to pets or animals, arthropod bites, cardiac abnormalities, prosthetic material, recent contact with ill persons, and possible sexually transmitted infections. Clarify the initial site of rash, pruritus or pain, and speed and direction of spread. Document associated symptoms including prodrome, fever, and itching. Physical examination should define lesion morphology (macules, papules, vesicles, plaques, nodules), configuration (annular, target), arrangement, and distribution (central versus peripheral).
Epidemiology
Infectious mononucleosis may present with generalized maculopapular, petechial, or urticarial rash, often after antibiotic exposure. Approximately one-fifth of erythema infectiosum cases occur in adults, though rash may resemble rubella. Up to half of patients with primary HIV infection develop a maculopapular rash within days of fever onset, typically involving the upper trunk and face. Rubella has been declared eliminated in the United States. Cutaneous leishmaniasis affects up to 1.5 million individuals annually worldwide. Rash occurs in about half of dengue cases. In early Lyme disease, erythema migrans develops at the tick bite site in most patients.
General Prevention
Women of reproductive age should be immunized against rubella. Pregnant women diagnosed with early rubella infection should receive counseling regarding fetal risks and management options.
Etiology
Common adult rash patterns include centrally distributed maculopapular eruptions (such as dengue, infectious mononucleosis, leptospirosis, Lyme disease, primary HIV infection, rubella, measles, typhoid fever, systemic lupus erythematosus, and various rickettsial infections), peripheral eruptions (including bacterial endocarditis, chronic meningococcemia, disseminated gonococcal infection, erythema multiforme, Rocky Mountain spotted fever, and secondary syphilis), confluent desquamative erythemas (graft-versus-host disease, Kawasaki disease, scarlet fever, staphylococcal and streptococcal toxic shock syndromes), vesiculobullous eruptions (disseminated Vibrio vulnificus infection, ecthyma gangrenosum, rickettsialpox), nodular eruptions (disseminated fungal or mycobacterial infections, erythema nodosum, Sweet syndrome), and purpuric eruptions (acute or chronic meningococcemia, disseminated gonococcal infection, enteroviral petechiae, Rocky Mountain spotted fever, thrombotic thrombocytopenic purpura).
Diagnosis
Rocky Mountain spotted fever (RMSF) typically presents with rash around day four of illness, beginning as blanching macules that may progress to purpura and necrosis; genital involvement may be suggestive. Rash may be absent in some cases and is associated with worse prognosis. Meningococcal disease often produces petechiae that evolve into palpable purpura, though other lesion types can occur. Fulminant meningococcemia with disseminated intravascular coagulation constitutes Waterhouse–Friderichsen syndrome. Cutaneous findings in infective endocarditis include vascular phenomena such as petechiae, splinter hemorrhages, and Janeway lesions, and immunologic signs such as Osler nodes and Roth spots. Lyme disease progresses from erythema migrans to neurologic or cardiac involvement and later arthritis or chronic skin changes. Ehrlichiosis often features headache and high fever, with variable rash. Staphylococcal toxic shock syndrome presents with diffuse erythematous rash resembling sunburn, followed by desquamation within two weeks, along with conjunctival injection, mucosal hyperemia, and strawberry tongue. Streptococcal toxic shock syndrome often arises from invasive soft-tissue infection. Dengue rash is typically maculopapular and appears within several days of illness onset.
Diagnostic Tests and Interpretation
Laboratory Studies
Gram stain and culture of pustular or bullous lesions should be performed when infection is suspected. Antibodies to Rickettsia rickettsii become detectable after the first week of RMSF. Meningococcal disease is confirmed by Gram stain and culture of blood or cerebrospinal fluid; skin biopsy may assist. Streptococcal toxic shock syndrome more commonly involves bacteremia than staphylococcal toxic shock syndrome.
Diagnostic Procedures/Other
Skin biopsy with culture and histopathologic examination may establish diagnosis in unclear cases.
Differential Diagnosis
Desquamating erythroderma is more common in staphylococcal than streptococcal toxic shock syndrome. Gonococcemia frequently causes a pustular hemorrhagic rash but may present with diverse lesion types.
Treatment
Management depends on the underlying etiology and may require urgent antimicrobial or supportive therapy.
Ongoing Care and Follow-Up
Serial documentation of rash progression with photography or ink demarcation can assist monitoring.
Complications
Untreated Rocky Mountain spotted fever carries high mortality, underscoring the importance of early recognition and treatment.
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