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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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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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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.
I’
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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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: 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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Emergency and Acute Medicine – Patellar Injuries
Patellar injuries encompass a spectrum of conditions involving the patella and its associated extensor mechanism, including patellar dislocation, patellar fracture, patellar tendon rupture, and patellar tendinitis. These injuries commonly result from traumatic forces, sudden deceleration, or repetitive overuse and are frequently encountered in athletic and emergency settings. Accurate recognition is essential, as management ranges from conservative treatment to urgent surgical intervention.
Patellar dislocation most often occurs due to sudden knee flexion combined with external rotation of the tibia on the femur, accompanied by a strong contraction of the quadriceps muscle. Lateral dislocation is by far the most common type, with the patella displaced over the lateral femoral condyle. Direct trauma to the patella is a less frequent cause. Risk factors include genu valgum, patella alta, shallow femoral trochlea, weak vastus medialis, pes planus, and structural abnormalities of the patella. Dislocations are particularly common in adolescent athletes, especially females, and younger age at first dislocation is associated with higher recurrence rates.
Patients with patellar dislocation typically report a sensation of the knee “giving way,” often accompanied by a popping or tearing feeling, immediate pain, swelling, and difficulty bearing weight. On examination, there may be an obvious lateral deformity of the patella, although spontaneous reduction frequently occurs before ED evaluation. Tenderness along the patella and a positive apprehension test (Fairbanks sign) are characteristic findings.
Patellar fractures are most commonly caused by direct trauma such as a fall or direct blow to the knee, often resulting in comminuted or minimally displaced fractures. Indirect mechanisms involve excessive tension through the extensor mechanism, leading to transverse or displaced fractures. Transverse fractures account for the majority of cases, followed by comminuted, longitudinal, and osteochondral fractures. Patients present with anterior knee pain, swelling, hemarthrosis, difficulty ambulating, and impaired knee extension. Palpable defects or crepitus may be present.
Patellar tendon rupture usually results from a forceful eccentric contraction of the quadriceps on a flexed knee, such as during landing from a jump or heavy lifting. It occurs more often in older athletes and in patients with predisposing conditions such as chronic patellar tendinitis, diabetes mellitus, inflammatory arthropathies, prior steroid injections, or previous knee surgery. Clinically, patients experience abrupt severe pain, inability to maintain knee extension, and a high-riding patella on examination or imaging.
Patellar tendinitis, also known as “jumper’s knee,” is an overuse injury caused by repetitive microtrauma from activities involving frequent jumping or rapid acceleration and deceleration. It is common in volleyball players, basketball players, runners, and high jumpers. Patients typically report localized pain at the inferior pole of the patella or proximal patellar tendon that worsens with stair climbing or rising from a seated position.
Radiographic evaluation is essential in suspected patellar injuries. Standard anteroposterior, lateral, and sunrise (axial) views of the knee should be obtained. In patellar dislocations, postreduction radiographs are important to exclude associated osteochondral fractures. A bipartite patella may mimic fracture and should be distinguished with comparison views if needed. In patellar tendon rupture, imaging may reveal a superiorly displaced patella. Radiographs are often normal in early patellar tendinitis.
Management depends on the specific injury. Simple lateral patellar dislocations are typically reduced by gentle knee extension, sometimes with medial pressure on the patella. Procedural analgesia or sedation may be required. Other dislocation types (superior, medial, or intra-articular) should not be reduced in the ED and require orthopedic consultation. Patellar fractures warrant orthopedic evaluation; nondisplaced fractures with intact extensor function may be treated nonoperatively with immobilization, while displaced or open fractures require surgical management. Patellar tendon rupture requires early orthopedic consultation and surgical repair, typically within two to six weeks. Patellar tendinitis is managed conservatively with rest, activity modification, NSAIDs, and physical therapy.
Patients with successfully reduced lateral patellar dislocations and normal postreduction imaging may be discharged with a knee immobilizer, crutches, and close orthopedic follow-up. Admission is indicated for irreducible dislocations, associated fractures, open injuries, or compromised extensor mechanism. Important clinical pearls include recognizing that patellar dislocations may spontaneously reduce prior to evaluation and that swelling may obscure a palpable defect in patellar tendon rupture.
Patellar injuries encompass a spectrum of conditions involving the patella and its associated extensor mechanism, including patellar dislocation, patellar fracture, patellar tendon rupture, and patellar tendinitis. These injuries commonly result from traumatic forces, sudden deceleration, or repetitive overuse and are frequently encountered in athletic and emergency settings. Accurate recognition is essential, as management ranges from conservative treatment to urgent surgical intervention.
Patellar dislocation most often occurs due to sudden knee flexion combined with external rotation of the tibia on the femur, accompanied by a strong contraction of the quadriceps muscle. Lateral dislocation is by far the most common type, with the patella displaced over the lateral femoral condyle. Direct trauma to the patella is a less frequent cause. Risk factors include genu valgum, patella alta, shallow femoral trochlea, weak vastus medialis, pes planus, and structural abnormalities of the patella. Dislocations are particularly common in adolescent athletes, especially females, and younger age at first dislocation is associated with higher recurrence rates.
Patients with patellar dislocation typically report a sensation of the knee “giving way,” often accompanied by a popping or tearing feeling, immediate pain, swelling, and difficulty bearing weight. On examination, there may be an obvious lateral deformity of the patella, although spontaneous reduction frequently occurs before ED evaluation. Tenderness along the patella and a positive apprehension test (Fairbanks sign) are characteristic findings.
Patellar fractures are most commonly caused by direct trauma such as a fall or direct blow to the knee, often resulting in comminuted or minimally displaced fractures. Indirect mechanisms involve excessive tension through the extensor mechanism, leading to transverse or displaced fractures. Transverse fractures account for the majority of cases, followed by comminuted, longitudinal, and osteochondral fractures. Patients present with anterior knee pain, swelling, hemarthrosis, difficulty ambulating, and impaired knee extension. Palpable defects or crepitus may be present.
Patellar tendon rupture usually results from a forceful eccentric contraction of the quadriceps on a flexed knee, such as during landing from a jump or heavy lifting. It occurs more often in older athletes and in patients with predisposing conditions such as chronic patellar tendinitis, diabetes mellitus, inflammatory arthropathies, prior steroid injections, or previous knee surgery. Clinically, patients experience abrupt severe pain, inability to maintain knee extension, and a high-riding patella on examination or imaging.
Patellar tendinitis, also known as “jumper’s knee,” is an overuse injury caused by repetitive microtrauma from activities involving frequent jumping or rapid acceleration and deceleration. It is common in volleyball players, basketball players, runners, and high jumpers. Patients typically report localized pain at the inferior pole of the patella or proximal patellar tendon that worsens with stair climbing or rising from a seated position.
Radiographic evaluation is essential in suspected patellar injuries. Standard anteroposterior, lateral, and sunrise (axial) views of the knee should be obtained. In patellar dislocations, postreduction radiographs are important to exclude associated osteochondral fractures. A bipartite patella may mimic fracture and should be distinguished with comparison views if needed. In patellar tendon rupture, imaging may reveal a superiorly displaced patella. Radiographs are often normal in early patellar tendinitis.
Management depends on the specific injury. Simple lateral patellar dislocations are typically reduced by gentle knee extension, sometimes with medial pressure on the patella. Procedural analgesia or sedation may be required. Other dislocation types (superior, medial, or intra-articular) should not be reduced in the ED and require orthopedic consultation. Patellar fractures warrant orthopedic evaluation; nondisplaced fractures with intact extensor function may be treated nonoperatively with immobilization, while displaced or open fractures require surgical management. Patellar tendon rupture requires early orthopedic consultation and surgical repair, typically within two to six weeks. Patellar tendinitis is managed conservatively with rest, activity modification, NSAIDs, and physical therapy.
Patients with successfully reduced lateral patellar dislocations and normal postreduction imaging may be discharged with a knee immobilizer, crutches, and close orthopedic follow-up. Admission is indicated for irreducible dislocations, associated fractures, open injuries, or compromised extensor mechanism. Important clinical pearls include recognizing that patellar dislocations may spontaneously reduce prior to evaluation and that swelling may obscure a palpable defect in patellar tendon rupture.
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Emergency and Acute Medicine – Pancreatic Trauma
Pancreatic trauma most commonly results from a direct epigastric blow that compresses the pancreas against the vertebral column in blunt trauma or from penetrating injury by a sharp object. Because of the retroperitoneal location of the pancreas, significant force is usually required to cause injury. In children, pancreatic trauma often reflects proportionately greater force to a smaller body mass, leading to multisystem injuries, and clinicians must consider nonaccidental trauma, malpositioned seat belts, and child abuse. Pediatric patients may present without hypotension despite serious injury.
Penetrating trauma is the most common mechanism overall, while blunt trauma typically involves steering wheels, seat belts, or bicycle handlebars impacting the upper abdomen. Pancreatic injury is rarely isolated, with approximately 90% of cases associated with injuries to adjacent structures including the liver, stomach, spleen, kidneys, duodenum, colon, small bowel, common bile duct, gallbladder, major vascular structures, and the spine, particularly Chance fractures.
Clinical presentation is often subtle and nonspecific, and the extent of pancreatic injury may not be apparent on initial evaluation. Patients typically report diffuse or epigastric abdominal pain that may be out of proportion to physical findings and vital signs. Associated findings include upper abdominal soft-tissue contusions, lower rib or costal cartilage injuries, hypotension, and signs of retroperitoneal hemorrhage such as Grey Turner or Cullen signs. Vascular injury is the leading cause of mortality and mandates immediate evaluation and surgical consideration when suspected.
Physical examination should be thorough and repeated serially, with inspection for abrasions, contusions, and penetrating wounds, including a complete log roll. Clinicians should assess bowel sounds, abdominal tenderness, guarding, rebound, and evaluate for occult bleeding with rectal or genital examinations as appropriate. Serial vital signs and examinations are essential, as early findings may be minimal despite significant injury.
Diagnostic evaluation is dictated by patient stability and associated injuries. Contrast-enhanced abdominal CT is the cornerstone of evaluation for pancreatic trauma, although imaging may still miss injuries, particularly ductal disruptions. MRCP is increasingly used in trauma centers to better assess pancreatic duct involvement. Laboratory testing includes hematocrit, complete metabolic profile, coagulation studies, and type and screen. Serum amylase and lipase are unreliable for ruling out pancreatic injury; normal levels do not exclude injury, while elevations are nonspecific but may raise suspicion. FAST ultrasound may identify associated injuries but is insensitive for pancreatic damage.
Initial management follows standard trauma principles with airway protection, hemodynamic resuscitation using crystalloids or blood products, and early surgical consultation. Nasogastric decompression may be beneficial. Broad-spectrum antibiotics are indicated for penetrating injuries or when operative intervention is required, with coverage for both aerobic and anaerobic enteric organisms. Early identification of ductal injury significantly reduces morbidity and mortality.
Definitive management depends on injury grade and patient stability. Minor pancreatic injuries are often managed with drainage, while higher-grade injuries involving ductal disruption may require resection and drainage, pancreaticoduodenectomy, or selective endoscopic interventions. There is insufficient evidence to support routine use of octreotide. All patients with suspected pancreatic injury require hospital admission, observation, and serial examinations, with unstable patients proceeding directly to operative exploration.
Complications may present in a delayed fashion and include pancreatitis, pseudocyst formation, fistulas, and vascular aneurysms. Long-term endocrine or exocrine dysfunction is uncommon unless extensive pancreatic tissue is destroyed or resected. A high index of suspicion, careful imaging selection, and early surgical involvement are essential to optimize outcomes in pancreatic trauma.
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Emergency and Acute Medicine – Paronychia
Paronychia is an inflammatory condition of the nail folds surrounding the nail plate that occurs when disruption of the protective seal between the nail plate and nail fold allows microorganisms to enter the eponychial space. This disruption commonly follows minor trauma and leads to localized infection and inflammation.
The etiology differs between acute and chronic paronychia. Acute paronychia is most commonly caused by *Staphylococcus aureus*, although streptococci, *Pseudomonas*, and anaerobic organisms may also be involved. Chronic paronychia is multifactorial and results from repeated exposure to allergens and irritants, with fungal organisms—most commonly *Candida albicans*—frequently coexisting alongside *Staphylococcus* species.
Clinically, paronychia presents with pain, warmth, swelling, and erythema of the proximal or lateral nail folds, usually developing two to five days after trauma. For symptoms to meet criteria for chronic paronychia, they must persist for more than six weeks. A careful history is important. Acute paronychia is often associated with nail biting, finger sucking, aggressive manicuring, or direct trauma. Chronic paronychia is commonly seen in individuals with occupations involving persistent moisture exposure, such as dishwashers or bartenders, and occurs more frequently in patients with diabetes or peripheral vascular disease. In children, infections often involve anaerobic oral flora due to nail biting.
On physical examination, early paronychia begins as localized erythema, swelling, and tenderness at the dorsolateral nail fold, which may bulge over the nail plate. As the condition progresses, a subcuticular or subungual abscess may form. Green discoloration of the nail suggests *Pseudomonas* infection, while nail plate hypertrophy raises concern for a fungal etiology.
The diagnosis of paronychia is primarily clinical and based on history and physical examination. Evaluation should include assessment for associated infections such as felon or cellulitis and confirmation of tetanus immunization status. Laboratory testing is generally not helpful, and cultures are not routinely indicated. If herpetic whitlow is suspected, a Tzanck smear or viral culture may be considered. Imaging with soft tissue radiographs is reserved for suspected foreign bodies or possible osteomyelitis. A digital pressure test, using opposing pressure between the thumb and affected finger, may help identify early subungual abscess formation.
Management depends on the stage and type of paronychia. Early acute paronychia without purulence can often be treated with warm-water soaks four times daily, with or without topical antibiotics or corticosteroids. If a superficial abscess is present, elevation of the eponychial fold using a small blade or needle may allow adequate drainage; local anesthesia or a digital nerve block may be required. When infection extends beneath the nail plate, partial nail removal may be necessary, while extensive subungual abscesses may require complete nail removal. Runaround abscesses involving both sides of the nail fold require partial proximal nail removal with packing to prevent re-adhesion.
Antibiotic therapy is recommended when there is cellulitis, abscess formation, or systemic signs of infection. Appropriate first-line oral agents include trimethoprim–sulfamethoxazole, dicloxacillin, or amoxicillin–clavulanate, typically for five to ten days depending on severity. Clindamycin or amoxicillin–clavulanate is preferred when infection is associated with nail biting or oral exposure. Chronic paronychia management focuses on avoidance of irritants and moisture, with topical corticosteroids considered first-line therapy, often combined with a broad-spectrum topical antifungal. Refractory cases may require surgical eponychial marsupialization or oral antifungal therapy.
Admission is rarely required for paronychia alone. Patients with uncomplicated infections may be discharged with appropriate wound care instructions and follow-up. Those with packing in place should be re-evaluated within 24 hours. Referral is indicated for chronic or recurrent paronychia that does not respond to standard therapy.
Key clinical pearls include recognizing that acute paronychia generally responds well to timely drainage with or without antibiotics, while chronic paronychia is usually driven by repeated exposure to irritants rather than infection alone. Conditions such as psoriasis, Reiter syndrome, and herpetic whitlow can mimic paronychia and should be considered in recurrent or atypical cases.
Paronychia is an inflammatory condition of the nail folds surrounding the nail plate that occurs when disruption of the protective seal between the nail plate and nail fold allows microorganisms to enter the eponychial space. This disruption commonly follows minor trauma and leads to localized infection and inflammation.
The etiology differs between acute and chronic paronychia. Acute paronychia is most commonly caused by *Staphylococcus aureus*, although streptococci, *Pseudomonas*, and anaerobic organisms may also be involved. Chronic paronychia is multifactorial and results from repeated exposure to allergens and irritants, with fungal organisms—most commonly *Candida albicans*—frequently coexisting alongside *Staphylococcus* species.
Clinically, paronychia presents with pain, warmth, swelling, and erythema of the proximal or lateral nail folds, usually developing two to five days after trauma. For symptoms to meet criteria for chronic paronychia, they must persist for more than six weeks. A careful history is important. Acute paronychia is often associated with nail biting, finger sucking, aggressive manicuring, or direct trauma. Chronic paronychia is commonly seen in individuals with occupations involving persistent moisture exposure, such as dishwashers or bartenders, and occurs more frequently in patients with diabetes or peripheral vascular disease. In children, infections often involve anaerobic oral flora due to nail biting.
On physical examination, early paronychia begins as localized erythema, swelling, and tenderness at the dorsolateral nail fold, which may bulge over the nail plate. As the condition progresses, a subcuticular or subungual abscess may form. Green discoloration of the nail suggests *Pseudomonas* infection, while nail plate hypertrophy raises concern for a fungal etiology.
The diagnosis of paronychia is primarily clinical and based on history and physical examination. Evaluation should include assessment for associated infections such as felon or cellulitis and confirmation of tetanus immunization status. Laboratory testing is generally not helpful, and cultures are not routinely indicated. If herpetic whitlow is suspected, a Tzanck smear or viral culture may be considered. Imaging with soft tissue radiographs is reserved for suspected foreign bodies or possible osteomyelitis. A digital pressure test, using opposing pressure between the thumb and affected finger, may help identify early subungual abscess formation.
Management depends on the stage and type of paronychia. Early acute paronychia without purulence can often be treated with warm-water soaks four times daily, with or without topical antibiotics or corticosteroids. If a superficial abscess is present, elevation of the eponychial fold using a small blade or needle may allow adequate drainage; local anesthesia or a digital nerve block may be required. When infection extends beneath the nail plate, partial nail removal may be necessary, while extensive subungual abscesses may require complete nail removal. Runaround abscesses involving both sides of the nail fold require partial proximal nail removal with packing to prevent re-adhesion.
Antibiotic therapy is recommended when there is cellulitis, abscess formation, or systemic signs of infection. Appropriate first-line oral agents include trimethoprim–sulfamethoxazole, dicloxacillin, or amoxicillin–clavulanate, typically for five to ten days depending on severity. Clindamycin or amoxicillin–clavulanate is preferred when infection is associated with nail biting or oral exposure. Chronic paronychia management focuses on avoidance of irritants and moisture, with topical corticosteroids considered first-line therapy, often combined with a broad-spectrum topical antifungal. Refractory cases may require surgical eponychial marsupialization or oral antifungal therapy.
Admission is rarely required for paronychia alone. Patients with uncomplicated infections may be discharged with appropriate wound care instructions and follow-up. Those with packing in place should be re-evaluated within 24 hours. Referral is indicated for chronic or recurrent paronychia that does not respond to standard therapy.
Key clinical pearls include recognizing that acute paronychia generally responds well to timely drainage with or without antibiotics, while chronic paronychia is usually driven by repeated exposure to irritants rather than infection alone. Conditions such as psoriasis, Reiter syndrome, and herpetic whitlow can mimic paronychia and should be considered in recurrent or atypical cases.
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Emergency and Acute Medicine – Parkinson Disease
Parkinson disease (PD) is a gradually progressive neurodegenerative disorder that typically affects individuals in middle or late life. It is characterized by degeneration of dopaminergic neurons in the substantia nigra, formation of Lewy bodies in remaining neurons, and accelerated cortical atrophy. Although symptoms often begin unilaterally, the disease usually progresses to symmetric involvement. Parkinson disease affects approximately 1% of people over 60 years of age and up to 4% of those over 80. Importantly, nonspecific symptoms such as fatigue, constipation, and hyposmia may precede the diagnosis by many years, sometimes up to two decades.
The etiology of Parkinson disease is most often sporadic or idiopathic. However, several other conditions can present with parkinsonism and must be considered, especially in the emergency setting. These include drug-induced causes such as neuroleptics and sudden withdrawal of dopaminergic medications leading to parkinsonism–hyperpyrexia syndrome, as well as exposure to toxins like carbon monoxide, methanol, cyanide, organophosphates, and MPTP. Structural brain lesions involving the basal ganglia or midbrain, hydrocephalus, infections such as viral encephalitis or Mycoplasma, and other neurologic conditions like central pontine myelinolysis and encephalitis lethargica can also produce parkinsonian features.
Clinical manifestations of Parkinson disease are divided into nonmotor and motor symptoms. Nonmotor symptoms include orthostatic hypotension, constipation, delayed gastric emptying, dysphagia, pain and sensory disturbances, depression, hallucinations, dementia, and sleep disorders. Motor symptoms are classically defined by resting “pill-rolling” tremor, cogwheel rigidity due to increased muscle tone, bradykinesia with marked slowness of movement, postural instability, stooped posture, and a reduced facial expression often described as a “masked face.” A sudden change in baseline motor function or mental status in a patient with known PD may be the only sign of an underlying systemic illness such as infection.
History is the cornerstone of diagnosis and emergency assessment. Important elements include the onset and progression of symptoms, whether the presentation was gradual or sudden, medication adherence, and exposure to drugs or toxins that may cause parkinsonism. Sudden withdrawal or noncompliance with dopaminergic therapy can precipitate parkinsonism–hyperpyrexia syndrome, a life-threatening condition marked by rigidity, hyperthermia, reduced consciousness, autonomic instability, and complications such as acute renal failure, rhabdomyolysis, venous thrombosis, and disseminated intravascular coagulation.
Physical examination typically reveals cogwheel rigidity, resting tremor, bradykinesia, and postural abnormalities. Diagnosis of Parkinson disease is primarily clinical, and no specific laboratory test is required to confirm it. In the emergency department, investigations are directed toward identifying alternative diagnoses, complications, or precipitants of deterioration. Laboratory studies may be indicated if parkinsonism–hyperpyrexia syndrome or infection is suspected. Neuroimaging with CT or MRI is not required to diagnose PD but may be performed to evaluate dementia or exclude other neurologic conditions. Chest radiography may be useful when respiratory infection is suspected.
The differential diagnosis of Parkinson disease is broad and includes essential tremor, benign familial tremor, major depression, Wilson disease, Huntington disease, Alzheimer disease, dementia with Lewy bodies, Creutzfeldt–Jakob disease, vitamin B12 deficiency, hypothyroidism, hydrocephalus, multi-infarct dementia, and toxic exposures such as carbon monoxide poisoning. Careful clinical assessment is essential to avoid misdiagnosis.
Management in the emergency department focuses on symptom control, identification and treatment of triggers, and prevention of complications. Antiparkinsonian medications may be initiated or adjusted in consultation with neurology. Patients with mild disease may not require immediate pharmacologic therapy, while those with moderate disease often benefit from dopaminergic or anticholinergic agents. Underlying infections or metabolic disturbances should be treated promptly. Parkinsonism–hyperpyrexia syndrome requires urgent replacement of dopaminergic therapy, supportive care, and management of associated complications.
Common medications used in Parkinson disease include carbidopa/levodopa as first-line therapy, dopamine agonists such as pramipexole and ropinirole, MAO-B inhibitors like selegiline and rasagiline, anticholinergics such as benztropine for tremor-dominant disease, and amantadine to stimulate dopamine release. Adjunctive agents like entacapone may be used to enhance levodopa bioavailability. In parkinsonism–hyperpyrexia syndrome, intravenous or enteral levodopa and bromocriptine are essential.
Admission is indicated for patients with Parkinson disease who present with serious medical conditions such as infection, trauma, cardiovascular or cerebrovascular emergencies, electrolyte disturbances, altered mental status, medication complications, failure to thrive, or suspected abuse. Patients with depression and suicidal intent or complications related to deep brain stimulation devices also require inpatient care. Stable patients with mild to moderate disease may be discharged with medications and urgent outpatient neurology follow-up.
Key clinical pearls include recognizing that Parkinson disease can be difficult to diagnose and is frequently confused with other neurologic conditions. Sudden withdrawal of dopaminergic medications is a medical emergency and must be avoided. In the emergency setting, vigilance for systemic illness, medication noncompliance, and life-threatening complications is critical to optimal patient outcomes.
Parkinson disease (PD) is a gradually progressive neurodegenerative disorder that typically affects individuals in middle or late life. It is characterized by degeneration of dopaminergic neurons in the substantia nigra, formation of Lewy bodies in remaining neurons, and accelerated cortical atrophy. Although symptoms often begin unilaterally, the disease usually progresses to symmetric involvement. Parkinson disease affects approximately 1% of people over 60 years of age and up to 4% of those over 80. Importantly, nonspecific symptoms such as fatigue, constipation, and hyposmia may precede the diagnosis by many years, sometimes up to two decades.
The etiology of Parkinson disease is most often sporadic or idiopathic. However, several other conditions can present with parkinsonism and must be considered, especially in the emergency setting. These include drug-induced causes such as neuroleptics and sudden withdrawal of dopaminergic medications leading to parkinsonism–hyperpyrexia syndrome, as well as exposure to toxins like carbon monoxide, methanol, cyanide, organophosphates, and MPTP. Structural brain lesions involving the basal ganglia or midbrain, hydrocephalus, infections such as viral encephalitis or Mycoplasma, and other neurologic conditions like central pontine myelinolysis and encephalitis lethargica can also produce parkinsonian features.
Clinical manifestations of Parkinson disease are divided into nonmotor and motor symptoms. Nonmotor symptoms include orthostatic hypotension, constipation, delayed gastric emptying, dysphagia, pain and sensory disturbances, depression, hallucinations, dementia, and sleep disorders. Motor symptoms are classically defined by resting “pill-rolling” tremor, cogwheel rigidity due to increased muscle tone, bradykinesia with marked slowness of movement, postural instability, stooped posture, and a reduced facial expression often described as a “masked face.” A sudden change in baseline motor function or mental status in a patient with known PD may be the only sign of an underlying systemic illness such as infection.
History is the cornerstone of diagnosis and emergency assessment. Important elements include the onset and progression of symptoms, whether the presentation was gradual or sudden, medication adherence, and exposure to drugs or toxins that may cause parkinsonism. Sudden withdrawal or noncompliance with dopaminergic therapy can precipitate parkinsonism–hyperpyrexia syndrome, a life-threatening condition marked by rigidity, hyperthermia, reduced consciousness, autonomic instability, and complications such as acute renal failure, rhabdomyolysis, venous thrombosis, and disseminated intravascular coagulation.
Physical examination typically reveals cogwheel rigidity, resting tremor, bradykinesia, and postural abnormalities. Diagnosis of Parkinson disease is primarily clinical, and no specific laboratory test is required to confirm it. In the emergency department, investigations are directed toward identifying alternative diagnoses, complications, or precipitants of deterioration. Laboratory studies may be indicated if parkinsonism–hyperpyrexia syndrome or infection is suspected. Neuroimaging with CT or MRI is not required to diagnose PD but may be performed to evaluate dementia or exclude other neurologic conditions. Chest radiography may be useful when respiratory infection is suspected.
The differential diagnosis of Parkinson disease is broad and includes essential tremor, benign familial tremor, major depression, Wilson disease, Huntington disease, Alzheimer disease, dementia with Lewy bodies, Creutzfeldt–Jakob disease, vitamin B12 deficiency, hypothyroidism, hydrocephalus, multi-infarct dementia, and toxic exposures such as carbon monoxide poisoning. Careful clinical assessment is essential to avoid misdiagnosis.
Management in the emergency department focuses on symptom control, identification and treatment of triggers, and prevention of complications. Antiparkinsonian medications may be initiated or adjusted in consultation with neurology. Patients with mild disease may not require immediate pharmacologic therapy, while those with moderate disease often benefit from dopaminergic or anticholinergic agents. Underlying infections or metabolic disturbances should be treated promptly. Parkinsonism–hyperpyrexia syndrome requires urgent replacement of dopaminergic therapy, supportive care, and management of associated complications.
Common medications used in Parkinson disease include carbidopa/levodopa as first-line therapy, dopamine agonists such as pramipexole and ropinirole, MAO-B inhibitors like selegiline and rasagiline, anticholinergics such as benztropine for tremor-dominant disease, and amantadine to stimulate dopamine release. Adjunctive agents like entacapone may be used to enhance levodopa bioavailability. In parkinsonism–hyperpyrexia syndrome, intravenous or enteral levodopa and bromocriptine are essential.
Admission is indicated for patients with Parkinson disease who present with serious medical conditions such as infection, trauma, cardiovascular or cerebrovascular emergencies, electrolyte disturbances, altered mental status, medication complications, failure to thrive, or suspected abuse. Patients with depression and suicidal intent or complications related to deep brain stimulation devices also require inpatient care. Stable patients with mild to moderate disease may be discharged with medications and urgent outpatient neurology follow-up.
Key clinical pearls include recognizing that Parkinson disease can be difficult to diagnose and is frequently confused with other neurologic conditions. Sudden withdrawal of dopaminergic medications is a medical emergency and must be avoided. In the emergency setting, vigilance for systemic illness, medication noncompliance, and life-threatening complications is critical to optimal patient outcomes.
- Published on
Emergency and Acute Medicine – Paraphimosis
Paraphimosis is a urologic emergency defined by entrapment of the retracted foreskin proximal to the glans penis. This entrapment leads to progressive lymphatic congestion and venous obstruction, which can ultimately compromise arterial blood flow to the glans. If not promptly recognized and treated, paraphimosis may result in ischemia, necrosis, and permanent penile injury.
The condition most commonly occurs when the foreskin is retracted and not returned to its normal position. Predisposing factors include phimosis, inflammation, trauma, and sexual inexperience, particularly in individuals unaware of the need to reduce the foreskin after intercourse. Paraphimosis is frequently iatrogenic, occurring after physical examination, urinary catheterization, cystoscopy, or genital hygiene when the foreskin is left retracted.
Patients typically present with penile pain, a visibly retracted foreskin, and a swollen, edematous glans. The glans may appear erythematous, dusky, or cyanotic as venous congestion progresses. Local cellulitis may be present, and in advanced or untreated cases, necrosis of the glans can develop. Physical examination should include careful inspection of the entire penis to exclude constricting foreign bodies or bands, such as hair tourniquets, wire, or string, which can mimic paraphimosis.
The diagnosis of paraphimosis is clinical and should be made based on history and physical examination alone. Treatment must not be delayed for laboratory or imaging studies. Imaging is generally unnecessary unless a foreign body is suspected, in which case radiographs may be obtained after restoration of adequate perfusion.
Initial management focuses on rapid reduction of edema and prompt return of the foreskin to its normal position to restore blood flow. Pain control is essential and may require local anesthesia, a penile nerve block, systemic analgesia, or conscious sedation, especially in children. Ice packs may be applied to the glans to reduce swelling while preparations for reduction are made. Manual reduction is the first-line treatment and involves circumferential compression of the edematous glans while simultaneously applying traction to advance the foreskin distally over the glans.
If manual reduction is unsuccessful, additional techniques may be employed to reduce edema. These include the multiple puncture technique, in which small-gauge needle punctures are made in the swollen foreskin to allow expression of edema fluid, followed by another attempt at manual reduction. Osmotic methods, such as application of gauze soaked in 50% dextrose, may also help decrease edema if immediate reduction is delayed. When noninvasive methods fail, a dorsal slit of the foreskin may be required to release the constricting ring. In some cases, suturing may be necessary after reduction if the incision is extensive.
Antibiotics are generally not required unless there is associated cellulitis or balanoposthitis. Once reduction is successful and symptoms resolve, most patients can be discharged with close urologic follow-up. Admission is indicated for patients with penile necrosis, severe infection, or inability to achieve reduction. Urologic consultation is recommended in all cases, and circumcision may be considered to prevent recurrence, although this remains a topic of clinical debate.
Patient education is essential to prevent recurrence. Patients should be instructed on proper foreskin hygiene and the importance of returning the foreskin to its normal position after retraction for cleaning, sexual activity, or medical procedures. Early recognition and prompt management are key to preventing serious complications of paraphimosis.
Paraphimosis is a urologic emergency defined by entrapment of the retracted foreskin proximal to the glans penis. This entrapment leads to progressive lymphatic congestion and venous obstruction, which can ultimately compromise arterial blood flow to the glans. If not promptly recognized and treated, paraphimosis may result in ischemia, necrosis, and permanent penile injury.
The condition most commonly occurs when the foreskin is retracted and not returned to its normal position. Predisposing factors include phimosis, inflammation, trauma, and sexual inexperience, particularly in individuals unaware of the need to reduce the foreskin after intercourse. Paraphimosis is frequently iatrogenic, occurring after physical examination, urinary catheterization, cystoscopy, or genital hygiene when the foreskin is left retracted.
Patients typically present with penile pain, a visibly retracted foreskin, and a swollen, edematous glans. The glans may appear erythematous, dusky, or cyanotic as venous congestion progresses. Local cellulitis may be present, and in advanced or untreated cases, necrosis of the glans can develop. Physical examination should include careful inspection of the entire penis to exclude constricting foreign bodies or bands, such as hair tourniquets, wire, or string, which can mimic paraphimosis.
The diagnosis of paraphimosis is clinical and should be made based on history and physical examination alone. Treatment must not be delayed for laboratory or imaging studies. Imaging is generally unnecessary unless a foreign body is suspected, in which case radiographs may be obtained after restoration of adequate perfusion.
Initial management focuses on rapid reduction of edema and prompt return of the foreskin to its normal position to restore blood flow. Pain control is essential and may require local anesthesia, a penile nerve block, systemic analgesia, or conscious sedation, especially in children. Ice packs may be applied to the glans to reduce swelling while preparations for reduction are made. Manual reduction is the first-line treatment and involves circumferential compression of the edematous glans while simultaneously applying traction to advance the foreskin distally over the glans.
If manual reduction is unsuccessful, additional techniques may be employed to reduce edema. These include the multiple puncture technique, in which small-gauge needle punctures are made in the swollen foreskin to allow expression of edema fluid, followed by another attempt at manual reduction. Osmotic methods, such as application of gauze soaked in 50% dextrose, may also help decrease edema if immediate reduction is delayed. When noninvasive methods fail, a dorsal slit of the foreskin may be required to release the constricting ring. In some cases, suturing may be necessary after reduction if the incision is extensive.
Antibiotics are generally not required unless there is associated cellulitis or balanoposthitis. Once reduction is successful and symptoms resolve, most patients can be discharged with close urologic follow-up. Admission is indicated for patients with penile necrosis, severe infection, or inability to achieve reduction. Urologic consultation is recommended in all cases, and circumcision may be considered to prevent recurrence, although this remains a topic of clinical debate.
Patient education is essential to prevent recurrence. Patients should be instructed on proper foreskin hygiene and the importance of returning the foreskin to its normal position after retraction for cleaning, sexual activity, or medical procedures. Early recognition and prompt management are key to preventing serious complications of paraphimosis.
