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.

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.

​Emergency and Acute Medicine – Panic Attack

Panic attacks are characterized by sudden episodes of intense fear accompanied by prominent physical symptoms that peak rapidly, usually within 10 minutes, and resolve within approximately 20–30 minutes. Some patients, particularly those with medical illness, may experience a nonfearful variant dominated by somatic symptoms. Panic disorder is defined by recurrent, unexpected panic attacks followed by at least one month of persistent concern about additional attacks, worry about their implications, or maladaptive behavioral changes such as avoidance. Panic disorder may occur with or without agoraphobia, which reflects anxiety related to fear of being unable to escape or obtain help. The condition is often episodic or chronic and is frequently comorbid with depression, substance use disorders, functional disability, and increased suicidal risk.

The underlying mechanism involves dysregulation of the limbic system with excessive norepinephrine release and altered serotonergic and benzodiazepine receptor function, triggering a maladaptive “fight-or-flight” response. Genetic factors play an important role, with family history of panic or anxiety disorders commonly reported. Risk factors include major life stressors in the year preceding onset, childhood shyness or separation anxiety, female sex, and stimulant use such as cocaine. Panic attacks may initially arise in the context of physical illness or substance use and persist even after the precipitating condition has resolved.

Clinical presentation reflects widespread autonomic activation. Cardiac symptoms include palpitations, tachycardia, and chest discomfort. Respiratory complaints such as shortness of breath, choking sensations, or smothering feelings are common. Neurologic and systemic symptoms include tremor, dizziness, lightheadedness, paresthesias, sweating, chills, flushing, and feelings of unreality or depersonalization. Gastrointestinal symptoms such as nausea, cramping, and abdominal pain may occur. Intense, stereotyped fears often center on imminent death, having a heart attack, losing control, or “going crazy.” A thorough history should explore medical conditions, medications (including over-the-counter and herbal products), substance and caffeine use, age at onset, triggering stressors, avoidance behaviors, prior treatment response, and family history of anxiety or substance use.

Physical examination should be complete and focused on cardiopulmonary and neurologic systems, guided by presenting symptoms. The essential workup is individualized and often minimal, aimed at excluding organic causes suggested by the history or exam. Laboratory evaluation may include basic metabolic studies, glucose, thyroid-stimulating hormone, and toxicology screening. Electrocardiography is appropriate for patients over 40 years of age, those with cardiac symptoms, or those taking tricyclic antidepressants. Additional testing such as Holter monitoring, arterial blood gases, or EEG is reserved for specific indications.

The differential diagnosis is broad and must be carefully considered, particularly in first presentations, late-onset cases, or atypical features. Cardiopulmonary causes include myocardial ischemia, arrhythmias, pulmonary embolism, asthma, and pneumonia. Metabolic and endocrine disorders include hypoglycemia, hyperthyroidism, electrolyte abnormalities, and pheochromocytoma. Neurologic conditions such as seizures or transient ischemic attack, medication effects, substance intoxication or withdrawal, and other psychiatric disorders including PTSD, obsessive-compulsive disorder, and somatoform disorders must also be considered.

Initial management focuses on calm reassurance and patient education. Most panic attacks resolve spontaneously, and excessive medical intervention may reinforce fear. Explaining the physiologic basis of symptoms can reduce distress and interrupt the cycle of escalating anxiety. In the emergency department, short-acting, high-potency benzodiazepines may be used for severe or persistent symptoms. Lorazepam is often preferred due to its rapid onset and smoother offset. Clonazepam is effective but has a slower onset and is better suited for maintenance therapy rather than acute control. Alprazolam should generally be avoided due to rapid offset and risk of rebound anxiety. Long-term management of recurrent panic attacks or panic disorder relies on cognitive–behavioral therapy and selective serotonin reuptake inhibitors, which should be initiated in the outpatient setting when follow-up is assured.

Admission is rarely required unless needed to exclude a serious medical condition or for psychiatric indications such as suicidality. Most patients can be safely discharged once symptoms resolve, with reassurance and clear follow-up plans. Referral to primary care or mental health services is recommended for recurrent attacks, interepisode anxiety, or avoidance behaviors. Patients should be counseled to avoid triggers such as caffeine, stimulants, and alcohol. Key pearls include recognizing that panic attacks are self-limited, maintaining a calm clinical approach, using medications judiciously, and emphasizing nonpharmacologic strategies such as cognitive–behavioral therapy to achieve durable symptom control.

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.

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.

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.

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.

Emergency and Acute Medicine – Patent Ductus Arteriosus

Patent ductus arteriosus (PDA) is a condition in which the fetal vessel connecting the pulmonary trunk to the descending aorta fails to close after birth. Normally, shortly after delivery, increased oxygen tension and changes in prostaglandin metabolism lead to ductal constriction, closure, and eventual fibrosis. In preterm infants, persistent patency may represent a physiologic and sometimes life-saving response related to hypoxia and immaturity. In contrast, persistence of the ductus in full-term infants represents a true congenital malformation due to structural deficiencies of the ductal wall.

As pulmonary vascular resistance falls after birth, blood is shunted from the aorta into the pulmonary artery, producing a left-to-right shunt. The magnitude of shunting depends on ductal size and the relative pulmonary and systemic vascular resistances, and in severe cases up to 70% of left ventricular output may pass through the ductus. Risk factors include prematurity, hypoxic conditions, high altitude, maternal rubella infection, and coexisting congenital heart disease, with a female predominance.

Clinical presentation varies with ductal size. Small PDAs may be asymptomatic, whereas larger shunts can lead to congestive heart failure, often within the first days of life. Typical findings include wide pulse pressure, a prominent apical impulse, a palpable thrill, and a characteristic continuous “machinery” murmur best heard at the second left intercostal space and radiating along the left sternal border. Additional features may include recurrent pulmonary infections and failure to thrive.

Diagnosis is primarily established through imaging. Chest radiography may be normal in infants but can show increased pulmonary vascular markings, cardiac chamber enlargement, and dilated great vessels in older patients. Electrocardiography may reveal left ventricular hypertrophy, with right ventricular hypertrophy indicating more severe disease. Echocardiography with Doppler is the diagnostic modality of choice, allowing visualization of ductal size, left atrial enlargement, and continuous aortic-to-pulmonary flow. Cardiac catheterization confirms shunting when needed and may be used therapeutically.

Management depends on patient age, symptoms, and ductal significance. Small, asymptomatic PDAs may be observed. In preterm infants, pharmacologic closure with prostaglandin synthesis inhibitors such as indomethacin is often effective during the first week of life. Full-term infants and children generally require definitive closure, as spontaneous resolution is rare; options include surgical ligation or transcatheter occlusion techniques. Supportive care includes oxygen for heart failure, fluid and sodium restriction, correction of anemia, and endocarditis prophylaxis when indicated.

Admission is required for patients with heart failure, pulmonary hypertension, or suspected endocarditis. Asymptomatic patients may be discharged with close cardiology follow-up and plans for elective closure. Key clinical points include recognition that heart failure may reduce renal perfusion and urine output, and that indomethacin therapy carries risks such as gastrointestinal bleeding.

Emergency and Acute Medicine – Nonsteroidal Anti-Inflammatory Poisoning

Nonsteroidal anti-inflammatory drugs (NSAIDs) exert their effects by inhibiting cyclooxygenase (COX), thereby blocking the conversion of arachidonic acid to prostaglandins. In most cases, NSAID ingestion results in low morbidity, and toxicity is usually mild. Much of the published toxicity data involves ibuprofen, largely because of its widespread over-the-counter availability. Fatal outcomes are rare but have been reported with massive ingestions. Patients with underlying congestive heart failure or renal insufficiency are at increased risk of toxicity because NSAIDs promote sodium and water retention and reduce renal blood flow. Experience with COX-2 inhibitors such as celecoxib in overdose is limited, but management is similar to that of traditional NSAIDs. Patients may still ingest rofecoxib or valdecoxib from stored supplies despite their withdrawal from the US market.

NSAIDs are available both by prescription and over the counter and include agents such as ibuprofen, naproxen, diclofenac, ketorolac, indomethacin, meloxicam, sulindac, piroxicam, and others. Toxic effects vary slightly among agents, but the overall clinical approach remains similar.

Clinical manifestations primarily involve the gastrointestinal and central nervous systems. Gastrointestinal symptoms include nausea, vomiting, and epigastric pain. Neurologic findings range from drowsiness, dizziness, and lethargy to aseptic meningitis and seizures in severe cases. Cardiovascular effects may include hypotension and tachycardia. Pulmonary complications such as eosinophilic pneumonia, apnea, or hyperventilation are uncommon but reported. Renal effects include acute renal failure, hyperkalemia, acute tubular necrosis, and acute interstitial nephritis. Hepatic injury may present as hepatocellular damage or cholestatic jaundice, particularly with diclofenac or sulindac. Metabolic effects are usually limited to a mild, transient metabolic acidosis. Hypersensitivity reactions can occur and include asthma exacerbations, angioedema, urticaria, and aseptic meningitis.

Evaluation begins with a focused history and assessment of the specific NSAID ingested, as subtle toxicologic differences exist between agents. Most cases result in mild toxicity, but identification of the drug is helpful because aseptic meningitis is more commonly associated with ibuprofen, while liver toxicity is more frequently seen with diclofenac and sulindac.

Laboratory evaluation should include electrolytes, blood urea nitrogen, creatinine, and glucose to assess baseline renal function and metabolic status. A complete blood count and arterial blood gas are indicated in large overdoses or if metabolic acidosis is suspected. Coagulation studies may be obtained, noting that etodolac can cause false-positive bilirubin or ketone dipstick results. Acetaminophen and salicylate levels should be obtained in all suspected NSAID ingestions, as patients often confuse these medications. Toxicology screens are not useful because NSAIDs are difficult to detect and results do not alter management.

The differential diagnosis includes other causes of metabolic acidosis, gastrointestinal irritation, and altered mental status, such as salicylate poisoning, isoniazid toxicity, ethylene glycol, methanol, and isopropanol ingestion.

Management is largely supportive. Prehospital care should focus on bringing all medication containers for identification. Initial stabilization follows standard airway, breathing, and circulation principles, with administration of naloxone, thiamine, and dextrose for altered mental status when indicated. In the emergency department, activated charcoal may be administered if the patient presents early after ingestion. Enhanced elimination techniques such as hemodialysis are not effective due to the high degree of plasma protein binding of NSAIDs.

Admission is indicated for patients with persistent vomiting, hematemesis, central nervous system depression, seizures, metabolic acidosis, hypotension or hypertension, congestive heart failure, or renal failure. Asymptomatic patients with nontoxic ingestions who remain well after 6–8 hours of observation may be safely discharged. Intentional ingestions warrant psychiatric evaluation and follow-up.

Key clinical points include the generally benign nature of NSAID poisoning, the importance of evaluating for coingestions, and the routine measurement of acetaminophen and salicylate levels. Massive overdoses and patients with underlying cardiac or renal disease carry a higher risk of significant toxicity and require closer monitoring.