Emergency and Acute Medicine – Transplant Rejection




Transplant rejection is an immune-mediated response against a transplanted organ due to recognition of genetically dissimilar antigens, most commonly related to human leukocyte antigen (HLA) incompatibility. Although blood group incompatibility plays a lesser role, it can still result in severe reactions such as hyperacute rejection, particularly in vascularized organs like the kidney and heart. Rejection remains a significant cause of morbidity in transplant recipients, although infection is a more common reason for emergency department presentation.


Rejection is classically divided into three phases. Hyperacute rejection occurs immediately after transplantation and is caused by preformed antibodies against donor antigens, leading to endothelial injury, platelet aggregation, thrombosis, and rapid graft necrosis. This form is now rare due to improved donor–recipient matching. Acute rejection typically occurs within the first three months but can happen at any time, especially with reduction or noncompliance with immunosuppressive therapy. It is primarily T-cell–mediated and results in inflammatory infiltration and destruction of the graft. Chronic rejection develops over months to years and leads to progressive fibrosis and eventual organ failure.


The epidemiology of transplantation shows that kidney transplants are the most common, followed by liver, heart, lung, and pancreas. Despite advances in immunosuppressive therapy, rejection still accounts for a portion of emergency visits and hospital admissions. A major contributing factor is medication noncompliance or drug interactions affecting levels of immunosuppressive agents such as cyclosporine or tacrolimus.


Clinical presentation varies depending on the transplanted organ. Renal transplant rejection may present with hypertension, decreased urine output, and sometimes swelling or fever, although symptoms may be subtle due to immunosuppression. Liver transplant rejection often manifests as fever, right upper quadrant pain, and jaundice. Heart transplant rejection may present with dyspnea, chest pain, arrhythmias, hypotension or hypertension, and can even be asymptomatic or lead to sudden death. Lung transplant rejection typically presents with cough, dyspnea, fever, and abnormal lung sounds. Bone marrow transplant rejection, including graft-versus-host disease, can involve multiple systems, presenting with fever, rash, gastrointestinal symptoms, pulmonary findings, and neurologic complications.


Evaluation requires a high index of suspicion, as symptoms may be mild or nonspecific. Laboratory testing includes complete blood count, immunosuppressant drug levels, and organ-specific markers such as creatinine for kidney transplants, liver function tests for liver transplants, and cardiac biomarkers for heart transplants. Imaging plays an important role, including chest radiography for lung involvement, ultrasound for renal or hepatic grafts, and echocardiography for cardiac function. In some cases, biopsy is required to distinguish rejection from infection. Opportunistic infections such as Cytomegalovirus infection or fungal infections like Aspergillosis may mimic rejection and must always be considered.


Management in the emergency setting begins with stabilization following standard ABC principles. Shock should be treated with fluids and vasopressors as needed, while hypertensive crises are managed according to standard protocols. A key principle is early communication with the transplant team before initiating or modifying therapy. High-dose corticosteroids are commonly used in suspected acute rejection, and stress-dose steroids should be considered in ill transplant patients. Care must be taken with medications such as NSAIDs and blood transfusions due to potential complications in this population.


Special considerations apply to specific organs. In heart transplant patients, atropine is ineffective for bradycardia due to lack of vagal innervation, and alternative therapies such as dopamine, epinephrine, or pacing are required. Lung transplant patients often require treatment for both infection and rejection simultaneously. Bone marrow transplant patients with graft-versus-host disease typically require systemic corticosteroids and adjustments in immunosuppressive therapy.


Disposition depends on severity. Most transplant patients presenting with symptoms suggestive of rejection, infection, or organ dysfunction require hospital admission, and many need ICU-level care. Patients who are stable and in whom serious causes have been excluded may be discharged with close follow-up in coordination with their transplant team.


Key clinical pearls include maintaining a broad differential diagnosis, as infection and drug toxicity frequently mimic rejection. Even minor complaints in transplant patients warrant thorough evaluation. Early consultation with transplant specialists is essential, and a low threshold for admission is appropriate given the high risk of complications.

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Emergency and Acute Medicine – Trauma, Multiple




Multiple trauma refers to patients with more than one serious injury requiring a structured and prioritized approach to maximize survival. Management follows a standardized system designed for rapid assessment and intervention, recognizing that life-threatening injuries must be addressed immediately. Although often described sequentially, many steps occur simultaneously in real clinical practice. Continuous reassessment is critical—any deterioration requires repeating the primary survey.


The causes of multiple trauma are varied and include motor vehicle and motorcycle crashes, falls from height, assaults, aviation or train accidents, and mass-casualty incidents such as terrorism. Triage decisions are guided by local protocols, but patients with unstable vital signs or those requiring surgical, neurosurgical, or orthopedic intervention should be transported to a Level I trauma center whenever possible.


Initial evaluation begins with the primary survey using the ABCDE approach. Airway assessment is the first priority, ensuring patency while maintaining cervical spine immobilization in patients with significant mechanisms of injury or altered mental status. Signs such as stridor, gurgling, or absent air movement indicate immediate airway intervention is required before proceeding further.


Breathing is assessed next by evaluating chest wall movement, breath sounds, respiratory rate, and oxygen saturation. Findings such as asymmetry, hypoxia, or decreased breath sounds may indicate life-threatening conditions like tension pneumothorax or hemothorax, which require immediate intervention such as needle thoracostomy followed by chest tube placement.


Circulation focuses on identifying and managing shock. Assessment includes blood pressure, heart rate, pulse quality, mental status, urine output, and capillary refill. Early signs like tachycardia and decreased urine output suggest evolving shock, while hypotension is a late and critical finding. Hemorrhage must be rapidly identified and controlled, including external bleeding with direct pressure and internal bleeding through appropriate imaging and intervention.


Disability involves a rapid neurologic assessment, commonly using the Glasgow Coma Scale. A score of 8 or less indicates severe brain injury and necessitates airway protection and intracranial pressure management. Pupillary size and reactivity help assess brainstem function, while motor function provides clues to spinal cord injury.


Exposure requires complete undressing of the patient to identify hidden injuries while preventing hypothermia. Once the patient is stabilized, a secondary survey is performed, consisting of a thorough head-to-toe examination and detailed history, often obtained from emergency medical services.


Diagnostic evaluation includes essential imaging such as cervical spine and chest radiographs, with pelvic imaging when indicated. Laboratory studies include hemoglobin, coagulation profile, arterial blood gases, and type and crossmatch. Advanced imaging depends on patient stability: hemodynamically stable patients typically undergo CT scanning, while unstable patients benefit from bedside ultrasound such as the FAST (Focused Assessment with Sonography for Trauma) exam. Many centers now use “pan-CT” imaging to reduce missed injuries, though this increases radiation exposure.


Treatment parallels the primary survey. Airway management may involve rapid sequence intubation or surgical airway if necessary. Breathing is supported with oxygen and interventions for conditions like pneumothorax or pulmonary contusion. Circulatory support includes large-bore IV access, aggressive fluid resuscitation, blood transfusion when needed, and control of hemorrhage. Special situations such as pericardial tamponade require emergent procedures like pericardiocentesis. Neurologic management includes measures to reduce intracranial pressure, such as head elevation and osmotic therapy.


Definitive management is often surgical, and early involvement of trauma surgeons and subspecialists is essential. Most patients with significant trauma require hospital admission, frequently to an intensive care unit for close monitoring. Patients with minor injuries and negative evaluations may be observed and discharged if stable.


Key principles include strict adherence to the ABCDE approach, maintaining a high suspicion for occult injuries, and rapid escalation of care when needed. Trauma systems rely on coordinated, multidisciplinary care to optimize outcomes, and early transfer to appropriate facilities plays a crucial role in survival.

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Emergency and Acute Medicine – Trichomonas




Trichomonas infection is a common sexually transmitted disease caused by the protozoan Trichomonas vaginalis. It primarily affects the urogenital tract and is associated with a high prevalence of coexisting sexually transmitted infections. It can lead to important complications, including premature rupture of membranes, preterm labor, and low-birth-weight infants in pregnancy, and it may facilitate transmission of HIV. The infection is widespread, with millions of cases annually, and many individuals remain asymptomatic.


Transmission occurs through sexual contact, and the organism is a flagellated protozoan that commonly resides in the urethra, bladder, and Skene glands. The incubation period ranges from 4 to 28 days. Despite its prevalence, a significant proportion of infected individuals—particularly men—remain asymptomatic, contributing to ongoing transmission.


In females, the infection often presents as vaginitis. Symptoms may include vaginal discharge, although this is present in fewer than one-third of patients. When present, the discharge is classically described as frothy and yellow-green or gray-white, often accompanied by vulvar itching, irritation, and malodor. Dysuria, urinary urgency, and dyspareunia may also occur. On examination, findings may include diffuse cervical erythema or the characteristic “strawberry cervix” caused by punctate hemorrhages, though this is relatively uncommon. Abdominal pain is not typical.


In males, infection is frequently asymptomatic or self-limited. When symptoms occur, they usually manifest as nongonococcal urethritis, with mild dysuria, urinary urgency, and scant urethral discharge. Complications can include prostatitis, epididymitis, and, rarely, reversible infertility. Male-to-male transmission is uncommon.


Diagnosis is often clinical but can be supported by laboratory testing. In females, a saline wet mount examination of vaginal or cervical secretions may reveal motile, pear-shaped, flagellated organisms, though sensitivity is only about 60–70% and requires immediate evaluation. Elevated vaginal pH (>4.5) is common but nonspecific. Culture remains highly sensitive (around 95%) and is useful when suspicion is high but microscopy is negative. PCR testing is highly accurate but not always widely available. In males, wet mount is less sensitive, and culture or PCR is more reliable.


The differential diagnosis includes urinary tract infection, gonorrhea, chlamydia, bacterial vaginosis, candidal vaginitis, and nonspecific vaginitis, as symptoms often overlap.


Treatment is straightforward and highly effective. First-line therapy is oral metronidazole 2 g as a single dose, achieving cure rates of 90–95%, or tinidazole 2 g as a single dose. A 7-day course of metronidazole may be used in certain cases, such as urethritis or in HIV-positive patients where single-dose therapy may be less effective. Topical metronidazole gel is not recommended due to lower efficacy.


All sexual partners must be treated simultaneously to prevent reinfection, and patients should abstain from sexual activity until both partners are asymptomatic and treatment is completed. Patients should also avoid alcohol during and for at least 24 hours after metronidazole due to the risk of a disulfiram-like reaction. Condom use should be encouraged to reduce transmission risk.


Most patients can be safely discharged after treatment. Follow-up is generally not required unless symptoms persist or recur.


Important clinical considerations include recognizing that standard treatments for nongonococcal urethritis, such as azithromycin or doxycycline, do not treat Trichomonas vaginalis. Persistent vaginitis or urethritis despite standard therapy should raise suspicion for trichomoniasis.

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Emergency and Acute Medicine – Tricyclic Antidepressant (TCA) Poisoning




Tricyclic antidepressant (TCA) poisoning is a life-threatening toxicologic emergency characterized by rapid clinical deterioration, primarily due to cardiac sodium channel blockade (a quinidine-like effect). Additional mechanisms include inhibition of norepinephrine reuptake, α-adrenergic blockade, and anticholinergic effects. Compared to TCAs, selective serotonin reuptake inhibitors (SSRIs) have a much wider safety margin and less cardiovascular toxicity, while serotonin–norepinephrine reuptake inhibitors (SNRIs), such as venlafaxine, may still cause seizures and dysrhythmias.


Common TCAs involved include amitriptyline, nortriptyline, imipramine, and doxepin. Toxicity can develop quickly after ingestion, and even initially well-appearing patients may deteriorate suddenly with seizures, arrhythmias, or coma.


Clinical manifestations affect multiple systems. In the central nervous system, patients may exhibit either stimulation (agitation, tremor, fasciculations, seizures) or depression (drowsiness, lethargy, coma). Seizures are particularly dangerous, as resulting acidemia worsens cardiotoxicity. Cardiovascular findings are the hallmark and include early sinus tachycardia due to anticholinergic and norepinephrine effects, followed by potential hypotension and late bradycardia from catecholamine depletion. ECG abnormalities are critical: QRS widening greater than 100 ms is associated with seizures, and greater than 160 ms predicts ventricular dysrhythmias. A characteristic finding is a prominent R wave in lead aVR (>3 mm), reflecting rightward terminal QRS axis deviation.


Anticholinergic effects such as dilated pupils, decreased bowel sounds, and urinary retention may occur but are less prominent than cardiac toxicity.


Evaluation centers on rapid recognition and cardiac monitoring. An ECG is the most important diagnostic tool and should be obtained immediately and repeated as needed. Continuous cardiac monitoring is essential. Laboratory tests include electrolytes, renal function, glucose, arterial blood gas, and toxicology screening to assess for coingestants. Serum TCA levels are not useful for guiding management, as they correlate poorly with severity.


Management requires aggressive and early intervention. Initial stabilization follows airway, breathing, and circulation principles, with a low threshold for intubation in patients with altered mental status. Intravenous fluids and oxygen are administered, and cardiac monitoring is continuous.


The cornerstone of treatment is sodium bicarbonate therapy. Indications include QRS widening greater than 100–120 ms or any evidence of cardiac toxicity. Boluses of sodium bicarbonate (1–2 mEq/kg) are given and repeated as needed, with the goal of narrowing the QRS and maintaining an arterial pH of 7.45–7.5. Hyperventilation may assist in achieving this alkalinization. If needed, a bicarbonate infusion can be started.


Dysrhythmias are treated with sodium bicarbonate first; lidocaine may be used as a second-line agent. Class IA and IC antiarrhythmics (e.g., procainamide) and physostigmine are contraindicated, as they can worsen toxicity. Hypotension is managed with IV fluids, and if refractory, norepinephrine is the preferred vasopressor due to its α-agonist effects.


Seizures are treated with benzodiazepines such as diazepam or lorazepam, followed by phenobarbital if needed. Refractory seizures may require neuromuscular paralysis and airway control.


Decontamination with activated charcoal is appropriate if the patient presents early and the airway is protected. Gastric lavage may be considered within 1 hour of ingestion in severe cases. Ipecac is contraindicated due to the risk of aspiration. Flumazenil should not be used, especially in mixed overdoses, as it may precipitate seizures.


Patients require close observation and disposition decisions depend on clinical status. Symptomatic patients, those with ECG abnormalities, altered mental status, seizures, or persistent tachycardia beyond 6 hours should be admitted, often to an intensive care setting. Asymptomatic patients with a normal ECG after 6 hours of observation may be considered for discharge, provided psychiatric evaluation is completed if the ingestion was intentional.


Key clinical points include recognizing that TCA poisoning can deteriorate rapidly, making early ECG monitoring essential. QRS widening is a critical marker of toxicity, and prompt treatment with sodium bicarbonate can be lifesaving.

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Emergency and Acute Medicine – Trigeminal Neuralgia




Trigeminal neuralgia is a distinct facial pain syndrome involving the trigeminal nerve, which provides sensory innervation to the face, oral cavity, nasal mucosa, and cornea. Also known as tic douloureux, the condition is characterized by brief, recurrent episodes of severe facial pain. It most commonly affects individuals over 50 years of age and occurs more frequently in women.


The disorder is divided into two forms. Classical trigeminal neuralgia occurs without an identifiable structural lesion and is typically caused by vascular compression of the nerve root, most often by the superior cerebellar artery. This compression leads to focal demyelination and abnormal nerve firing. Symptomatic trigeminal neuralgia presents with similar clinical features but is caused by an identifiable pathology such as multiple sclerosis, tumors (e.g., cerebellopontine angle tumors), aneurysms, or arteriovenous malformations.


Clinically, patients describe sudden, severe, “electric shock–like” pain affecting one or more divisions of the trigeminal nerve. The maxillary (V2) division is most commonly involved, followed by the mandibular (V3) and ophthalmic (V1) divisions. Pain is usually unilateral and may occur spontaneously or be triggered by light stimuli such as talking, chewing, brushing teeth, shaving, or even gentle touch. Episodes last from a fraction of a second up to 2 minutes and can occur multiple times per day. Between episodes, patients are typically pain-free, although chronic cases may develop a persistent dull ache.


The diagnosis is primarily clinical and based on a characteristic history. Physical examination is usually normal; the presence of neurologic deficits or atypical features—such as bilateral symptoms, prolonged pain, or abnormal cranial nerve findings—should prompt evaluation for secondary causes. Trigger points that reproduce the pain are considered highly suggestive of the diagnosis.


Imaging is not always required in classic cases but is recommended when atypical features are present or when secondary causes are suspected. MRI of the brain is particularly useful for identifying structural lesions such as tumors or demyelinating disease like multiple sclerosis.


Management focuses on pain control. First-line therapy is carbamazepine, an anticonvulsant that is highly effective in reducing symptoms. Alternative or adjunctive medications include gabapentin, oxcarbazepine, lamotrigine, phenytoin, and valproic acid, particularly in refractory cases.


Patients who do not respond to medical therapy may require referral for procedural or surgical interventions. These include percutaneous nerve blocks, radiofrequency ablation, or microvascular decompression, which can provide long-term relief in a significant proportion of patients.


Disposition depends on severity and associated findings. Patients with typical features and good response to treatment can be managed as outpatients with follow-up by a primary care physician or neurologist. Admission is indicated if there are focal neurologic deficits, concerning imaging findings, or refractory pain requiring advanced intervention.


Key clinical points include recognizing the classic presentation of unilateral, paroxysmal, shock-like facial pain and identifying trigger points. It is essential to exclude secondary causes, particularly in younger patients or those with abnormal neurologic findings. Carbamazepine remains the cornerstone of therapy, and early treatment can significantly improve quality of life.

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Emergency and Acute Medicine: Tularemia




Tularemia is an acute febrile zoonotic illness caused by Francisella tularensis, a highly infectious, small aerobic gram-negative intracellular coccobacillus. It is notable for its extreme infectivity—very few organisms are required to cause disease—and lack of person-to-person transmission. Humans acquire infection through environmental exposure, including bites from infected ticks, deerflies, or mosquitoes; direct contact with infected animal tissue (especially rabbits); ingestion of contaminated food or water; or inhalation of aerosolized organisms (e.g., during lawn mowing or farming activities).


There are multiple subspecies of the organism, with Francisella tularensis subspecies tularensis (type A) being more virulent and common in North America, and Francisella tularensis subspecies holartica (type B) causing milder disease. Natural reservoirs include rabbits, rodents, and various wild and domestic animals, while vectors include ticks, biting flies, and mosquitoes. Due to its high virulence and ability to be aerosolized, tularemia has historically been studied as a potential biologic weapon.


Tularemia primarily affects individuals with outdoor exposure in endemic regions, such as farmers, hunters, forestry workers, and those handling animal carcasses. It is most common in the northern hemisphere and peaks during warmer months (June to October). Although relatively rare, it carries a mortality rate of 5–15% if untreated, which decreases to about 1% with appropriate therapy. Pediatric cases account for approximately 25% of infections.


Clinical presentation varies depending on the route of entry, with an incubation period typically of 3–5 days. The most common form is ulceroglandular tularemia, accounting for 70–80% of cases. It begins as a papule at the inoculation site that progresses to a painful ulcer, followed by regional lymphadenopathy and systemic symptoms such as fever, chills, headache, and myalgias. Glandular tularemia presents similarly but without a visible skin lesion. Oculoglandular tularemia occurs when the organism enters through the eye, causing conjunctivitis, chemosis, and regional lymphadenopathy. Pharyngeal tularemia results from ingestion of contaminated material and presents with severe exudative pharyngitis and lymphadenitis.


Pneumonic tularemia arises from inhalation and presents with fever, dry cough, pleuritic chest pain, and potentially severe pneumonia. Typhoidal tularemia is the most severe form, characterized by systemic illness without a clear entry site, often progressing to sepsis, multiorgan failure, and potentially death—particularly with type A strains.


Diagnosis is often challenging due to nonspecific laboratory findings and the absence of rapid diagnostic tests. Routine labs may be normal or show mild inflammatory changes. Blood cultures are often negative due to the organism’s fastidious growth requirements. Definitive diagnosis relies on serology, with antibody titers typically becoming diagnostic only after 10–14 days. Polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) are available in specialized laboratories. Imaging, such as chest radiography, may reveal pneumonia, pleural effusions, or hilar adenopathy in pulmonary cases.


Management in the emergency setting focuses on supportive care and early antibiotic therapy. Initial stabilization includes airway, breathing, and circulation (ABCs), oxygen supplementation for hypoxia, and intravenous fluids for dehydration or septic shock. First-line antimicrobial therapy consists of aminoglycosides, particularly gentamicin or streptomycin, administered for approximately 10 days. Alternative agents include ciprofloxacin or doxycycline, though these are bacteriostatic and associated with higher relapse rates. Importantly, β-lactam antibiotics and carbapenems are ineffective against F. tularensis.


Disposition depends on disease severity. Patients with severe illness, hemodynamic instability, hypoxemia, or typhoidal tularemia require ICU admission. Mild cases may be managed as outpatients with close follow-up and appropriate antibiotic therapy. Infectious disease consultation is recommended, particularly in severe or unclear cases.


Key clinical pearls include maintaining a high index of suspicion in patients presenting with fever and regional lymphadenopathy—especially when accompanied by a skin ulcer or conjunctivitis—and considering epidemiologic exposure history. Diagnosis is often delayed due to reliance on serology, and early empiric treatment is crucial. Tularemia remains a category A bioterrorism agent due to its high infectivity and potential for aerosol dissemination.

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Emergency and Acute Medicine – Toothache




Toothache is a common presentation caused by irritation of the nerve endings within the dental pulp, which contains the tooth’s neurovascular supply. Although most causes are odontogenic, pain may also originate from non-dental sources and be referred to the oral cavity via the distribution of the trigeminal nerve.


The most common etiologies are dental in origin. Dental caries, resulting from bacterial demineralization of tooth structures, can progress to pulpitis, which may be reversible or irreversible depending on severity. Reversible pulpitis causes mild inflammation and transient pain, whereas irreversible pulpitis leads to severe, persistent, and poorly localized pain. If untreated, this may progress to a periapical abscess involving necrotic pulp and surrounding tissues. Other dental causes include periodontal disease (gingivitis and periodontitis), periodontal abscess, pericoronitis (often associated with partially erupted wisdom teeth), cracked-tooth syndrome, postextraction complications such as dry socket, and mucosal conditions such as aphthous ulcers or herpetic gingivostomatitis.


Patients typically present with localized or referred tooth pain that may radiate to the jaw, ear, face, eye, or neck. The pain is often exacerbated by chewing, temperature changes, or lying flat. Associated symptoms may include foul taste, bad breath, fever, or facial swelling. A detailed history should include onset, duration, prior treatments, and associated systemic symptoms.


Physical examination should be thorough and systematic. Findings may include visible dental decay, gingival inflammation, swelling, or trismus (reduced mouth opening). The clinician should inspect and palpate oral structures, assess for lymphadenopathy, and evaluate for signs of deep-space infection such as floor-of-mouth swelling or voice changes. Percussion of teeth may reveal tenderness, and examination for fractures, mobility, or missing teeth is essential. Facial and neck examination should assess for cellulitis, warmth, and stiffness.


Diagnosis is primarily clinical. Laboratory tests are generally not required unless there are signs of systemic toxicity or deep-space infection, in which case inflammatory markers and cultures may be considered. Imaging such as panoramic or periapical radiographs may help identify abscesses or fractures, while CT or MRI is reserved for suspected deep infections. Dental nerve blocks can provide both diagnostic and therapeutic benefit in selected cases.


Management focuses on pain control and treatment of the underlying cause. NSAIDs are first-line therapy for uncomplicated dental pain, with opioids reserved for severe cases. Local or regional dental nerve blocks using long-acting anesthetics such as bupivacaine can provide effective relief. If infection is present, antibiotics are indicated, with penicillin as first-line therapy and clindamycin for penicillin-allergic patients or suspected anaerobic infections.


Localized abscesses should be incised, drained, and irrigated, followed by saline rinses and prompt dental follow-up. Most patients can be discharged with appropriate analgesia, antibiotics if indicated, and referral to a dentist or oral surgeon. However, admission is required for serious complications such as deep-space infections (e.g., Ludwig angina), facial cellulitis near the eye, significant trismus, inability to maintain hydration, or systemic toxicity.


Key clinical pearls include recognizing that dental pain can be referred from non-dental sources such as sinusitis, temporomandibular joint disorders, or even cardiac ischemia. Failure to identify deep-space infections can lead to life-threatening complications, so careful assessment is essential. Prompt dental follow-up is critical, as emergency department treatment is only temporizing and does not address the definitive underlying pathology.

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Emergency and Acute Medicine – Tinea Infections (Cutaneous)




Cutaneous tinea infections are superficial fungal infections involving the hair, skin, or nails, typically confined to the stratum corneum. They are among the most common diseases worldwide and require keratin for growth, which explains why mucosal surfaces are not affected. These infections are named according to their anatomical location. The causative organisms are dermatophytes, primarily species of Microsporum, Trichophyton, and Epidermophyton. In contrast, tinea versicolor is caused by Malassezia furfur, a yeast, and is not a true dermatophyte infection. Transmission may occur via direct contact with infected individuals, animals, or contaminated soil, and skin trauma or maceration facilitates fungal entry. In children, spread can occur through shared items such as toys or brushes, while nail infections are uncommon unless associated with conditions like immunosuppression or Down syndrome.


Clinical presentation varies depending on the site of infection but is generally characterized by itching as the main symptom. Tinea capitis primarily affects children and presents with scalp involvement, including alopecia, scaling, and characteristic “black dots” from broken hairs. Inflammatory forms such as kerion may appear as boggy, purulent masses with associated lymphadenopathy. Tinea corporis, or ringworm, presents as annular lesions with raised, well-demarcated borders and central clearing, commonly affecting the trunk and extremities. Tinea cruris involves the groin, thighs, and buttocks, producing erythematous, scaly patches that typically spare the scrotum and penis, helping differentiate it from candidiasis. Tinea pedis, the most common form in adults, manifests as scaling, maceration, and fissuring between the toes, often associated with moisture and poor foot hygiene. Tinea unguium (onychomycosis) causes thickened, discolored nails with subungual debris and nail separation. Tinea versicolor presents with hypo- or hyperpigmented macules on the upper trunk, arms, and neck, especially in warm climates.


Diagnosis is primarily clinical, based on history and physical examination. If uncertainty exists, confirmation can be achieved through microscopy using potassium hydroxide (KOH) preparation, which demonstrates fungal elements such as septate hyphae in dermatophyte infections or the characteristic “spaghetti and meatballs” pattern in Malassezia. Fungal cultures are generally not necessary due to slow growth. Wood lamp examination has limited utility, as most dermatophytes do not fluoresce, although Microsporum species may appear green and Malassezia yellow-green.


Treatment depends on the site and severity of infection. Most superficial infections such as tinea corporis, cruris, and pedis respond well to topical antifungals, including terbinafine or imidazoles like clotrimazole and miconazole. Keeping the affected area dry and maintaining hygiene are important adjuncts. In contrast, infections involving hair or nails, such as tinea capitis and tinea unguium, require systemic therapy because topical agents do not adequately penetrate these structures. Oral terbinafine is commonly used and is considered first-line for tinea capitis, while longer treatment durations are required for nail infections. Selenium sulfide or ketoconazole shampoos may reduce transmission in scalp infections. Tinea versicolor is typically treated with topical agents such as selenium sulfide shampoo or topical azoles, with oral therapy reserved for extensive or refractory cases.


Most patients improve within 1–2 weeks of treatment, although hair and nail infections require prolonged therapy lasting several months. Patients can usually be managed as outpatients, with hospital admission reserved for rare cases of invasive infection in immunocompromised individuals or complicated kerion with secondary bacterial infection. Follow-up is important for patients on oral antifungal therapy to monitor for adverse effects, particularly hepatotoxicity.


Key clinical pearls include recognizing tinea capitis as the most common dermatophyte infection in children and understanding that itching is the predominant symptom across most forms. Tinea pedis can predispose to cellulitis, and recurrence of infections, particularly in the feet and groin, is common. Preventive measures such as proper hygiene and avoiding sharing personal items are essential to reduce reinfection and transmission.

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Emergency and Acute Medicine – Tick Bite




Tick bites are a common presentation, but the actual risk of acquiring a tick-borne infection is low, even in endemic areas. Most patients seek care because of concern about Lyme disease, proper tick removal, or local skin reactions rather than true systemic illness.


Ticks belong to two main groups: soft ticks (such as Ornithodoros), which feed briefly and are rarely noticed, and hard ticks (especially Ixodes and Dermacentor), which feed for several days and are more clinically relevant. Lyme disease is most commonly transmitted by the nymph stage of Ixodes scapularis (deer tick). Transmission generally requires prolonged attachment, typically 24–48 hours, and the degree of tick engorgement serves as an important indicator of duration and risk.


Clinically, patients usually present with a visible tick attached to the skin and are often otherwise asymptomatic. There may be mild local irritation, redness, or swelling. Patient anxiety about infection is very common. However, red flags include fever after a tick bite, neurologic symptoms (particularly in children, where tick paralysis must be considered), or signs of systemic illness such as hypotension or sepsis, which may suggest serious infections like Rocky Mountain spotted fever, anaplasmosis, or babesiosis. Because early diagnostic tests are often not helpful, these conditions are largely diagnosed based on clinical presentation and epidemiologic context.


Routine laboratory testing is not indicated for simple tick bites. Lyme serology is not useful immediately after a bite because it reflects prior exposure rather than acute infection, and testing the tick itself is not recommended. Management therefore focuses primarily on proper tick removal and clinical observation.


The most important step in management is early and proper removal of the tick. This is done using fine forceps, grasping the tick as close to the skin as possible, and applying slow, steady upward traction over 30–120 seconds. The tick should not be squeezed, twisted, burned, or covered with substances such as petroleum jelly, as these methods may increase the risk of pathogen transmission. If mouthparts remain embedded in the skin, they may cause local irritation or a foreign body reaction but do not increase the risk of systemic infection.


Antibiotic prophylaxis for Lyme disease is only indicated in specific circumstances. These include identification of an engorged Ixodes scapularis tick, likely attachment for at least 24–48 hours, and removal within 72 hours. In such cases, a single dose of doxycycline 200 mg is recommended. In children, a single-dose regimen is not well studied, and amoxicillin for 10 days may be used instead. There is no evidence to support prophylactic antibiotics for other tick-borne diseases.


Supportive care consists of wound cleaning, reassurance, and education. Most patients can be safely discharged after tick removal. Admission is reserved for those with signs of systemic illness, tick paralysis, or severe tick-borne infection.


Patients should be advised to seek medical attention if they develop fever, rash (particularly an expanding rash suggestive of erythema migrans), joint pain, or neurologic symptoms. Preventive counseling is important and includes the use of insect repellents such as DEET and wearing permethrin-treated clothing in endemic areas.


Key clinical pearls include the importance of early tick removal in reducing infection risk and the selective—not routine—use of antibiotic prophylaxis. Clinicians should always inquire about tick exposure in febrile patients. In children presenting with unexplained weakness, especially girls with long hair, careful scalp examination is essential to rule out tick paralysis.

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​Infectious Disease And Microbiology – Endophthalmitis


Endophthalmitis is a severe infectious condition involving the ocular (vitreous) cavity, while panophthalmitis refers to inflammation affecting all structures of the eye. It is a vision-threatening emergency most commonly occurring after ocular surgery, trauma, or via hematogenous spread from a distant infection.


The incidence of endophthalmitis after cataract surgery ranges from 0.1–0.3%, whereas it is significantly higher after penetrating ocular trauma (3–30%), especially when intraocular foreign bodies are present. Major risk factors include untreated eyelid disease (such as blepharitis), poor surgical technique, prolonged operative time, and intraoperative complications. Endogenous endophthalmitis is more likely in chronically ill, diabetic, or immunocompromised patients, particularly those with indwelling intravenous catheters or bloodstream infections.


Prevention strategies include routine postoperative use of topical fluoroquinolones after cataract surgery, although definitive evidence of benefit is limited. Intracameral cefuroxime has been shown to reduce postoperative risk. In high-risk penetrating ocular injuries, systemic prophylaxis with vancomycin or moxifloxacin may be used. For anterior segment trauma, intensive topical antibiotics or subconjunctival injections may achieve adequate antimicrobial levels. Patients with systemic infections, especially fungemia due to Candida species, should be monitored for possible endogenous spread to the eye.


The pathophysiology differs depending on the source. In postoperative cases, organisms from the eyelid or conjunctiva may enter through surgical wounds. In endogenous cases, pathogens disseminate hematogenously and initially involve the choroid before extending into the vitreous cavity.


Endophthalmitis may be caused by bacteria, fungi, or parasites. Common bacterial pathogens include Staphylococcus, Streptococcus, Pseudomonas, and Escherichia coli. Fungal causes include Candida, Aspergillus, and Fusarium. Parasitic causes include Taenia solium, Toxocara canis, and Toxoplasma gondii. Acute postoperative cases are most often due to Gram-positive organisms, whereas more severe infections and worse outcomes are associated with Gram-negative bacteria and streptococci. Trauma-related infections frequently involve mixed organisms, especially in rural injuries contaminated with organic material.


Clinically, most patients present with ocular pain, redness (conjunctival injection), photophobia, and reduced vision. In some cases, visual loss may be the only symptom. More aggressive infections, such as those caused by Bacillus cereus, can present rapidly with severe pain and profound vision loss. Panophthalmitis may cause pain with eye movement.


On examination, key findings include vitreous opacities, which are essential for diagnosis, and hypopyon (layering of white blood cells in the anterior chamber). Chorioretinal infiltrates are characteristic of endogenous infection.


Diagnosis involves obtaining aqueous and vitreous samples for microscopy and culture. Smears should be stained using Gram, Giemsa, and special fungal stains, and cultured for aerobic and anaerobic bacteria, mycobacteria, and fungi. Culture positivity is approximately 70% in postoperative cases. Imaging with ocular ultrasonography or CT scan is useful when visualization is limited or when a retained intraocular foreign body is suspected.


The differential diagnosis includes noninfectious causes such as uveitis, toxic anterior segment syndrome (TASS), and sterile postoperative inflammation due to retained lens fragments.


Management is an ophthalmologic emergency requiring immediate treatment. First-line therapy for acute postoperative bacterial endophthalmitis includes intravitreal injection of vancomycin for Gram-positive coverage and ceftazidime (or amikacin in β-lactam allergy) for Gram-negative coverage. Intensive topical antibiotics are also used. Systemic antibiotics are generally not beneficial in routine postoperative cases but may be considered with newer fluoroquinolones due to good ocular penetration.


In endogenous endophthalmitis, systemic antimicrobial therapy targeting the primary source is essential in addition to intravitreal treatment. For fungal infections, intravitreal amphotericin B is commonly used, though retinal toxicity must be considered. Systemic antifungal therapy is required in endogenous disease, with alternatives such as fluconazole, voriconazole, or caspofungin.


Supportive treatment includes pain management and cycloplegic eye drops. Corticosteroids may be used topically or periocularly to reduce inflammation, although systemic or intravitreal use remains controversial. Early referral to an ophthalmologist is critical.


Surgical intervention with pars plana vitrectomy is indicated in severe cases, especially when visual acuity is limited to light perception or worse. This procedure helps remove infectious material, toxins, and inflammatory debris, thereby improving outcomes.


Patients are typically managed as outpatients unless special circumstances require admission. Close daily follow-up is essential. If there is no improvement or worsening within 48 hours, repeat intravitreal antibiotics and/or vitrectomy should be considered.


Prognosis varies depending on the cause. Postoperative endophthalmitis has better outcomes than traumatic cases. After cataract surgery, approximately 50% of patients may achieve visual acuity of 20/40 or better, while outcomes are poorer in traumatic infections. Infections caused by Bacillus cereus have a particularly poor prognosis. Complications include permanent vision loss, retinal detachment, secondary glaucoma, and phthisis bulbi.