Emergency and Acute Medicine: Tympanic Membrane Perforation




Tympanic membrane (TM) perforation refers to a disruption or hole in the eardrum and can be classified by duration, location, and extent. Acute perforations are defined as those present for less than 3 months, whereas chronic perforations persist beyond this period. Anatomically, perforations may involve the pars tensa or pars flaccida, and the extent may range from small defects confined to one quadrant to total perforations involving the entire membrane.


The most common cause of acute TM perforation is infection, particularly acute otitis media, where increased middle ear pressure leads to rupture. Trauma is another frequent cause and may be blunt, such as a slap to the ear (often seen in assaults or domestic violence), or penetrating, such as injury from cotton swabs (Q-tips). Rapid pressure changes from activities like diving or flying can also cause rupture (barotrauma), as can blast injuries, extreme noise exposure, lightning strikes, and thermal injuries such as slag burns during welding. Less commonly, perforation may result from surgical procedures (e.g., myringotomy or tympanostomy tube placement) or infections like acute necrotizing myringitis.


Patients typically present with mild ear pain, though severe pain or complete hearing loss may indicate more serious associated injury. Other common symptoms include tinnitus, vertigo (especially if injury occurs in water), and partial hearing loss. On physical examination, findings may include visible perforation on otoscopy, decreased hearing, and purulent or bloody discharge from the ear canal. Small perforations may only be detected by decreased mobility of the tympanic membrane during pneumatic otoscopy. Special tests such as the Weber and Rinne tuning fork tests help differentiate conductive from sensorineural hearing loss. The presence of nystagmus or vertigo during pressure testing may suggest a more serious inner ear injury such as a labyrinthine fistula.


Diagnosis is primarily clinical, based on direct visualization of the tympanic membrane and hearing assessment. If discharge is present, culture may be considered. Imaging, particularly CT of the temporal bone, is reserved for cases where a temporal bone fracture or more severe injury is suspected.


Management in the emergency setting focuses on supportive care and prevention of complications. Initial stabilization follows standard trauma principles when indicated. The ear canal should be gently cleared of debris using suction or manual removal, but irrigation must be avoided to prevent forcing contaminants into the middle ear. Routine prophylactic antibiotics are not necessary; however, antibiotics should be prescribed if there is evidence of infection or contamination (e.g., water exposure). Common options include amoxicillin or amoxicillin-clavulanate. Ototopical antibiotics—particularly fluoroquinolone drops such as ciprofloxacin with dexamethasone—are preferred in cases of chronic suppurative otitis media or when contamination is suspected, as they are safer with respect to ototoxicity compared to other agents.


Urgent ENT consultation is indicated in patients with concerning features such as vertigo, sensorineural hearing loss, severe tinnitus, significant bleeding, or facial nerve paralysis. Most patients can be safely discharged with outpatient follow-up. Nearly all tympanic membrane perforations heal spontaneously, especially small ones—many within weeks to months. Surgical repair (e.g., tympanoplasty) is reserved for the minority (10–20%) that fail to heal.


Patients should be given clear discharge instructions to prevent complications. They should keep the ear dry by occluding it during showering, avoid swimming unless protected, and refrain from forceful nose blowing. Prognosis is generally excellent, though complications such as infection, ossicular disruption, perilymph leakage, or cholesteatoma can occur in some cases.


Key clinical pearls include recognizing acute otitis media as the most common cause, avoiding irrigation of the ear, and understanding that most perforations heal without intervention. Proper protection of the ear from water and contaminants is essential to promote healing and prevent infection.

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Emergency and Acute Medicine: Ultraviolet Keratitis




Ultraviolet keratitis is a painful ocular condition caused by corneal epithelial damage following exposure to ultraviolet (UV) light. Also known as photokeratitis, snow blindness, UV conjunctivitis, or welder’s flash, it results from absorption of UV radiation—particularly at wavelengths around 290 nm—by the corneal epithelium. This exposure damages epithelial cells and penetrates to nociceptor nerve endings, leading to intense pain due to subepithelial nerve stimulation.


The condition is commonly associated with occupational exposures such as welding, electrical work, and mechanical tasks, as well as recreational exposures including skiing, snowboarding, water sports, and use of tanning beds. The severity of injury is directly related to the intensity and duration of UV exposure. Importantly, patients are often unaware of the exposure at the time of injury.


Symptoms typically develop with a delay of 6–12 hours after exposure. Patients usually present with bilateral eye pain, photophobia, tearing, and redness. A foreign-body sensation is commonly reported, but purulent discharge is absent. Additional findings may include eyelid edema, facial erythema, and blepharospasm. On examination, visual acuity may be mildly decreased. Conjunctival injection, chemosis, and excessive tearing are typical. Slit-lamp examination with fluorescein staining reveals multiple superficial punctate epithelial lesions across the cornea, which are characteristic of the condition.


Diagnosis is clinical and relies heavily on history and physical examination. A key diagnostic clue is a history of UV exposure several hours prior to symptom onset. Evaluation should include assessment of visual acuity, extraocular movements, and a detailed ocular exam with fluorescein staining. Lid eversion is important to rule out retained foreign bodies, and the anterior chamber should be assessed for signs of inflammation such as cells or flare. Laboratory tests and imaging are generally not required unless other injuries are suspected.


Management is primarily supportive, as ultraviolet keratitis is a self-limited condition. In the emergency setting, topical anesthetics may be used to facilitate examination but should not be prescribed for outpatient use due to the risk of delayed healing and corneal ulceration. Treatment includes oral analgesics such as ibuprofen or acetaminophen (with or without opioids for severe pain), topical antibiotic ointment (e.g., erythromycin) to prevent secondary infection, and short-acting cycloplegic agents to relieve ciliary spasm. Eye patching may provide comfort but does not accelerate healing.


Disposition is generally outpatient, as most cases resolve completely within 24–72 hours. Admission is rarely required but may be considered in cases of severe visual impairment, inability to care for oneself, or when both eyes are patched and functional vision is significantly impaired. Follow-up with an ophthalmologist within 24–48 hours is recommended to ensure proper healing and symptom resolution.


Key clinical pearls include recognizing the delayed onset of symptoms after UV exposure, which is critical for diagnosis, and understanding that the condition, while extremely painful, is typically benign and self-limited. Preventive measures are essential—individuals at risk should use appropriate UV-protective eyewear, as regular glasses or contact lenses do not provide adequate protection.

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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 – Toxic Shock Syndrome (TSS)




Toxic shock syndrome (TSS) is a severe, acute, life-threatening illness caused by toxin-producing bacteria, most commonly Staphylococcus aureus and less commonly Group A Streptococcus (referred to as streptococcal toxic shock syndrome, STSS). These organisms produce exotoxins such as toxic shock syndrome toxin (TSST-1) and streptococcal pyrogenic exotoxins, which act as superantigens. These toxins trigger massive cytokine release, leading to fever, immune dysregulation, and profound vasodilation with capillary leak, ultimately resulting in hypotension and shock.


The etiology of TSS has evolved over time. Initially associated with menstruating women using highly absorbent tampons, modern cases are now frequently nonmenstrual. These include infections related to surgical wounds, postpartum infections, burns, nasal packing, mastitis, osteomyelitis, and soft tissue infections. Many individuals are asymptomatic carriers of S. aureus in areas such as the nasal passages, skin, or genital tract. In streptococcal TSS, infection often follows minor trauma and may present with severe pain even before visible signs of infection appear.


Clinically, TSS is diagnosed using criteria established by the CDC. Patients typically present with high fever (>38.9°C), hypotension, and a diffuse blanching macular erythroderma rash. This rash is followed 1–2 weeks later by desquamation, especially of the palms and soles. Multisystem involvement is a hallmark and includes gastrointestinal symptoms (vomiting, diarrhea), musculoskeletal involvement (severe myalgias or elevated creatine phosphokinase), mucosal hyperemia (conjunctival, oral, or vaginal), renal dysfunction, hepatic involvement, hematologic abnormalities such as thrombocytopenia, and central nervous system symptoms including confusion or hallucinations.


Streptococcal TSS differs slightly in presentation and diagnostic criteria. It requires isolation of Group A Streptococcus from a sterile site, hypotension, and evidence of organ dysfunction such as renal failure, coagulopathy, liver dysfunction, acute respiratory distress syndrome, or soft tissue necrosis. A key distinguishing feature is severe pain, often out of proportion to physical findings, which may indicate deep soft tissue infection such as necrotizing fasciitis.


Laboratory findings are nonspecific but reflect systemic inflammation and organ dysfunction. These may include leukocytosis or leukopenia, elevated creatinine and liver enzymes, thrombocytopenia, electrolyte abnormalities (such as hypocalcemia), and elevated creatine phosphokinase. Cultures from blood or suspected infection sites should be obtained, although blood cultures are not always positive in staphylococcal TSS. Imaging such as chest radiography or CT may help identify the source of infection or complications.


The differential diagnosis includes Kawasaki disease, Scarlet fever, Stevens-Johnson syndrome, Rocky Mountain spotted fever, and meningococcemia. Differentiation is essential because management strategies differ significantly.


Management of TSS is a medical emergency and focuses on rapid stabilization and source control. Prehospital care includes airway management, IV access, and fluid resuscitation. In the emergency department, aggressive management of shock is critical, often requiring large volumes of intravenous fluids (up to 4–20 L in the first 24 hours). If hypotension persists, vasopressors such as norepinephrine or dopamine are initiated.


Identifying and removing the source of infection is essential, such as removing tampons, nasal packing, or infected wound material. Early surgical consultation is necessary if drainage or debridement is required, particularly in cases of suspected necrotizing infection.


Antibiotic therapy should be initiated promptly. Regimens typically include clindamycin or linezolid to suppress toxin production, combined with agents such as vancomycin for broad coverage. For confirmed methicillin-sensitive S. aureus, oxacillin or nafcillin may be used. In streptococcal TSS, broader-spectrum regimens including beta-lactams and clindamycin are recommended. Intravenous immunoglobulin (IVIG) may be considered, particularly in streptococcal TSS or refractory shock.


All patients with TSS require hospital admission, and most require intensive care due to the risk of rapid progression to multiorgan failure.


Key clinical pearls include recognizing the combination of fever, rash, hypotension, and multisystem involvement, and initiating aggressive supportive care immediately. Early antibiotic therapy, toxin suppression, and prompt source control are critical for survival.

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Emergency and Acute Medicine – Toxoplasmosis

Emergency and Acute Medicine – Toxoplasmosis


Toxoplasmosis is an infection caused by Toxoplasma gondii, an intracellular protozoan that exists in three forms: tachyzoites (actively replicating), tissue cysts (chronic latent form), and oocysts (shed in cat feces). Transmission occurs primarily through ingestion of undercooked meat containing tissue cysts, ingestion of food or water contaminated with oocysts, or contact with cat feces or contaminated soil. Less common routes include transplacental transmission, blood transfusion, and organ transplantation.


Toxoplasmosis is extremely common worldwide, with approximately 70% of adults demonstrating prior exposure. Most immunocompetent individuals remain asymptomatic. Cats serve as the definitive host, and the incubation period typically ranges from 4 to 21 days.


Clinical manifestations vary depending on the host’s immune status and the type of infection. In immunocompromised patients, particularly those with HIV/AIDS, toxoplasmosis most commonly presents as encephalitis. Symptoms are typically subacute and include headache, fever, altered mental status, seizures, cranial nerve deficits, and focal neurologic signs. Neuropsychiatric symptoms such as psychosis, paranoia, or dementia may also occur. Pulmonary involvement may present as pneumonitis with dyspnea and nonproductive cough.


In immunocompetent individuals, approximately 90% of infections are asymptomatic. When symptoms occur, they usually present as a self-limited mononucleosis-like illness with cervical lymphadenopathy, fever, malaise, sore throat, and occasionally hepatosplenomegaly or rash. Rarely, severe complications such as encephalitis or pneumonitis may occur.


Ocular toxoplasmosis is an important manifestation, often presenting with blurred vision, scotoma, pain, and photophobia. Examination may reveal chorioretinitis with characteristic yellow-white retinal lesions. This form is particularly common in individuals with untreated congenital infection and may lead to long-term visual impairment.


Congenital toxoplasmosis results from maternal infection during pregnancy. Infection during the first trimester is associated with severe outcomes such as miscarriage or stillbirth, while later infections are more likely to be transmitted to the fetus but may present with delayed manifestations. Many affected infants are asymptomatic at birth but later develop neurologic or ocular complications, including blindness, seizures, or developmental delay.


Diagnosis involves a combination of clinical suspicion and laboratory testing. Detection of the organism may be achieved through analysis of blood, cerebrospinal fluid, bronchoalveolar lavage, or amniotic fluid. Serologic testing for IgM and IgG antibodies is commonly used, although interpretation can be challenging due to false positives and negatives. Imaging plays a key role in CNS disease: CT or MRI typically shows multiple bilateral ring-enhancing lesions. Chest radiography may reveal a reticulonodular pattern in pulmonary involvement.


The differential diagnosis includes Cryptococcal meningitis, Primary CNS lymphoma, Pneumocystis pneumonia, Cytomegalovirus retinitis, and mycobacterial infections, particularly in immunocompromised patients.


Management depends on disease severity and host immune status. Immunocompetent patients with mild disease typically require no treatment. Symptomatic or severe cases are treated with a combination of pyrimethamine, sulfadiazine, and folinic acid, or alternatively clindamycin in patients with sulfa allergy.


Immunocompromised patients require prompt and aggressive therapy, often initiated empirically when characteristic brain lesions are present. Treatment typically continues for 4–6 weeks after symptom resolution, and long-term prophylaxis may be necessary, particularly in patients with HIV.


Ocular disease is treated similarly, often with the addition of corticosteroids in cases involving the macula or optic nerve. In pregnancy, management is complex and requires specialist consultation; spiramycin is typically used early in pregnancy to reduce fetal transmission risk.


Patients with severe systemic disease, CNS involvement, or immunocompromise require hospital admission. Immunocompetent patients with mild disease can usually be managed as outpatients with follow-up.


Key clinical pearls include recognizing that toxoplasmosis is often asymptomatic in healthy individuals but can cause life-threatening disease in immunocompromised patients. CNS toxoplasmosis should always be suspected in patients with HIV presenting with focal neurologic deficits and ring-enhancing brain lesions. Prevention, particularly in pregnant women, includes avoiding undercooked meat and exposure to cat litter or contaminated soil.

Emergency and Acute Medicine – Transfusion Complications




Transfusion complications are relatively common clinical events associated with blood product administration, ranging from mild allergic reactions to life-threatening conditions. Approximately 5–6% of hospitalized patients receive transfusions, and about 2% of transfused units result in some type of reaction within 24 hours. Although mortality is rare, complications can be severe, especially with acute hemolytic reactions or pulmonary syndromes.


Noninfectious complications are more common than infectious ones. Febrile nonhemolytic reactions occur in approximately 1 in 500 red blood cell transfusions and are characterized by fever and chills due to antigen–antibody reactions involving leukocytes or cytokines. Allergic reactions are relatively frequent and usually mild, presenting with urticaria or pruritus, while anaphylaxis is rare but potentially fatal. Acute hemolytic transfusion reactions, often due to ABO incompatibility, are uncommon but dangerous, occurring in roughly 1 in 38,000 to 70,000 transfusions. Delayed hemolytic reactions occur days later and are typically less severe.


Transfusion-associated circulatory overload (TACO) is relatively common, particularly in elderly or volume-sensitive patients, and presents with signs of fluid overload such as dyspnea and hypertension. Transfusion-related acute lung injury (TRALI) is a serious complication presenting within 6 hours of transfusion with acute respiratory distress, bilateral pulmonary infiltrates, and normal cardiac function. It is a leading cause of transfusion-related mortality and must be distinguished from TACO and Acute Respiratory Distress Syndrome.


Other important complications include electrolyte disturbances such as hypocalcemia (due to citrate binding calcium) and hyperkalemia (from stored blood breakdown), iron overload with repeated transfusions, and rare but fatal graft-versus-host disease. Infectious complications are now rare due to screening but include transmission of viruses such as HIV, Hepatitis B, and Hepatitis C, as well as bacterial contamination (especially in platelet transfusions), which remains the most common infectious cause of mortality.


Acute intravascular hemolytic transfusion reactions are the most severe form and typically occur immediately due to ABO incompatibility, often from clerical or identification errors. Even small volumes (5–20 mL) can trigger symptoms. These reactions result in rapid destruction of transfused red blood cells, triggering a cascade involving cytokine release, activation of the coagulation system, and potential progression to shock, disseminated intravascular coagulation, renal failure, and respiratory failure.


Clinical manifestations of transfusion reactions vary widely but commonly include fever, chills, urticaria, dyspnea, hypotension, chest pain, nausea, and hemoglobinuria. Severe reactions may present with shock, bleeding, renal failure, or respiratory distress. The classic triad of fever, flank pain, and dark urine in hemolytic reactions is uncommon but highly suggestive when present.


Evaluation begins with immediate recognition of symptoms and verification of patient and blood product identity. Laboratory testing includes CBC, electrolytes, renal function, coagulation studies, bilirubin, and a direct Coombs test. Hemolysis may be indicated by hemoglobinemia or hemoglobinuria. Imaging such as chest x-ray is useful when pulmonary complications like TRALI are suspected, typically showing bilateral infiltrates without cardiomegaly.


Management requires immediate cessation of the transfusion as the first and most critical step. Supportive care follows the ABC approach, including oxygen supplementation and hemodynamic stabilization. Intravenous fluids with normal saline are used for hypotension, while avoiding lactated solutions or dextrose-containing fluids. Maintaining adequate urine output is essential to prevent renal failure, often requiring diuretics such as furosemide or osmotic agents like mannitol.


Febrile reactions are treated with antipyretics, while allergic reactions are managed with antihistamines such as diphenhydramine. Severe allergic or anaphylactic reactions require prompt administration of epinephrine and corticosteroids. In cases of electrolyte disturbances, calcium replacement may be necessary. If disseminated intravascular coagulation develops, it must be treated accordingly.


Patients with severe reactions, including hemolysis, anaphylaxis, pulmonary complications, or sepsis, require ICU admission and close monitoring. Mild febrile or allergic reactions may be managed conservatively and discharged with appropriate follow-up.


Key clinical pearls include the importance of strict patient identification and cross-matching procedures to prevent catastrophic hemolytic reactions. Clinicians should always suspect hemolysis when hypotension, dark urine, or unexplained bleeding occurs during transfusion. Additionally, transfusions should be used judiciously, as they carry significant risks despite their lifesaving potential.

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Emergency and Acute Medicine – Transient Global Amnesia




Transient global amnesia (TGA) is a sudden, temporary episode of memory loss characterized by abrupt onset of profound anterograde amnesia without other focal neurologic deficits. Patients are unable to form new memories during the episode, resulting in repetitive questioning and confusion about recent events. Despite this, personal identity—such as name, birth date, and address—remains intact. After recovery, there is typically a permanent memory gap corresponding to the duration of the episode, while previously stored memories gradually return.


TGA is relatively uncommon, with an incidence of approximately 3–8 cases per 100,000 people, most often affecting individuals between 50 and 70 years of age. It is rare in patients younger than 40. Episodes usually last between 1 and 8 hours, although durations can range from 15 minutes up to 24 hours, and by definition must resolve within that time frame.


The exact cause of TGA remains unclear. Imaging studies such as MRI, SPECT, and PET have demonstrated transient abnormalities in the hippocampus, a brain region critical for memory formation. Proposed mechanisms include transient venous congestion of the hippocampus during Valsalva-like activities, vasoconstriction related to hyperventilation, and migraine-associated phenomena. Importantly, there is no established link between TGA and thromboembolic stroke or other forms of Cerebrovascular disease.


Diagnosis is clinical and relies on strict criteria. The episode must be witnessed, with sudden onset of anterograde amnesia and no alteration in consciousness. There should be no focal neurologic deficits, seizure activity, or recent head trauma. Cognitive function remains intact aside from memory impairment, and the patient retains awareness of self. The episode must resolve within 24 hours, and alternative causes of amnesia must be excluded.


Patients often present after a triggering event such as physical exertion, emotional stress, sexual activity, temperature extremes, or Valsalva maneuvers. They may repeatedly ask questions like “Where am I?” or “How did I get here?” while remaining cooperative and able to follow complex commands. Associated symptoms such as mild headache, dizziness, or nausea may occur at onset.


On examination, patients demonstrate marked anterograde amnesia but are otherwise neurologically normal. They are alert, attentive, and oriented to personal identity. They can perform complex tasks and do not exhibit aphasia, apraxia, or agnosia. Importantly, they are not globally confused, somnolent, or inattentive—features that would suggest alternative diagnoses such as encephalopathy.


In classic cases, no diagnostic testing is required. However, if the diagnosis is uncertain, further evaluation may include laboratory testing to rule out metabolic or toxic causes, imaging such as MRI (which may show transient hippocampal lesions), CT scan for structural pathology, EEG for seizure activity, or lumbar puncture if encephalitis is suspected.


The differential diagnosis includes transient ischemic attack involving posterior circulation, complex partial seizures, psychogenic amnesia, metabolic encephalopathy, and early dementia such as Alzheimer disease. These conditions can usually be distinguished by additional neurologic findings, altered consciousness, shorter or recurrent episodes, or broader cognitive impairment.


Management of TGA is supportive, as the condition is self-limited and benign. Patients should be observed until symptoms resolve, and reassurance should be provided to both the patient and family. No specific pharmacologic treatment is indicated.


Disposition depends on clinical certainty and recovery. Patients with a clear diagnosis and resolving symptoms, along with good social support, can be safely discharged. Admission is appropriate for patients with uncertain diagnosis, incomplete resolution, or inadequate support at home.


The recurrence rate of TGA is relatively low, around 8%. Patients with recurrent episodes should be referred to a neurologist for further evaluation, including possible EEG to exclude seizure disorders.


Key clinical pearls include recognizing TGA as a benign condition characterized by isolated anterograde amnesia with preserved identity and normal neurologic exam. Clinicians must remain vigilant for red flags such as focal deficits, impaired consciousness, or recurrent brief episodes, which may indicate more serious conditions like seizure, encephalitis, or vascular events.

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Emergency and Acute Medicine – Transient Ischemic Attack (TIA)




A transient ischemic attack (TIA) is a brief episode of neurologic dysfunction caused by a temporary reduction in blood flow to a region of the central nervous system. Traditionally defined as symptoms lasting less than 24 hours, most TIAs resolve within one hour. Importantly, TIA is a major warning sign for impending stroke, with approximately 12–30% of strokes preceded by a TIA.


The underlying mechanism involves transient cerebral hypoperfusion. Common causes include atherosclerotic thrombosis in large or medium arteries, small vessel disease, and emboli originating from the heart—particularly in conditions such as Atrial fibrillation. Less common causes include arterial dissection, vasculitis, and hypercoagulable states, while in a significant proportion of patients, no clear etiology is identified.


Clinical presentation depends on the vascular territory affected. Large-vessel TIAs produce characteristic focal deficits. For example, involvement of the middle cerebral artery causes contralateral weakness and sensory loss affecting the face and arm more than the leg, often accompanied by aphasia (dominant hemisphere) or neglect (nondominant hemisphere). Posterior circulation TIAs may present with vertigo, ataxia, diplopia, or cranial nerve deficits. Transient monocular blindness, known as amaurosis fugax, reflects involvement of the ophthalmic branch of the internal carotid artery. Small-vessel (lacunar) TIAs typically produce isolated motor or sensory deficits without cortical signs.


The history is critical in diagnosis. TIAs typically have sudden onset, short duration, and produce “negative” neurologic symptoms such as weakness, vision loss, or aphasia due to loss of function. In contrast, gradual onset or “positive” symptoms such as tingling, jerking, or visual scintillations suggest alternative diagnoses like migraine or seizure.


Physical examination should include a detailed neurologic assessment, evaluating strength, sensation, coordination, speech, and visual fields. By definition, neurologic deficits resolve in TIA; persistent deficits indicate an acute Ischemic stroke rather than TIA. Standardized tools such as the NIH Stroke Scale can aid in assessment and monitoring.


Initial evaluation in the emergency setting focuses on excluding mimics and identifying risk factors. A rapid bedside glucose test is essential, as hypoglycemia can mimic focal neurologic deficits. A noncontrast CT scan of the head should be obtained urgently to exclude intracranial hemorrhage. MRI with diffusion-weighted imaging is more sensitive and may reveal infarction in up to 50% of patients initially thought to have TIA. Vascular imaging of the head and neck—via CT angiography, MR angiography, or carotid ultrasound—is important, as nearly half of patients have significant arterial stenosis or occlusion.


Additional workup includes ECG to detect arrhythmias such as atrial fibrillation and echocardiography to evaluate for cardiac sources of emboli. Laboratory tests assess metabolic abnormalities,

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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: 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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