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 – 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 – 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 – 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 – 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 – 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 – 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 – 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 – 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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