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Emergency And Acute Medicine – Reperfusion Therapy, Cardiac
Cardiac reperfusion therapy is indicated for patients presenting with ST-segment elevation myocardial infarction (STEMI), which results from acute occlusion of an epicardial coronary artery, usually due to thrombus formation. Early restoration of coronary blood flow reduces myocardial necrosis, morbidity, and mortality. The two primary reperfusion strategies are percutaneous coronary intervention (PCI) and fibrinolytic therapy. In unstable angina (UA) and non–ST-segment elevation myocardial infarction (NSTEMI), early PCI may be considered, but fibrinolytics are not indicated.
Primary PCI is the preferred reperfusion method when it can be performed in a timely fashion. The goal is a door-to-balloon time of 90 minutes from first medical contact in STEMI patients presenting to PCI-capable centers, or within 120 minutes if transfer from a non-PCI facility is required. PCI includes balloon angioplasty, stent placement, and thrombus removal. It achieves higher rates of coronary patency, lower mortality and reinfarction rates, reduced bleeding risk compared with fibrinolytics, and immediate assessment of coronary anatomy. Stent placement decreases early and late luminal loss compared with balloon angioplasty alone. PCI should also be strongly considered within 48 hours for NSTEMI patients after cardiology consultation. Post–cardiac arrest patients may undergo therapeutic hypothermia prior to or during PCI.
Fibrinolytic therapy is indicated in STEMI when PCI cannot be performed within 120 minutes. The goal is a door-to-needle time of 30 minutes. Earlier administration results in greater myocardial salvage. Fibrinolytics are contraindicated in patients with active bleeding, recent hemorrhagic stroke, recent intracranial surgery or trauma, intracranial neoplasm or vascular malformation, severe uncontrolled hypertension, pregnancy, or recent major trauma or surgery.
Adjunctive pharmacotherapy is essential in both PCI and fibrinolytic strategies. Aspirin should be administered immediately. Dual antiplatelet therapy with clopidogrel, prasugrel (contraindicated in prior stroke), or ticagrelor should be added. Anticoagulation with unfractionated heparin, low-molecular-weight heparin (such as enoxaparin), or bivalirudin is indicated in STEMI (whether treated with PCI or fibrinolytics) and in UA/NSTEMI. Low-molecular-weight heparin has more predictable pharmacokinetics and lower bleeding risk compared with unfractionated heparin. Glycoprotein IIb/IIIa inhibitors may be used in patients undergoing PCI but are not indicated in STEMI without PCI. Statin therapy should be initiated early as it reduces subsequent cardiovascular events.
Patients typically present with chest pain described as pressure or heaviness, dyspnea, radiation to the arm, neck, or back, diaphoresis, nausea, vomiting, weakness, palpitations, or syncope. Diagnosis relies on history and ECG findings. STEMI is defined by new ST-segment elevation at the J point in two contiguous leads meeting sex-specific criteria or new ST changes consistent with acute infarction. Left bundle branch block may obscure diagnosis; Sgarbossa criteria can aid interpretation. ECGs may initially be normal and should be repeated if suspicion remains high. Troponin is the preferred cardiac biomarker. Baseline creatinine, hematocrit, and coagulation studies are also obtained. Chest radiograph may be helpful if aortic dissection is suspected.
Prehospital care includes intravenous access, oxygen if hypoxic, cardiac monitoring, sublingual nitroglycerin (unless phosphodiesterase inhibitors were recently used), and aspirin 162–325 mg nonenteric coated. STEMI patients should be transported preferentially to PCI-capable facilities. In the emergency department, continuous cardiac monitoring, blood pressure monitoring, oxygen, nitrates, and analgesia are initiated. β-blockers such as metoprolol may be administered unless contraindicated. Fibrinolytics are given only when PCI is unavailable within the recommended timeframe and no contraindications exist.
All patients undergoing reperfusion therapy require hospital admission to a cardiac catheterization laboratory, intensive care unit, or telemetry unit. No patient considered for reperfusion therapy should be discharged from the emergency department.
The central goal of reperfusion therapy in STEMI is rapid restoration of coronary blood flow, preferably with primary PCI within 90 minutes of first medical contact. If PCI cannot be achieved within 120 minutes, fibrinolytic therapy should be administered within 30 minutes of arrival. Prompt recognition, rapid decision-making, and adherence to time targets are critical determinants of survival.
Cardiac reperfusion therapy is indicated for patients presenting with ST-segment elevation myocardial infarction (STEMI), which results from acute occlusion of an epicardial coronary artery, usually due to thrombus formation. Early restoration of coronary blood flow reduces myocardial necrosis, morbidity, and mortality. The two primary reperfusion strategies are percutaneous coronary intervention (PCI) and fibrinolytic therapy. In unstable angina (UA) and non–ST-segment elevation myocardial infarction (NSTEMI), early PCI may be considered, but fibrinolytics are not indicated.
Primary PCI is the preferred reperfusion method when it can be performed in a timely fashion. The goal is a door-to-balloon time of 90 minutes from first medical contact in STEMI patients presenting to PCI-capable centers, or within 120 minutes if transfer from a non-PCI facility is required. PCI includes balloon angioplasty, stent placement, and thrombus removal. It achieves higher rates of coronary patency, lower mortality and reinfarction rates, reduced bleeding risk compared with fibrinolytics, and immediate assessment of coronary anatomy. Stent placement decreases early and late luminal loss compared with balloon angioplasty alone. PCI should also be strongly considered within 48 hours for NSTEMI patients after cardiology consultation. Post–cardiac arrest patients may undergo therapeutic hypothermia prior to or during PCI.
Fibrinolytic therapy is indicated in STEMI when PCI cannot be performed within 120 minutes. The goal is a door-to-needle time of 30 minutes. Earlier administration results in greater myocardial salvage. Fibrinolytics are contraindicated in patients with active bleeding, recent hemorrhagic stroke, recent intracranial surgery or trauma, intracranial neoplasm or vascular malformation, severe uncontrolled hypertension, pregnancy, or recent major trauma or surgery.
Adjunctive pharmacotherapy is essential in both PCI and fibrinolytic strategies. Aspirin should be administered immediately. Dual antiplatelet therapy with clopidogrel, prasugrel (contraindicated in prior stroke), or ticagrelor should be added. Anticoagulation with unfractionated heparin, low-molecular-weight heparin (such as enoxaparin), or bivalirudin is indicated in STEMI (whether treated with PCI or fibrinolytics) and in UA/NSTEMI. Low-molecular-weight heparin has more predictable pharmacokinetics and lower bleeding risk compared with unfractionated heparin. Glycoprotein IIb/IIIa inhibitors may be used in patients undergoing PCI but are not indicated in STEMI without PCI. Statin therapy should be initiated early as it reduces subsequent cardiovascular events.
Patients typically present with chest pain described as pressure or heaviness, dyspnea, radiation to the arm, neck, or back, diaphoresis, nausea, vomiting, weakness, palpitations, or syncope. Diagnosis relies on history and ECG findings. STEMI is defined by new ST-segment elevation at the J point in two contiguous leads meeting sex-specific criteria or new ST changes consistent with acute infarction. Left bundle branch block may obscure diagnosis; Sgarbossa criteria can aid interpretation. ECGs may initially be normal and should be repeated if suspicion remains high. Troponin is the preferred cardiac biomarker. Baseline creatinine, hematocrit, and coagulation studies are also obtained. Chest radiograph may be helpful if aortic dissection is suspected.
Prehospital care includes intravenous access, oxygen if hypoxic, cardiac monitoring, sublingual nitroglycerin (unless phosphodiesterase inhibitors were recently used), and aspirin 162–325 mg nonenteric coated. STEMI patients should be transported preferentially to PCI-capable facilities. In the emergency department, continuous cardiac monitoring, blood pressure monitoring, oxygen, nitrates, and analgesia are initiated. β-blockers such as metoprolol may be administered unless contraindicated. Fibrinolytics are given only when PCI is unavailable within the recommended timeframe and no contraindications exist.
All patients undergoing reperfusion therapy require hospital admission to a cardiac catheterization laboratory, intensive care unit, or telemetry unit. No patient considered for reperfusion therapy should be discharged from the emergency department.
The central goal of reperfusion therapy in STEMI is rapid restoration of coronary blood flow, preferably with primary PCI within 90 minutes of first medical contact. If PCI cannot be achieved within 120 minutes, fibrinolytic therapy should be administered within 30 minutes of arrival. Prompt recognition, rapid decision-making, and adherence to time targets are critical determinants of survival.
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Emergency And Acute Medicine – Cerebral Reperfusion Therapy
Cerebral reperfusion therapy is indicated for acute ischemic stroke, defined as a sudden interruption of regional cerebral blood flow resulting in focal neurologic deficits. Reperfusion strategies include intravenous thrombolysis to dissolve thromboembolic occlusion, intra-arterial thrombolysis, and mechanical thrombectomy. The primary goal is rapid restoration of cerebral perfusion to salvage ischemic penumbra and reduce long-term disability. “Time is brain,” and treatment decisions are highly time dependent.
Ischemic stroke may be thrombotic, embolic, or due to other vascular occlusive processes. Thrombotic stroke results from in situ thrombosis, often at an ulcerated atherosclerotic plaque or from hypercoagulable states such as antithrombin III, protein C, or protein S deficiency. Sludging syndromes such as sickle cell disease or polycythemia vera may also contribute. Embolic stroke commonly arises from cardiac sources including atrial fibrillation, mural thrombus after myocardial infarction, cardiomyopathy, ventricular aneurysm, or prosthetic valves. Arterial sources include aortic or carotid atherosclerotic plaques. Other causes include vascular dissection and vasospasm from subarachnoid hemorrhage or vasoconstrictive agents such as cocaine.
Patients typically present with acute focal neurologic deficits within 4.5 hours of onset. Determining the exact time of symptom onset is critical. If unknown, the time last known well is used. Symptoms correspond to vascular territories. Middle cerebral artery involvement may cause contralateral hemiplegia (face and arm more than leg), hemisensory loss, homonymous hemianopsia, aphasia in the dominant hemisphere, or neglect. Posterior cerebral artery infarction may cause visual field deficits or visual agnosia. Vertebrobasilar strokes can present with vertigo, nystagmus, dysarthria, cranial nerve deficits, ataxia, and crossed sensory findings. Anterior cerebral artery infarction typically affects the contralateral leg more than the arm and may produce apraxia or behavioral changes. Lacunar infarcts may produce pure motor or pure sensory syndromes. Stroke severity is quantified using the National Institutes of Health Stroke Scale (NIHSS), which standardizes neurologic assessment and helps predict prognosis and hemorrhagic risk.
Initial evaluation includes immediate bedside glucose testing to exclude hypoglycemia. Laboratory studies include CBC and coagulation studies (PT/PTT) to assess bleeding risk prior to thrombolysis. A noncontrast head CT scan must be obtained emergently to exclude intracranial hemorrhage. Early ischemic changes may be subtle or absent in the first hours. Additional studies may include ECG to assess for arrhythmia or myocardial ischemia, serum electrolytes, renal function, pregnancy testing, and toxicology screening when indicated. Advanced imaging such as diffusion-weighted MRI, CT perfusion, CT angiography, or MR angiography may identify salvageable tissue and vascular occlusion but should not delay timely thrombolysis when indicated.
Intravenous alteplase (tPA) is indicated in eligible patients aged 18 years or older with clearly defined symptom onset within 4.5 hours and no evidence of hemorrhage on CT. Absolute contraindications include recent stroke or intracranial surgery within 3 months, prior intracranial hemorrhage, suspected subarachnoid hemorrhage, active bleeding, severe uncontrolled hypertension (>185/110 mm Hg), coagulopathy, thrombocytopenia, elevated INR, recent heparin with elevated aPTT, hypoglycemia <50 mg />L, or large established infarction involving more than one third of a cerebral hemisphere. Between 3 and 4.5 hours, additional exclusion criteria apply, including age over 80 years, oral anticoagulant use, NIHSS greater than 25, large MCA territory involvement, or history of both stroke and diabetes.
Blood pressure must be controlled to ≤185/110 mm Hg before thrombolysis and maintained below 180/105 mm Hg after treatment. Labetalol or nicardipine are commonly used. Alteplase is administered at 0.9 mg/kg (maximum 90 mg), with 10% given as an initial bolus over 1 minute and the remainder infused over 60 minutes. Antiplatelet and anticoagulant agents should be withheld for 24 hours. Blood pressure and neurologic status must be monitored frequently during and after infusion. Complications include intracranial hemorrhage, which occurs in up to 6% of treated patients and more commonly in those with severe strokes. If hemorrhage is suspected, tPA should be discontinued and emergent CT performed. Management includes reversal with cryoprecipitate, fibrinogen, platelets, and neurosurgical consultation.
Mechanical thrombectomy or intra-arterial therapy may be considered in selected patients with large vessel occlusion, often within 6 hours of onset, and sometimes beyond in specialized centers based on advanced imaging criteria. These approaches are particularly valuable in patients who are ineligible for IV thrombolysis or who have persistent large vessel occlusion despite treatment.
All patients receiving reperfusion therapy must be admitted to an intensive care or dedicated stroke unit for close neurologic and hemodynamic monitoring. Rapid recognition, precise determination of symptom onset, strict adherence to inclusion and exclusion criteria, and careful blood pressure management are critical. Even brief delays in therapy can significantly reduce the likelihood of meaningful neurologic recovery.
Cerebral reperfusion therapy is indicated for acute ischemic stroke, defined as a sudden interruption of regional cerebral blood flow resulting in focal neurologic deficits. Reperfusion strategies include intravenous thrombolysis to dissolve thromboembolic occlusion, intra-arterial thrombolysis, and mechanical thrombectomy. The primary goal is rapid restoration of cerebral perfusion to salvage ischemic penumbra and reduce long-term disability. “Time is brain,” and treatment decisions are highly time dependent.
Ischemic stroke may be thrombotic, embolic, or due to other vascular occlusive processes. Thrombotic stroke results from in situ thrombosis, often at an ulcerated atherosclerotic plaque or from hypercoagulable states such as antithrombin III, protein C, or protein S deficiency. Sludging syndromes such as sickle cell disease or polycythemia vera may also contribute. Embolic stroke commonly arises from cardiac sources including atrial fibrillation, mural thrombus after myocardial infarction, cardiomyopathy, ventricular aneurysm, or prosthetic valves. Arterial sources include aortic or carotid atherosclerotic plaques. Other causes include vascular dissection and vasospasm from subarachnoid hemorrhage or vasoconstrictive agents such as cocaine.
Patients typically present with acute focal neurologic deficits within 4.5 hours of onset. Determining the exact time of symptom onset is critical. If unknown, the time last known well is used. Symptoms correspond to vascular territories. Middle cerebral artery involvement may cause contralateral hemiplegia (face and arm more than leg), hemisensory loss, homonymous hemianopsia, aphasia in the dominant hemisphere, or neglect. Posterior cerebral artery infarction may cause visual field deficits or visual agnosia. Vertebrobasilar strokes can present with vertigo, nystagmus, dysarthria, cranial nerve deficits, ataxia, and crossed sensory findings. Anterior cerebral artery infarction typically affects the contralateral leg more than the arm and may produce apraxia or behavioral changes. Lacunar infarcts may produce pure motor or pure sensory syndromes. Stroke severity is quantified using the National Institutes of Health Stroke Scale (NIHSS), which standardizes neurologic assessment and helps predict prognosis and hemorrhagic risk.
Initial evaluation includes immediate bedside glucose testing to exclude hypoglycemia. Laboratory studies include CBC and coagulation studies (PT/PTT) to assess bleeding risk prior to thrombolysis. A noncontrast head CT scan must be obtained emergently to exclude intracranial hemorrhage. Early ischemic changes may be subtle or absent in the first hours. Additional studies may include ECG to assess for arrhythmia or myocardial ischemia, serum electrolytes, renal function, pregnancy testing, and toxicology screening when indicated. Advanced imaging such as diffusion-weighted MRI, CT perfusion, CT angiography, or MR angiography may identify salvageable tissue and vascular occlusion but should not delay timely thrombolysis when indicated.
Intravenous alteplase (tPA) is indicated in eligible patients aged 18 years or older with clearly defined symptom onset within 4.5 hours and no evidence of hemorrhage on CT. Absolute contraindications include recent stroke or intracranial surgery within 3 months, prior intracranial hemorrhage, suspected subarachnoid hemorrhage, active bleeding, severe uncontrolled hypertension (>185/110 mm Hg), coagulopathy, thrombocytopenia, elevated INR, recent heparin with elevated aPTT, hypoglycemia <50 mg />L, or large established infarction involving more than one third of a cerebral hemisphere. Between 3 and 4.5 hours, additional exclusion criteria apply, including age over 80 years, oral anticoagulant use, NIHSS greater than 25, large MCA territory involvement, or history of both stroke and diabetes.
Blood pressure must be controlled to ≤185/110 mm Hg before thrombolysis and maintained below 180/105 mm Hg after treatment. Labetalol or nicardipine are commonly used. Alteplase is administered at 0.9 mg/kg (maximum 90 mg), with 10% given as an initial bolus over 1 minute and the remainder infused over 60 minutes. Antiplatelet and anticoagulant agents should be withheld for 24 hours. Blood pressure and neurologic status must be monitored frequently during and after infusion. Complications include intracranial hemorrhage, which occurs in up to 6% of treated patients and more commonly in those with severe strokes. If hemorrhage is suspected, tPA should be discontinued and emergent CT performed. Management includes reversal with cryoprecipitate, fibrinogen, platelets, and neurosurgical consultation.
Mechanical thrombectomy or intra-arterial therapy may be considered in selected patients with large vessel occlusion, often within 6 hours of onset, and sometimes beyond in specialized centers based on advanced imaging criteria. These approaches are particularly valuable in patients who are ineligible for IV thrombolysis or who have persistent large vessel occlusion despite treatment.
All patients receiving reperfusion therapy must be admitted to an intensive care or dedicated stroke unit for close neurologic and hemodynamic monitoring. Rapid recognition, precise determination of symptom onset, strict adherence to inclusion and exclusion criteria, and careful blood pressure management are critical. Even brief delays in therapy can significantly reduce the likelihood of meaningful neurologic recovery.
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Emergency And Acute Medicine – Respiratory Distress
Respiratory distress, shortness of breath, or dyspnea is a frequent and potentially life-threatening emergency department presentation. It represents a symptom rather than a diagnosis and may arise from airway, pulmonary, cardiac, neuromuscular, metabolic, toxic, traumatic, or psychogenic causes. Rapid identification of life-threatening conditions and early airway management are critical to prevent respiratory failure and cardiac arrest.
Etiologies include upper airway obstruction such as epiglottitis, croup, foreign body, angioedema, or retropharyngeal abscess. Cardiovascular causes include congestive heart failure with pulmonary edema, dysrhythmias, myocardial ischemia, pulmonary embolism, pericarditis, tamponade, and air embolism. Pulmonary causes include asthma, chronic obstructive pulmonary disease (COPD), pneumonia, influenza, bronchiolitis, aspiration, acute respiratory distress syndrome (ARDS), pleural effusion, toxic inhalation, and trauma such as pneumothorax or pulmonary contusion. Neuromuscular disorders such as Guillain–Barré syndrome or myasthenia gravis may impair ventilation. Metabolic and systemic causes include anaphylaxis, anemia, acidosis, sepsis, salicylate toxicity, stimulant overdose, and severe obesity. Anxiety and hyperventilation syndrome may mimic organic disease but should be diagnoses of exclusion.
Patients commonly present with tachypnea, dyspnea, tachycardia, anxiety, diaphoresis, cough, stridor, wheezing, crackles, increased work of breathing, accessory muscle use, hypoxemia, or cyanosis. Severe cases may show respiratory acidosis, altered mental status, lethargy, or obtundation. History should focus on prior lung or cardiac disease, recent infection, trauma, toxic exposure, chest pain, fever, or foreign-body aspiration. Intravenous drug use and indwelling catheters raise suspicion for septic emboli. Physical examination should assess mental status, work of breathing, jugular venous distention, heart sounds, lung sounds, chest wall movement, peripheral edema, and signs of trauma.
Initial evaluation includes pulse oximetry, cardiac and blood pressure monitoring, and electrocardiography when cardiac causes are suspected. Arterial blood gas may help determine severity and acid–base status. Laboratory studies may include CBC, metabolic panel, blood cultures if febrile, BNP for suspected heart failure, toxicology testing, and D-dimer or other evaluation for pulmonary embolism when appropriate. Chest radiography is often essential to identify pneumonia, pneumothorax, hyperinflation, pulmonary edema, or effusion. Bedside ultrasound can rapidly assess pneumothorax, pleural effusion, cardiac tamponade, right ventricular strain, or heart failure. CT angiography is indicated when pulmonary embolism is strongly suspected.
Prehospital management prioritizes airway positioning, high-flow oxygen, and assisted ventilation with bag-valve mask if needed. Needle decompression should be performed immediately if tension pneumothorax is suspected. In the emergency department, airway, breathing, and circulation are addressed first. Oxygen is administered, with caution in patients with chronic CO₂ retention. Intubation is indicated for severe respiratory distress, hypoxia refractory to oxygen, or altered mental status. Intravenous fluids are given for hypotension, and advanced cardiac life support protocols are followed for dysrhythmias or arrest.
Definitive treatment targets the underlying cause. Heart failure and pulmonary edema are managed with diuretics, nitrates, noninvasive positive-pressure ventilation, and vasodilators when hypertensive. Asthma and COPD exacerbations require bronchodilators, systemic corticosteroids, oxygen, and antibiotics if infection is suspected. Severe cases may require noninvasive ventilation or intubation. Pneumonia is treated with appropriate antibiotics and respiratory isolation when tuberculosis is suspected. Pneumothorax requires immediate decompression if tension is present, followed by tube thoracostomy. Anaphylaxis and angioedema require epinephrine, antihistamines, corticosteroids, and early airway protection. Epiglottitis requires urgent airway stabilization in a controlled setting and intravenous antibiotics. Pulmonary embolism requires anticoagulation and, in select cases, thrombolysis. Neuromuscular causes require ventilatory support and disease-specific therapy.
Patients require admission if they have persistent oxygen requirements, airway instability, hemodynamic compromise, significant comorbid conditions, or need for repeated treatments or monitoring. Discharge is appropriate only when the underlying cause has been addressed, oxygen is no longer required, and the airway is stable.
Early recognition, aggressive supportive care, and prompt treatment of the underlying etiology are essential. Immunocompromised states, emerging viral infections, and early administration of antibiotics in suspected bacterial pneumonia are important considerations. Respiratory distress can deteriorate rapidly, and continuous reassessment is vital to prevent progression to respiratory failure.
Respiratory distress, shortness of breath, or dyspnea is a frequent and potentially life-threatening emergency department presentation. It represents a symptom rather than a diagnosis and may arise from airway, pulmonary, cardiac, neuromuscular, metabolic, toxic, traumatic, or psychogenic causes. Rapid identification of life-threatening conditions and early airway management are critical to prevent respiratory failure and cardiac arrest.
Etiologies include upper airway obstruction such as epiglottitis, croup, foreign body, angioedema, or retropharyngeal abscess. Cardiovascular causes include congestive heart failure with pulmonary edema, dysrhythmias, myocardial ischemia, pulmonary embolism, pericarditis, tamponade, and air embolism. Pulmonary causes include asthma, chronic obstructive pulmonary disease (COPD), pneumonia, influenza, bronchiolitis, aspiration, acute respiratory distress syndrome (ARDS), pleural effusion, toxic inhalation, and trauma such as pneumothorax or pulmonary contusion. Neuromuscular disorders such as Guillain–Barré syndrome or myasthenia gravis may impair ventilation. Metabolic and systemic causes include anaphylaxis, anemia, acidosis, sepsis, salicylate toxicity, stimulant overdose, and severe obesity. Anxiety and hyperventilation syndrome may mimic organic disease but should be diagnoses of exclusion.
Patients commonly present with tachypnea, dyspnea, tachycardia, anxiety, diaphoresis, cough, stridor, wheezing, crackles, increased work of breathing, accessory muscle use, hypoxemia, or cyanosis. Severe cases may show respiratory acidosis, altered mental status, lethargy, or obtundation. History should focus on prior lung or cardiac disease, recent infection, trauma, toxic exposure, chest pain, fever, or foreign-body aspiration. Intravenous drug use and indwelling catheters raise suspicion for septic emboli. Physical examination should assess mental status, work of breathing, jugular venous distention, heart sounds, lung sounds, chest wall movement, peripheral edema, and signs of trauma.
Initial evaluation includes pulse oximetry, cardiac and blood pressure monitoring, and electrocardiography when cardiac causes are suspected. Arterial blood gas may help determine severity and acid–base status. Laboratory studies may include CBC, metabolic panel, blood cultures if febrile, BNP for suspected heart failure, toxicology testing, and D-dimer or other evaluation for pulmonary embolism when appropriate. Chest radiography is often essential to identify pneumonia, pneumothorax, hyperinflation, pulmonary edema, or effusion. Bedside ultrasound can rapidly assess pneumothorax, pleural effusion, cardiac tamponade, right ventricular strain, or heart failure. CT angiography is indicated when pulmonary embolism is strongly suspected.
Prehospital management prioritizes airway positioning, high-flow oxygen, and assisted ventilation with bag-valve mask if needed. Needle decompression should be performed immediately if tension pneumothorax is suspected. In the emergency department, airway, breathing, and circulation are addressed first. Oxygen is administered, with caution in patients with chronic CO₂ retention. Intubation is indicated for severe respiratory distress, hypoxia refractory to oxygen, or altered mental status. Intravenous fluids are given for hypotension, and advanced cardiac life support protocols are followed for dysrhythmias or arrest.
Definitive treatment targets the underlying cause. Heart failure and pulmonary edema are managed with diuretics, nitrates, noninvasive positive-pressure ventilation, and vasodilators when hypertensive. Asthma and COPD exacerbations require bronchodilators, systemic corticosteroids, oxygen, and antibiotics if infection is suspected. Severe cases may require noninvasive ventilation or intubation. Pneumonia is treated with appropriate antibiotics and respiratory isolation when tuberculosis is suspected. Pneumothorax requires immediate decompression if tension is present, followed by tube thoracostomy. Anaphylaxis and angioedema require epinephrine, antihistamines, corticosteroids, and early airway protection. Epiglottitis requires urgent airway stabilization in a controlled setting and intravenous antibiotics. Pulmonary embolism requires anticoagulation and, in select cases, thrombolysis. Neuromuscular causes require ventilatory support and disease-specific therapy.
Patients require admission if they have persistent oxygen requirements, airway instability, hemodynamic compromise, significant comorbid conditions, or need for repeated treatments or monitoring. Discharge is appropriate only when the underlying cause has been addressed, oxygen is no longer required, and the airway is stable.
Early recognition, aggressive supportive care, and prompt treatment of the underlying etiology are essential. Immunocompromised states, emerging viral infections, and early administration of antibiotics in suspected bacterial pneumonia are important considerations. Respiratory distress can deteriorate rapidly, and continuous reassessment is vital to prevent progression to respiratory failure.
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Emergency And Acute Medicine – Resuscitation, Neonate
Neonatal resuscitation addresses failure of the newborn to successfully transition from placental oxygenation to effective pulmonary respiration. Globally, nearly one million deaths annually are related to birth asphyxia. Approximately 10% of newborns require some assistance at birth, and about 1% require extensive resuscitation. In certain circumstances, resuscitation may be withheld after careful discussion with the family and care team, such as confirmed gestational age under 23 weeks, birth weight under 400 g, anencephaly, or confirmed trisomy 13 or 18. APGAR scores do not guide resuscitation and should not delay intervention. They are used to assess the infant’s response at 1 and 5 minutes but should never determine whether resuscitation is initiated.
The pathophysiology centers on hypoxia during the transition to extrauterine life. Initial hypoxia produces tachypnea followed by primary apnea, during which stimulation may restore breathing. Continued hypoxia results in secondary apnea, which does not respond to stimulation and requires assisted ventilation. Numerous antepartum and intrapartum risk factors increase the likelihood of resuscitation, including maternal hypertension, diabetes, infection, substance use, abnormal fetal heart tracings, emergency cesarean delivery, prematurity, meconium-stained amniotic fluid, and placental complications.
Compromised newborns may exhibit decreased muscle tone, inadequate respiratory effort, bradycardia, hypotension, cyanosis, or poor perfusion. Immediate assessment focuses on respirations, heart rate by auscultation or umbilical palpation, tone, and color. The essential first steps follow airway, breathing, and circulation principles while ensuring warmth. Heat loss is a significant risk, particularly in premature or low-birth-weight infants.
Initial stabilization includes warming, positioning the airway in a neutral “sniffing” position, clearing secretions if necessary, drying, and gentle stimulation. For term infants, room air is recommended initially to avoid hyperoxia. Premature infants may require blended oxygen with pulse oximetry monitoring. If apnea or heart rate less than 100 beats per minute persists after initial steps, positive-pressure ventilation is initiated at 40 to 60 breaths per minute using a properly fitting mask. Peak pressures may initially require 30 to 40 cm H₂O. If ventilation is prolonged, a nasogastric tube should be placed to reduce gastric distention.
If heart rate remains below 60 beats per minute after 30 seconds of effective ventilation, chest compressions are started using the two-thumb encircling technique or two-finger method. Compressions should depress the chest approximately one third of the anterior–posterior diameter. The compression-to-ventilation ratio is 3:1, achieving 120 events per minute (90 compressions and 30 breaths). If the heart rate remains below 60 beats per minute despite adequate ventilation and compressions, epinephrine should be administered via intravenous umbilical vein catheter or, if necessary, via the endotracheal tube.
Special situations require additional management. Nonvigorous infants with meconium-stained fluid may require endotracheal intubation and suctioning. Suspected hypovolemia warrants volume expansion with normal saline, lactated Ringer solution, or O-negative blood at 10 mL/kg. Hypoglycemia should be treated with intravenous dextrose. Severe metabolic acidosis may be addressed with sodium bicarbonate after ensuring adequate ventilation. Naloxone may be considered if maternal narcotic exposure occurred within four hours and the infant shows respiratory depression, but it is contraindicated in infants of opioid-dependent mothers due to risk of seizures. Persistent respiratory distress after resuscitation may indicate pneumothorax or congenital diaphragmatic hernia, the latter requiring immediate intubation and gastric decompression. Consider discontinuing resuscitation if there is persistent asystole after 10 minutes of adequate efforts.
Medication dosing includes epinephrine 0.01 to 0.03 mg/kg (0.1 to 0.3 mL/kg of 1:10,000 solution), dextrose 2 to 4 mL/kg of D10W, sodium bicarbonate 2 mEq/kg given slowly, naloxone 0.1 mg/kg, and volume expanders at 10 mL/kg. All medications are preferably administered via an umbilical venous catheter.
All newborns require hospital admission, and those requiring significant resuscitation should be admitted to a neonatal intensive care unit. Low-birth-weight and very-low-birth-weight infants are at risk for complications such as intraventricular hemorrhage, chronic lung disease, thermoregulatory instability, and retinopathy of prematurity. Excess oxygen exposure in very-low-birth-weight infants increases oxidative stress; therefore, careful titration of oxygen concentration is essential.
Successful neonatal resuscitation depends on anticipation of risk factors, preparation of equipment, rapid assessment, effective ventilation, and coordinated team response. Early and adequate ventilation remains the most critical intervention in preventing neonatal morbidity and mortality.
Neonatal resuscitation addresses failure of the newborn to successfully transition from placental oxygenation to effective pulmonary respiration. Globally, nearly one million deaths annually are related to birth asphyxia. Approximately 10% of newborns require some assistance at birth, and about 1% require extensive resuscitation. In certain circumstances, resuscitation may be withheld after careful discussion with the family and care team, such as confirmed gestational age under 23 weeks, birth weight under 400 g, anencephaly, or confirmed trisomy 13 or 18. APGAR scores do not guide resuscitation and should not delay intervention. They are used to assess the infant’s response at 1 and 5 minutes but should never determine whether resuscitation is initiated.
The pathophysiology centers on hypoxia during the transition to extrauterine life. Initial hypoxia produces tachypnea followed by primary apnea, during which stimulation may restore breathing. Continued hypoxia results in secondary apnea, which does not respond to stimulation and requires assisted ventilation. Numerous antepartum and intrapartum risk factors increase the likelihood of resuscitation, including maternal hypertension, diabetes, infection, substance use, abnormal fetal heart tracings, emergency cesarean delivery, prematurity, meconium-stained amniotic fluid, and placental complications.
Compromised newborns may exhibit decreased muscle tone, inadequate respiratory effort, bradycardia, hypotension, cyanosis, or poor perfusion. Immediate assessment focuses on respirations, heart rate by auscultation or umbilical palpation, tone, and color. The essential first steps follow airway, breathing, and circulation principles while ensuring warmth. Heat loss is a significant risk, particularly in premature or low-birth-weight infants.
Initial stabilization includes warming, positioning the airway in a neutral “sniffing” position, clearing secretions if necessary, drying, and gentle stimulation. For term infants, room air is recommended initially to avoid hyperoxia. Premature infants may require blended oxygen with pulse oximetry monitoring. If apnea or heart rate less than 100 beats per minute persists after initial steps, positive-pressure ventilation is initiated at 40 to 60 breaths per minute using a properly fitting mask. Peak pressures may initially require 30 to 40 cm H₂O. If ventilation is prolonged, a nasogastric tube should be placed to reduce gastric distention.
If heart rate remains below 60 beats per minute after 30 seconds of effective ventilation, chest compressions are started using the two-thumb encircling technique or two-finger method. Compressions should depress the chest approximately one third of the anterior–posterior diameter. The compression-to-ventilation ratio is 3:1, achieving 120 events per minute (90 compressions and 30 breaths). If the heart rate remains below 60 beats per minute despite adequate ventilation and compressions, epinephrine should be administered via intravenous umbilical vein catheter or, if necessary, via the endotracheal tube.
Special situations require additional management. Nonvigorous infants with meconium-stained fluid may require endotracheal intubation and suctioning. Suspected hypovolemia warrants volume expansion with normal saline, lactated Ringer solution, or O-negative blood at 10 mL/kg. Hypoglycemia should be treated with intravenous dextrose. Severe metabolic acidosis may be addressed with sodium bicarbonate after ensuring adequate ventilation. Naloxone may be considered if maternal narcotic exposure occurred within four hours and the infant shows respiratory depression, but it is contraindicated in infants of opioid-dependent mothers due to risk of seizures. Persistent respiratory distress after resuscitation may indicate pneumothorax or congenital diaphragmatic hernia, the latter requiring immediate intubation and gastric decompression. Consider discontinuing resuscitation if there is persistent asystole after 10 minutes of adequate efforts.
Medication dosing includes epinephrine 0.01 to 0.03 mg/kg (0.1 to 0.3 mL/kg of 1:10,000 solution), dextrose 2 to 4 mL/kg of D10W, sodium bicarbonate 2 mEq/kg given slowly, naloxone 0.1 mg/kg, and volume expanders at 10 mL/kg. All medications are preferably administered via an umbilical venous catheter.
All newborns require hospital admission, and those requiring significant resuscitation should be admitted to a neonatal intensive care unit. Low-birth-weight and very-low-birth-weight infants are at risk for complications such as intraventricular hemorrhage, chronic lung disease, thermoregulatory instability, and retinopathy of prematurity. Excess oxygen exposure in very-low-birth-weight infants increases oxidative stress; therefore, careful titration of oxygen concentration is essential.
Successful neonatal resuscitation depends on anticipation of risk factors, preparation of equipment, rapid assessment, effective ventilation, and coordinated team response. Early and adequate ventilation remains the most critical intervention in preventing neonatal morbidity and mortality.
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Emergency And Acute Medicine – Resuscitation, Neonate
Neonatal resuscitation addresses failure of the newborn to successfully transition from placental oxygenation to effective pulmonary respiration. Globally, nearly one million deaths annually are related to birth asphyxia. Approximately 10% of newborns require some assistance at birth, and about 1% require extensive resuscitation. In certain circumstances, resuscitation may be withheld after careful discussion with the family and care team, such as confirmed gestational age under 23 weeks, birth weight under 400 g, anencephaly, or confirmed trisomy 13 or 18. APGAR scores do not guide resuscitation and should not delay intervention. They are used to assess the infant’s response at 1 and 5 minutes but should never determine whether resuscitation is initiated.
The pathophysiology centers on hypoxia during the transition to extrauterine life. Initial hypoxia produces tachypnea followed by primary apnea, during which stimulation may restore breathing. Continued hypoxia results in secondary apnea, which does not respond to stimulation and requires assisted ventilation. Numerous antepartum and intrapartum risk factors increase the likelihood of resuscitation, including maternal hypertension, diabetes, infection, substance use, abnormal fetal heart tracings, emergency cesarean delivery, prematurity, meconium-stained amniotic fluid, and placental complications.
Compromised newborns may exhibit decreased muscle tone, inadequate respiratory effort, bradycardia, hypotension, cyanosis, or poor perfusion. Immediate assessment focuses on respirations, heart rate by auscultation or umbilical palpation, tone, and color. The essential first steps follow airway, breathing, and circulation principles while ensuring warmth. Heat loss is a significant risk, particularly in premature or low-birth-weight infants.
Initial stabilization includes warming, positioning the airway in a neutral “sniffing” position, clearing secretions if necessary, drying, and gentle stimulation. For term infants, room air is recommended initially to avoid hyperoxia. Premature infants may require blended oxygen with pulse oximetry monitoring. If apnea or heart rate less than 100 beats per minute persists after initial steps, positive-pressure ventilation is initiated at 40 to 60 breaths per minute using a properly fitting mask. Peak pressures may initially require 30 to 40 cm H₂O. If ventilation is prolonged, a nasogastric tube should be placed to reduce gastric distention.
If heart rate remains below 60 beats per minute after 30 seconds of effective ventilation, chest compressions are started using the two-thumb encircling technique or two-finger method. Compressions should depress the chest approximately one third of the anterior–posterior diameter. The compression-to-ventilation ratio is 3:1, achieving 120 events per minute (90 compressions and 30 breaths). If the heart rate remains below 60 beats per minute despite adequate ventilation and compressions, epinephrine should be administered via intravenous umbilical vein catheter or, if necessary, via the endotracheal tube.
Special situations require additional management. Nonvigorous infants with meconium-stained fluid may require endotracheal intubation and suctioning. Suspected hypovolemia warrants volume expansion with normal saline, lactated Ringer solution, or O-negative blood at 10 mL/kg. Hypoglycemia should be treated with intravenous dextrose. Severe metabolic acidosis may be addressed with sodium bicarbonate after ensuring adequate ventilation. Naloxone may be considered if maternal narcotic exposure occurred within four hours and the infant shows respiratory depression, but it is contraindicated in infants of opioid-dependent mothers due to risk of seizures. Persistent respiratory distress after resuscitation may indicate pneumothorax or congenital diaphragmatic hernia, the latter requiring immediate intubation and gastric decompression. Consider discontinuing resuscitation if there is persistent asystole after 10 minutes of adequate efforts.
Medication dosing includes epinephrine 0.01 to 0.03 mg/kg (0.1 to 0.3 mL/kg of 1:10,000 solution), dextrose 2 to 4 mL/kg of D10W, sodium bicarbonate 2 mEq/kg given slowly, naloxone 0.1 mg/kg, and volume expanders at 10 mL/kg. All medications are preferably administered via an umbilical venous catheter.
All newborns require hospital admission, and those requiring significant resuscitation should be admitted to a neonatal intensive care unit. Low-birth-weight and very-low-birth-weight infants are at risk for complications such as intraventricular hemorrhage, chronic lung disease, thermoregulatory instability, and retinopathy of prematurity. Excess oxygen exposure in very-low-birth-weight infants increases oxidative stress; therefore, careful titration of oxygen concentration is essential.
Successful neonatal resuscitation depends on anticipation of risk factors, preparation of equipment, rapid assessment, effective ventilation, and coordinated team response. Early and adequate ventilation remains the most critical intervention in preventing neonatal morbidity and mortality.
Neonatal resuscitation addresses failure of the newborn to successfully transition from placental oxygenation to effective pulmonary respiration. Globally, nearly one million deaths annually are related to birth asphyxia. Approximately 10% of newborns require some assistance at birth, and about 1% require extensive resuscitation. In certain circumstances, resuscitation may be withheld after careful discussion with the family and care team, such as confirmed gestational age under 23 weeks, birth weight under 400 g, anencephaly, or confirmed trisomy 13 or 18. APGAR scores do not guide resuscitation and should not delay intervention. They are used to assess the infant’s response at 1 and 5 minutes but should never determine whether resuscitation is initiated.
The pathophysiology centers on hypoxia during the transition to extrauterine life. Initial hypoxia produces tachypnea followed by primary apnea, during which stimulation may restore breathing. Continued hypoxia results in secondary apnea, which does not respond to stimulation and requires assisted ventilation. Numerous antepartum and intrapartum risk factors increase the likelihood of resuscitation, including maternal hypertension, diabetes, infection, substance use, abnormal fetal heart tracings, emergency cesarean delivery, prematurity, meconium-stained amniotic fluid, and placental complications.
Compromised newborns may exhibit decreased muscle tone, inadequate respiratory effort, bradycardia, hypotension, cyanosis, or poor perfusion. Immediate assessment focuses on respirations, heart rate by auscultation or umbilical palpation, tone, and color. The essential first steps follow airway, breathing, and circulation principles while ensuring warmth. Heat loss is a significant risk, particularly in premature or low-birth-weight infants.
Initial stabilization includes warming, positioning the airway in a neutral “sniffing” position, clearing secretions if necessary, drying, and gentle stimulation. For term infants, room air is recommended initially to avoid hyperoxia. Premature infants may require blended oxygen with pulse oximetry monitoring. If apnea or heart rate less than 100 beats per minute persists after initial steps, positive-pressure ventilation is initiated at 40 to 60 breaths per minute using a properly fitting mask. Peak pressures may initially require 30 to 40 cm H₂O. If ventilation is prolonged, a nasogastric tube should be placed to reduce gastric distention.
If heart rate remains below 60 beats per minute after 30 seconds of effective ventilation, chest compressions are started using the two-thumb encircling technique or two-finger method. Compressions should depress the chest approximately one third of the anterior–posterior diameter. The compression-to-ventilation ratio is 3:1, achieving 120 events per minute (90 compressions and 30 breaths). If the heart rate remains below 60 beats per minute despite adequate ventilation and compressions, epinephrine should be administered via intravenous umbilical vein catheter or, if necessary, via the endotracheal tube.
Special situations require additional management. Nonvigorous infants with meconium-stained fluid may require endotracheal intubation and suctioning. Suspected hypovolemia warrants volume expansion with normal saline, lactated Ringer solution, or O-negative blood at 10 mL/kg. Hypoglycemia should be treated with intravenous dextrose. Severe metabolic acidosis may be addressed with sodium bicarbonate after ensuring adequate ventilation. Naloxone may be considered if maternal narcotic exposure occurred within four hours and the infant shows respiratory depression, but it is contraindicated in infants of opioid-dependent mothers due to risk of seizures. Persistent respiratory distress after resuscitation may indicate pneumothorax or congenital diaphragmatic hernia, the latter requiring immediate intubation and gastric decompression. Consider discontinuing resuscitation if there is persistent asystole after 10 minutes of adequate efforts.
Medication dosing includes epinephrine 0.01 to 0.03 mg/kg (0.1 to 0.3 mL/kg of 1:10,000 solution), dextrose 2 to 4 mL/kg of D10W, sodium bicarbonate 2 mEq/kg given slowly, naloxone 0.1 mg/kg, and volume expanders at 10 mL/kg. All medications are preferably administered via an umbilical venous catheter.
All newborns require hospital admission, and those requiring significant resuscitation should be admitted to a neonatal intensive care unit. Low-birth-weight and very-low-birth-weight infants are at risk for complications such as intraventricular hemorrhage, chronic lung disease, thermoregulatory instability, and retinopathy of prematurity. Excess oxygen exposure in very-low-birth-weight infants increases oxidative stress; therefore, careful titration of oxygen concentration is essential.
Successful neonatal resuscitation depends on anticipation of risk factors, preparation of equipment, rapid assessment, effective ventilation, and coordinated team response. Early and adequate ventilation remains the most critical intervention in preventing neonatal morbidity and mortality.
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Emergency And Acute Medicine – Retinal Detachment
Retinal detachment occurs when the sensory retina separates from the underlying retinal pigment epithelium, disrupting photoreceptor function and threatening permanent vision loss. There are three main types with a common final pathway of retinal separation: rhegmatogenous, tractional, and exudative. Rhegmatogenous retinal detachment (RRD) is the most common and results from a retinal break or tear that allows vitreous fluid to enter the subretinal space. It is typically an acute event and often associated with flashes of light from traction on retinal nerve fibers and floaters from associated vitreous hemorrhage. Tractional retinal detachment (TRD) occurs when fibrous vitreous bands contract and pull the retina away, usually as a chronic, progressive process related to prior pathology. Exudative retinal detachment (ERD) results from accumulation of subretinal fluid without a retinal tear and is often secondary to systemic or inflammatory disease; it usually does not require surgical repair.
Risk factors for RRD include myopia, prior cataract surgery, trauma, connective tissue disorders such as Marfan syndrome, and degenerative changes in the vitreous or retina. TRD is commonly associated with proliferative diabetic retinopathy, vasculopathies, penetrating trauma, retinopathy of prematurity, sickle cell disease, and chronic inflammatory processes. ERD is often caused by malignant hypertension, preeclampsia, intraocular tumors such as melanoma or retinoblastoma, and inflammatory conditions including posterior scleritis or Harada disease.
Patients typically present with painless visual disturbances. Common symptoms include flashes of light (photopsias), new floaters, and a progressive “curtain” or “veil” descending across the visual field. Visual loss often begins peripherally and advances centrally if untreated. Visual acuity may initially remain normal if the macula is spared. History should focus on onset, progression, prior eye disease, surgery, trauma, and systemic conditions.
Physical examination begins with assessment of visual acuity and visual fields before dilation. A field defect usually corresponds to the opposite side of the detachment. An afferent pupillary defect may be present in extensive detachments. Loss of the red reflex may be noted. Fundoscopic examination may reveal a pale, elevated, wrinkled retina; however, fundoscopy alone is insufficient to rule out detachment. Slit-lamp examination may reveal anterior vitreous pigment granules, known as “tobacco dust,” which strongly suggests a retinal tear. Intraocular pressure is often lower in the affected eye. Ocular ultrasound performed by trained emergency physicians is highly sensitive and can confirm the diagnosis when visualization is limited.
The differential diagnosis includes central retinal artery occlusion, central retinal vein occlusion, vitreous hemorrhage, migraine with aura, choroidal detachment, toxic exposures such as methanol poisoning, and other retinal or central nervous system pathology. A thorough neurologic examination is important to exclude cerebrovascular events when symptoms are atypical.
Management in the emergency setting includes placing the patient at bed rest and positioning with the side of the detachment dependent, which may help limit progression. Emergent ophthalmology consultation is required. Detachments involving the macula require surgical repair within 24 hours to optimize visual outcomes. Chronic detachments may be repaired on a less urgent timeline based on ophthalmologic assessment. Exudative detachments are treated by addressing the underlying systemic condition.
Early recognition of retinal tears allows prophylactic intervention and may prevent progression to full detachment. The presence of “tobacco dust” carries a high risk of retinal tear. Clinicians must also avoid missing central retinal artery occlusion, which carries an increased risk of stroke in patients with carotid or cardioembolic disease. Prompt diagnosis and referral are essential to preserve vision.
Retinal detachment occurs when the sensory retina separates from the underlying retinal pigment epithelium, disrupting photoreceptor function and threatening permanent vision loss. There are three main types with a common final pathway of retinal separation: rhegmatogenous, tractional, and exudative. Rhegmatogenous retinal detachment (RRD) is the most common and results from a retinal break or tear that allows vitreous fluid to enter the subretinal space. It is typically an acute event and often associated with flashes of light from traction on retinal nerve fibers and floaters from associated vitreous hemorrhage. Tractional retinal detachment (TRD) occurs when fibrous vitreous bands contract and pull the retina away, usually as a chronic, progressive process related to prior pathology. Exudative retinal detachment (ERD) results from accumulation of subretinal fluid without a retinal tear and is often secondary to systemic or inflammatory disease; it usually does not require surgical repair.
Risk factors for RRD include myopia, prior cataract surgery, trauma, connective tissue disorders such as Marfan syndrome, and degenerative changes in the vitreous or retina. TRD is commonly associated with proliferative diabetic retinopathy, vasculopathies, penetrating trauma, retinopathy of prematurity, sickle cell disease, and chronic inflammatory processes. ERD is often caused by malignant hypertension, preeclampsia, intraocular tumors such as melanoma or retinoblastoma, and inflammatory conditions including posterior scleritis or Harada disease.
Patients typically present with painless visual disturbances. Common symptoms include flashes of light (photopsias), new floaters, and a progressive “curtain” or “veil” descending across the visual field. Visual loss often begins peripherally and advances centrally if untreated. Visual acuity may initially remain normal if the macula is spared. History should focus on onset, progression, prior eye disease, surgery, trauma, and systemic conditions.
Physical examination begins with assessment of visual acuity and visual fields before dilation. A field defect usually corresponds to the opposite side of the detachment. An afferent pupillary defect may be present in extensive detachments. Loss of the red reflex may be noted. Fundoscopic examination may reveal a pale, elevated, wrinkled retina; however, fundoscopy alone is insufficient to rule out detachment. Slit-lamp examination may reveal anterior vitreous pigment granules, known as “tobacco dust,” which strongly suggests a retinal tear. Intraocular pressure is often lower in the affected eye. Ocular ultrasound performed by trained emergency physicians is highly sensitive and can confirm the diagnosis when visualization is limited.
The differential diagnosis includes central retinal artery occlusion, central retinal vein occlusion, vitreous hemorrhage, migraine with aura, choroidal detachment, toxic exposures such as methanol poisoning, and other retinal or central nervous system pathology. A thorough neurologic examination is important to exclude cerebrovascular events when symptoms are atypical.
Management in the emergency setting includes placing the patient at bed rest and positioning with the side of the detachment dependent, which may help limit progression. Emergent ophthalmology consultation is required. Detachments involving the macula require surgical repair within 24 hours to optimize visual outcomes. Chronic detachments may be repaired on a less urgent timeline based on ophthalmologic assessment. Exudative detachments are treated by addressing the underlying systemic condition.
Early recognition of retinal tears allows prophylactic intervention and may prevent progression to full detachment. The presence of “tobacco dust” carries a high risk of retinal tear. Clinicians must also avoid missing central retinal artery occlusion, which carries an increased risk of stroke in patients with carotid or cardioembolic disease. Prompt diagnosis and referral are essential to preserve vision.
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Emergency And Acute Medicine – Retro-Orbital Hematoma
Retro-orbital hematoma (ROH), also known as retrobulbar hematoma, is a rare but vision-threatening complication of orbital trauma or facial surgery. It involves accumulation of blood behind the globe, leading to rapidly increasing intraorbital pressure and orbital compartment syndrome. Elevated pressure compromises venous outflow and arterial inflow to the retina and optic nerve, resulting in tissue ischemia. Permanent vision loss may occur within 90 minutes, with irreversible damage possible by 120 minutes. Prompt recognition and immediate decompression, often via lateral canthotomy and inferior cantholysis, are critical and may need to be performed in the emergency department. Frequent reassessment is mandatory because hematoma progression can be rapid, and some patients may be unconscious or unable to report symptoms.
Retro-orbital hematoma may occur following blunt or penetrating orbital trauma, orbital wall fractures, facial fracture repair, blepharoplasty, endoscopic sinus surgery, retrobulbar anesthesia, or other periocular procedures. Rapid bleeding into the confined orbital space increases pressure, leading to proptosis and stretching of the optic nerve, further contributing to decreased visual acuity.
Patients typically present with a history of recent orbital trauma or facial surgery and complaints of eye pain and vision changes. Examination findings include decreased visual acuity, proptosis, increased intraocular pressure (IOP), diplopia, pain with eye movement, decreased extraocular movements, and a relative afferent pupillary defect with preserved consensual response. Nausea and vomiting may occur due to increased orbital pressure. Because patients may be unconscious after trauma, a high index of suspicion is essential.
Diagnosis is primarily clinical. Immediate evaluation should include assessment of visual acuity, pupillary response, extraocular movements, and IOP measurement. CT scan of the orbits is the imaging gold standard but should never delay emergent decompression if orbital compartment syndrome is suspected. Bedside ultrasound may demonstrate the “guitar-pick” sign, reflecting posterior globe tenting, but sensitivity and specificity are not well established. There are no diagnostic laboratory tests.
The differential diagnosis includes orbital fracture, retro-orbital edema, orbital emphysema, blow-in fractures, orbital roof fractures with brain herniation, intracranial hemorrhage, globe rupture, and other causes of post-traumatic visual loss. A ruptured globe is a contraindication to lateral canthotomy and must be excluded before performing the procedure.
Management begins with airway, breathing, and circulation stabilization. Immediate ophthalmology consultation is required; however, consultation should not delay decompression when indicated. Emergent lateral canthotomy and inferior cantholysis is the definitive treatment for orbital compartment syndrome. Indications include markedly elevated IOP (typically >40 mm Hg), proptosis with decreased vision, afferent pupillary defect, or a tense orbit in an unconscious patient. The procedure involves antiseptic preparation, local anesthesia, clamping and incising the lateral canthus, and releasing the inferior canthal tendon to relieve pressure. Prompt decompression can be sight-saving.
Adjunctive medical therapies may include intravenous mannitol to reduce intraocular pressure, acetazolamide (unless contraindicated), and high-dose methylprednisolone, although these should not replace surgical decompression. Hyperbaric oxygen has been described but is not first-line therapy.
All patients with suspected retro-orbital hematoma require hospital admission for observation, definitive management, and evaluation for associated injuries. They should not be discharged from the emergency department. Delayed diagnosis is a major pitfall and may occur due to inadequate examination, lack of suspicion, absence of tonometry equipment, waiting for imaging, or delayed specialist arrival. Early recognition and rapid decompression are essential to prevent permanent vision loss.
Retro-orbital hematoma (ROH), also known as retrobulbar hematoma, is a rare but vision-threatening complication of orbital trauma or facial surgery. It involves accumulation of blood behind the globe, leading to rapidly increasing intraorbital pressure and orbital compartment syndrome. Elevated pressure compromises venous outflow and arterial inflow to the retina and optic nerve, resulting in tissue ischemia. Permanent vision loss may occur within 90 minutes, with irreversible damage possible by 120 minutes. Prompt recognition and immediate decompression, often via lateral canthotomy and inferior cantholysis, are critical and may need to be performed in the emergency department. Frequent reassessment is mandatory because hematoma progression can be rapid, and some patients may be unconscious or unable to report symptoms.
Retro-orbital hematoma may occur following blunt or penetrating orbital trauma, orbital wall fractures, facial fracture repair, blepharoplasty, endoscopic sinus surgery, retrobulbar anesthesia, or other periocular procedures. Rapid bleeding into the confined orbital space increases pressure, leading to proptosis and stretching of the optic nerve, further contributing to decreased visual acuity.
Patients typically present with a history of recent orbital trauma or facial surgery and complaints of eye pain and vision changes. Examination findings include decreased visual acuity, proptosis, increased intraocular pressure (IOP), diplopia, pain with eye movement, decreased extraocular movements, and a relative afferent pupillary defect with preserved consensual response. Nausea and vomiting may occur due to increased orbital pressure. Because patients may be unconscious after trauma, a high index of suspicion is essential.
Diagnosis is primarily clinical. Immediate evaluation should include assessment of visual acuity, pupillary response, extraocular movements, and IOP measurement. CT scan of the orbits is the imaging gold standard but should never delay emergent decompression if orbital compartment syndrome is suspected. Bedside ultrasound may demonstrate the “guitar-pick” sign, reflecting posterior globe tenting, but sensitivity and specificity are not well established. There are no diagnostic laboratory tests.
The differential diagnosis includes orbital fracture, retro-orbital edema, orbital emphysema, blow-in fractures, orbital roof fractures with brain herniation, intracranial hemorrhage, globe rupture, and other causes of post-traumatic visual loss. A ruptured globe is a contraindication to lateral canthotomy and must be excluded before performing the procedure.
Management begins with airway, breathing, and circulation stabilization. Immediate ophthalmology consultation is required; however, consultation should not delay decompression when indicated. Emergent lateral canthotomy and inferior cantholysis is the definitive treatment for orbital compartment syndrome. Indications include markedly elevated IOP (typically >40 mm Hg), proptosis with decreased vision, afferent pupillary defect, or a tense orbit in an unconscious patient. The procedure involves antiseptic preparation, local anesthesia, clamping and incising the lateral canthus, and releasing the inferior canthal tendon to relieve pressure. Prompt decompression can be sight-saving.
Adjunctive medical therapies may include intravenous mannitol to reduce intraocular pressure, acetazolamide (unless contraindicated), and high-dose methylprednisolone, although these should not replace surgical decompression. Hyperbaric oxygen has been described but is not first-line therapy.
All patients with suspected retro-orbital hematoma require hospital admission for observation, definitive management, and evaluation for associated injuries. They should not be discharged from the emergency department. Delayed diagnosis is a major pitfall and may occur due to inadequate examination, lack of suspicion, absence of tonometry equipment, waiting for imaging, or delayed specialist arrival. Early recognition and rapid decompression are essential to prevent permanent vision loss.
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Emergency And Acute Medicine – Retropharyngeal Abscess
Retropharyngeal abscess is a deep neck space infection involving the retropharyngeal space, a potential space located between the buccopharyngeal fascia anteriorly and the alar fascia posteriorly, extending from the skull base to approximately the level of T2. Infection may spread through the poorly resistant alar fascia into the “danger space” and descend into the posterior mediastinum, leading to life-threatening complications. It is primarily a pediatric disease, with peak incidence between ages 3 and 5 years when retropharyngeal lymph nodes are most prominent, but cases in adults are increasing. Prognosis is favorable with early recognition, intravenous antibiotics, and surgical drainage when indicated. Airway compromise is the most common and serious complication. Other complications include aspiration pneumonia from rupture, mediastinitis, sepsis, necrotizing fasciitis, internal jugular vein thrombosis (including Lemierre syndrome), carotid artery erosion, epidural abscess, cranial nerve palsies, and recurrent abscess formation.
Most cases arise from spread of infection from the nasopharynx, paranasal sinuses, or middle ear to retropharyngeal lymph nodes. Trauma, foreign bodies, and iatrogenic instrumentation are more common causes in adults. Diabetes and immunosuppression increase risk. The infection is typically polymicrobial, involving aerobic and anaerobic organisms. Common pathogens include Streptococcus pyogenes, viridans streptococci, Staphylococcus aureus (including MRSA), and anaerobes such as Prevotella and Fusobacterium. Less common organisms include Haemophilus species, Klebsiella, Escherichia coli, Mycobacterium tuberculosis, and fungal pathogens.
Presentation may differ between children and adults. Common symptoms include sore throat, neck pain or stiffness, dysphagia, odynophagia, and fever. Patients may also develop stridor, dyspnea, muffled voice, trismus, or drooling. Young children may present only with irritability, poor oral intake, lethargy, or cough. Physical examination in adults may reveal posterior pharyngeal edema, cervical adenopathy, drooling, dysphonia, and tenderness with lateral movement of the larynx (tracheal rock sign). Children often have limited neck extension, torticollis, retropharyngeal bulge, agitation, and signs of respiratory distress.
Airway assessment is the priority. A normal examination does not exclude the diagnosis. Laboratory tests are nonspecific, though leukocytosis is common. Blood cultures should be obtained. Imaging is essential when suspicion is high. Lateral neck radiographs may show widening of the prevertebral soft tissue space, especially if the retropharyngeal space anterior to C2 exceeds 7 mm or is more than twice the vertebral body diameter, or if the space anterior to C6 exceeds 14 mm in preschool children or 22 mm in adults. CT of the neck with intravenous contrast is the preferred imaging modality, showing a hypodense lesion with peripheral ring enhancement. CT assists in determining abscess size and extent but may not reliably distinguish abscess from cellulitis. MRI is more sensitive and useful for evaluating vascular complications such as jugular thrombosis. Imaging should not delay airway management.
The differential diagnosis includes epiglottitis, peritonsillar abscess, croup, tracheitis, meningitis, cervical osteomyelitis, dental infection, mononucleosis, epidural abscess, and other deep neck infections.
Management begins with airway stabilization. The child should be kept in a position of comfort, as forced positioning may worsen obstruction. Supplemental oxygen and close monitoring are required. Early endotracheal intubation or tracheostomy may be necessary in cases of respiratory distress or impending airway obstruction. Induction must be performed cautiously, as sedation may precipitate complete obstruction. Rescue airway equipment must be readily available.
Empiric intravenous antibiotic therapy should begin promptly and cover group A streptococci, Staphylococcus aureus (including MRSA when indicated), and anaerobes. Regimens may include clindamycin, ampicillin-sulbactam, piperacillin-tazobactam, or penicillin plus metronidazole. Vancomycin or linezolid should be added if MRSA is suspected or if there is poor clinical response. Antibiotics should be tailored once culture results are available. The role of corticosteroids remains controversial and should be considered only in consultation with specialists.
All patients require hospital admission for intravenous antibiotics and monitoring. Surgical drainage in the operating room is indicated for airway compromise, large abscesses (typically greater than 2 cm on imaging), failure to improve with antibiotics, or development of complications. Intensive care admission is required for airway compromise, sepsis, hemodynamic instability, altered mental status, or significant comorbidities.
A high index of suspicion is essential, particularly in children presenting with fever, stiff neck, or dysphagia. Early imaging, prompt antibiotic therapy, and early surgical consultation are critical to prevent airway compromise and extension into mediastinal structures.
Retropharyngeal abscess is a deep neck space infection involving the retropharyngeal space, a potential space located between the buccopharyngeal fascia anteriorly and the alar fascia posteriorly, extending from the skull base to approximately the level of T2. Infection may spread through the poorly resistant alar fascia into the “danger space” and descend into the posterior mediastinum, leading to life-threatening complications. It is primarily a pediatric disease, with peak incidence between ages 3 and 5 years when retropharyngeal lymph nodes are most prominent, but cases in adults are increasing. Prognosis is favorable with early recognition, intravenous antibiotics, and surgical drainage when indicated. Airway compromise is the most common and serious complication. Other complications include aspiration pneumonia from rupture, mediastinitis, sepsis, necrotizing fasciitis, internal jugular vein thrombosis (including Lemierre syndrome), carotid artery erosion, epidural abscess, cranial nerve palsies, and recurrent abscess formation.
Most cases arise from spread of infection from the nasopharynx, paranasal sinuses, or middle ear to retropharyngeal lymph nodes. Trauma, foreign bodies, and iatrogenic instrumentation are more common causes in adults. Diabetes and immunosuppression increase risk. The infection is typically polymicrobial, involving aerobic and anaerobic organisms. Common pathogens include Streptococcus pyogenes, viridans streptococci, Staphylococcus aureus (including MRSA), and anaerobes such as Prevotella and Fusobacterium. Less common organisms include Haemophilus species, Klebsiella, Escherichia coli, Mycobacterium tuberculosis, and fungal pathogens.
Presentation may differ between children and adults. Common symptoms include sore throat, neck pain or stiffness, dysphagia, odynophagia, and fever. Patients may also develop stridor, dyspnea, muffled voice, trismus, or drooling. Young children may present only with irritability, poor oral intake, lethargy, or cough. Physical examination in adults may reveal posterior pharyngeal edema, cervical adenopathy, drooling, dysphonia, and tenderness with lateral movement of the larynx (tracheal rock sign). Children often have limited neck extension, torticollis, retropharyngeal bulge, agitation, and signs of respiratory distress.
Airway assessment is the priority. A normal examination does not exclude the diagnosis. Laboratory tests are nonspecific, though leukocytosis is common. Blood cultures should be obtained. Imaging is essential when suspicion is high. Lateral neck radiographs may show widening of the prevertebral soft tissue space, especially if the retropharyngeal space anterior to C2 exceeds 7 mm or is more than twice the vertebral body diameter, or if the space anterior to C6 exceeds 14 mm in preschool children or 22 mm in adults. CT of the neck with intravenous contrast is the preferred imaging modality, showing a hypodense lesion with peripheral ring enhancement. CT assists in determining abscess size and extent but may not reliably distinguish abscess from cellulitis. MRI is more sensitive and useful for evaluating vascular complications such as jugular thrombosis. Imaging should not delay airway management.
The differential diagnosis includes epiglottitis, peritonsillar abscess, croup, tracheitis, meningitis, cervical osteomyelitis, dental infection, mononucleosis, epidural abscess, and other deep neck infections.
Management begins with airway stabilization. The child should be kept in a position of comfort, as forced positioning may worsen obstruction. Supplemental oxygen and close monitoring are required. Early endotracheal intubation or tracheostomy may be necessary in cases of respiratory distress or impending airway obstruction. Induction must be performed cautiously, as sedation may precipitate complete obstruction. Rescue airway equipment must be readily available.
Empiric intravenous antibiotic therapy should begin promptly and cover group A streptococci, Staphylococcus aureus (including MRSA when indicated), and anaerobes. Regimens may include clindamycin, ampicillin-sulbactam, piperacillin-tazobactam, or penicillin plus metronidazole. Vancomycin or linezolid should be added if MRSA is suspected or if there is poor clinical response. Antibiotics should be tailored once culture results are available. The role of corticosteroids remains controversial and should be considered only in consultation with specialists.
All patients require hospital admission for intravenous antibiotics and monitoring. Surgical drainage in the operating room is indicated for airway compromise, large abscesses (typically greater than 2 cm on imaging), failure to improve with antibiotics, or development of complications. Intensive care admission is required for airway compromise, sepsis, hemodynamic instability, altered mental status, or significant comorbidities.
A high index of suspicion is essential, particularly in children presenting with fever, stiff neck, or dysphagia. Early imaging, prompt antibiotic therapy, and early surgical consultation are critical to prevent airway compromise and extension into mediastinal structures.
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Emergency And Acute Medicine – Reye Syndrome
Reye syndrome is a rare but potentially fatal, reversible clinicopathologic syndrome characterized by acute noninflammatory encephalopathy and hepatic dysfunction with fatty infiltration. It is believed to involve primary mitochondrial injury leading to impaired oxidative phosphorylation and decreased activity of enzymes involved in the Krebs cycle, gluconeogenesis, and urea synthesis. The result is hyperammonemia, hypoglycemia, and hepatic dysfunction without significant inflammation. Rapid neurologic deterioration is due to cerebral cytotoxic edema and increased intracranial pressure (ICP), with herniation being the most common cause of death. Survivors often recover normal liver and neurologic function.
The condition primarily affects children, with peak incidence between ages 4 and 11 years and an average age of 7 years. It is extremely rare in individuals older than 18 years. Fewer than 10% of cases occur before age 1 year. Incidence is highest in winter and early spring and has historically been associated with antecedent viral infections such as influenza A or B and varicella. Epidemiologic evidence strongly links exposure to salicylates during viral illness as a major risk factor. Genetic susceptibility and other environmental factors may contribute. Reye-like syndromes describe similar presentations due to inborn errors of metabolism or toxic exposures affecting fatty acid oxidation and urea metabolism.
Patients typically present with a biphasic illness. An initial viral prodrome is followed several days later by persistent, profuse vomiting and rapid onset of neurologic symptoms. The patient is usually afebrile at presentation. Early manifestations include lethargy, behavioral changes, irritability, confusion, delirium, and combativeness. As cerebral edema worsens, patients may develop hyperventilation, decorticate or decerebrate posturing, seizures, and coma. Hepatomegaly is present in about 40% of cases. No focal neurologic deficits are typically found. Infants may present atypically with tachypnea, apnea, hypoglycemia, irritability, or seizures.
Laboratory evaluation demonstrates elevated liver transaminases (at least three times normal), elevated serum ammonia, hypoglycemia (particularly in infants), prolonged prothrombin time due to decreased clotting factor synthesis, and elevated blood urea nitrogen. Serum bilirubin is usually normal or only mildly elevated. Ammonia levels often peak 24 to 48 hours after onset of neurologic symptoms; levels greater than 300 μg/dL are associated with poor prognosis. Platelet count and peripheral smear are usually normal. Toxicology screening should be performed to exclude other causes. Head CT may demonstrate diffuse cerebral edema. Lumbar puncture is not contraindicated but typically shows fewer than 8 leukocytes/mm³. Liver biopsy confirms the diagnosis by demonstrating microvesicular fatty infiltration but should not delay treatment.
The differential diagnosis includes inborn errors of metabolism (urea cycle defects, fatty acid oxidation disorders, organic acidemias), toxin exposures, drug intoxications such as acetaminophen or salicylates, hypoglycemia, sepsis, meningitis, encephalitis, and head trauma.
Management is supportive and aimed primarily at controlling intracranial pressure and correcting metabolic derangements. All patients require intensive care admission in a facility capable of ICP monitoring. Airway protection with rapid-sequence intubation is indicated for significant encephalopathy. Supplemental oxygen and cardiorespiratory monitoring are essential. Intravenous glucose should be administered promptly for altered mental status, and serum glucose should be maintained between 125 and 175 mg/dL with careful monitoring. Overhydration should be avoided.
Elevated ICP is managed with head elevation, controlled hyperventilation, osmotic therapy such as mannitol, and, in severe cases, barbiturate coma. Intracranial pressure monitoring via subarachnoid bolt or intraventricular catheter may be required in advanced stages. Vitamin K is administered if prothrombin time is prolonged, and fresh-frozen plasma may be given for severe coagulopathy or bleeding. Diuretics such as furosemide may be used adjunctively. Treatment should be initiated promptly without waiting for liver biopsy confirmation.
All children with suspected Reye syndrome should be admitted to the intensive care unit. Discharge decisions are individualized and depend on stabilization of mental status and laboratory values. Long-term follow-up with hepatology and neurology is recommended, including neuropsychological assessment.
A critical preventive point is the avoidance of aspirin and salicylate-containing products in children and adolescents with viral illnesses. Clinicians must maintain vigilance for alternative diagnoses and aggressively manage intracranial pressure, as neurologic complications are the primary determinant of outcome.
Reye syndrome is a rare but potentially fatal, reversible clinicopathologic syndrome characterized by acute noninflammatory encephalopathy and hepatic dysfunction with fatty infiltration. It is believed to involve primary mitochondrial injury leading to impaired oxidative phosphorylation and decreased activity of enzymes involved in the Krebs cycle, gluconeogenesis, and urea synthesis. The result is hyperammonemia, hypoglycemia, and hepatic dysfunction without significant inflammation. Rapid neurologic deterioration is due to cerebral cytotoxic edema and increased intracranial pressure (ICP), with herniation being the most common cause of death. Survivors often recover normal liver and neurologic function.
The condition primarily affects children, with peak incidence between ages 4 and 11 years and an average age of 7 years. It is extremely rare in individuals older than 18 years. Fewer than 10% of cases occur before age 1 year. Incidence is highest in winter and early spring and has historically been associated with antecedent viral infections such as influenza A or B and varicella. Epidemiologic evidence strongly links exposure to salicylates during viral illness as a major risk factor. Genetic susceptibility and other environmental factors may contribute. Reye-like syndromes describe similar presentations due to inborn errors of metabolism or toxic exposures affecting fatty acid oxidation and urea metabolism.
Patients typically present with a biphasic illness. An initial viral prodrome is followed several days later by persistent, profuse vomiting and rapid onset of neurologic symptoms. The patient is usually afebrile at presentation. Early manifestations include lethargy, behavioral changes, irritability, confusion, delirium, and combativeness. As cerebral edema worsens, patients may develop hyperventilation, decorticate or decerebrate posturing, seizures, and coma. Hepatomegaly is present in about 40% of cases. No focal neurologic deficits are typically found. Infants may present atypically with tachypnea, apnea, hypoglycemia, irritability, or seizures.
Laboratory evaluation demonstrates elevated liver transaminases (at least three times normal), elevated serum ammonia, hypoglycemia (particularly in infants), prolonged prothrombin time due to decreased clotting factor synthesis, and elevated blood urea nitrogen. Serum bilirubin is usually normal or only mildly elevated. Ammonia levels often peak 24 to 48 hours after onset of neurologic symptoms; levels greater than 300 μg/dL are associated with poor prognosis. Platelet count and peripheral smear are usually normal. Toxicology screening should be performed to exclude other causes. Head CT may demonstrate diffuse cerebral edema. Lumbar puncture is not contraindicated but typically shows fewer than 8 leukocytes/mm³. Liver biopsy confirms the diagnosis by demonstrating microvesicular fatty infiltration but should not delay treatment.
The differential diagnosis includes inborn errors of metabolism (urea cycle defects, fatty acid oxidation disorders, organic acidemias), toxin exposures, drug intoxications such as acetaminophen or salicylates, hypoglycemia, sepsis, meningitis, encephalitis, and head trauma.
Management is supportive and aimed primarily at controlling intracranial pressure and correcting metabolic derangements. All patients require intensive care admission in a facility capable of ICP monitoring. Airway protection with rapid-sequence intubation is indicated for significant encephalopathy. Supplemental oxygen and cardiorespiratory monitoring are essential. Intravenous glucose should be administered promptly for altered mental status, and serum glucose should be maintained between 125 and 175 mg/dL with careful monitoring. Overhydration should be avoided.
Elevated ICP is managed with head elevation, controlled hyperventilation, osmotic therapy such as mannitol, and, in severe cases, barbiturate coma. Intracranial pressure monitoring via subarachnoid bolt or intraventricular catheter may be required in advanced stages. Vitamin K is administered if prothrombin time is prolonged, and fresh-frozen plasma may be given for severe coagulopathy or bleeding. Diuretics such as furosemide may be used adjunctively. Treatment should be initiated promptly without waiting for liver biopsy confirmation.
All children with suspected Reye syndrome should be admitted to the intensive care unit. Discharge decisions are individualized and depend on stabilization of mental status and laboratory values. Long-term follow-up with hepatology and neurology is recommended, including neuropsychological assessment.
A critical preventive point is the avoidance of aspirin and salicylate-containing products in children and adolescents with viral illnesses. Clinicians must maintain vigilance for alternative diagnoses and aggressively manage intracranial pressure, as neurologic complications are the primary determinant of outcome.
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Infectious Disease and Microbiology – Septic Bursitis
Bursitis refers to inflammation of a bursa, one of more than 150 sac-like structures in the body that cushion soft tissues over bony prominences. Bursitis may result from infection (pyogenic), crystal deposition due to trauma or gout, or inflammatory arthritis such as rheumatoid arthritis. Septic bursitis most commonly involves superficial bursae and frequently affects the olecranon, prepatellar, subdeltoid, ischial, and trochanteric bursae.
The most important predisposing factor for septic bursitis is trauma, which accounts for approximately 70% of cases. Repetitive microtrauma is common in certain activities and occupations. Specific associations include ischial bursitis in individuals with spinal cord injuries, malleolar bursitis in ice skaters, and subdeltoid bursitis following injections. Additional risk factors include diabetes mellitus, alcohol abuse, chronic skin conditions, intravenous drug use, and invasive procedures such as acupuncture or joint injections, which have been associated with outbreaks of methicillin-resistant Staphylococcus aureus (MRSA).
The most common causative organism is Staphylococcus aureus. Streptococcal species account for 5–30% of cases. Gram-negative bacteria and fungi are rare causes. Prototheca wickerhamii, an environmental algae, has been reported in immunocompromised individuals. In endemic regions, brucellosis should be considered in the differential diagnosis, and tuberculous bursitis may occur as part of disseminated disease.
Clinically, septic bursitis presents with localized painful swelling, erythema, warmth, and tenderness over the affected bursa. Fever may be present. Overlying cellulitis may extend beyond the bursa. Deep bursal infections are more likely to be associated with systemic signs of infection and bacteremia.
Aspiration of bursal fluid is the diagnostic procedure of choice. Fluid analysis typically shows elevated white blood cell counts, often below 20,000 cells/mm³ in septic bursitis. Gram stain positivity varies widely, and culture of aspirated fluid has high sensitivity and specificity. Use of liquid media may improve culture yield. Crystal analysis should be performed, as crystal-induced bursitis can coexist with infection. Laboratory blood tests may show inflammatory markers, but they are nonspecific.
Imaging may support the diagnosis. Plain radiographs can demonstrate soft tissue swelling and subcutaneous edema. Ultrasound is useful in identifying fluid collections and guiding aspiration. MRI may show a fluid-filled bursa with rim enhancement after gadolinium administration, while surrounding structures are typically spared unless there is extension of infection.
The differential diagnosis includes cellulitis, fasciitis, acute monoarthritis, gout, pseudogout, and traumatic injury.
Management includes repeated needle aspiration, often daily, until the bursa is no longer fluctuant. Empiric antibiotic therapy should cover staphylococci and streptococci. For methicillin-sensitive Staphylococcus aureus, intravenous oxacillin or nafcillin is recommended. For MRSA, vancomycin is indicated. Antibiotic therapy is generally continued for at least 14 days, although shorter courses (7 days) may be sufficient in selected non-immunocompromised patients with severe infection requiring hospitalization. The choice between intravenous and oral therapy depends on severity and systemic involvement. Immobilization of the affected joint is advised during acute treatment.
If medical therapy fails, or if there is persistent swelling, pain, or loculated infection, surgical incision and drainage may be necessary. In chronic or recurrent cases, excision of the bursa may be required.
Follow-up care includes rehabilitation to prevent limitation of joint movement and ensure restoration of function.
Bursitis refers to inflammation of a bursa, one of more than 150 sac-like structures in the body that cushion soft tissues over bony prominences. Bursitis may result from infection (pyogenic), crystal deposition due to trauma or gout, or inflammatory arthritis such as rheumatoid arthritis. Septic bursitis most commonly involves superficial bursae and frequently affects the olecranon, prepatellar, subdeltoid, ischial, and trochanteric bursae.
The most important predisposing factor for septic bursitis is trauma, which accounts for approximately 70% of cases. Repetitive microtrauma is common in certain activities and occupations. Specific associations include ischial bursitis in individuals with spinal cord injuries, malleolar bursitis in ice skaters, and subdeltoid bursitis following injections. Additional risk factors include diabetes mellitus, alcohol abuse, chronic skin conditions, intravenous drug use, and invasive procedures such as acupuncture or joint injections, which have been associated with outbreaks of methicillin-resistant Staphylococcus aureus (MRSA).
The most common causative organism is Staphylococcus aureus. Streptococcal species account for 5–30% of cases. Gram-negative bacteria and fungi are rare causes. Prototheca wickerhamii, an environmental algae, has been reported in immunocompromised individuals. In endemic regions, brucellosis should be considered in the differential diagnosis, and tuberculous bursitis may occur as part of disseminated disease.
Clinically, septic bursitis presents with localized painful swelling, erythema, warmth, and tenderness over the affected bursa. Fever may be present. Overlying cellulitis may extend beyond the bursa. Deep bursal infections are more likely to be associated with systemic signs of infection and bacteremia.
Aspiration of bursal fluid is the diagnostic procedure of choice. Fluid analysis typically shows elevated white blood cell counts, often below 20,000 cells/mm³ in septic bursitis. Gram stain positivity varies widely, and culture of aspirated fluid has high sensitivity and specificity. Use of liquid media may improve culture yield. Crystal analysis should be performed, as crystal-induced bursitis can coexist with infection. Laboratory blood tests may show inflammatory markers, but they are nonspecific.
Imaging may support the diagnosis. Plain radiographs can demonstrate soft tissue swelling and subcutaneous edema. Ultrasound is useful in identifying fluid collections and guiding aspiration. MRI may show a fluid-filled bursa with rim enhancement after gadolinium administration, while surrounding structures are typically spared unless there is extension of infection.
The differential diagnosis includes cellulitis, fasciitis, acute monoarthritis, gout, pseudogout, and traumatic injury.
Management includes repeated needle aspiration, often daily, until the bursa is no longer fluctuant. Empiric antibiotic therapy should cover staphylococci and streptococci. For methicillin-sensitive Staphylococcus aureus, intravenous oxacillin or nafcillin is recommended. For MRSA, vancomycin is indicated. Antibiotic therapy is generally continued for at least 14 days, although shorter courses (7 days) may be sufficient in selected non-immunocompromised patients with severe infection requiring hospitalization. The choice between intravenous and oral therapy depends on severity and systemic involvement. Immobilization of the affected joint is advised during acute treatment.
If medical therapy fails, or if there is persistent swelling, pain, or loculated infection, surgical incision and drainage may be necessary. In chronic or recurrent cases, excision of the bursa may be required.
Follow-up care includes rehabilitation to prevent limitation of joint movement and ensure restoration of function.
