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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 – 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 – 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 – 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.
- Published on
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 – 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 – Renal Failure (Acute Kidney Injury)
Acute kidney injury (AKI) is the preferred term for what was previously called acute renal failure. It represents a spectrum of acute changes in glomerular filtration rate and urine output, resulting in accumulation of nitrogenous waste products. Severity is defined by the RIFLE criteria: Risk (creatinine increase ×1.5 or GFR decrease >25%, urine output <0.5 ml />g/h for >6 hours), Injury (creatinine ×2 or GFR decrease >50%, urine output <0.5 ml />g/h for >12 hours), and Failure (creatinine ×3 or GFR decrease >75% or creatinine ≥4 mg/dL with acute rise ≥0.5 mg/dL, urine output <0.3 ml />g/h for 24 hours or anuria for 12 hours). Outcome stages include Loss (>4 weeks of renal dysfunction) and ESRD (>3 months). Higher RIFLE stages correlate with increased short- and intermediate-term mortality.
AKI is categorized as prerenal, intrinsic (intrarenal), or postrenal. Prerenal AKI results from renal hypoperfusion without intrinsic parenchymal damage unless prolonged. Causes include hypovolemia, heart failure, systemic vasodilation from sepsis or anaphylaxis, and low cardiac output states. Intrinsic AKI results from parenchymal disease such as acute tubular necrosis (ATN), glomerulonephritis, vasculitis, allergic interstitial nephritis, hemolytic uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP), rhabdomyolysis, nephrotoxins, or renal vascular thrombosis. Iatrogenic causes include aminoglycosides, radiocontrast, NSAIDs, ACE inhibitors, and angiotensin receptor blockers. Postrenal AKI is due to urinary tract obstruction, commonly from prostatic hypertrophy, prostatitis, stones, or malignancy.
AKI is often asymptomatic and detected incidentally on laboratory testing. Oliguria (<400 ml />ay) may be present. Fluid overload may cause dyspnea, hypertension, jugular venous distention, pulmonary edema, peripheral edema, ascites, pleural effusions, or pericardial effusion. Uremic symptoms include nausea, vomiting, pruritus, confusion, asterixis, seizures, and pericarditis. Fever and rash suggest allergic interstitial nephritis. Flank pain may indicate renal vein thrombosis. Postrenal obstruction may present with abdominal pain, distended bladder, oliguria, or anuria. Hyperkalemia and metabolic acidosis are potentially life-threatening complications.
History should include prior kidney disease, recent illness, medication exposure (especially nephrotoxins), fluid losses, and weight changes. Physical examination evaluates mental status, volume status, cardiac findings (S3, jugular venous distention), pulmonary crackles, abdominal or flank tenderness, edema, and skin changes. Elderly patients are particularly vulnerable to prerenal causes and medication toxicity, and baseline creatinine may underestimate renal impairment due to reduced muscle mass.
Essential evaluation includes serum electrolytes (including calcium, magnesium, and phosphate), BUN, creatinine, CBC, urinalysis with microscopy, and ECG. Fractional excretion of sodium (FENa) or urea may help differentiate prerenal from intrinsic causes. Postvoid residual measurement or renal ultrasound is necessary to exclude obstruction, particularly in older men.
In prerenal AKI, urinalysis typically shows high specific gravity (>1.018), urine osmolality >500 mmol/kg, low urine sodium (<10 mmol />), hyaline casts, BUN/creatinine ratio >20, and FENa <1%, with improvement after restoration of perfusion. intrinsic aki often shows bun />reatinine ratio <10-15 and fena>2%. ATN is associated with brown granular casts, urine sodium >20 mmol/L, and urine osmolality <350 mmol />g. Glomerulonephritis presents with red cell casts and proteinuria. Allergic interstitial nephritis shows white blood cells and WBC casts with possible eosinophilia. Postrenal AKI often has relatively normal urinalysis and is confirmed by imaging showing obstruction. Ultrasound is highly sensitive for detecting obstruction.
Initial management focuses on airway, breathing, and circulation, oxygen for hypoxia, and intravenous normal saline for volume depletion. Nephrotoxic medications should be discontinued. Monitor urine output closely. Indications for emergent dialysis include intractable hypertension, refractory volume overload, uremic encephalopathy, uremic bleeding or pericarditis, BUN >100 mg/dL, severe metabolic acidosis (pH <7.2), and refractory hyperkalemia.< />pan>
Hyperkalemia requires prompt treatment. For potassium >6.5 mEq/L or ECG changes, administer calcium (calcium gluconate in awake patients, calcium chloride in pulseless patients) to stabilize myocardium, followed by insulin with dextrose, nebulized albuterol, and loop diuretics if not anuric. Dialysis is required for refractory cases. Sodium polystyrene sulfonate or calcium polystyrene sulfonate may be used in less urgent cases. Sodium bicarbonate may be considered for severe metabolic acidosis but should be used cautiously due to sodium load, especially in oliguric or anuric patients.
Prerenal AKI is treated with volume resuscitation and correction of underlying hypoperfusion. Intrinsic causes require targeted therapy such as glucocorticoids or plasma exchange for glomerulonephritis, supportive care for ATN, aggressive fluids for rhabdomyolysis, and management of electrolyte disturbances. Postrenal AKI requires relief of obstruction.
Admission is required for new-onset AKI, significant electrolyte abnormalities, hyperkalemia, volume overload with hypoxia, uremia, or altered mental status. Stable patients with mild laboratory abnormalities may be managed with close follow-up. Key pitfalls include inappropriate use of nephrotoxic medications, failure to recognize hyperkalemia, and underdosing insulin in renal or liver disease leading to hypoglycemia. Contrast exposure should be avoided whenever possible in patients with AKI.
Acute kidney injury (AKI) is the preferred term for what was previously called acute renal failure. It represents a spectrum of acute changes in glomerular filtration rate and urine output, resulting in accumulation of nitrogenous waste products. Severity is defined by the RIFLE criteria: Risk (creatinine increase ×1.5 or GFR decrease >25%, urine output <0.5 ml />g/h for >6 hours), Injury (creatinine ×2 or GFR decrease >50%, urine output <0.5 ml />g/h for >12 hours), and Failure (creatinine ×3 or GFR decrease >75% or creatinine ≥4 mg/dL with acute rise ≥0.5 mg/dL, urine output <0.3 ml />g/h for 24 hours or anuria for 12 hours). Outcome stages include Loss (>4 weeks of renal dysfunction) and ESRD (>3 months). Higher RIFLE stages correlate with increased short- and intermediate-term mortality.
AKI is categorized as prerenal, intrinsic (intrarenal), or postrenal. Prerenal AKI results from renal hypoperfusion without intrinsic parenchymal damage unless prolonged. Causes include hypovolemia, heart failure, systemic vasodilation from sepsis or anaphylaxis, and low cardiac output states. Intrinsic AKI results from parenchymal disease such as acute tubular necrosis (ATN), glomerulonephritis, vasculitis, allergic interstitial nephritis, hemolytic uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP), rhabdomyolysis, nephrotoxins, or renal vascular thrombosis. Iatrogenic causes include aminoglycosides, radiocontrast, NSAIDs, ACE inhibitors, and angiotensin receptor blockers. Postrenal AKI is due to urinary tract obstruction, commonly from prostatic hypertrophy, prostatitis, stones, or malignancy.
AKI is often asymptomatic and detected incidentally on laboratory testing. Oliguria (<400 ml />ay) may be present. Fluid overload may cause dyspnea, hypertension, jugular venous distention, pulmonary edema, peripheral edema, ascites, pleural effusions, or pericardial effusion. Uremic symptoms include nausea, vomiting, pruritus, confusion, asterixis, seizures, and pericarditis. Fever and rash suggest allergic interstitial nephritis. Flank pain may indicate renal vein thrombosis. Postrenal obstruction may present with abdominal pain, distended bladder, oliguria, or anuria. Hyperkalemia and metabolic acidosis are potentially life-threatening complications.
History should include prior kidney disease, recent illness, medication exposure (especially nephrotoxins), fluid losses, and weight changes. Physical examination evaluates mental status, volume status, cardiac findings (S3, jugular venous distention), pulmonary crackles, abdominal or flank tenderness, edema, and skin changes. Elderly patients are particularly vulnerable to prerenal causes and medication toxicity, and baseline creatinine may underestimate renal impairment due to reduced muscle mass.
Essential evaluation includes serum electrolytes (including calcium, magnesium, and phosphate), BUN, creatinine, CBC, urinalysis with microscopy, and ECG. Fractional excretion of sodium (FENa) or urea may help differentiate prerenal from intrinsic causes. Postvoid residual measurement or renal ultrasound is necessary to exclude obstruction, particularly in older men.
In prerenal AKI, urinalysis typically shows high specific gravity (>1.018), urine osmolality >500 mmol/kg, low urine sodium (<10 mmol />), hyaline casts, BUN/creatinine ratio >20, and FENa <1%, with improvement after restoration of perfusion. intrinsic aki often shows bun />reatinine ratio <10-15 and fena>2%. ATN is associated with brown granular casts, urine sodium >20 mmol/L, and urine osmolality <350 mmol />g. Glomerulonephritis presents with red cell casts and proteinuria. Allergic interstitial nephritis shows white blood cells and WBC casts with possible eosinophilia. Postrenal AKI often has relatively normal urinalysis and is confirmed by imaging showing obstruction. Ultrasound is highly sensitive for detecting obstruction.
Initial management focuses on airway, breathing, and circulation, oxygen for hypoxia, and intravenous normal saline for volume depletion. Nephrotoxic medications should be discontinued. Monitor urine output closely. Indications for emergent dialysis include intractable hypertension, refractory volume overload, uremic encephalopathy, uremic bleeding or pericarditis, BUN >100 mg/dL, severe metabolic acidosis (pH <7.2), and refractory hyperkalemia.< />pan>
Hyperkalemia requires prompt treatment. For potassium >6.5 mEq/L or ECG changes, administer calcium (calcium gluconate in awake patients, calcium chloride in pulseless patients) to stabilize myocardium, followed by insulin with dextrose, nebulized albuterol, and loop diuretics if not anuric. Dialysis is required for refractory cases. Sodium polystyrene sulfonate or calcium polystyrene sulfonate may be used in less urgent cases. Sodium bicarbonate may be considered for severe metabolic acidosis but should be used cautiously due to sodium load, especially in oliguric or anuric patients.
Prerenal AKI is treated with volume resuscitation and correction of underlying hypoperfusion. Intrinsic causes require targeted therapy such as glucocorticoids or plasma exchange for glomerulonephritis, supportive care for ATN, aggressive fluids for rhabdomyolysis, and management of electrolyte disturbances. Postrenal AKI requires relief of obstruction.
Admission is required for new-onset AKI, significant electrolyte abnormalities, hyperkalemia, volume overload with hypoxia, uremia, or altered mental status. Stable patients with mild laboratory abnormalities may be managed with close follow-up. Key pitfalls include inappropriate use of nephrotoxic medications, failure to recognize hyperkalemia, and underdosing insulin in renal or liver disease leading to hypoglycemia. Contrast exposure should be avoided whenever possible in patients with AKI.
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Emergency And Acute Medicine – Renal Injury
Renal injury is the most common urologic injury and occurs in approximately 8–10% of all abdominal trauma. The kidneys are retroperitoneal organs extending from the lower thoracic to upper lumbar vertebrae, with the left kidney positioned slightly higher than the right. They are mobile structures supported by the renal vessels and surrounding adipose tissue within Gerota fascia. Because they are not rigidly fixed, rapid deceleration and displacement forces contribute significantly to traumatic injury.
Blunt trauma accounts for 80–85% of renal injuries and is about five times more common than penetrating trauma. Common mechanisms include motor vehicle collisions, falls, contact sports, and interpersonal violence. Approximately 20% of cases are associated with intraperitoneal injuries, and significant renal trauma rarely occurs in isolation. Penetrating trauma results from gunshot wounds, stab wounds, or impalement and involves a combination of kinetic energy and shear forces. In children, the kidney is the most frequently injured organ in blunt abdominal trauma due to relatively larger kidney size and incomplete rib ossification. Major abdominal injury in nonaccidental trauma is uncommon but carries high mortality.
Renal injuries are graded according to the American Association for the Surgery of Trauma (AAST) scale. Grade I includes contusion with microscopic or gross hematuria and normal imaging, or a nonexpanding subcapsular hematoma. Grade II includes nonexpanding perirenal hematoma or cortical laceration less than 1 cm without urinary extravasation. Grade III includes cortical laceration greater than 1 cm without collecting system involvement. Grade IV includes lacerations extending into the collecting system with urinary extravasation or injury to the main renal artery or vein with contained hemorrhage. Grade V includes shattered kidney or avulsion of the renal hilum resulting in devascularization.
History should focus on mechanism and kinematics of injury. In blunt trauma, the direction and magnitude of deceleration or compression are important. In penetrating trauma, the type of weapon, caliber, blade length, and distance from the source should be documented. Most renal injuries are associated with other abdominal or thoracic injuries.
Hematuria is the most common indicator of urinary tract injury, but the severity of hematuria does not correlate with injury grade. Absence of hematuria does not exclude renal injury. Microscopic hematuria with hypotension (systolic blood pressure ≤90 mm Hg) increases suspicion for significant injury. Additional findings may include flank ecchymosis, flank or abdominal tenderness, palpable mass, lower rib or transverse process fractures, nausea, and vomiting.
Evaluation guidelines for blunt renal trauma recommend imaging in adults with gross hematuria, or microscopic hematuria with shock, or a history of significant deceleration injury even without hematuria. These guidelines do not apply to penetrating trauma or pediatric patients. In penetrating trauma, imaging decisions depend primarily on wound location and trajectory; any hematuria warrants imaging. Children may sustain significant renal injury without gross hematuria or shock due to physiologic compensation. In pediatric blunt trauma, imaging may be omitted when microscopic hematuria is less than 50 RBCs per high-power field and there are no other major injuries.
Urinalysis is essential. Gross hematuria or significant microscopic hematuria (>50 RBCs/HPF in adults, >20 RBCs/HPF in children) suggests renal injury. Baseline hematocrit and renal function tests should be obtained. Plain radiographs may reveal rib or vertebral fractures or loss of the psoas shadow but are nonspecific. Intravenous pyelography may be used where CT is unavailable but has largely been replaced by contrast-enhanced CT.
Contrast-enhanced helical CT scan is the diagnostic modality of choice, with approximately 98% accuracy. It provides excellent anatomic detail, detects parenchymal lacerations, urinary extravasation, vascular injury, and associated intra-abdominal injuries. Ultrasound, including FAST examination, may identify perirenal hematoma but has limited sensitivity for retroperitoneal injury.
Initial management follows Advanced Trauma Life Support principles with airway protection, cervical spine immobilization, adequate intravenous access, and fluid resuscitation with crystalloids followed by blood products as needed. Life-threatening injuries take priority over renal injury. Immediate laparotomy is indicated in hemodynamically unstable patients with suspected hemoperitoneum and renal injury.
The vast majority of blunt renal injuries (approximately 98%) can be managed nonoperatively. Grades I and II injuries with stable vital signs are treated conservatively with observation. Management of grade III injuries remains individualized based on imaging findings and clinical stability. Grades IV and V injuries, particularly those involving shattered kidney, renal pedicle injury, or hemodynamic instability, require emergent surgical intervention. Selective renal angiography and embolization have an increasing role in managing vascular injuries in stable patients. Ureteral injuries require operative repair. Nonoperative management of penetrating injuries may be appropriate for grades I–III in stable patients without other intra-abdominal injuries.
Patients with significant renal injury require hospitalization for observation or operative management. Adult blunt trauma patients without hematuria, shock, or radiographic injury may be discharged. Adults with isolated microscopic hematuria and no shock may also be discharged with follow-up. Pediatric patients with ≤50 RBCs/HPF and no other major injuries may not require imaging. Outpatient urologic follow-up is recommended for patients with persistent microscopic hematuria. Urinoma formation is the most common complication, occurring in 1–7% of cases, and most resolve spontaneously.
Key considerations include recognizing that hematuria severity does not predict injury grade and that absence of hematuria does not exclude significant renal trauma, particularly in children and penetrating injuries.
Renal injury is the most common urologic injury and occurs in approximately 8–10% of all abdominal trauma. The kidneys are retroperitoneal organs extending from the lower thoracic to upper lumbar vertebrae, with the left kidney positioned slightly higher than the right. They are mobile structures supported by the renal vessels and surrounding adipose tissue within Gerota fascia. Because they are not rigidly fixed, rapid deceleration and displacement forces contribute significantly to traumatic injury.
Blunt trauma accounts for 80–85% of renal injuries and is about five times more common than penetrating trauma. Common mechanisms include motor vehicle collisions, falls, contact sports, and interpersonal violence. Approximately 20% of cases are associated with intraperitoneal injuries, and significant renal trauma rarely occurs in isolation. Penetrating trauma results from gunshot wounds, stab wounds, or impalement and involves a combination of kinetic energy and shear forces. In children, the kidney is the most frequently injured organ in blunt abdominal trauma due to relatively larger kidney size and incomplete rib ossification. Major abdominal injury in nonaccidental trauma is uncommon but carries high mortality.
Renal injuries are graded according to the American Association for the Surgery of Trauma (AAST) scale. Grade I includes contusion with microscopic or gross hematuria and normal imaging, or a nonexpanding subcapsular hematoma. Grade II includes nonexpanding perirenal hematoma or cortical laceration less than 1 cm without urinary extravasation. Grade III includes cortical laceration greater than 1 cm without collecting system involvement. Grade IV includes lacerations extending into the collecting system with urinary extravasation or injury to the main renal artery or vein with contained hemorrhage. Grade V includes shattered kidney or avulsion of the renal hilum resulting in devascularization.
History should focus on mechanism and kinematics of injury. In blunt trauma, the direction and magnitude of deceleration or compression are important. In penetrating trauma, the type of weapon, caliber, blade length, and distance from the source should be documented. Most renal injuries are associated with other abdominal or thoracic injuries.
Hematuria is the most common indicator of urinary tract injury, but the severity of hematuria does not correlate with injury grade. Absence of hematuria does not exclude renal injury. Microscopic hematuria with hypotension (systolic blood pressure ≤90 mm Hg) increases suspicion for significant injury. Additional findings may include flank ecchymosis, flank or abdominal tenderness, palpable mass, lower rib or transverse process fractures, nausea, and vomiting.
Evaluation guidelines for blunt renal trauma recommend imaging in adults with gross hematuria, or microscopic hematuria with shock, or a history of significant deceleration injury even without hematuria. These guidelines do not apply to penetrating trauma or pediatric patients. In penetrating trauma, imaging decisions depend primarily on wound location and trajectory; any hematuria warrants imaging. Children may sustain significant renal injury without gross hematuria or shock due to physiologic compensation. In pediatric blunt trauma, imaging may be omitted when microscopic hematuria is less than 50 RBCs per high-power field and there are no other major injuries.
Urinalysis is essential. Gross hematuria or significant microscopic hematuria (>50 RBCs/HPF in adults, >20 RBCs/HPF in children) suggests renal injury. Baseline hematocrit and renal function tests should be obtained. Plain radiographs may reveal rib or vertebral fractures or loss of the psoas shadow but are nonspecific. Intravenous pyelography may be used where CT is unavailable but has largely been replaced by contrast-enhanced CT.
Contrast-enhanced helical CT scan is the diagnostic modality of choice, with approximately 98% accuracy. It provides excellent anatomic detail, detects parenchymal lacerations, urinary extravasation, vascular injury, and associated intra-abdominal injuries. Ultrasound, including FAST examination, may identify perirenal hematoma but has limited sensitivity for retroperitoneal injury.
Initial management follows Advanced Trauma Life Support principles with airway protection, cervical spine immobilization, adequate intravenous access, and fluid resuscitation with crystalloids followed by blood products as needed. Life-threatening injuries take priority over renal injury. Immediate laparotomy is indicated in hemodynamically unstable patients with suspected hemoperitoneum and renal injury.
The vast majority of blunt renal injuries (approximately 98%) can be managed nonoperatively. Grades I and II injuries with stable vital signs are treated conservatively with observation. Management of grade III injuries remains individualized based on imaging findings and clinical stability. Grades IV and V injuries, particularly those involving shattered kidney, renal pedicle injury, or hemodynamic instability, require emergent surgical intervention. Selective renal angiography and embolization have an increasing role in managing vascular injuries in stable patients. Ureteral injuries require operative repair. Nonoperative management of penetrating injuries may be appropriate for grades I–III in stable patients without other intra-abdominal injuries.
Patients with significant renal injury require hospitalization for observation or operative management. Adult blunt trauma patients without hematuria, shock, or radiographic injury may be discharged. Adults with isolated microscopic hematuria and no shock may also be discharged with follow-up. Pediatric patients with ≤50 RBCs/HPF and no other major injuries may not require imaging. Outpatient urologic follow-up is recommended for patients with persistent microscopic hematuria. Urinoma formation is the most common complication, occurring in 1–7% of cases, and most resolve spontaneously.
Key considerations include recognizing that hematuria severity does not predict injury grade and that absence of hematuria does not exclude significant renal trauma, particularly in children and penetrating injuries.
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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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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.
