- Published on
Emergency And Acute Medicine – Knee Dislocation
Basics Description
Knee dislocation is defined by displacement of the tibia relative to the distal femur and represents a true orthopedic emergency because of the high risk of vascular and neurologic injury. Anterior dislocation is the most common type, accounting for approximately 60% of cases, and typically results from hyperextension. Rupture of the posterior capsule may occur at 30° of hyperextension, with disruption of the posterior cruciate ligament and potential popliteal artery injury at greater degrees. Posterior dislocation usually results from a direct blow to the anterior tibia with the knee flexed, such as a dashboard injury. Medial and lateral dislocations occur from varus or valgus stress, respectively, and are associated with multiligamentous injuries.
Popliteal artery injury occurs in up to 35% of knee dislocations and is the most limb-threatening complication. Anterior dislocations commonly cause traction-related intimal injury with delayed thrombosis, whereas posterior dislocations are more likely to cause direct arterial transection and immediate thrombosis. Peroneal nerve injury is less common but clinically significant and often accompanies arterial injury, particularly in medial or rotational dislocations.
Etiology
Knee dislocations typically result from high-energy mechanisms such as motor vehicle collisions, auto–pedestrian trauma, or athletic injuries, most commonly football.
Diagnosis Signs And Symptoms
Patients may present with a grossly deformed or unstable knee, though spontaneous reduction can mask deformity. Absence of distal pulses or signs of ischemia such as pallor, paresthesia, pain, paralysis, or poikilothermia raise immediate concern for popliteal artery injury. Neurologic deficits may include decreased sensation in the first web space or inability to dorsiflex the foot. A careful history of the mechanism of injury and repeated neurovascular examinations are essential.
Essential Workup
Evaluation requires a detailed history and thorough physical examination with emphasis on vascular and neurologic status. Distal pulses should be assessed by palpation and Doppler, capillary refill documented, and ankle–brachial index calculated. Neurologic examination should assess peroneal nerve function. Repeat examinations are mandatory, especially after reduction.
Diagnosis Tests And Interpretation
AP and lateral knee radiographs are required to confirm alignment and exclude associated fractures. MRI within one week is useful for defining ligamentous injury. An ABI ≥0.9 suggests low likelihood of major arterial injury, but abnormal findings warrant further evaluation. Vascular ultrasound or arteriography should be considered when pulses are diminished, ischemic symptoms persist, or peroneal nerve injury is present.
Differential Diagnosis
Conditions to consider include tibial plateau fracture, supracondylar femoral fracture, and ligamentous or tendinous avulsion injuries.
Treatment Pre Hospital
Initial management focuses on airway, breathing, and circulation. Distal pulses and motor function must be documented. The knee should be splinted in slight flexion to minimize popliteal artery tension.
Initial Stabilization Therapy
Address ABCs, particularly in polytrauma patients. Hypotension should be corrected, as it may obscure vascular compromise. Immediate closed reduction is indicated for any evidence of limb ischemia, with early orthopedic and vascular consultation.
Ed Treatment Procedures
Closed reduction is performed using longitudinal traction with gentle realignment, avoiding pressure in the popliteal fossa. The knee is immobilized in 15–20° of flexion. Neurovascular status must be reassessed immediately after reduction and monitored frequently. IV analgesia should be provided, and surgical consultation obtained for open injuries, vascular compromise, or irreducible dislocations.
Medication
IV narcotic analgesia is first-line. Oral medications should be avoided due to the high likelihood of operative intervention.
Follow-Up Disposition
All patients with knee dislocation require admission for observation and management of potential vascular injury. Discharge from the ED is not appropriate.
Follow-Up Recommendations
Orthopedic follow-up is required for staged ligamentous repair, typically delayed until swelling subsides. Vascular surgery follow-up is necessary if popliteal artery injury is identified.
Pearls And Pitfalls
Failure to restore popliteal artery flow within 6–8 hours carries an amputation risk approaching 90%. Peroneal nerve injury has a poor prognosis for recovery. Delayed compartment syndrome may occur and requires vigilant monitoring.
Basics Description
Knee dislocation is defined by displacement of the tibia relative to the distal femur and represents a true orthopedic emergency because of the high risk of vascular and neurologic injury. Anterior dislocation is the most common type, accounting for approximately 60% of cases, and typically results from hyperextension. Rupture of the posterior capsule may occur at 30° of hyperextension, with disruption of the posterior cruciate ligament and potential popliteal artery injury at greater degrees. Posterior dislocation usually results from a direct blow to the anterior tibia with the knee flexed, such as a dashboard injury. Medial and lateral dislocations occur from varus or valgus stress, respectively, and are associated with multiligamentous injuries.
Popliteal artery injury occurs in up to 35% of knee dislocations and is the most limb-threatening complication. Anterior dislocations commonly cause traction-related intimal injury with delayed thrombosis, whereas posterior dislocations are more likely to cause direct arterial transection and immediate thrombosis. Peroneal nerve injury is less common but clinically significant and often accompanies arterial injury, particularly in medial or rotational dislocations.
Etiology
Knee dislocations typically result from high-energy mechanisms such as motor vehicle collisions, auto–pedestrian trauma, or athletic injuries, most commonly football.
Diagnosis Signs And Symptoms
Patients may present with a grossly deformed or unstable knee, though spontaneous reduction can mask deformity. Absence of distal pulses or signs of ischemia such as pallor, paresthesia, pain, paralysis, or poikilothermia raise immediate concern for popliteal artery injury. Neurologic deficits may include decreased sensation in the first web space or inability to dorsiflex the foot. A careful history of the mechanism of injury and repeated neurovascular examinations are essential.
Essential Workup
Evaluation requires a detailed history and thorough physical examination with emphasis on vascular and neurologic status. Distal pulses should be assessed by palpation and Doppler, capillary refill documented, and ankle–brachial index calculated. Neurologic examination should assess peroneal nerve function. Repeat examinations are mandatory, especially after reduction.
Diagnosis Tests And Interpretation
AP and lateral knee radiographs are required to confirm alignment and exclude associated fractures. MRI within one week is useful for defining ligamentous injury. An ABI ≥0.9 suggests low likelihood of major arterial injury, but abnormal findings warrant further evaluation. Vascular ultrasound or arteriography should be considered when pulses are diminished, ischemic symptoms persist, or peroneal nerve injury is present.
Differential Diagnosis
Conditions to consider include tibial plateau fracture, supracondylar femoral fracture, and ligamentous or tendinous avulsion injuries.
Treatment Pre Hospital
Initial management focuses on airway, breathing, and circulation. Distal pulses and motor function must be documented. The knee should be splinted in slight flexion to minimize popliteal artery tension.
Initial Stabilization Therapy
Address ABCs, particularly in polytrauma patients. Hypotension should be corrected, as it may obscure vascular compromise. Immediate closed reduction is indicated for any evidence of limb ischemia, with early orthopedic and vascular consultation.
Ed Treatment Procedures
Closed reduction is performed using longitudinal traction with gentle realignment, avoiding pressure in the popliteal fossa. The knee is immobilized in 15–20° of flexion. Neurovascular status must be reassessed immediately after reduction and monitored frequently. IV analgesia should be provided, and surgical consultation obtained for open injuries, vascular compromise, or irreducible dislocations.
Medication
IV narcotic analgesia is first-line. Oral medications should be avoided due to the high likelihood of operative intervention.
Follow-Up Disposition
All patients with knee dislocation require admission for observation and management of potential vascular injury. Discharge from the ED is not appropriate.
Follow-Up Recommendations
Orthopedic follow-up is required for staged ligamentous repair, typically delayed until swelling subsides. Vascular surgery follow-up is necessary if popliteal artery injury is identified.
Pearls And Pitfalls
Failure to restore popliteal artery flow within 6–8 hours carries an amputation risk approaching 90%. Peroneal nerve injury has a poor prognosis for recovery. Delayed compartment syndrome may occur and requires vigilant monitoring.
- Published on
Infectious Diseases and Microbiology: Ear Pain
Basics
Description
Otalgia denotes pain originating in or perceived in the ear. Evaluation should consider patient age and associated symptoms such as sore throat, fever, headache, visual changes, and symptom duration. A systematic ear examination is essential, beginning with the auricle and external auditory meatus, followed by inspection of the auditory canal and tympanic membrane to guide the differential diagnosis. A complete head and neck examination may uncover lymphadenopathy, pharyngeal or nasal inflammation, thyroid disease, or dental and oral pathology. Cerumen can obstruct visualization of the tympanic membrane and should be gently removed when necessary. Any exudate within the auditory canal should be cultured. Pain elicited by movement of the pinna suggests otitis externa, foreign body, or impacted cerumen. Perichondritis, an infectious process of the outer ear cartilage, must be differentiated from relapsing polychondritis, a noninfectious rheumatologic condition.
Epidemiology
Approximately half of ear pain cases are referred from non-otologic sources. Acute otitis externa, commonly termed swimmer’s ear, occurs more frequently during summer months. Recurrent acute otitis media affects about one-fifth of children. Head and neck malignancies typically occur after age 50 but may present earlier, even without classic risk factors; several forms of nasopharyngeal carcinoma are associated with Epstein–Barr virus infection. Auricular cellulitis often follows minor trauma. Perichondritis usually develops after burns, trauma, or upper-ear piercings and is most commonly caused by Pseudomonas aeruginosa or Staphylococcus aureus. Chronic otitis externa often results from repeated minor trauma such as scratching or cotton swab use, and chronic middle-ear drainage may be mistaken for this condition. Malignant otitis externa is a destructive infection of the external canal and skull base.
Etiology
Ear pain is frequently referred because the ear receives sensory innervation from cranial nerves V, VII, VIII, IX, and X. Referred otalgia may arise from dental disease, gingival abscesses, nasopharyngeal or laryngeal inflammation or tumors, sinusitis, temporomandibular joint disorders, tonsillitis, tongue lesions, cervical spine disease, neural irritation such as trigeminal neuralgia or acoustic neuroma, gastroesophageal reflux in infants, thyroiditis, lateral sinus thrombosis, posterior fossa inflammation, or medication effects. Primary ear pathology causing otalgia includes acute or chronic otitis media, tympanic membrane rupture, anterior canal wall fracture, mastoiditis, Ménière disease, and eustachian tube dysfunction. Malignant otitis externa is almost always due to Pseudomonas aeruginosa. Otalgia may also accompany migraine, atypical facial pain, and herpes simplex infection of cranial nerves V, VII, or IX. Herpes zoster affecting the external auditory canal may produce ipsilateral facial paralysis, known as Ramsay Hunt syndrome, from involvement of the geniculate ganglion. Facial nerve palsy may also occur with Lyme disease. Neoplasms of the infratemporal fossa may present solely with ear pain. Acute otitis externa is most often caused by Pseudomonas aeruginosa, Staphylococcus aureus, or streptococcal species, with swimming and canal trauma as major risk factors.
Diagnosis
Clinical Manifestations
Auricular cellulitis presents with a swollen, erythematous, warm, mildly tender ear. Perichondritis causes marked swelling, redness, heat, and severe tenderness of the pinna with relative sparing of the lobule. Chronic otitis externa more commonly causes itching than pain. Nasopharyngeal carcinoma may be asymptomatic early but often produces unilateral serous otitis media from eustachian tube obstruction, nasal blockage, or epistaxis, and advanced disease may cause cranial nerve palsies, especially involving nerves III, IV, VI, and VII. Malignant otitis externa typically affects elderly patients with diabetes or individuals with HIV and presents with severe otalgia, otorrhea, possible hearing loss, tender pinna, trismus from temporomandibular involvement, and sometimes cranial nerve palsies, most often of nerve VII. Fever and weight loss are uncommon. Examination reveals canal edema, erythema, purulent discharge, debris, and granulation tissue. Vesicular lesions in the external canal suggest herpes zoster and warrant evaluation for facial nerve palsy. Hearing loss with abnormal tympanic membrane findings indicates serous or bacterial otitis media or cholesteatoma. Nasal polyps, marked septal deviation, or nasopharyngeal tumors may be associated with otitis media.
Physical Examination
Findings such as an erythematous canal with discharge, preauricular lymphadenopathy, and pain on tragal or pinna manipulation suggest otitis externa. Fever, irritability in children, and a bulging or erythematous tympanic membrane with loss of the cone of light indicate otitis media, sometimes with canal pus if perforation is present. Altered mental status or meningeal signs such as headache and neck stiffness indicate possible central nervous system involvement and require urgent management.
Diagnostic Tests and Interpretation
Laboratory Studies
Peripheral leukocytosis is uncommon in malignant otitis externa, whereas erythrocyte sedimentation rate is typically elevated. Cerebrospinal fluid analysis may occasionally show pleocytosis and increased protein.
Imaging
Dental pathology can be assessed with panoramic radiography. In malignant otitis externa, CT of the temporal bone or mastoid often demonstrates bony erosion and new bone formation, while MRI more accurately defines soft-tissue extension and skull-base involvement.
Treatment
Medications
Acute otitis externa is managed with careful canal cleaning and topical therapy using antiseptics or antibiotic drops such as polymyxin–neomycin, along with counseling on ear hygiene and water avoidance. Malignant otitis externa requires urgent otolaryngology consultation and prolonged antipseudomonal therapy with agents such as cefepime, ceftazidime, carbapenems, or fluoroquinolones, typically for at least three to four weeks and longer if bone involvement is present. Auricular cellulitis is treated with warm compresses and intravenous antibiotics targeting staphylococci and streptococci. Severe perichondritis requires extended antibiotic therapy, often with agents such as piperacillin–tazobactam or nafcillin combined with ciprofloxacin, and may benefit from incision and drainage. Ramsay Hunt syndrome is treated with acyclovir and corticosteroids, and early therapy improves facial nerve outcomes; ophthalmologic evaluation is recommended to assess ocular involvement.
Ongoing Care and Follow-Up
Referral to an otolaryngologist is advised when ear pain persists despite appropriate initial evaluation and management.
Complications
Otitis media can lead to mastoiditis, epidural abscess, dural venous sinus thrombosis, meningitis, or brain abscess. Malignant otitis externa may extend to the cavernous sinus or contralateral petrous apex, and although meningitis and brain abscess are uncommon, they are serious potential sequelae.
Basics
Description
Otalgia denotes pain originating in or perceived in the ear. Evaluation should consider patient age and associated symptoms such as sore throat, fever, headache, visual changes, and symptom duration. A systematic ear examination is essential, beginning with the auricle and external auditory meatus, followed by inspection of the auditory canal and tympanic membrane to guide the differential diagnosis. A complete head and neck examination may uncover lymphadenopathy, pharyngeal or nasal inflammation, thyroid disease, or dental and oral pathology. Cerumen can obstruct visualization of the tympanic membrane and should be gently removed when necessary. Any exudate within the auditory canal should be cultured. Pain elicited by movement of the pinna suggests otitis externa, foreign body, or impacted cerumen. Perichondritis, an infectious process of the outer ear cartilage, must be differentiated from relapsing polychondritis, a noninfectious rheumatologic condition.
Epidemiology
Approximately half of ear pain cases are referred from non-otologic sources. Acute otitis externa, commonly termed swimmer’s ear, occurs more frequently during summer months. Recurrent acute otitis media affects about one-fifth of children. Head and neck malignancies typically occur after age 50 but may present earlier, even without classic risk factors; several forms of nasopharyngeal carcinoma are associated with Epstein–Barr virus infection. Auricular cellulitis often follows minor trauma. Perichondritis usually develops after burns, trauma, or upper-ear piercings and is most commonly caused by Pseudomonas aeruginosa or Staphylococcus aureus. Chronic otitis externa often results from repeated minor trauma such as scratching or cotton swab use, and chronic middle-ear drainage may be mistaken for this condition. Malignant otitis externa is a destructive infection of the external canal and skull base.
Etiology
Ear pain is frequently referred because the ear receives sensory innervation from cranial nerves V, VII, VIII, IX, and X. Referred otalgia may arise from dental disease, gingival abscesses, nasopharyngeal or laryngeal inflammation or tumors, sinusitis, temporomandibular joint disorders, tonsillitis, tongue lesions, cervical spine disease, neural irritation such as trigeminal neuralgia or acoustic neuroma, gastroesophageal reflux in infants, thyroiditis, lateral sinus thrombosis, posterior fossa inflammation, or medication effects. Primary ear pathology causing otalgia includes acute or chronic otitis media, tympanic membrane rupture, anterior canal wall fracture, mastoiditis, Ménière disease, and eustachian tube dysfunction. Malignant otitis externa is almost always due to Pseudomonas aeruginosa. Otalgia may also accompany migraine, atypical facial pain, and herpes simplex infection of cranial nerves V, VII, or IX. Herpes zoster affecting the external auditory canal may produce ipsilateral facial paralysis, known as Ramsay Hunt syndrome, from involvement of the geniculate ganglion. Facial nerve palsy may also occur with Lyme disease. Neoplasms of the infratemporal fossa may present solely with ear pain. Acute otitis externa is most often caused by Pseudomonas aeruginosa, Staphylococcus aureus, or streptococcal species, with swimming and canal trauma as major risk factors.
Diagnosis
Clinical Manifestations
Auricular cellulitis presents with a swollen, erythematous, warm, mildly tender ear. Perichondritis causes marked swelling, redness, heat, and severe tenderness of the pinna with relative sparing of the lobule. Chronic otitis externa more commonly causes itching than pain. Nasopharyngeal carcinoma may be asymptomatic early but often produces unilateral serous otitis media from eustachian tube obstruction, nasal blockage, or epistaxis, and advanced disease may cause cranial nerve palsies, especially involving nerves III, IV, VI, and VII. Malignant otitis externa typically affects elderly patients with diabetes or individuals with HIV and presents with severe otalgia, otorrhea, possible hearing loss, tender pinna, trismus from temporomandibular involvement, and sometimes cranial nerve palsies, most often of nerve VII. Fever and weight loss are uncommon. Examination reveals canal edema, erythema, purulent discharge, debris, and granulation tissue. Vesicular lesions in the external canal suggest herpes zoster and warrant evaluation for facial nerve palsy. Hearing loss with abnormal tympanic membrane findings indicates serous or bacterial otitis media or cholesteatoma. Nasal polyps, marked septal deviation, or nasopharyngeal tumors may be associated with otitis media.
Physical Examination
Findings such as an erythematous canal with discharge, preauricular lymphadenopathy, and pain on tragal or pinna manipulation suggest otitis externa. Fever, irritability in children, and a bulging or erythematous tympanic membrane with loss of the cone of light indicate otitis media, sometimes with canal pus if perforation is present. Altered mental status or meningeal signs such as headache and neck stiffness indicate possible central nervous system involvement and require urgent management.
Diagnostic Tests and Interpretation
Laboratory Studies
Peripheral leukocytosis is uncommon in malignant otitis externa, whereas erythrocyte sedimentation rate is typically elevated. Cerebrospinal fluid analysis may occasionally show pleocytosis and increased protein.
Imaging
Dental pathology can be assessed with panoramic radiography. In malignant otitis externa, CT of the temporal bone or mastoid often demonstrates bony erosion and new bone formation, while MRI more accurately defines soft-tissue extension and skull-base involvement.
Treatment
Medications
Acute otitis externa is managed with careful canal cleaning and topical therapy using antiseptics or antibiotic drops such as polymyxin–neomycin, along with counseling on ear hygiene and water avoidance. Malignant otitis externa requires urgent otolaryngology consultation and prolonged antipseudomonal therapy with agents such as cefepime, ceftazidime, carbapenems, or fluoroquinolones, typically for at least three to four weeks and longer if bone involvement is present. Auricular cellulitis is treated with warm compresses and intravenous antibiotics targeting staphylococci and streptococci. Severe perichondritis requires extended antibiotic therapy, often with agents such as piperacillin–tazobactam or nafcillin combined with ciprofloxacin, and may benefit from incision and drainage. Ramsay Hunt syndrome is treated with acyclovir and corticosteroids, and early therapy improves facial nerve outcomes; ophthalmologic evaluation is recommended to assess ocular involvement.
Ongoing Care and Follow-Up
Referral to an otolaryngologist is advised when ear pain persists despite appropriate initial evaluation and management.
Complications
Otitis media can lead to mastoiditis, epidural abscess, dural venous sinus thrombosis, meningitis, or brain abscess. Malignant otitis externa may extend to the cavernous sinus or contralateral petrous apex, and although meningitis and brain abscess are uncommon, they are serious potential sequelae.
- Published on
Emergency and Acute Medicine – Iritis (Anterior Uveitis)
Basics and description
Iritis is an inflammatory condition of the anterior uveal tract and is synonymous with anterior uveitis. When the inflammation occurs after blunt or penetrating eye injury, it is referred to as traumatic iritis. The condition may present acutely or follow a chronic, relapsing course and can threaten vision if not recognized and treated appropriately.
Etiology
Most cases of iritis are idiopathic, but many are associated with trauma, systemic inflammatory diseases, infections, malignancies, or drug reactions. Noninfectious systemic associations include ankylosing spondylitis, reactive arthritis (Reiter syndrome), sarcoidosis, Behçet disease, inflammatory bowel disease, juvenile rheumatoid arthritis, Kawasaki syndrome, interstitial nephritis, IgA nephropathy, Sjögren syndrome, and psoriatic arthritis. Infectious causes include viral pathogens such as herpes simplex virus, herpes zoster virus, cytomegalovirus, HIV, rubella, measles, mumps, varicella, adenovirus, and West Nile virus; bacterial causes such as tuberculosis, syphilis, Lyme disease, chlamydia, gonorrhea, brucellosis, pertussis, rickettsial infections, and leprosy; and less commonly fungal infections. Other associations include leukemia, lymphoma, multiple sclerosis, malignant melanoma, cocaine use, pesticide exposure, corneal foreign bodies, and blunt ocular trauma.
Diagnosis and clinical presentation
Acute iritis typically presents with ocular pain, a red eye, photophobia (often consensual), tearing, and mildly decreased visual acuity. On examination, characteristic findings include ciliary flush (perilimbal injection), miosis, inflammatory cells and protein “flare” in the anterior chamber, and sometimes hypopyon. Posterior synechiae, which are adhesions between the iris and the lens, may develop. Intraocular pressure is often low but can occasionally be elevated. Chronic iritis may present with recurrent episodes and few acute symptoms, making diagnosis more challenging.
Essential workup and evaluation
A thorough history and review of systems are critical, as up to half of patients have an associated systemic disease. Slit-lamp examination is diagnostic and reveals leukocytes (“cells”) and protein leakage (“flare”) in the anterior chamber; these findings are best appreciated with a short, wide beam of light. Intraocular pressure should be measured. Relief of pain with topical anesthetic suggests a superficial process and makes iritis less likely.
Diagnostic tests and interpretation
Routine laboratory testing is usually not required in the emergency setting. Further outpatient evaluation should be guided by clinical suspicion and coordinated with ophthalmology and other specialists. Targeted testing may include inflammatory markers, HLA-B27 typing, autoimmune serologies, tuberculosis screening, syphilis testing, Lyme serologies, ACE levels, or imaging such as chest radiography or sacroiliac joint films, depending on suspected systemic disease. Ultrasound biomicroscopy may assist in selected cases.
Differential diagnosis
Conditions that can mimic iritis include acute angle-closure glaucoma, conjunctivitis, corneal abrasion or foreign body, episcleritis, keratitis, intraocular foreign body, posterior segment tumors, and traumatic globe rupture. These must be carefully excluded because management differs significantly.
Treatment and emergency management
The primary goals of treatment are to reduce inflammation, relieve pain, prevent posterior synechiae, and preserve vision. Cycloplegic agents are the cornerstone of initial therapy, as they decrease ciliary muscle spasm, relieve pain and photophobia, and prevent synechiae formation. Topical corticosteroids may be indicated but should only be started in consultation with an ophthalmologist because of the risk of worsening infectious keratitis, particularly herpes simplex virus infection. Secondary glaucoma should be treated if present. Supportive care includes warm compresses, dark glasses, and appropriate analgesia. Identification and treatment of any underlying systemic or infectious cause are essential.
Medications
Cyclopentolate 1–2% is commonly used for mild to moderate inflammation, typically one drop three times daily. Homatropine 2–5% may be used for moderate inflammation. Atropine 1% is reserved for moderate to severe cases and should only be used with ophthalmology guidance. Prednisolone acetate 1% topical drops may be used for inflammation under ophthalmologic supervision. Analgesics such as acetaminophen or acetaminophen with codeine may be given for pain control.
Pediatric considerations
Cycloplegic agents are generally not recommended in children under 6 years of age because of the risk of systemic anticholinergic toxicity, which may cause flushing, tachycardia, hypotension, blurred vision, and hallucinations.
Disposition and follow-up
Hospital admission is rarely required unless there is a significant associated systemic illness. All patients with suspected iritis should be referred to an ophthalmologist within 24 hours for confirmation of diagnosis, monitoring, and adjustment of therapy. Referral to rheumatology, gastroenterology, or other specialists may be necessary when a systemic disease is identified.
Pearls and pitfalls
If topical anesthetic relieves eye pain, iritis is unlikely. Iritis must be distinguished from other causes of painful red eye that can rapidly threaten vision, including keratitis, herpes simplex conjunctivitis, bacterial conjunctivitis, acute angle-closure glaucoma, and globe rupture. Early recognition and appropriate referral are critical to preventing complications and vision loss.
Basics and description
Iritis is an inflammatory condition of the anterior uveal tract and is synonymous with anterior uveitis. When the inflammation occurs after blunt or penetrating eye injury, it is referred to as traumatic iritis. The condition may present acutely or follow a chronic, relapsing course and can threaten vision if not recognized and treated appropriately.
Etiology
Most cases of iritis are idiopathic, but many are associated with trauma, systemic inflammatory diseases, infections, malignancies, or drug reactions. Noninfectious systemic associations include ankylosing spondylitis, reactive arthritis (Reiter syndrome), sarcoidosis, Behçet disease, inflammatory bowel disease, juvenile rheumatoid arthritis, Kawasaki syndrome, interstitial nephritis, IgA nephropathy, Sjögren syndrome, and psoriatic arthritis. Infectious causes include viral pathogens such as herpes simplex virus, herpes zoster virus, cytomegalovirus, HIV, rubella, measles, mumps, varicella, adenovirus, and West Nile virus; bacterial causes such as tuberculosis, syphilis, Lyme disease, chlamydia, gonorrhea, brucellosis, pertussis, rickettsial infections, and leprosy; and less commonly fungal infections. Other associations include leukemia, lymphoma, multiple sclerosis, malignant melanoma, cocaine use, pesticide exposure, corneal foreign bodies, and blunt ocular trauma.
Diagnosis and clinical presentation
Acute iritis typically presents with ocular pain, a red eye, photophobia (often consensual), tearing, and mildly decreased visual acuity. On examination, characteristic findings include ciliary flush (perilimbal injection), miosis, inflammatory cells and protein “flare” in the anterior chamber, and sometimes hypopyon. Posterior synechiae, which are adhesions between the iris and the lens, may develop. Intraocular pressure is often low but can occasionally be elevated. Chronic iritis may present with recurrent episodes and few acute symptoms, making diagnosis more challenging.
Essential workup and evaluation
A thorough history and review of systems are critical, as up to half of patients have an associated systemic disease. Slit-lamp examination is diagnostic and reveals leukocytes (“cells”) and protein leakage (“flare”) in the anterior chamber; these findings are best appreciated with a short, wide beam of light. Intraocular pressure should be measured. Relief of pain with topical anesthetic suggests a superficial process and makes iritis less likely.
Diagnostic tests and interpretation
Routine laboratory testing is usually not required in the emergency setting. Further outpatient evaluation should be guided by clinical suspicion and coordinated with ophthalmology and other specialists. Targeted testing may include inflammatory markers, HLA-B27 typing, autoimmune serologies, tuberculosis screening, syphilis testing, Lyme serologies, ACE levels, or imaging such as chest radiography or sacroiliac joint films, depending on suspected systemic disease. Ultrasound biomicroscopy may assist in selected cases.
Differential diagnosis
Conditions that can mimic iritis include acute angle-closure glaucoma, conjunctivitis, corneal abrasion or foreign body, episcleritis, keratitis, intraocular foreign body, posterior segment tumors, and traumatic globe rupture. These must be carefully excluded because management differs significantly.
Treatment and emergency management
The primary goals of treatment are to reduce inflammation, relieve pain, prevent posterior synechiae, and preserve vision. Cycloplegic agents are the cornerstone of initial therapy, as they decrease ciliary muscle spasm, relieve pain and photophobia, and prevent synechiae formation. Topical corticosteroids may be indicated but should only be started in consultation with an ophthalmologist because of the risk of worsening infectious keratitis, particularly herpes simplex virus infection. Secondary glaucoma should be treated if present. Supportive care includes warm compresses, dark glasses, and appropriate analgesia. Identification and treatment of any underlying systemic or infectious cause are essential.
Medications
Cyclopentolate 1–2% is commonly used for mild to moderate inflammation, typically one drop three times daily. Homatropine 2–5% may be used for moderate inflammation. Atropine 1% is reserved for moderate to severe cases and should only be used with ophthalmology guidance. Prednisolone acetate 1% topical drops may be used for inflammation under ophthalmologic supervision. Analgesics such as acetaminophen or acetaminophen with codeine may be given for pain control.
Pediatric considerations
Cycloplegic agents are generally not recommended in children under 6 years of age because of the risk of systemic anticholinergic toxicity, which may cause flushing, tachycardia, hypotension, blurred vision, and hallucinations.
Disposition and follow-up
Hospital admission is rarely required unless there is a significant associated systemic illness. All patients with suspected iritis should be referred to an ophthalmologist within 24 hours for confirmation of diagnosis, monitoring, and adjustment of therapy. Referral to rheumatology, gastroenterology, or other specialists may be necessary when a systemic disease is identified.
Pearls and pitfalls
If topical anesthetic relieves eye pain, iritis is unlikely. Iritis must be distinguished from other causes of painful red eye that can rapidly threaten vision, including keratitis, herpes simplex conjunctivitis, bacterial conjunctivitis, acute angle-closure glaucoma, and globe rupture. Early recognition and appropriate referral are critical to preventing complications and vision loss.
- Published on
Emergency and Acute Medicine – Irritable infant
Irritability in infants is common and often part of normal development. Most infants have a predictable period of increased fussiness, usually in the evening. Normal crying peaks around 6 weeks of age, with infants crying 1–4 hours per day on average, and gradually improves over the first 6 months of life. Irritability is defined relative to the infant’s usual behavior. Colic is the most common cause of inconsolable crying, affecting up to 25% of otherwise healthy infants. It typically begins at 2–3 weeks of age, may last until 12 weeks, and is characterized by paroxysms of intense crying with knee flexion and passage of flatus. Colic is a diagnosis of exclusion.
The differential diagnosis of an irritable infant is broad and includes both benign and life-threatening conditions. Causes include gastrointestinal disorders such as gastroenteritis, gastroesophageal reflux, cow’s milk protein intolerance, constipation, anal fissure, volvulus, malrotation, intussusception, and appendicitis. Genitourinary causes include urinary tract infection, testicular torsion, incarcerated hernia, urinary retention, and genital tourniquets. Neurologic causes include increased intracranial pressure from hemorrhage, hydrocephalus, mass lesions, subdural or epidural hematomas, skull fracture, and meningitis. Cardiovascular causes include supraventricular tachycardia, congestive heart failure, myocarditis, endocarditis, anomalous coronary arteries, and coarctation of the aorta. Other important considerations include trauma, child abuse, infections (otitis media, pneumonia, thrush, gingivostomatitis), metabolic or endocrine abnormalities (hypoglycemia, hypocalcemia, hypernatremia, metabolic acidosis, inborn errors of metabolism, hyperthyroidism), toxicologic exposures, medication reactions, iron deficiency, sickle cell crisis, burns, bites, corneal abrasion or foreign body, hair or fiber tourniquets, splinters, and vaccine reactions.
Evaluation begins with careful assessment of vital signs, chief complaint, and the chronology of symptoms. A complete history should include prenatal and neonatal history, feeding patterns, stooling, sleep, recent illnesses, medications, immunizations, and caregiver concerns. Physical examination must be thorough and performed with the infant completely undressed. Measurement and plotting of weight, length, and head circumference are essential, along with rectal temperature and pulse oximetry.
Diagnostic testing is guided by the history and physical examination. Laboratory studies such as CBC, urinalysis, serum chemistries, cultures, bedside glucose testing, or stool hemoccult may be indicated. Imaging may include chest radiograph for cardiopulmonary disease, skeletal survey when abuse is suspected, CT imaging directed by neurologic findings, or contrast studies such as barium enema when intussusception is suspected. Targeted procedures may include fluorescein eye examination or ECG.
Management focuses first on identifying and stabilizing any life-threatening conditions using standard airway, breathing, and circulation principles. Immediate correction of reversible causes such as hair tourniquets or splinters is essential. If serious pathology is excluded, management is supportive. Colic is treated with reassurance, soothing rhythmic activities, reduction of environmental stimulation, and parental support. Dietary interventions such as trial of soy or hydrolyzed formula may offer temporary benefit in select infants. No medication has proven consistently effective for colic, though probiotics may help some infants. Observation in the emergency department is often appropriate.
Admission is indicated for infants with life-threatening conditions or when significant parental stress raises safety concerns. Discharge may be considered when no serious cause is identified, the infant appears well, the family is functional and supported, and close follow-up is assured. Parents must feel heard and supported, and clear return precautions are essential.
A critical pitfall is failure to recognize serious underlying disease. Cardiovascular, neurologic, gastrointestinal, metabolic, genitourinary, pulmonary, toxicologic, traumatic, ophthalmologic, and abuse-related causes must be actively considered. In noncritically ill infants, a meticulous history and complete physical examination should precede extensive laboratory or radiologic testing.
Irritability in infants is common and often part of normal development. Most infants have a predictable period of increased fussiness, usually in the evening. Normal crying peaks around 6 weeks of age, with infants crying 1–4 hours per day on average, and gradually improves over the first 6 months of life. Irritability is defined relative to the infant’s usual behavior. Colic is the most common cause of inconsolable crying, affecting up to 25% of otherwise healthy infants. It typically begins at 2–3 weeks of age, may last until 12 weeks, and is characterized by paroxysms of intense crying with knee flexion and passage of flatus. Colic is a diagnosis of exclusion.
The differential diagnosis of an irritable infant is broad and includes both benign and life-threatening conditions. Causes include gastrointestinal disorders such as gastroenteritis, gastroesophageal reflux, cow’s milk protein intolerance, constipation, anal fissure, volvulus, malrotation, intussusception, and appendicitis. Genitourinary causes include urinary tract infection, testicular torsion, incarcerated hernia, urinary retention, and genital tourniquets. Neurologic causes include increased intracranial pressure from hemorrhage, hydrocephalus, mass lesions, subdural or epidural hematomas, skull fracture, and meningitis. Cardiovascular causes include supraventricular tachycardia, congestive heart failure, myocarditis, endocarditis, anomalous coronary arteries, and coarctation of the aorta. Other important considerations include trauma, child abuse, infections (otitis media, pneumonia, thrush, gingivostomatitis), metabolic or endocrine abnormalities (hypoglycemia, hypocalcemia, hypernatremia, metabolic acidosis, inborn errors of metabolism, hyperthyroidism), toxicologic exposures, medication reactions, iron deficiency, sickle cell crisis, burns, bites, corneal abrasion or foreign body, hair or fiber tourniquets, splinters, and vaccine reactions.
Evaluation begins with careful assessment of vital signs, chief complaint, and the chronology of symptoms. A complete history should include prenatal and neonatal history, feeding patterns, stooling, sleep, recent illnesses, medications, immunizations, and caregiver concerns. Physical examination must be thorough and performed with the infant completely undressed. Measurement and plotting of weight, length, and head circumference are essential, along with rectal temperature and pulse oximetry.
Diagnostic testing is guided by the history and physical examination. Laboratory studies such as CBC, urinalysis, serum chemistries, cultures, bedside glucose testing, or stool hemoccult may be indicated. Imaging may include chest radiograph for cardiopulmonary disease, skeletal survey when abuse is suspected, CT imaging directed by neurologic findings, or contrast studies such as barium enema when intussusception is suspected. Targeted procedures may include fluorescein eye examination or ECG.
Management focuses first on identifying and stabilizing any life-threatening conditions using standard airway, breathing, and circulation principles. Immediate correction of reversible causes such as hair tourniquets or splinters is essential. If serious pathology is excluded, management is supportive. Colic is treated with reassurance, soothing rhythmic activities, reduction of environmental stimulation, and parental support. Dietary interventions such as trial of soy or hydrolyzed formula may offer temporary benefit in select infants. No medication has proven consistently effective for colic, though probiotics may help some infants. Observation in the emergency department is often appropriate.
Admission is indicated for infants with life-threatening conditions or when significant parental stress raises safety concerns. Discharge may be considered when no serious cause is identified, the infant appears well, the family is functional and supported, and close follow-up is assured. Parents must feel heard and supported, and clear return precautions are essential.
A critical pitfall is failure to recognize serious underlying disease. Cardiovascular, neurologic, gastrointestinal, metabolic, genitourinary, pulmonary, toxicologic, traumatic, ophthalmologic, and abuse-related causes must be actively considered. In noncritically ill infants, a meticulous history and complete physical examination should precede extensive laboratory or radiologic testing.
- Published on
Emergency and Acute Medicine – Iron Poisoning
Basics and pathophysiology
Iron poisoning is a potentially life-threatening toxicologic emergency, most commonly seen in pediatric accidental ingestions and adult intentional overdoses. Peak serum iron concentrations usually occur 2–4 hours after ingestion. Serum iron levels obtained more than 4–6 hours after ingestion may be misleading because iron rapidly redistributes into tissues; enteric-coated or sustained-release preparations require serial measurements. After absorption, free iron shifts intracellularly, causing direct cellular injury. The gastrointestinal tract sustains corrosive injury that can lead to hemorrhage, profound fluid loss, shock, and perforation. The liver receives the highest iron load via portal circulation, resulting in hemorrhagic periportal necrosis. Free iron disrupts mitochondrial oxidative phosphorylation, catalyzes lipid peroxidation and free radical formation, increases anaerobic metabolism, and produces metabolic acidosis. Cardiovascular depression, venodilation, cerebral edema, and acidemia result from these mechanisms.
Etiology and toxic doses
Toxicity depends on the amount of elemental iron ingested. Doses below 20 mg/kg are generally nontoxic, while ingestions greater than 40 mg/kg are associated with moderate to severe toxicity. Lethality is possible at doses exceeding 60 mg/kg. Elemental iron content varies by formulation: ferrous sulfate contains approximately 20% elemental iron (a 325-mg tablet contains 65 mg elemental iron), ferrous gluconate contains 12%, and ferrous fumarate contains 33%. Prenatal vitamins may contain 60–90 mg elemental iron per tablet, whereas children’s vitamins usually contain 5–18 mg per tablet. Historically, iron poisoning carried one of the highest pediatric mortality rates due to adult iron products; modern children’s chewable preparations are considerably safer.
Clinical presentation
Iron poisoning classically progresses through five stages, though patients may skip stages or present at any point. Stage 1 (0.5–6 hours) is characterized by gastrointestinal symptoms including abdominal pain, vomiting, diarrhea, hematemesis, and hematochezia. Stage 2 (6–24 hours) is a deceptive latent phase during which GI symptoms improve despite ongoing cellular injury; hypotension and acidosis may develop. Stage 3 (6–72 hours) involves shock and systemic toxicity with hypoperfusion, severe metabolic acidosis, coma, and coagulopathy. Stage 4 (2–3 days) is marked by hepatic failure with hypoglycemia, jaundice, coagulopathy, and markedly elevated transaminases. Stage 5 (2–4 weeks) presents with gastric outlet or small bowel obstruction due to scarring. Absence of symptoms within the first 6 hours makes a significant ingestion unlikely.
Diagnosis and essential workup
Acute iron poisoning is primarily a clinical diagnosis, and treatment decisions should not rely solely on laboratory values. Serum iron levels peak between 2 and 6 hours after ingestion, with 4 hours being the most common peak; delayed peaks occur with sustained-release formulations. Laboratory evaluation typically reveals an anion gap metabolic acidosis, early hyperglycemia followed by late hypoglycemia, leukocytosis, anemia if bleeding is significant, abnormal liver function tests, and coagulopathy in severe cases. Total iron-binding capacity is not useful and should not be obtained. Abdominal radiographs may reveal radiopaque tablets, although absence of pill fragments does not exclude severe poisoning. Imaging is also useful for detecting perforation.
Differential diagnosis
The differential diagnosis includes sepsis, acetaminophen toxicity, gastrointestinal bleeding from other causes, and toxic ingestions that cause anion gap metabolic acidosis such as salicylates, cyanide, methanol, ethylene glycol, heavy metals, mushrooms, and theophylline.
Emergency management
Initial management focuses on airway, breathing, and circulation. Patients with altered mental status or hemodynamic instability may require intubation. Establish venous access, initiate aggressive fluid resuscitation for hypotension, and place the patient on cardiac monitoring and pulse oximetry. Activated charcoal is ineffective for iron and should not be used. Gastric lavage has not shown outcome benefit. Sodium bicarbonate, phosphate preparations, and oral deferoxamine are not recommended. If tablets are visualized on abdominal radiograph or there is a history of significant ingestion, whole bowel irrigation with polyethylene glycol solution via nasogastric tube may be considered, with careful monitoring for gastrointestinal bleeding or perforation. Endoscopic or surgical removal may be required for massive ingestions with bezoar formation.
Chelation therapy
Deferoxamine (DFO) is the treatment of choice for significant iron poisoning and should be administered as early as possible, ideally within 24 hours. It chelates free iron, forming a complex excreted in urine, which may turn a characteristic “vin rose” color. Intravenous infusion is preferred and should be titrated carefully due to the risk of hypotension; infusion rates may be increased to 15 mg/kg/hour and adjusted as tolerated. Treatment decisions should be based on clinical status as well as laboratory data, especially in late presenters, because serum iron levels may be deceptively low after redistribution. Prolonged DFO therapy beyond 24–48 hours increases the risk of acute respiratory distress syndrome and should be used cautiously. Resolution of acidosis and systemic toxicity is the best endpoint for therapy. Regional poison control consultation is strongly recommended for moderate to severe cases.
Disposition and follow-up
Patients with gastrointestinal symptoms, dehydration, altered mental status, hypotension, metabolic acidosis, shock, serum iron levels above 500 mg/dL, rising iron levels, or those requiring deferoxamine therapy should be admitted. ICU admission is indicated for coma, severe acidosis, shock, or extremely elevated iron levels. Patients who remain asymptomatic after 6 hours of observation, have normal radiographs, minimal symptoms, and serum iron levels below 350 mg/dL may be discharged with careful instructions. Follow-up is important for patients at risk of delayed gastric outlet obstruction. Psychiatric evaluation is required for intentional ingestions.
Pearls and pitfalls
Resolution of early gastrointestinal symptoms does not exclude ongoing or worsening toxicity. Deferoxamine may be indicated even in late presentations with relatively low serum iron levels if there is evidence of intracellular poisoning such as metabolic acidosis. Clinical status, not laboratory values alone, should guide management decisions.
Basics and pathophysiology
Iron poisoning is a potentially life-threatening toxicologic emergency, most commonly seen in pediatric accidental ingestions and adult intentional overdoses. Peak serum iron concentrations usually occur 2–4 hours after ingestion. Serum iron levels obtained more than 4–6 hours after ingestion may be misleading because iron rapidly redistributes into tissues; enteric-coated or sustained-release preparations require serial measurements. After absorption, free iron shifts intracellularly, causing direct cellular injury. The gastrointestinal tract sustains corrosive injury that can lead to hemorrhage, profound fluid loss, shock, and perforation. The liver receives the highest iron load via portal circulation, resulting in hemorrhagic periportal necrosis. Free iron disrupts mitochondrial oxidative phosphorylation, catalyzes lipid peroxidation and free radical formation, increases anaerobic metabolism, and produces metabolic acidosis. Cardiovascular depression, venodilation, cerebral edema, and acidemia result from these mechanisms.
Etiology and toxic doses
Toxicity depends on the amount of elemental iron ingested. Doses below 20 mg/kg are generally nontoxic, while ingestions greater than 40 mg/kg are associated with moderate to severe toxicity. Lethality is possible at doses exceeding 60 mg/kg. Elemental iron content varies by formulation: ferrous sulfate contains approximately 20% elemental iron (a 325-mg tablet contains 65 mg elemental iron), ferrous gluconate contains 12%, and ferrous fumarate contains 33%. Prenatal vitamins may contain 60–90 mg elemental iron per tablet, whereas children’s vitamins usually contain 5–18 mg per tablet. Historically, iron poisoning carried one of the highest pediatric mortality rates due to adult iron products; modern children’s chewable preparations are considerably safer.
Clinical presentation
Iron poisoning classically progresses through five stages, though patients may skip stages or present at any point. Stage 1 (0.5–6 hours) is characterized by gastrointestinal symptoms including abdominal pain, vomiting, diarrhea, hematemesis, and hematochezia. Stage 2 (6–24 hours) is a deceptive latent phase during which GI symptoms improve despite ongoing cellular injury; hypotension and acidosis may develop. Stage 3 (6–72 hours) involves shock and systemic toxicity with hypoperfusion, severe metabolic acidosis, coma, and coagulopathy. Stage 4 (2–3 days) is marked by hepatic failure with hypoglycemia, jaundice, coagulopathy, and markedly elevated transaminases. Stage 5 (2–4 weeks) presents with gastric outlet or small bowel obstruction due to scarring. Absence of symptoms within the first 6 hours makes a significant ingestion unlikely.
Diagnosis and essential workup
Acute iron poisoning is primarily a clinical diagnosis, and treatment decisions should not rely solely on laboratory values. Serum iron levels peak between 2 and 6 hours after ingestion, with 4 hours being the most common peak; delayed peaks occur with sustained-release formulations. Laboratory evaluation typically reveals an anion gap metabolic acidosis, early hyperglycemia followed by late hypoglycemia, leukocytosis, anemia if bleeding is significant, abnormal liver function tests, and coagulopathy in severe cases. Total iron-binding capacity is not useful and should not be obtained. Abdominal radiographs may reveal radiopaque tablets, although absence of pill fragments does not exclude severe poisoning. Imaging is also useful for detecting perforation.
Differential diagnosis
The differential diagnosis includes sepsis, acetaminophen toxicity, gastrointestinal bleeding from other causes, and toxic ingestions that cause anion gap metabolic acidosis such as salicylates, cyanide, methanol, ethylene glycol, heavy metals, mushrooms, and theophylline.
Emergency management
Initial management focuses on airway, breathing, and circulation. Patients with altered mental status or hemodynamic instability may require intubation. Establish venous access, initiate aggressive fluid resuscitation for hypotension, and place the patient on cardiac monitoring and pulse oximetry. Activated charcoal is ineffective for iron and should not be used. Gastric lavage has not shown outcome benefit. Sodium bicarbonate, phosphate preparations, and oral deferoxamine are not recommended. If tablets are visualized on abdominal radiograph or there is a history of significant ingestion, whole bowel irrigation with polyethylene glycol solution via nasogastric tube may be considered, with careful monitoring for gastrointestinal bleeding or perforation. Endoscopic or surgical removal may be required for massive ingestions with bezoar formation.
Chelation therapy
Deferoxamine (DFO) is the treatment of choice for significant iron poisoning and should be administered as early as possible, ideally within 24 hours. It chelates free iron, forming a complex excreted in urine, which may turn a characteristic “vin rose” color. Intravenous infusion is preferred and should be titrated carefully due to the risk of hypotension; infusion rates may be increased to 15 mg/kg/hour and adjusted as tolerated. Treatment decisions should be based on clinical status as well as laboratory data, especially in late presenters, because serum iron levels may be deceptively low after redistribution. Prolonged DFO therapy beyond 24–48 hours increases the risk of acute respiratory distress syndrome and should be used cautiously. Resolution of acidosis and systemic toxicity is the best endpoint for therapy. Regional poison control consultation is strongly recommended for moderate to severe cases.
Disposition and follow-up
Patients with gastrointestinal symptoms, dehydration, altered mental status, hypotension, metabolic acidosis, shock, serum iron levels above 500 mg/dL, rising iron levels, or those requiring deferoxamine therapy should be admitted. ICU admission is indicated for coma, severe acidosis, shock, or extremely elevated iron levels. Patients who remain asymptomatic after 6 hours of observation, have normal radiographs, minimal symptoms, and serum iron levels below 350 mg/dL may be discharged with careful instructions. Follow-up is important for patients at risk of delayed gastric outlet obstruction. Psychiatric evaluation is required for intentional ingestions.
Pearls and pitfalls
Resolution of early gastrointestinal symptoms does not exclude ongoing or worsening toxicity. Deferoxamine may be indicated even in late presentations with relatively low serum iron levels if there is evidence of intracellular poisoning such as metabolic acidosis. Clinical status, not laboratory values alone, should guide management decisions.
- Published on
Emergency And Acute Medicine – Intussusception
Basics
Description Intussusception occurs when a proximal segment of bowel telescopes into a distal segment, leading to bowel obstruction, ischemia, infarction, and possible gangrene. More than 80% of cases involve the ileocecal region. It is the most common cause of intestinal obstruction in the first 2 years of life. Mortality is less than 1% with prompt treatment, but morbidity increases significantly with delayed diagnosis.
Epidemiology Most cases occur between 5 and 9 months of age, with an incidence of approximately 2.4 per 1,000 live births. There is a male predominance of about 2:1. Children older than 2 years are more likely to have a pathologic lead point, and in children older than 6 years, lymphoma is the most common lead point. Adults almost always have an identifiable pathologic lead point.
Alert Any infant or child presenting with episodic abdominal pain, vomiting, lethargy or altered mental status, or heme-positive stool should be evaluated for intussusception.
Etiology Most cases, particularly in infants, are idiopathic. In older children and adults, intussusception is often caused by a lead point such as lymphoma, polyps, lipomas, hypertrophied lymphoid tissue, Meckel diverticulum, viral infections such as adenovirus or rotavirus, parasites, foreign bodies, Henoch–Schönlein purpura, or underlying conditions such as celiac disease or cystic fibrosis.
Diagnosis
Signs and symptoms The classic triad of abdominal pain, vomiting, and bloody “currant jelly” stools occurs in fewer than half of patients. Abdominal pain is typically sudden, severe, intermittent, and associated with screaming and drawing up of the legs. Vomiting may be bilious. Stools may be grossly bloody or only occult blood positive. Mental status changes such as irritability, lethargy, or listlessness are common and may precede abdominal findings. Fever and abdominal distention may occur as the disease progresses.
Physical exam The abdomen may be distended and tender, and a sausage-shaped mass is sometimes palpable in the right upper quadrant. The right lower quadrant may feel empty. Rectal examination may reveal blood or a mass. In advanced cases, signs of peritonitis or sepsis from bowel perforation may be present.
Essential workup The diagnosis is suggested by the clinical presentation and confirmed radiographically. A heme-positive stool can support the diagnosis, particularly in patients presenting with lethargy.
Diagnosis tests and interpretation Laboratory studies typically include a CBC, electrolytes, BUN, and type and cross-match if surgery is anticipated. Abdominal radiographs are abnormal in only 35–40% of cases but may show decreased gas in the right colon, bowel obstruction, or free air if perforation has occurred. Ultrasound is the preferred initial diagnostic test and is highly sensitive and specific, demonstrating a “target” or “donut” sign. Contrast or air enema is both diagnostic and therapeutic and is successful in approximately 75–80% of cases when performed within 24 hours of symptom onset. Enema reduction is contraindicated in patients with perforation, peritonitis, or hemodynamic instability. Surgical intervention is required when enema reduction fails or is contraindicated, or when a pathologic lead point is suspected.
Differential diagnosis Conditions to consider include acute gastroenteritis, appendicitis, pneumonia, pyelonephritis, colic, malrotation with volvulus, strangulated hernia, Hirschsprung disease, inflammatory bowel disease, Henoch–Schönlein purpura, trauma, and intestinal ischemia.
Treatment
Prehospital care Management includes establishing IV access and administering isotonic fluid boluses for hypovolemia when indicated. The diagnosis is rarely confirmed in the prehospital setting.
Initial stabilization In the emergency department, IV access is obtained, fluid resuscitation initiated, and a nasogastric tube placed for decompression if needed. Early surgical consultation is essential.
Emergency department management Stabilization of airway, breathing, and circulation is followed by imaging and radiologic reduction with air or contrast enema when appropriate. Broad-spectrum antibiotics are initiated if there is concern for perforation, peritonitis, or sepsis. Surgical reduction is required if nonoperative management fails.
Follow-up and disposition Patients who undergo successful enema reduction should be admitted for observation due to the risk of recurrence. All patients requiring surgery should be admitted. Discharge may be considered only after prolonged observation, complete resolution of symptoms, normal mental status, and reliable caregivers who understand the signs of recurrence.
Pearls and pitfalls Intussusception may present primarily with lethargy rather than abdominal pain, and the classic triad is often absent. Delayed diagnosis increases the risk of bowel necrosis, perforation, and sepsis. Recurrence occurs in up to 10% of cases and may still be amenable to repeat enema reduction.
Basics
Description Intussusception occurs when a proximal segment of bowel telescopes into a distal segment, leading to bowel obstruction, ischemia, infarction, and possible gangrene. More than 80% of cases involve the ileocecal region. It is the most common cause of intestinal obstruction in the first 2 years of life. Mortality is less than 1% with prompt treatment, but morbidity increases significantly with delayed diagnosis.
Epidemiology Most cases occur between 5 and 9 months of age, with an incidence of approximately 2.4 per 1,000 live births. There is a male predominance of about 2:1. Children older than 2 years are more likely to have a pathologic lead point, and in children older than 6 years, lymphoma is the most common lead point. Adults almost always have an identifiable pathologic lead point.
Alert Any infant or child presenting with episodic abdominal pain, vomiting, lethargy or altered mental status, or heme-positive stool should be evaluated for intussusception.
Etiology Most cases, particularly in infants, are idiopathic. In older children and adults, intussusception is often caused by a lead point such as lymphoma, polyps, lipomas, hypertrophied lymphoid tissue, Meckel diverticulum, viral infections such as adenovirus or rotavirus, parasites, foreign bodies, Henoch–Schönlein purpura, or underlying conditions such as celiac disease or cystic fibrosis.
Diagnosis
Signs and symptoms The classic triad of abdominal pain, vomiting, and bloody “currant jelly” stools occurs in fewer than half of patients. Abdominal pain is typically sudden, severe, intermittent, and associated with screaming and drawing up of the legs. Vomiting may be bilious. Stools may be grossly bloody or only occult blood positive. Mental status changes such as irritability, lethargy, or listlessness are common and may precede abdominal findings. Fever and abdominal distention may occur as the disease progresses.
Physical exam The abdomen may be distended and tender, and a sausage-shaped mass is sometimes palpable in the right upper quadrant. The right lower quadrant may feel empty. Rectal examination may reveal blood or a mass. In advanced cases, signs of peritonitis or sepsis from bowel perforation may be present.
Essential workup The diagnosis is suggested by the clinical presentation and confirmed radiographically. A heme-positive stool can support the diagnosis, particularly in patients presenting with lethargy.
Diagnosis tests and interpretation Laboratory studies typically include a CBC, electrolytes, BUN, and type and cross-match if surgery is anticipated. Abdominal radiographs are abnormal in only 35–40% of cases but may show decreased gas in the right colon, bowel obstruction, or free air if perforation has occurred. Ultrasound is the preferred initial diagnostic test and is highly sensitive and specific, demonstrating a “target” or “donut” sign. Contrast or air enema is both diagnostic and therapeutic and is successful in approximately 75–80% of cases when performed within 24 hours of symptom onset. Enema reduction is contraindicated in patients with perforation, peritonitis, or hemodynamic instability. Surgical intervention is required when enema reduction fails or is contraindicated, or when a pathologic lead point is suspected.
Differential diagnosis Conditions to consider include acute gastroenteritis, appendicitis, pneumonia, pyelonephritis, colic, malrotation with volvulus, strangulated hernia, Hirschsprung disease, inflammatory bowel disease, Henoch–Schönlein purpura, trauma, and intestinal ischemia.
Treatment
Prehospital care Management includes establishing IV access and administering isotonic fluid boluses for hypovolemia when indicated. The diagnosis is rarely confirmed in the prehospital setting.
Initial stabilization In the emergency department, IV access is obtained, fluid resuscitation initiated, and a nasogastric tube placed for decompression if needed. Early surgical consultation is essential.
Emergency department management Stabilization of airway, breathing, and circulation is followed by imaging and radiologic reduction with air or contrast enema when appropriate. Broad-spectrum antibiotics are initiated if there is concern for perforation, peritonitis, or sepsis. Surgical reduction is required if nonoperative management fails.
Follow-up and disposition Patients who undergo successful enema reduction should be admitted for observation due to the risk of recurrence. All patients requiring surgery should be admitted. Discharge may be considered only after prolonged observation, complete resolution of symptoms, normal mental status, and reliable caregivers who understand the signs of recurrence.
Pearls and pitfalls Intussusception may present primarily with lethargy rather than abdominal pain, and the classic triad is often absent. Delayed diagnosis increases the risk of bowel necrosis, perforation, and sepsis. Recurrence occurs in up to 10% of cases and may still be amenable to repeat enema reduction.
- Published on
Emergency And Acute Medicine – Influenza
Basics
Description Influenza is an acute, usually self-limited viral respiratory infection transmitted via small-particle aerosols from coughing, sneezing, or talking. The virus infects respiratory epithelium after deposition in the airway. Incubation is 1–4 days (average 2), with a mean illness duration of approximately 4 days in adults. Seasonal outbreaks peak most commonly in winter, often February. Mortality is largely due to pulmonary complications. Complications include primary viral pneumonia, secondary bacterial pneumonia, COPD exacerbations, otitis media and sinusitis in children, reactive airway disease, and rarely myositis, myocarditis, pericarditis, Guillain–Barré syndrome, aseptic meningitis, ARDS, and multisystem organ failure.
Etiology
Influenza is caused primarily by influenza A or B viruses, with influenza A generally producing more severe disease. Influenza A is classified by hemagglutinin (H1, H2, H3) and neuraminidase subtypes. Annual epidemics result from antigenic drift, while pandemics result from antigenic shift. Waterfowl serve as the primary reservoir. Vaccine targets circulating subtype antigens.
Diagnosis
Signs and symptoms Influenza-like illness is defined as fever with cough or sore throat without another clear diagnosis. Fever and cough together are somewhat specific but insensitive. Children often have higher fevers, more lower respiratory involvement, calf myalgias, and febrile seizures. Elderly patients may present atypically with confusion, lassitude, or minimal respiratory symptoms. Local epidemic activity is the strongest predictor of disease.
Essential workup
Diagnosis is primarily clinical during influenza season when community prevalence is high.
Diagnosis tests and interpretation
Lab CBC may show normal or mildly decreased WBC count. Pulse oximetry or ABG is indicated for significant respiratory symptoms.
Imaging Chest radiograph is indicated for lower respiratory findings and may be normal or show bilateral interstitial infiltrates.
Diagnostic procedures Rapid antigen tests are specific but poorly sensitive. PCR testing is both sensitive and specific and can differentiate subtypes. Viral culture is not useful for ED decision-making.
Differential diagnosis
Other respiratory viral infections, bronchitis, atypical pneumonia, infectious mononucleosis, and rarely anthrax.
Treatment
Initial stabilization Provide supplemental oxygen, IV fluids, and ventilatory support as indicated.
Emergency department management Treatment is primarily supportive with antipyretics, hydration, and bronchodilators for bronchospasm. Avoid aspirin, especially in children. Neuraminidase inhibitors (oseltamivir, zanamivir) are most effective when started within 48 hours of symptom onset and reduce symptom duration by less than one day. Antivirals are recommended for severe illness, hospitalized patients, immunocompromised individuals, and those at high risk for complications.
Medication
Oseltamivir 75 mg PO BID for treatment or 75 mg PO daily for postexposure prophylaxis. Zanamivir inhalation 10 mg q12h. Albuterol for associated bronchospasm.
Prevention
Annual inactivated influenza vaccination is recommended for high-risk groups, health care workers, pregnant women, and children. Live attenuated intranasal vaccine is approved for healthy individuals aged 2–49 years but contraindicated in pregnancy, immunocompromise, and certain comorbidities. Chemoprophylaxis may be used in selected high-risk exposures.
Follow-up and disposition
Admission criteria Hypoxia, pneumonia, severe dehydration, altered mental status, or inability to tolerate oral intake.
Discharge criteria Stable patients tolerating fluids with mild disease.
Follow-up recommendations Outpatient follow-up and return precautions for worsening respiratory symptoms.
Pearls and pitfalls
Local influenza prevalence is the most important diagnostic clue. Most patients do not require testing or antivirals. Consider concurrent reactive airway disease in patients with wheezing or hypoxia. Stay updated with seasonal CDC guidance.
Basics
Description Influenza is an acute, usually self-limited viral respiratory infection transmitted via small-particle aerosols from coughing, sneezing, or talking. The virus infects respiratory epithelium after deposition in the airway. Incubation is 1–4 days (average 2), with a mean illness duration of approximately 4 days in adults. Seasonal outbreaks peak most commonly in winter, often February. Mortality is largely due to pulmonary complications. Complications include primary viral pneumonia, secondary bacterial pneumonia, COPD exacerbations, otitis media and sinusitis in children, reactive airway disease, and rarely myositis, myocarditis, pericarditis, Guillain–Barré syndrome, aseptic meningitis, ARDS, and multisystem organ failure.
Etiology
Influenza is caused primarily by influenza A or B viruses, with influenza A generally producing more severe disease. Influenza A is classified by hemagglutinin (H1, H2, H3) and neuraminidase subtypes. Annual epidemics result from antigenic drift, while pandemics result from antigenic shift. Waterfowl serve as the primary reservoir. Vaccine targets circulating subtype antigens.
Diagnosis
Signs and symptoms Influenza-like illness is defined as fever with cough or sore throat without another clear diagnosis. Fever and cough together are somewhat specific but insensitive. Children often have higher fevers, more lower respiratory involvement, calf myalgias, and febrile seizures. Elderly patients may present atypically with confusion, lassitude, or minimal respiratory symptoms. Local epidemic activity is the strongest predictor of disease.
Essential workup
Diagnosis is primarily clinical during influenza season when community prevalence is high.
Diagnosis tests and interpretation
Lab CBC may show normal or mildly decreased WBC count. Pulse oximetry or ABG is indicated for significant respiratory symptoms.
Imaging Chest radiograph is indicated for lower respiratory findings and may be normal or show bilateral interstitial infiltrates.
Diagnostic procedures Rapid antigen tests are specific but poorly sensitive. PCR testing is both sensitive and specific and can differentiate subtypes. Viral culture is not useful for ED decision-making.
Differential diagnosis
Other respiratory viral infections, bronchitis, atypical pneumonia, infectious mononucleosis, and rarely anthrax.
Treatment
Initial stabilization Provide supplemental oxygen, IV fluids, and ventilatory support as indicated.
Emergency department management Treatment is primarily supportive with antipyretics, hydration, and bronchodilators for bronchospasm. Avoid aspirin, especially in children. Neuraminidase inhibitors (oseltamivir, zanamivir) are most effective when started within 48 hours of symptom onset and reduce symptom duration by less than one day. Antivirals are recommended for severe illness, hospitalized patients, immunocompromised individuals, and those at high risk for complications.
Medication
Oseltamivir 75 mg PO BID for treatment or 75 mg PO daily for postexposure prophylaxis. Zanamivir inhalation 10 mg q12h. Albuterol for associated bronchospasm.
Prevention
Annual inactivated influenza vaccination is recommended for high-risk groups, health care workers, pregnant women, and children. Live attenuated intranasal vaccine is approved for healthy individuals aged 2–49 years but contraindicated in pregnancy, immunocompromise, and certain comorbidities. Chemoprophylaxis may be used in selected high-risk exposures.
Follow-up and disposition
Admission criteria Hypoxia, pneumonia, severe dehydration, altered mental status, or inability to tolerate oral intake.
Discharge criteria Stable patients tolerating fluids with mild disease.
Follow-up recommendations Outpatient follow-up and return precautions for worsening respiratory symptoms.
Pearls and pitfalls
Local influenza prevalence is the most important diagnostic clue. Most patients do not require testing or antivirals. Consider concurrent reactive airway disease in patients with wheezing or hypoxia. Stay updated with seasonal CDC guidance.
- Published on
Emergency and Acute Medicine – Irritable bowel syndrome
Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder characterized by chronic abdominal pain or discomfort associated with altered bowel habits, without identifiable structural or biochemical pathology to explain the symptoms. It is common, with an estimated prevalence of 10–20% of the population.
The pathophysiology of IBS is uncertain and likely multifactorial. Proposed mechanisms include altered gastrointestinal motility and increased gut sensitivity (visceral hyperalgesia), leading to exaggerated pain responses to normal bowel activity. Mucosal inflammation may play a role, particularly in postinfectious IBS, which can occur in up to 10% of patients following bacterial enteritis and is associated with mucosal lymphocyte infiltration. Altered intestinal microflora has also been described. Food sensitivity is frequently reported by patients but remains unproven as a primary cause. Psychosocial factors are important in some patients, especially those who seek medical care, with higher rates of anxiety, somatoform disorders, and prior abuse histories; however, there is no clear increase in psychiatric illness among individuals with IBS who do not seek care.
Clinically, IBS presents with recurrent abdominal pain or discomfort that is often relieved by defecation and associated with changes in stool frequency or consistency. Common accompanying symptoms include bloating or abdominal distention, passage of mucus, and a sensation of incomplete evacuation. The Rome III criteria define IBS as recurrent abdominal pain or discomfort at least 3 days per month over the past 3 months, associated with at least two of the following: improvement with defecation, onset associated with a change in stool frequency, or onset associated with a change in stool form. IBS is more common in women than men, particularly among those who seek medical attention.
A careful history is central to diagnosis, as IBS is a clinical diagnosis. Alarm features that warrant further evaluation include onset after age 50, nocturnal symptoms, unintentional weight loss, iron-deficiency anemia, hematochezia, or a family history of colorectal cancer, inflammatory bowel disease, or celiac disease. Physical examination is usually normal, though mild sigmoid tenderness or a palpable sigmoid cord may be noted.
Laboratory testing is typically normal and is not required to establish the diagnosis. When indicated to exclude alternative diagnoses, basic studies such as a CBC (to rule out anemia or leukocytosis), ESR or CRP (to exclude inflammatory disease), and selective stool studies for diarrhea may be considered. Testing for celiac disease may be appropriate in the outpatient setting. Imaging and endoscopic evaluation are reserved for patients with alarm features or diagnostic uncertainty.
Management in the emergency setting is supportive and focused on reassurance. Establishing an empathetic physician–patient relationship is essential. Treatment is individualized and symptom based. Lifestyle interventions such as regular exercise may improve constipation and overall symptoms. Dietary modification can be empirically attempted, including exclusion of lactose or gluten and avoidance of gas-producing foods if these worsen symptoms. Constipation-predominant symptoms may benefit from increased dietary fiber or fiber supplementation. Abdominal pain may improve with short-term use of antispasmodics such as dicyclomine or hyoscyamine. Probiotics, particularly those containing bifidobacteria, may provide benefit. Low-dose tricyclic antidepressants or selective serotonin reuptake inhibitors can reduce global IBS symptoms and abdominal pain, and psychological therapies are effective in selected patients.
Most patients with IBS can be safely discharged from the emergency department with reassurance and outpatient follow-up. Admission is rarely indicated and should be reserved for patients with diagnostic uncertainty or concern for emergent abdominal pathology. Ongoing care with a primary care physician is critical, and some patients may benefit from gastroenterology or mental health referral.
A key pitfall is prematurely attributing symptoms to IBS without adequately considering alternative or emergent diagnoses. Although IBS is common and often underlies repeated emergency evaluations, alarm features or atypical presentations should prompt further investigation.
Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder characterized by chronic abdominal pain or discomfort associated with altered bowel habits, without identifiable structural or biochemical pathology to explain the symptoms. It is common, with an estimated prevalence of 10–20% of the population.
The pathophysiology of IBS is uncertain and likely multifactorial. Proposed mechanisms include altered gastrointestinal motility and increased gut sensitivity (visceral hyperalgesia), leading to exaggerated pain responses to normal bowel activity. Mucosal inflammation may play a role, particularly in postinfectious IBS, which can occur in up to 10% of patients following bacterial enteritis and is associated with mucosal lymphocyte infiltration. Altered intestinal microflora has also been described. Food sensitivity is frequently reported by patients but remains unproven as a primary cause. Psychosocial factors are important in some patients, especially those who seek medical care, with higher rates of anxiety, somatoform disorders, and prior abuse histories; however, there is no clear increase in psychiatric illness among individuals with IBS who do not seek care.
Clinically, IBS presents with recurrent abdominal pain or discomfort that is often relieved by defecation and associated with changes in stool frequency or consistency. Common accompanying symptoms include bloating or abdominal distention, passage of mucus, and a sensation of incomplete evacuation. The Rome III criteria define IBS as recurrent abdominal pain or discomfort at least 3 days per month over the past 3 months, associated with at least two of the following: improvement with defecation, onset associated with a change in stool frequency, or onset associated with a change in stool form. IBS is more common in women than men, particularly among those who seek medical attention.
A careful history is central to diagnosis, as IBS is a clinical diagnosis. Alarm features that warrant further evaluation include onset after age 50, nocturnal symptoms, unintentional weight loss, iron-deficiency anemia, hematochezia, or a family history of colorectal cancer, inflammatory bowel disease, or celiac disease. Physical examination is usually normal, though mild sigmoid tenderness or a palpable sigmoid cord may be noted.
Laboratory testing is typically normal and is not required to establish the diagnosis. When indicated to exclude alternative diagnoses, basic studies such as a CBC (to rule out anemia or leukocytosis), ESR or CRP (to exclude inflammatory disease), and selective stool studies for diarrhea may be considered. Testing for celiac disease may be appropriate in the outpatient setting. Imaging and endoscopic evaluation are reserved for patients with alarm features or diagnostic uncertainty.
Management in the emergency setting is supportive and focused on reassurance. Establishing an empathetic physician–patient relationship is essential. Treatment is individualized and symptom based. Lifestyle interventions such as regular exercise may improve constipation and overall symptoms. Dietary modification can be empirically attempted, including exclusion of lactose or gluten and avoidance of gas-producing foods if these worsen symptoms. Constipation-predominant symptoms may benefit from increased dietary fiber or fiber supplementation. Abdominal pain may improve with short-term use of antispasmodics such as dicyclomine or hyoscyamine. Probiotics, particularly those containing bifidobacteria, may provide benefit. Low-dose tricyclic antidepressants or selective serotonin reuptake inhibitors can reduce global IBS symptoms and abdominal pain, and psychological therapies are effective in selected patients.
Most patients with IBS can be safely discharged from the emergency department with reassurance and outpatient follow-up. Admission is rarely indicated and should be reserved for patients with diagnostic uncertainty or concern for emergent abdominal pathology. Ongoing care with a primary care physician is critical, and some patients may benefit from gastroenterology or mental health referral.
A key pitfall is prematurely attributing symptoms to IBS without adequately considering alternative or emergent diagnoses. Although IBS is common and often underlies repeated emergency evaluations, alarm features or atypical presentations should prompt further investigation.
- Published on
Emergency And Acute Medicine – Inflammatory Bowel Disease
Basics
Description Inflammatory bowel disease (IBD) consists of idiopathic, chronic inflammatory disorders of the gastrointestinal tract with frequent extraintestinal involvement. It includes ulcerative colitis (UC), Crohn disease, and intermediate forms. Disease may present as new onset or as an acute exacerbation. Crohn disease often presents subtly and requires a high index of suspicion. In UC, inflammation is continuous, begins in the rectum, and is limited to the colon and submucosa. Crohn disease may affect any region from mouth to anus, is discontinuous, and involves transmural inflammation. Both conditions are associated with an increased risk of colon cancer after more than 10 years of disease. Age distribution is bimodal, with peaks in early adulthood and around 60 years of age. Pediatric cases may present early in life, often with prominent extraintestinal features.
Etiology
The cause is unknown. IBD is multifactorial, involving genetic susceptibility, environmental influences, and dysregulated immune responses. Family history is common. No definitive infectious cause has been identified, though psychosocial stress may exacerbate symptoms.
Diagnosis
Signs and symptoms Crohn disease may manifest as inflammatory, fibrostenotic, or fistulizing disease. Ulcerative colitis ranges from mild to fulminant colitis. Constitutional symptoms include fever, fatigue, night sweats, and weight loss, particularly in Crohn disease, with growth or pubertal delay in children. Gastrointestinal manifestations include abdominal pain, diarrhea, and bleeding. Crohn disease pain is often episodic and periumbilical or right lower quadrant, while UC pain is more generalized and often associated with defecation. Diarrhea in UC is typically bloody with mucus, urgency, and tenesmus. Extraintestinal manifestations include arthritis, uveitis, episcleritis, aphthous ulcers, erythema nodosum, and pyoderma gangrenosum. Perianal disease such as fissures, abscesses, and fistulas is characteristic of Crohn disease and absent in UC.
Essential workup
IBD should be considered in patients with chronic diarrhea, abdominal pain, weight loss, anemia, or extraintestinal inflammatory findings, especially with recurrent or unexplained presentations.
Diagnosis tests and interpretation
Lab No single diagnostic test exists. Common findings include anemia, elevated ESR, electrolyte abnormalities, and inflammatory markers. Stool studies should exclude infectious etiologies including Clostridioides difficile.
Imaging Upright abdominal and chest radiographs assess for toxic megacolon, obstruction, or perforation. CT or MRI of the abdomen helps identify abscesses, inflammatory masses, and complications, with MRI preferred when available to limit radiation exposure. Colonoscopy with biopsy confirms diagnosis but should be deferred in severe disease due to perforation risk.
Differential diagnosis
Infectious colitis, pseudomembranous colitis, appendicitis, diverticulitis, ischemic colitis, colorectal cancer, functional bowel disease, sexually transmitted proctitis, HIV, vasculitis, and lymphoma.
Treatment
Initial stabilization Provide IV isotonic fluids for dehydration and transfuse if there is significant blood loss.
Emergency department management Insert nasogastric tube if obstruction or toxic dilation is suspected. Administer broad-spectrum antibiotics in fulminant disease, suspected perforation, or sepsis. Stress-dose steroids may be required in patients recently on chronic steroids. Surgical consultation is mandatory for perforation, uncontrolled hemorrhage, obstruction, or toxic megacolon. Medical therapy is generally continued or resumed rather than initiated in the ED unless previously established, with gastroenterology consultation recommended.
Medication
Therapies depend on disease severity and prior diagnosis and may include aminosalicylates, corticosteroids, antibiotics such as metronidazole or ciprofloxacin for Crohn disease, and immunomodulators or biologics under specialist guidance.
Follow-up and disposition
Admission criteria Indications include perforation, obstruction, toxic megacolon, massive bleeding, severe pain, dehydration, electrolyte imbalance, high fever, or severe flare requiring intensive therapy.
Discharge criteria Mild symptoms without toxicity, obstruction, significant bleeding, or dehydration, with reliable follow-up and established care.
Follow-up recommendations Gastroenterology follow-up is essential, with surgical consultation for complications or refractory disease.
Pearls and pitfalls
Always exclude toxic megacolon in severe flares. Avoid antidiarrheal agents in severe ulcerative colitis. Consider Crohn disease in children with growth delay or perianal disease. Always rule out C. difficile during disease exacerbations.
Basics
Description Inflammatory bowel disease (IBD) consists of idiopathic, chronic inflammatory disorders of the gastrointestinal tract with frequent extraintestinal involvement. It includes ulcerative colitis (UC), Crohn disease, and intermediate forms. Disease may present as new onset or as an acute exacerbation. Crohn disease often presents subtly and requires a high index of suspicion. In UC, inflammation is continuous, begins in the rectum, and is limited to the colon and submucosa. Crohn disease may affect any region from mouth to anus, is discontinuous, and involves transmural inflammation. Both conditions are associated with an increased risk of colon cancer after more than 10 years of disease. Age distribution is bimodal, with peaks in early adulthood and around 60 years of age. Pediatric cases may present early in life, often with prominent extraintestinal features.
Etiology
The cause is unknown. IBD is multifactorial, involving genetic susceptibility, environmental influences, and dysregulated immune responses. Family history is common. No definitive infectious cause has been identified, though psychosocial stress may exacerbate symptoms.
Diagnosis
Signs and symptoms Crohn disease may manifest as inflammatory, fibrostenotic, or fistulizing disease. Ulcerative colitis ranges from mild to fulminant colitis. Constitutional symptoms include fever, fatigue, night sweats, and weight loss, particularly in Crohn disease, with growth or pubertal delay in children. Gastrointestinal manifestations include abdominal pain, diarrhea, and bleeding. Crohn disease pain is often episodic and periumbilical or right lower quadrant, while UC pain is more generalized and often associated with defecation. Diarrhea in UC is typically bloody with mucus, urgency, and tenesmus. Extraintestinal manifestations include arthritis, uveitis, episcleritis, aphthous ulcers, erythema nodosum, and pyoderma gangrenosum. Perianal disease such as fissures, abscesses, and fistulas is characteristic of Crohn disease and absent in UC.
Essential workup
IBD should be considered in patients with chronic diarrhea, abdominal pain, weight loss, anemia, or extraintestinal inflammatory findings, especially with recurrent or unexplained presentations.
Diagnosis tests and interpretation
Lab No single diagnostic test exists. Common findings include anemia, elevated ESR, electrolyte abnormalities, and inflammatory markers. Stool studies should exclude infectious etiologies including Clostridioides difficile.
Imaging Upright abdominal and chest radiographs assess for toxic megacolon, obstruction, or perforation. CT or MRI of the abdomen helps identify abscesses, inflammatory masses, and complications, with MRI preferred when available to limit radiation exposure. Colonoscopy with biopsy confirms diagnosis but should be deferred in severe disease due to perforation risk.
Differential diagnosis
Infectious colitis, pseudomembranous colitis, appendicitis, diverticulitis, ischemic colitis, colorectal cancer, functional bowel disease, sexually transmitted proctitis, HIV, vasculitis, and lymphoma.
Treatment
Initial stabilization Provide IV isotonic fluids for dehydration and transfuse if there is significant blood loss.
Emergency department management Insert nasogastric tube if obstruction or toxic dilation is suspected. Administer broad-spectrum antibiotics in fulminant disease, suspected perforation, or sepsis. Stress-dose steroids may be required in patients recently on chronic steroids. Surgical consultation is mandatory for perforation, uncontrolled hemorrhage, obstruction, or toxic megacolon. Medical therapy is generally continued or resumed rather than initiated in the ED unless previously established, with gastroenterology consultation recommended.
Medication
Therapies depend on disease severity and prior diagnosis and may include aminosalicylates, corticosteroids, antibiotics such as metronidazole or ciprofloxacin for Crohn disease, and immunomodulators or biologics under specialist guidance.
Follow-up and disposition
Admission criteria Indications include perforation, obstruction, toxic megacolon, massive bleeding, severe pain, dehydration, electrolyte imbalance, high fever, or severe flare requiring intensive therapy.
Discharge criteria Mild symptoms without toxicity, obstruction, significant bleeding, or dehydration, with reliable follow-up and established care.
Follow-up recommendations Gastroenterology follow-up is essential, with surgical consultation for complications or refractory disease.
Pearls and pitfalls
Always exclude toxic megacolon in severe flares. Avoid antidiarrheal agents in severe ulcerative colitis. Consider Crohn disease in children with growth delay or perianal disease. Always rule out C. difficile during disease exacerbations.
- Published on
Emergency And Acute Medicine – Intracerebral Hemorrhage
Basics
Description Intracerebral hemorrhage is bleeding into the brain parenchyma causing direct compression of brain tissue. Secondary injury results from cerebral edema, rising intracranial pressure, and risk of brain herniation.
Etiology
Intracerebral hemorrhage may be spontaneous or traumatic. Common causes include uncontrolled or acute hypertension (most common), vascular malformations (arteriovenous malformations, venous angiomas), ruptured cerebral aneurysms, intracranial neoplasms (especially melanoma and glioma), anticoagulant or thrombolytic therapy, illicit drug use (cocaine, amphetamines), bleeding disorders, cerebral amyloid angiopathy, and blunt or penetrating head trauma.
Diagnosis
Signs and symptoms Sudden severe headache, seizures, vomiting, neck stiffness, altered mental status, or coma. Neurologic deficits depend on hemorrhage location. Putaminal hemorrhage causes contralateral hemiparesis and sensory loss. Lobar hemorrhage causes variable focal deficits. Cerebellar hemorrhage presents with vomiting, ataxia, and nystagmus. Thalamic hemorrhage causes motor and sensory deficits with eye movement abnormalities. Pontine hemorrhage presents with quadriplegia and pinpoint pupils.
Essential workup
Secure airway if indicated and obtain immediate noncontrast CT of the head, which shows acute hemorrhage as a hyperdense lesion.
Diagnosis tests and interpretation
Lab CBC, electrolytes, BUN/creatinine, coagulation studies (PT, PTT, INR, platelets), pregnancy test when appropriate, ECG, and toxicology screen if indicated.
Imaging Noncontrast CT is diagnostic. CT angiography may identify an underlying vascular lesion and contrast extravasation (“spot sign”), which predicts hematoma expansion and worse outcomes. MRI may be useful later but is not first line in the ED.
Differential diagnosis
Seizure with postictal paralysis, ischemic stroke, CNS infection, intracranial mass, electrolyte or metabolic abnormalities, intoxication, migraine, transient ischemic attack, and traumatic intracranial hemorrhages.
Treatment
Prehospital Maintain cervical spine precautions if trauma suspected, elevate head with spinal alignment, and document neurologic deficits for comparison.
Initial stabilization Manage airway and breathing aggressively. Early neurosurgical and neurologic consultation is essential.
Emergency department management Control blood pressure cautiously to avoid reducing cerebral perfusion. Gradually lower diastolic blood pressure by approximately 10%, avoiding rapid normalization. Treat elevated intracranial pressure with head elevation, controlled ventilation, osmotic therapy, and fluid management. Reverse coagulopathies promptly using vitamin K, fresh frozen plasma, platelets, or prothrombin complex concentrates as indicated. Consider anticonvulsants for seizure management or prophylaxis.
Medication
Common agents include labetalol, nicardipine, esmolol, or enalapril for blood pressure control; mannitol or furosemide for intracranial pressure; phenytoin or fosphenytoin for seizures; and appropriate blood products for anticoagulation reversal.
Follow-up and disposition
Admission criteria All patients with intracerebral hemorrhage require admission. ICU care is indicated for altered mental status, intubation, or continuous blood pressure infusions.
Discharge criteria Discharge is not appropriate for intracerebral hemorrhage.
Follow-up recommendations Long-term blood pressure control, smoking and substance cessation, and rehabilitation planning are critical to reduce recurrence and improve functional recovery.
Key points
Early brain imaging is essential in patients with headache, hypertension, or altered mental status. Blood pressure reduction must be cautious to preserve cerebral perfusion. Delayed hemorrhage should be considered in anticoagulated patients with head trauma.
Basics
Description Intracerebral hemorrhage is bleeding into the brain parenchyma causing direct compression of brain tissue. Secondary injury results from cerebral edema, rising intracranial pressure, and risk of brain herniation.
Etiology
Intracerebral hemorrhage may be spontaneous or traumatic. Common causes include uncontrolled or acute hypertension (most common), vascular malformations (arteriovenous malformations, venous angiomas), ruptured cerebral aneurysms, intracranial neoplasms (especially melanoma and glioma), anticoagulant or thrombolytic therapy, illicit drug use (cocaine, amphetamines), bleeding disorders, cerebral amyloid angiopathy, and blunt or penetrating head trauma.
Diagnosis
Signs and symptoms Sudden severe headache, seizures, vomiting, neck stiffness, altered mental status, or coma. Neurologic deficits depend on hemorrhage location. Putaminal hemorrhage causes contralateral hemiparesis and sensory loss. Lobar hemorrhage causes variable focal deficits. Cerebellar hemorrhage presents with vomiting, ataxia, and nystagmus. Thalamic hemorrhage causes motor and sensory deficits with eye movement abnormalities. Pontine hemorrhage presents with quadriplegia and pinpoint pupils.
Essential workup
Secure airway if indicated and obtain immediate noncontrast CT of the head, which shows acute hemorrhage as a hyperdense lesion.
Diagnosis tests and interpretation
Lab CBC, electrolytes, BUN/creatinine, coagulation studies (PT, PTT, INR, platelets), pregnancy test when appropriate, ECG, and toxicology screen if indicated.
Imaging Noncontrast CT is diagnostic. CT angiography may identify an underlying vascular lesion and contrast extravasation (“spot sign”), which predicts hematoma expansion and worse outcomes. MRI may be useful later but is not first line in the ED.
Differential diagnosis
Seizure with postictal paralysis, ischemic stroke, CNS infection, intracranial mass, electrolyte or metabolic abnormalities, intoxication, migraine, transient ischemic attack, and traumatic intracranial hemorrhages.
Treatment
Prehospital Maintain cervical spine precautions if trauma suspected, elevate head with spinal alignment, and document neurologic deficits for comparison.
Initial stabilization Manage airway and breathing aggressively. Early neurosurgical and neurologic consultation is essential.
Emergency department management Control blood pressure cautiously to avoid reducing cerebral perfusion. Gradually lower diastolic blood pressure by approximately 10%, avoiding rapid normalization. Treat elevated intracranial pressure with head elevation, controlled ventilation, osmotic therapy, and fluid management. Reverse coagulopathies promptly using vitamin K, fresh frozen plasma, platelets, or prothrombin complex concentrates as indicated. Consider anticonvulsants for seizure management or prophylaxis.
Medication
Common agents include labetalol, nicardipine, esmolol, or enalapril for blood pressure control; mannitol or furosemide for intracranial pressure; phenytoin or fosphenytoin for seizures; and appropriate blood products for anticoagulation reversal.
Follow-up and disposition
Admission criteria All patients with intracerebral hemorrhage require admission. ICU care is indicated for altered mental status, intubation, or continuous blood pressure infusions.
Discharge criteria Discharge is not appropriate for intracerebral hemorrhage.
Follow-up recommendations Long-term blood pressure control, smoking and substance cessation, and rehabilitation planning are critical to reduce recurrence and improve functional recovery.
Key points
Early brain imaging is essential in patients with headache, hypertension, or altered mental status. Blood pressure reduction must be cautious to preserve cerebral perfusion. Delayed hemorrhage should be considered in anticoagulated patients with head trauma.
