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Infectious Diseases and Microbiology: Fever of Unknown Origin
Basics
Description
Fever of unknown origin (FUO) describes persistent fever that lasts longer than expected for a typical acute febrile illness and is meant to exclude self-limited infections, conditions identified on basic initial testing, and benign fevers below 38.3°C. Current criteria, revised from the 1961 Petersdorf and Beeson definition, require illness duration of at least three weeks, documented temperatures above 38.3°C on multiple occasions, and no diagnosis despite a thorough evaluation. Durack and Street proposed FUO subtypes reflecting differing causes and workups: classical FUO, immune-deficient FUO, healthcare-associated FUO, and HIV-related FUO. Using this framework, immune-deficient patients, hospitalized patients who were afebrile before admission, and patients with HIV may meet FUO criteria after three to five inpatient days of evaluation with 48 hours of negative cultures.
Approach to the Patient
FUO is clinically difficult for both patients and clinicians, and management centers on identifying a cause, reaching a diagnosis efficiently and safely with appropriate testing, and initiating targeted therapy once a diagnosis is established or, when necessary, performing a therapeutic trial. Evaluation should be individualized to avoid both excessive testing for unlikely causes and missed evaluation of likely ones, so rigid algorithms are discouraged. Key aims are to confirm true fever and define its pattern, assess illness tempo and severity, look for localizing symptoms, place the illness in context of comorbidities and medications, and identify exposure risks such as travel, occupational and sexual history, animal contact, vaccination status, and intravenous drug use. Minimum baseline evaluation should include detailed history, repeated physical examination, complete blood count with smear, differential and platelets, routine chemistries including liver enzymes, LDH and bilirubin, urinalysis with microscopy and culture, chest radiograph, ESR and CRP, ANA, rheumatoid factor and anti-CCP, three sets of blood cultures obtained off antibiotics, tuberculosis testing with TST or IGRA, CT abdomen and pelvis, and infectious serologies guided by the clinical scenario.
Special Populations
Geriatric Considerations
Consider polymyalgia rheumatica and recognize that the distribution of undiagnosed etiologies differs in older adults.
Pediatric Considerations
Herpesviruses HHV-6/7/8 are common in infants and children. Ultrasound is preferred over CT to limit radiation and because pediatric imaging resolution is favorable. Connective tissue disease and neoplasia are uncommon under 12 months, Kawasaki disease is common under 5 years, Still’s disease often affects children and young adults, and arthritis in children should be treated as a marker of potentially serious disease. Periodic fever and other entities to consider include hyper-IgD syndrome, cyclic neutropenia, and nephroma.
Pregnancy Considerations
Pregnancy increases venous thromboembolism risk. Consider septic pelvic thrombophlebitis after obstetric surgery, sexually transmitted infections including HIV and syphilis, and pyometra.
Epidemiology
True FUO is uncommon. Reported etiologic frequencies vary by population, geography, institution, age, local disease prevalence, and practice patterns. Over time, the proportion of infectious and malignant causes has decreased while the proportion of undiagnosed cases has increased.
Diagnosis
FUO evaluation relies on iterative history-taking, repeated examinations, laboratory studies, and imaging.
History
History should cover alcohol use, medications, occupational and sexual exposures, pets, travel, family conditions, and prior illnesses. Although fever patterns are described for many disorders, truly distinctive patterns are rare in practice; classic patterns such as malaria are uncommon in many settings, and patterns considered characteristic for other diseases, such as Pel–Ebstein fever in lymphoma, are infrequently observed.
Physical Examination
Repeated comprehensive examination is central and should specifically assess the oropharynx for dental abscess, thyroid for thyroiditis, temporal regions for arteritis, cardiac auscultation for murmurs suggesting endocarditis or atrial myxoma, skin for vasculitis and Whipple disease clues, all wounds and vascular access sites with dressings removed for inspection, regional lymph nodes, and the genitoperineal region, sometimes requiring rectal or vaginal examination. Relative bradycardia can be a clue but is nonspecific and occurs in diverse conditions including brucellosis, drug fever, factitious fever, hepatitis A, Legionella infection, leptospirosis, malignancy, psittacosis, subacute necrotizing lymphadenitis, and typhoid fever. Fever from solid tumors and many connective tissue diseases may abate with NSAIDs, whereas fever from other causes may not. Symptoms such as sweats, chills, and weight loss do not reliably distinguish etiologies. Clues suggesting factitious fever include lack of tachycardia or tachypnea, temperatures exceeding 41°C, absent diurnal variation, and lack of sweating after defervescence.
Diagnostic Tests and Interpretation
Laboratory Studies
Noninvasive tests yield a diagnosis in roughly one-quarter of cases and include serologies for infectious and rheumatologic disease, biochemical markers such as ferritin for Still’s disease, and genetic markers such as those used for familial Mediterranean fever.
Imaging
Imaging is primarily used to localize targets for further evaluation. Abdominal CT has improved diagnostic yield when followed by invasive sampling, though false negatives can occur even with solid-organ abscesses. MRI is preferred when spinal or paraspinal pathology is suspected. Nuclear imaging with gallium-67 or indium-111 labeled leukocytes can sometimes help when infection or malignancy is suspected, but limitations include false-negative gallium scans in secondarily infected lesions, poor detection of splenic abscess due to background uptake, and low positive predictive value with indium studies. FDG PET/CT can help establish malignant, inflammatory, or infectious diagnoses in at least one-third of cases. If imaging and serologies are unrevealing, invasive investigations such as liver and bone marrow biopsy should be considered, and fewer than half of diagnoses are ultimately made via biopsy or laparotomy. Temporal artery biopsy is often high yield in older adults with markedly elevated ESR even without obvious local symptoms. Disseminated tuberculosis is a highly treatable lethal cause of FUO and warrants aggressive pursuit; TST and IGRA can be negative in up to half of cases, sputum smears are only intermittently positive, and confirmation often requires biopsy of lymph node, bone marrow, or liver. Excisional lymph node biopsy is helpful when nodes are enlarged, though inguinal nodes are commonly palpable and usually not diagnostically useful.
Differential Diagnosis
The major etiologic categories and approximate frequencies include infections, malignancies, connective tissue or inflammatory disorders, miscellaneous causes, and undiagnosed cases. Unusual presentations of common diseases and conditions that are difficult to confirm account for more FUO cases than truly rare diseases, and thinking in terms of FUO subtype helps prioritize causes.
Classical FUO
Common infectious drivers remain tuberculosis, bacterial endocarditis, and intraabdominal collections. Systemic bacterial causes include bartonellosis, brucellosis, Campylobacter infection, cat-scratch disease or bacillary angiomatosis, ehrlichiosis, gonococcemia, HACEK organisms, Legionella infection, leptospirosis, listeriosis, Lyme disease, meningococcemia, rat-bite fever, relapsing fever due to Borrelia recurrentis, salmonellosis including typhoid, syphilis, tularemia, and yersiniosis, along with chlamydial, fungal, parasitic, and viral infections. Localized infections include intravascular infections such as endocarditis, aortitis, catheter infections, septic jugular phlebitis, and vascular graft infection; intraabdominal infections such as appendicitis, cholangitis, cholecystitis, diverticulitis, and diverse abscesses (subphrenic, hepatic, splenic, pancreatic, perinephric, pelvic), mesenteric lymphadenitis, pelvic inflammatory disease, and pyometra; prosthesis-related infections involving joint prostheses, pacemakers, defibrillators, shunts, and vascular access; and other focal infections including dental, intracranial, pulmonary, mastoid, middle ear, sinus, prostatic, and wound infections. Common noninfectious causes include malignancies such as renal cell carcinoma, hepatocellular carcinoma, Hodgkin and non-Hodgkin lymphoma, colon cancer, leukemia, malignant histiocytosis, pancreatic cancer, and sarcoma; benign tumors such as atrial myxoma; inflammatory disorders such as adult Still’s disease, Behçet syndrome, and cryoglobulinemia; and miscellaneous conditions including neuroleptic malignant syndrome, hematoma, recurrent pulmonary embolism, aortic dissection, post–myocardial infarction fever syndromes, subacute thyroiditis, hyperthyroidism, adrenal insufficiency, drug fever, factitious fever, gout, pseudogout, hypersensitivity pneumonitis, stroke, familial Mediterranean fever, and pheochromocytoma.
Healthcare-Associated FUO
Infectious causes include intravascular catheter infection, septic thrombophlebitis, prosthetic device infection, deep postoperative wound infections and intraabdominal collections, C. difficile colitis that may present with ileus rather than diarrhea in severe disease, septic pelvic thrombophlebitis after obstetric or gynecologic surgery, acalculous cholecystitis, and ICU-associated sinusitis related to nasogastric tubes and endotracheal intubation. Miscellaneous causes include venous thromboembolism, drug fever often without rash or eosinophilia and commonly triggered by antimicrobials and multiple other medication classes, factitious fever, and postoperative inflammatory fever without a defined diagnosis.
Immune-Deficient FUO
Most cases are infectious, with pathogen identification in a large fraction, and the likely infections depend on the type and duration of immunodeficiency. Persistent fever can reflect progressive or relapsed malignancy in hematology-oncology patients, inflammatory causes such as graft-versus-host disease, or miscellaneous etiologies including venous thromboembolism, drug fever, and adrenal insufficiency.
HIV-Related FUO
Most cases are infectious, though FUO has decreased in the antiretroviral era due to fewer opportunistic infections, and likely etiologies depend strongly on CD4 count. Scenarios include HIV seroconversion illness, opportunistic infections such as mycobacterial disease, Pneumocystis jirovecii, cytomegalovirus, toxoplasmosis, histoplasmosis, and leishmaniasis, inflammatory syndromes such as immune reconstitution, Castleman disease, and hemophagocytic lymphohistiocytosis, malignancies such as lymphoma and Kaposi sarcoma, and drug fever.
Treatment
Medications
Management is determined by the underlying cause. If TST or IGRA is positive or if granulomatous disease with possible anergy is suspected, a therapeutic trial for tuberculosis is recommended and may be continued for up to six weeks; persistent fever beyond this period suggests an alternate diagnosis. Glucocorticoids and NSAIDs can suppress fever and obscure diagnosis while allowing infection to progress and should be avoided unless infection has largely been excluded. In severely immune-deficient patients, empiric antimicrobial therapy is often necessary because infections are common and associated with high mortality.
Ongoing Care and Follow-Up
Hospitalized patients with FUO require close monitoring for evolving symptoms or new physical findings that may provide diagnostic direction.
Basics
Description
Fever of unknown origin (FUO) describes persistent fever that lasts longer than expected for a typical acute febrile illness and is meant to exclude self-limited infections, conditions identified on basic initial testing, and benign fevers below 38.3°C. Current criteria, revised from the 1961 Petersdorf and Beeson definition, require illness duration of at least three weeks, documented temperatures above 38.3°C on multiple occasions, and no diagnosis despite a thorough evaluation. Durack and Street proposed FUO subtypes reflecting differing causes and workups: classical FUO, immune-deficient FUO, healthcare-associated FUO, and HIV-related FUO. Using this framework, immune-deficient patients, hospitalized patients who were afebrile before admission, and patients with HIV may meet FUO criteria after three to five inpatient days of evaluation with 48 hours of negative cultures.
Approach to the Patient
FUO is clinically difficult for both patients and clinicians, and management centers on identifying a cause, reaching a diagnosis efficiently and safely with appropriate testing, and initiating targeted therapy once a diagnosis is established or, when necessary, performing a therapeutic trial. Evaluation should be individualized to avoid both excessive testing for unlikely causes and missed evaluation of likely ones, so rigid algorithms are discouraged. Key aims are to confirm true fever and define its pattern, assess illness tempo and severity, look for localizing symptoms, place the illness in context of comorbidities and medications, and identify exposure risks such as travel, occupational and sexual history, animal contact, vaccination status, and intravenous drug use. Minimum baseline evaluation should include detailed history, repeated physical examination, complete blood count with smear, differential and platelets, routine chemistries including liver enzymes, LDH and bilirubin, urinalysis with microscopy and culture, chest radiograph, ESR and CRP, ANA, rheumatoid factor and anti-CCP, three sets of blood cultures obtained off antibiotics, tuberculosis testing with TST or IGRA, CT abdomen and pelvis, and infectious serologies guided by the clinical scenario.
Special Populations
Geriatric Considerations
Consider polymyalgia rheumatica and recognize that the distribution of undiagnosed etiologies differs in older adults.
Pediatric Considerations
Herpesviruses HHV-6/7/8 are common in infants and children. Ultrasound is preferred over CT to limit radiation and because pediatric imaging resolution is favorable. Connective tissue disease and neoplasia are uncommon under 12 months, Kawasaki disease is common under 5 years, Still’s disease often affects children and young adults, and arthritis in children should be treated as a marker of potentially serious disease. Periodic fever and other entities to consider include hyper-IgD syndrome, cyclic neutropenia, and nephroma.
Pregnancy Considerations
Pregnancy increases venous thromboembolism risk. Consider septic pelvic thrombophlebitis after obstetric surgery, sexually transmitted infections including HIV and syphilis, and pyometra.
Epidemiology
True FUO is uncommon. Reported etiologic frequencies vary by population, geography, institution, age, local disease prevalence, and practice patterns. Over time, the proportion of infectious and malignant causes has decreased while the proportion of undiagnosed cases has increased.
Diagnosis
FUO evaluation relies on iterative history-taking, repeated examinations, laboratory studies, and imaging.
History
History should cover alcohol use, medications, occupational and sexual exposures, pets, travel, family conditions, and prior illnesses. Although fever patterns are described for many disorders, truly distinctive patterns are rare in practice; classic patterns such as malaria are uncommon in many settings, and patterns considered characteristic for other diseases, such as Pel–Ebstein fever in lymphoma, are infrequently observed.
Physical Examination
Repeated comprehensive examination is central and should specifically assess the oropharynx for dental abscess, thyroid for thyroiditis, temporal regions for arteritis, cardiac auscultation for murmurs suggesting endocarditis or atrial myxoma, skin for vasculitis and Whipple disease clues, all wounds and vascular access sites with dressings removed for inspection, regional lymph nodes, and the genitoperineal region, sometimes requiring rectal or vaginal examination. Relative bradycardia can be a clue but is nonspecific and occurs in diverse conditions including brucellosis, drug fever, factitious fever, hepatitis A, Legionella infection, leptospirosis, malignancy, psittacosis, subacute necrotizing lymphadenitis, and typhoid fever. Fever from solid tumors and many connective tissue diseases may abate with NSAIDs, whereas fever from other causes may not. Symptoms such as sweats, chills, and weight loss do not reliably distinguish etiologies. Clues suggesting factitious fever include lack of tachycardia or tachypnea, temperatures exceeding 41°C, absent diurnal variation, and lack of sweating after defervescence.
Diagnostic Tests and Interpretation
Laboratory Studies
Noninvasive tests yield a diagnosis in roughly one-quarter of cases and include serologies for infectious and rheumatologic disease, biochemical markers such as ferritin for Still’s disease, and genetic markers such as those used for familial Mediterranean fever.
Imaging
Imaging is primarily used to localize targets for further evaluation. Abdominal CT has improved diagnostic yield when followed by invasive sampling, though false negatives can occur even with solid-organ abscesses. MRI is preferred when spinal or paraspinal pathology is suspected. Nuclear imaging with gallium-67 or indium-111 labeled leukocytes can sometimes help when infection or malignancy is suspected, but limitations include false-negative gallium scans in secondarily infected lesions, poor detection of splenic abscess due to background uptake, and low positive predictive value with indium studies. FDG PET/CT can help establish malignant, inflammatory, or infectious diagnoses in at least one-third of cases. If imaging and serologies are unrevealing, invasive investigations such as liver and bone marrow biopsy should be considered, and fewer than half of diagnoses are ultimately made via biopsy or laparotomy. Temporal artery biopsy is often high yield in older adults with markedly elevated ESR even without obvious local symptoms. Disseminated tuberculosis is a highly treatable lethal cause of FUO and warrants aggressive pursuit; TST and IGRA can be negative in up to half of cases, sputum smears are only intermittently positive, and confirmation often requires biopsy of lymph node, bone marrow, or liver. Excisional lymph node biopsy is helpful when nodes are enlarged, though inguinal nodes are commonly palpable and usually not diagnostically useful.
Differential Diagnosis
The major etiologic categories and approximate frequencies include infections, malignancies, connective tissue or inflammatory disorders, miscellaneous causes, and undiagnosed cases. Unusual presentations of common diseases and conditions that are difficult to confirm account for more FUO cases than truly rare diseases, and thinking in terms of FUO subtype helps prioritize causes.
Classical FUO
Common infectious drivers remain tuberculosis, bacterial endocarditis, and intraabdominal collections. Systemic bacterial causes include bartonellosis, brucellosis, Campylobacter infection, cat-scratch disease or bacillary angiomatosis, ehrlichiosis, gonococcemia, HACEK organisms, Legionella infection, leptospirosis, listeriosis, Lyme disease, meningococcemia, rat-bite fever, relapsing fever due to Borrelia recurrentis, salmonellosis including typhoid, syphilis, tularemia, and yersiniosis, along with chlamydial, fungal, parasitic, and viral infections. Localized infections include intravascular infections such as endocarditis, aortitis, catheter infections, septic jugular phlebitis, and vascular graft infection; intraabdominal infections such as appendicitis, cholangitis, cholecystitis, diverticulitis, and diverse abscesses (subphrenic, hepatic, splenic, pancreatic, perinephric, pelvic), mesenteric lymphadenitis, pelvic inflammatory disease, and pyometra; prosthesis-related infections involving joint prostheses, pacemakers, defibrillators, shunts, and vascular access; and other focal infections including dental, intracranial, pulmonary, mastoid, middle ear, sinus, prostatic, and wound infections. Common noninfectious causes include malignancies such as renal cell carcinoma, hepatocellular carcinoma, Hodgkin and non-Hodgkin lymphoma, colon cancer, leukemia, malignant histiocytosis, pancreatic cancer, and sarcoma; benign tumors such as atrial myxoma; inflammatory disorders such as adult Still’s disease, Behçet syndrome, and cryoglobulinemia; and miscellaneous conditions including neuroleptic malignant syndrome, hematoma, recurrent pulmonary embolism, aortic dissection, post–myocardial infarction fever syndromes, subacute thyroiditis, hyperthyroidism, adrenal insufficiency, drug fever, factitious fever, gout, pseudogout, hypersensitivity pneumonitis, stroke, familial Mediterranean fever, and pheochromocytoma.
Healthcare-Associated FUO
Infectious causes include intravascular catheter infection, septic thrombophlebitis, prosthetic device infection, deep postoperative wound infections and intraabdominal collections, C. difficile colitis that may present with ileus rather than diarrhea in severe disease, septic pelvic thrombophlebitis after obstetric or gynecologic surgery, acalculous cholecystitis, and ICU-associated sinusitis related to nasogastric tubes and endotracheal intubation. Miscellaneous causes include venous thromboembolism, drug fever often without rash or eosinophilia and commonly triggered by antimicrobials and multiple other medication classes, factitious fever, and postoperative inflammatory fever without a defined diagnosis.
Immune-Deficient FUO
Most cases are infectious, with pathogen identification in a large fraction, and the likely infections depend on the type and duration of immunodeficiency. Persistent fever can reflect progressive or relapsed malignancy in hematology-oncology patients, inflammatory causes such as graft-versus-host disease, or miscellaneous etiologies including venous thromboembolism, drug fever, and adrenal insufficiency.
HIV-Related FUO
Most cases are infectious, though FUO has decreased in the antiretroviral era due to fewer opportunistic infections, and likely etiologies depend strongly on CD4 count. Scenarios include HIV seroconversion illness, opportunistic infections such as mycobacterial disease, Pneumocystis jirovecii, cytomegalovirus, toxoplasmosis, histoplasmosis, and leishmaniasis, inflammatory syndromes such as immune reconstitution, Castleman disease, and hemophagocytic lymphohistiocytosis, malignancies such as lymphoma and Kaposi sarcoma, and drug fever.
Treatment
Medications
Management is determined by the underlying cause. If TST or IGRA is positive or if granulomatous disease with possible anergy is suspected, a therapeutic trial for tuberculosis is recommended and may be continued for up to six weeks; persistent fever beyond this period suggests an alternate diagnosis. Glucocorticoids and NSAIDs can suppress fever and obscure diagnosis while allowing infection to progress and should be avoided unless infection has largely been excluded. In severely immune-deficient patients, empiric antimicrobial therapy is often necessary because infections are common and associated with high mortality.
Ongoing Care and Follow-Up
Hospitalized patients with FUO require close monitoring for evolving symptoms or new physical findings that may provide diagnostic direction.
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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.
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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.
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Emergency and Acute Medicine – Isoniazid poisoning
Isoniazid (INH) poisoning results from disruption of normal vitamin B6–dependent neurotransmitter metabolism. INH complexes with and inactivates pyridoxal-5-phosphate, the active form of pyridoxine, and inhibits pyridoxine phosphokinase, preventing conversion of pyridoxine to its active form. This leads to decreased production of γ-aminobutyric acid (GABA), causing cerebral excitability and refractory seizures. INH also inhibits lactate dehydrogenase, impairing conversion of lactate to pyruvate and contributing to profound anion gap metabolic acidosis. Chronic toxicity interferes with niacin synthesis and may cause a pellagra-like syndrome after months of therapy. Rare neuropsychiatric effects include mania, depression, obsessive–compulsive symptoms, and psychosis. INH is rapidly absorbed, with peak levels in 1–2 hours, has low protein binding, and is renally excreted after hepatic acetylation. Toxicity is more severe in slow acetylators.
High-risk populations include immigrants, homeless individuals, patients with HIV, alcohol use disorder, and those of lower socioeconomic status. Slow acetylators are more prone to chronic toxicity. Ingestions less than 1.5 g usually cause mild toxicity, whereas ingestions of 10 g or more are often fatal.
Acute toxicity typically presents with neurologic findings, most notably seizures that are refractory to standard anticonvulsant therapy, along with altered mental status, agitation, coma, ataxia, hyperreflexia, hallucinations, and psychosis. Gastrointestinal symptoms include nausea and vomiting. Cardiovascular manifestations include hypotension, tachycardia, shock, and cyanosis. Metabolic findings are dominated by severe anion gap metabolic acidosis with elevated lactate and hyperthermia. Chronic toxicity presents with peripheral neuropathy, optic neuritis or atrophy, vertigo, psychosis, insomnia, and gastrointestinal or hepatic injury including hepatitis and liver failure.
Initial evaluation should focus on any patient with unexplained refractory seizures, altered mental status, or severe metabolic acidosis. Laboratory studies typically show profound metabolic acidosis on arterial blood gas, elevated anion gap, hyperglycemia, and leukocytosis in acute toxicity. Chronic toxicity may show agranulocytosis, anemia, hemolysis, and eosinophilia. Imaging is guided by clinical presentation, with chest radiography sometimes suggesting underlying tuberculosis and helping evaluate aspiration.
Management begins with airway, breathing, and circulation stabilization, supplemental oxygen, IV access, cardiac monitoring, and bedside glucose assessment. The specific antidote is pyridoxine (vitamin B6). The recommended dose is 1 g of pyridoxine for every gram of INH ingested; if the amount ingested is unknown, administer 5 g IV. Pyridoxine may be repeated if seizures or coma persist. If IV pyridoxine is unavailable, crushed tablets may be given via nasogastric tube. Benzodiazepines are used adjunctively for seizure control, but phenytoin is ineffective. Gastric decontamination with activated charcoal may be considered after stabilization, and gastric lavage is reserved for life-threatening ingestions presenting within one hour with a protected airway. Hemodialysis may be considered for persistent symptoms or renal failure. Acidosis generally resolves once seizures are controlled and does not usually require aggressive bicarbonate therapy.
Patients with refractory seizures, severe acidosis, coma, or unclear ingestion history require ICU admission. Asymptomatic patients may be discharged after a minimum of six hours of observation. Psychiatric evaluation is required for intentional ingestions.
Key pitfalls include failure to recognize INH poisoning in patients with seizures refractory to standard therapy and severe lactic acidosis. Pyridoxine should be given gram for gram relative to the suspected ingestion, and additional doses may be required if coma persists. Never paralyze a seizing patient without continuous EEG monitoring.
Isoniazid (INH) poisoning results from disruption of normal vitamin B6–dependent neurotransmitter metabolism. INH complexes with and inactivates pyridoxal-5-phosphate, the active form of pyridoxine, and inhibits pyridoxine phosphokinase, preventing conversion of pyridoxine to its active form. This leads to decreased production of γ-aminobutyric acid (GABA), causing cerebral excitability and refractory seizures. INH also inhibits lactate dehydrogenase, impairing conversion of lactate to pyruvate and contributing to profound anion gap metabolic acidosis. Chronic toxicity interferes with niacin synthesis and may cause a pellagra-like syndrome after months of therapy. Rare neuropsychiatric effects include mania, depression, obsessive–compulsive symptoms, and psychosis. INH is rapidly absorbed, with peak levels in 1–2 hours, has low protein binding, and is renally excreted after hepatic acetylation. Toxicity is more severe in slow acetylators.
High-risk populations include immigrants, homeless individuals, patients with HIV, alcohol use disorder, and those of lower socioeconomic status. Slow acetylators are more prone to chronic toxicity. Ingestions less than 1.5 g usually cause mild toxicity, whereas ingestions of 10 g or more are often fatal.
Acute toxicity typically presents with neurologic findings, most notably seizures that are refractory to standard anticonvulsant therapy, along with altered mental status, agitation, coma, ataxia, hyperreflexia, hallucinations, and psychosis. Gastrointestinal symptoms include nausea and vomiting. Cardiovascular manifestations include hypotension, tachycardia, shock, and cyanosis. Metabolic findings are dominated by severe anion gap metabolic acidosis with elevated lactate and hyperthermia. Chronic toxicity presents with peripheral neuropathy, optic neuritis or atrophy, vertigo, psychosis, insomnia, and gastrointestinal or hepatic injury including hepatitis and liver failure.
Initial evaluation should focus on any patient with unexplained refractory seizures, altered mental status, or severe metabolic acidosis. Laboratory studies typically show profound metabolic acidosis on arterial blood gas, elevated anion gap, hyperglycemia, and leukocytosis in acute toxicity. Chronic toxicity may show agranulocytosis, anemia, hemolysis, and eosinophilia. Imaging is guided by clinical presentation, with chest radiography sometimes suggesting underlying tuberculosis and helping evaluate aspiration.
Management begins with airway, breathing, and circulation stabilization, supplemental oxygen, IV access, cardiac monitoring, and bedside glucose assessment. The specific antidote is pyridoxine (vitamin B6). The recommended dose is 1 g of pyridoxine for every gram of INH ingested; if the amount ingested is unknown, administer 5 g IV. Pyridoxine may be repeated if seizures or coma persist. If IV pyridoxine is unavailable, crushed tablets may be given via nasogastric tube. Benzodiazepines are used adjunctively for seizure control, but phenytoin is ineffective. Gastric decontamination with activated charcoal may be considered after stabilization, and gastric lavage is reserved for life-threatening ingestions presenting within one hour with a protected airway. Hemodialysis may be considered for persistent symptoms or renal failure. Acidosis generally resolves once seizures are controlled and does not usually require aggressive bicarbonate therapy.
Patients with refractory seizures, severe acidosis, coma, or unclear ingestion history require ICU admission. Asymptomatic patients may be discharged after a minimum of six hours of observation. Psychiatric evaluation is required for intentional ingestions.
Key pitfalls include failure to recognize INH poisoning in patients with seizures refractory to standard therapy and severe lactic acidosis. Pyridoxine should be given gram for gram relative to the suspected ingestion, and additional doses may be required if coma persists. Never paralyze a seizing patient without continuous EEG monitoring.
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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.
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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.
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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.
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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.
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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.
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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.
