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Infectious Diseases and Microbiology: Low Back Pain and Fever
Basics
Description
Back pain refers to acute or chronic pain arising from the spine or paraspinal structures. The combination of back pain and fever requires careful evaluation for nonmechanical causes. History should specifically assess weight loss, pain worse when lying down, morning stiffness, and sudden severe or colicky pain. Serial spinal and neurologic examinations are crucial, and any spinal tenderness or focal pain warrants full diagnostic assessment. Vertebral osteomyelitis is commonly suggested by pain worsened by movement and not relieved by rest, focal vertebral tenderness, and elevated erythrocyte sedimentation rate. Pain from neoplastic nerve infiltration is typically constant, progressively worse, and persists at night without relief, whereas mechanical low back pain usually improves with rest. Work-up often begins with plain radiography followed by bone scintigraphy, MRI, CT, laboratory testing, and biopsy based on abnormal findings.
Epidemiology
A definitive pain source is difficult to establish and is identified in fewer than one-quarter of cases. Mechanical causes account for about 97% of low back pain, with degenerative disk disease and lumbar sprain/strain comprising most cases. The spine is a frequent site of bone metastasis. Vertebral osteomyelitis is uncommon at roughly 1 per 100,000 persons annually, with rising rates attributed to vascular devices and intravenous drug use; it occurs more often in early childhood and in adults over 50. Spinal epidural abscess occurs in about 1 per 10,000 hospital admissions per year, and MRSA-related vertebral osteomyelitis and epidural abscess are increasingly reported. Despite global increases in tuberculosis, the rate of extrapulmonary spinal disease remains relatively stable; Pott disease, typically involving the lower thoracic vertebrae, is the most common musculoskeletal extrapulmonary manifestation. Improved survival in sickle cell disease has been accompanied by more Salmonella vertebral osteomyelitis.
Risk Factors
Infectious complications can follow bites from many animals, often linked to occupational exposure (farmers, laboratory workers, veterinarians) or recreation (hunters, campers, exotic pet owners). Systemic infection after animal or human bites is more likely with extremity edema or impaired lymphatic drainage and in immunocompromised hosts. Fever after a dog bite in an immunosuppressed patient should prompt concern for invasive Capnocytophaga canimorsus infection.
Etiology
Infectious sources of back pain with fever include biliary tract infection, chronic prostatitis, herpes zoster, pyelonephritis, retroperitoneal abscess, spinal epidural abscess, and vertebral osteomyelitis. Noninfectious causes include colonic cancer, pancreatic disease, histiocytosis X, metastatic malignancy (breast, lung, prostate, thyroid, kidney, gastrointestinal tract), multiple myeloma, neoplastic invasion of pelvic nerves, lymphoma, pregnancy, vertebral fracture, renal artery or vein thrombosis, renal stones, retroperitoneal hemorrhage or tumors, and tumors of the posterior stomach or duodenum. Staphylococcus aureus is the leading cause of spinal epidural abscess, accounting for most reported cases, with additional pathogens including Actinomyces israelii, Aspergillus, Blastomyces, Brucella, Cryptococcus, Haemophilus parainfluenzae, Mycobacterium tuberculosis, and Streptococcus milleri. Vertebral osteomyelitis is most often due to staphylococci but may be caused by other bacteria or tuberculosis; one multicenter retrospective study from southern Spain reported a high proportion due to Brucella, with the remainder split between pyogenic and tuberculous disease.
Commonly Associated Conditions
Vertebral osteomyelitis and spinal epidural abscess are frequently associated with diabetes, injection drug use, chronic renal failure, alcohol use disorder, bacteremia or focal infections, and malignancy. Most epidural abscesses arise via hematogenous spread from skin or mucosal sources, though direct extension from adjacent infection is also recognized. Postoperative abscesses account for a substantial minority, and epidural catheter placement is another risk factor. Blunt trauma may precede symptoms and may lead to an epidural hematoma that later becomes infected.
Diagnosis
Spinal epidural abscess classically presents with fever, spinal pain and tenderness, and radicular pain progressing to limb weakness, with pain being the most consistent feature. Early on, spinal pain with or without fever may be the only findings before sudden neurologic decline. When sepsis dominates or when patients are bedbound, neurologic deficits may be missed. Fever is absent in a notable minority of pyogenic vertebral osteomyelitis cases and is even more commonly absent in tuberculous vertebral osteomyelitis.
History
Key elements include age; systemic symptoms such as fever, weakness, weight loss, and night sweats; prior trauma, infection, or cancer; pain characteristics; immune status; glycemic control in diabetes; and injection drug use. Screen for neurologic complaints including weakness, paresthesias, numbness, and bowel, bladder, or sexual dysfunction. Risk is higher in patients over 50, those using steroids, individuals with HIV, those on immunosuppressants, and those with prior surgery.
Physical Examination
Assess general appearance, vital signs, peripheral pulses, and perform a focused cardiopulmonary and abdominal evaluation in unstable patients. Look for referred pain by examining potential primary sources of tenderness. Perform a complete neurologic examination to evaluate for spinal cord compromise and localize deficits; lesions below T12 can produce lower motor neuron findings, and cauda equina syndrome may include bowel or bladder incontinence. In older adults, fever may be low-grade and does not reliably indicate severity. Percussion of spinous processes may reveal focal vertebral tenderness due to trauma, malignancy, or infection. Examine for signs of endocarditis and septic emboli.
Diagnostic Tests and Interpretation
Laboratory Studies
Routine blood tests are often nonspecific for vertebral osteomyelitis, but leukocytosis, neutrophilia, and markedly elevated ESR and C-reactive protein support pyogenic disease. Blood cultures are the most useful routine test and identify the organism in about half of pyogenic and Brucella vertebral osteomyelitis cases. Bone biopsy is often required to confirm the diagnosis, especially in tuberculous disease.
Imaging
Plain spinal radiographs may be normal early in vertebral osteomyelitis. MRI best defines the extent and location of spinal epidural abscess. MRI or CT myelography is preferred when spinal metastasis is suspected.
Diagnostic Procedures/Other
CT-guided needle biopsy reliably diagnoses carcinoma but is less dependable for lymphoma, though performance has improved with CT guidance, immunophenotyping, and larger needles; false-negative rates remain significant. Establishing an etiologic diagnosis of vertebral osteomyelitis often requires percutaneous or surgical vertebral biopsy.
Differential Diagnosis
Tuberculosis may appear early as an opportunistic infection in AIDS and can be AIDS-defining, while Mycobacterium avium complex typically occurs later with very low CD4 counts. Pertussis should be considered when cough is the predominant symptom, particularly with paroxysms, inspiratory whoop, posttussive vomiting, sleep-disrupting cough, or exposure to similar illness.
Treatment
Medications
Suspected vertebral osteomyelitis or epidural abscess warrants empiric vancomycin to cover MRSA, with addition of a third- or fourth-generation cephalosporin when gram-negative bacteremia is suspected, especially with concurrent pyelonephritis. Therapy should be narrowed once the pathogen is identified; for methicillin-sensitive S. aureus, options include nafcillin, oxacillin, or cefazolin. Typical duration is at least six weeks. Management of tuberculous, brucellar, and salmonella bone disease follows their respective regimens. Corticosteroids may help in acute spinal cord compression. NSAIDs provide symptomatic analgesia, and bisphosphonates may be used for fractures related to breast cancer metastases.
Additional Treatment
Prompt diagnosis with targeted therapy is essential. Epidural abscess requires urgent surgical management with early decompression plus antibiotics. Spinal cord compression is a neurosurgical emergency, and decompression via surgery or radiotherapy within 24 hours of symptom onset is needed to reduce permanent neurologic injury. In suspected spinal or paraspinal infection, bactericidal empiric antibiotics should be started immediately.
.
Ongoing Care and Follow-Up
If symptoms persist beyond six weeks, repeat laboratory testing and imaging are recommended. After six weeks of antibiotics for osteomyelitis or epidural abscess, reassessment is needed to determine whether treatment should continue. Ongoing monitoring for medication toxicity is important, particularly in older adults who are more susceptible to adverse drug effects.
Basics
Description
Back pain refers to acute or chronic pain arising from the spine or paraspinal structures. The combination of back pain and fever requires careful evaluation for nonmechanical causes. History should specifically assess weight loss, pain worse when lying down, morning stiffness, and sudden severe or colicky pain. Serial spinal and neurologic examinations are crucial, and any spinal tenderness or focal pain warrants full diagnostic assessment. Vertebral osteomyelitis is commonly suggested by pain worsened by movement and not relieved by rest, focal vertebral tenderness, and elevated erythrocyte sedimentation rate. Pain from neoplastic nerve infiltration is typically constant, progressively worse, and persists at night without relief, whereas mechanical low back pain usually improves with rest. Work-up often begins with plain radiography followed by bone scintigraphy, MRI, CT, laboratory testing, and biopsy based on abnormal findings.
Epidemiology
A definitive pain source is difficult to establish and is identified in fewer than one-quarter of cases. Mechanical causes account for about 97% of low back pain, with degenerative disk disease and lumbar sprain/strain comprising most cases. The spine is a frequent site of bone metastasis. Vertebral osteomyelitis is uncommon at roughly 1 per 100,000 persons annually, with rising rates attributed to vascular devices and intravenous drug use; it occurs more often in early childhood and in adults over 50. Spinal epidural abscess occurs in about 1 per 10,000 hospital admissions per year, and MRSA-related vertebral osteomyelitis and epidural abscess are increasingly reported. Despite global increases in tuberculosis, the rate of extrapulmonary spinal disease remains relatively stable; Pott disease, typically involving the lower thoracic vertebrae, is the most common musculoskeletal extrapulmonary manifestation. Improved survival in sickle cell disease has been accompanied by more Salmonella vertebral osteomyelitis.
Risk Factors
Infectious complications can follow bites from many animals, often linked to occupational exposure (farmers, laboratory workers, veterinarians) or recreation (hunters, campers, exotic pet owners). Systemic infection after animal or human bites is more likely with extremity edema or impaired lymphatic drainage and in immunocompromised hosts. Fever after a dog bite in an immunosuppressed patient should prompt concern for invasive Capnocytophaga canimorsus infection.
Etiology
Infectious sources of back pain with fever include biliary tract infection, chronic prostatitis, herpes zoster, pyelonephritis, retroperitoneal abscess, spinal epidural abscess, and vertebral osteomyelitis. Noninfectious causes include colonic cancer, pancreatic disease, histiocytosis X, metastatic malignancy (breast, lung, prostate, thyroid, kidney, gastrointestinal tract), multiple myeloma, neoplastic invasion of pelvic nerves, lymphoma, pregnancy, vertebral fracture, renal artery or vein thrombosis, renal stones, retroperitoneal hemorrhage or tumors, and tumors of the posterior stomach or duodenum. Staphylococcus aureus is the leading cause of spinal epidural abscess, accounting for most reported cases, with additional pathogens including Actinomyces israelii, Aspergillus, Blastomyces, Brucella, Cryptococcus, Haemophilus parainfluenzae, Mycobacterium tuberculosis, and Streptococcus milleri. Vertebral osteomyelitis is most often due to staphylococci but may be caused by other bacteria or tuberculosis; one multicenter retrospective study from southern Spain reported a high proportion due to Brucella, with the remainder split between pyogenic and tuberculous disease.
Commonly Associated Conditions
Vertebral osteomyelitis and spinal epidural abscess are frequently associated with diabetes, injection drug use, chronic renal failure, alcohol use disorder, bacteremia or focal infections, and malignancy. Most epidural abscesses arise via hematogenous spread from skin or mucosal sources, though direct extension from adjacent infection is also recognized. Postoperative abscesses account for a substantial minority, and epidural catheter placement is another risk factor. Blunt trauma may precede symptoms and may lead to an epidural hematoma that later becomes infected.
Diagnosis
Spinal epidural abscess classically presents with fever, spinal pain and tenderness, and radicular pain progressing to limb weakness, with pain being the most consistent feature. Early on, spinal pain with or without fever may be the only findings before sudden neurologic decline. When sepsis dominates or when patients are bedbound, neurologic deficits may be missed. Fever is absent in a notable minority of pyogenic vertebral osteomyelitis cases and is even more commonly absent in tuberculous vertebral osteomyelitis.
History
Key elements include age; systemic symptoms such as fever, weakness, weight loss, and night sweats; prior trauma, infection, or cancer; pain characteristics; immune status; glycemic control in diabetes; and injection drug use. Screen for neurologic complaints including weakness, paresthesias, numbness, and bowel, bladder, or sexual dysfunction. Risk is higher in patients over 50, those using steroids, individuals with HIV, those on immunosuppressants, and those with prior surgery.
Physical Examination
Assess general appearance, vital signs, peripheral pulses, and perform a focused cardiopulmonary and abdominal evaluation in unstable patients. Look for referred pain by examining potential primary sources of tenderness. Perform a complete neurologic examination to evaluate for spinal cord compromise and localize deficits; lesions below T12 can produce lower motor neuron findings, and cauda equina syndrome may include bowel or bladder incontinence. In older adults, fever may be low-grade and does not reliably indicate severity. Percussion of spinous processes may reveal focal vertebral tenderness due to trauma, malignancy, or infection. Examine for signs of endocarditis and septic emboli.
Diagnostic Tests and Interpretation
Laboratory Studies
Routine blood tests are often nonspecific for vertebral osteomyelitis, but leukocytosis, neutrophilia, and markedly elevated ESR and C-reactive protein support pyogenic disease. Blood cultures are the most useful routine test and identify the organism in about half of pyogenic and Brucella vertebral osteomyelitis cases. Bone biopsy is often required to confirm the diagnosis, especially in tuberculous disease.
Imaging
Plain spinal radiographs may be normal early in vertebral osteomyelitis. MRI best defines the extent and location of spinal epidural abscess. MRI or CT myelography is preferred when spinal metastasis is suspected.
Diagnostic Procedures/Other
CT-guided needle biopsy reliably diagnoses carcinoma but is less dependable for lymphoma, though performance has improved with CT guidance, immunophenotyping, and larger needles; false-negative rates remain significant. Establishing an etiologic diagnosis of vertebral osteomyelitis often requires percutaneous or surgical vertebral biopsy.
Differential Diagnosis
Tuberculosis may appear early as an opportunistic infection in AIDS and can be AIDS-defining, while Mycobacterium avium complex typically occurs later with very low CD4 counts. Pertussis should be considered when cough is the predominant symptom, particularly with paroxysms, inspiratory whoop, posttussive vomiting, sleep-disrupting cough, or exposure to similar illness.
Treatment
Medications
Suspected vertebral osteomyelitis or epidural abscess warrants empiric vancomycin to cover MRSA, with addition of a third- or fourth-generation cephalosporin when gram-negative bacteremia is suspected, especially with concurrent pyelonephritis. Therapy should be narrowed once the pathogen is identified; for methicillin-sensitive S. aureus, options include nafcillin, oxacillin, or cefazolin. Typical duration is at least six weeks. Management of tuberculous, brucellar, and salmonella bone disease follows their respective regimens. Corticosteroids may help in acute spinal cord compression. NSAIDs provide symptomatic analgesia, and bisphosphonates may be used for fractures related to breast cancer metastases.
Additional Treatment
Prompt diagnosis with targeted therapy is essential. Epidural abscess requires urgent surgical management with early decompression plus antibiotics. Spinal cord compression is a neurosurgical emergency, and decompression via surgery or radiotherapy within 24 hours of symptom onset is needed to reduce permanent neurologic injury. In suspected spinal or paraspinal infection, bactericidal empiric antibiotics should be started immediately.
.
Ongoing Care and Follow-Up
If symptoms persist beyond six weeks, repeat laboratory testing and imaging are recommended. After six weeks of antibiotics for osteomyelitis or epidural abscess, reassessment is needed to determine whether treatment should continue. Ongoing monitoring for medication toxicity is important, particularly in older adults who are more susceptible to adverse drug effects.
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Emergency And Acute Medicine – Hirschsprung Disease
Basics
Condition Overview
First described in 1886 by Harold Hirschsprung as a cause of severe constipation in early infancy. Hirschsprung disease is a congenital aganglionic megacolon occurring in approximately 1:5,000 live births. Mortality associated with Hirschsprung-related enterocolitis remains high at 35–50%.
Etiology And Pathogenesis
The disease is caused by absence of enteric ganglion cells in the distal bowel. Normally, neural crest cells migrate along the gastrointestinal tract, reaching the proximal colon by 8 weeks of gestation and the rectum by 12 weeks. Failure of migration into the parasympathetic Meissner (submucosal) and Auerbach (myenteric) plexuses results in an aganglionic segment and clinical disease.
The affected bowel typically begins at the internal anal sphincter and involves the rectosigmoid colon in about 75% of cases, though it may extend proximally and, in rare cases, involve the entire GI tract, which is often fatal. The aganglionic segment remains chronically contracted, producing functional obstruction, while proximal bowel dilates to accommodate retained stool. Anal stimulation may temporarily allow stool passage.
Genetic associations include mutations of the RET proto-oncogene in both familial and sporadic forms. The male-to-female ratio is approximately 4:1. About 8% have a positive family history, with 5–12% of siblings affected. Chromosomal abnormalities occur in 5–15%, most commonly trisomy 21 (Down syndrome). Other congenital anomalies are present in approximately 18%, including gastrointestinal, cardiac, craniofacial abnormalities, cleft palate, and congenital deafness.
Diagnosis
Clinical Features
Most patients are diagnosed by 2 years of age, with presentation varying by age.
Neonatal presentation
Abdominal distension, failure to pass meconium within the first 48 hours of life, vomiting, enterocolitis characterized by abdominal pain, fever, foul-smelling and/or bloody diarrhea, vomiting progressing to sepsis and possible intestinal perforation, and sepsis.
Infancy
Chronic constipation, progressive abdominal distension, vomiting, failure to thrive, enterocolitis, and possible toxic megacolon.
Later childhood And Adulthood
Chronic constipation with obstruction, often refractory to standard treatment, rare overflow incontinence, abdominal distension, bloody foul-smelling diarrhea, malnutrition, and episodes of enterocolitis with systemic toxicity.
History
Frequent need for rectal stimulation or enemas to achieve bowel movements, narrow-caliber stools, encopresis and diarrhea are uncommon, and absence of typical triggers for functional constipation such as fissures, toilet training issues, or dietary factors.
Physical Examination
Possible palpable colon on the left, abdominal distension with signs of obstruction, findings consistent with malnutrition or failure to thrive, and an empty rectal vault on digital rectal examination.
Initial Evaluation
Plain abdominal radiographs commonly show distended small bowel and proximal colon (megacolon) with an empty rectum and a transition zone into a narrowed rectosigmoid segment. Neonates often demonstrate a distal obstructive pattern. In chronic constipation, imaging may show only fecal loading. In enterocolitis, bowel wall edema or pneumatosis intestinalis may be present.
Diagnostic Studies And Interpretation
Laboratory Studies
CBC, electrolytes, glucose, BUN, creatinine, urinalysis, and blood cultures if the patient appears toxic.
Imaging
Barium enema should be obtained after stabilization and is contraindicated if perforation or severe enterocolitis is suspected. Findings include a dilated proximal colon with a narrowed aganglionic distal segment, uncoordinated peristalsis, and a transition zone. A nondistensible rectum and delayed barium evacuation are classic findings. The transition zone may be absent in neonates or in infants who have undergone repeated rectal exams or enemas.
Procedures And Surgical Diagnosis
Rectal manometry may assist in diagnosis but is often abnormal in long-standing constipation; affected patients fail to demonstrate reflex relaxation of the internal anal sphincter with rectal balloon inflation. Definitive diagnosis requires a full-thickness rectal biopsy demonstrating absence of ganglion cells, which remains the diagnostic gold standard.
Differential Diagnosis
Neonates
Meconium ileus or meconium plug syndrome associated with cystic fibrosis, intestinal or anal atresia or hypoplasia, malrotation or duplication with volvulus, necrotizing enterocolitis, and sepsis.
Infants And Children
Functional constipation, toxic etiologies such as opiates or anticholinergics, infectious causes including botulism, acquired aganglionic colon, metabolic or endocrine disorders such as hypothyroidism, parathyroid or adrenal disease, electrolyte abnormalities, spinal cord defects, and abdominal masses.
Treatment
Initial Stabilization And Support
Airway, breathing, and circulation management with appropriate monitoring. Administer isotonic IV fluid bolus (20 mL/kg) for dehydration, shock, or sepsis.
Emergency Department Management
Infants should be treated as having bowel obstruction; nasogastric decompression is indicated if vomiting is present. Early consultation with a pediatric surgeon is essential. Broad-spectrum triple antibiotics are indicated for toxic patients or those with enterocolitis. Unstable patients may require emergent decompression with a loop colostomy. Stable patients may complete diagnostic evaluation as outpatients.
Definitive treatment consists of surgical resection of the aganglionic bowel with pull-through of normally innervated bowel to within 1 cm of the anal opening. Enterocolitis may occur before or after surgical intervention.
Medications
Ampicillin 50 mg/kg IV divided every 6 hours.
Gentamicin 2.5 mg/kg IV divided every 12–24 hours.
Metronidazole 7.5 mg/kg IV divided every 12–48 hours.
Follow-Up And Disposition
Admission Criteria
Neonates and infants with bowel obstruction, any patient with enterocolitis, and ill-appearing infants requiring NICU or PICU care with pediatric surgical support.
Discharge Criteria
Well-hydrated patients tolerating oral intake, typically older children presenting primarily with constipation, with reliable caregivers and close outpatient follow-up arranged.
Referral Considerations
Ongoing care should be coordinated with pediatric gastroenterology and pediatric surgery.
Key Clinical Insights And Common Pitfalls
Clinical presentation varies widely with age, ranging from neonatal obstruction to chronic constipation. The disease exists on a spectrum from mild constipation to life-threatening enterocolitis. Toxic patients require immediate stabilization, antibiotics, urgent imaging, and surgical consultation. Failure to recognize enterocolitis can result in rapid deterioration and death.
Basics
Condition Overview
First described in 1886 by Harold Hirschsprung as a cause of severe constipation in early infancy. Hirschsprung disease is a congenital aganglionic megacolon occurring in approximately 1:5,000 live births. Mortality associated with Hirschsprung-related enterocolitis remains high at 35–50%.
Etiology And Pathogenesis
The disease is caused by absence of enteric ganglion cells in the distal bowel. Normally, neural crest cells migrate along the gastrointestinal tract, reaching the proximal colon by 8 weeks of gestation and the rectum by 12 weeks. Failure of migration into the parasympathetic Meissner (submucosal) and Auerbach (myenteric) plexuses results in an aganglionic segment and clinical disease.
The affected bowel typically begins at the internal anal sphincter and involves the rectosigmoid colon in about 75% of cases, though it may extend proximally and, in rare cases, involve the entire GI tract, which is often fatal. The aganglionic segment remains chronically contracted, producing functional obstruction, while proximal bowel dilates to accommodate retained stool. Anal stimulation may temporarily allow stool passage.
Genetic associations include mutations of the RET proto-oncogene in both familial and sporadic forms. The male-to-female ratio is approximately 4:1. About 8% have a positive family history, with 5–12% of siblings affected. Chromosomal abnormalities occur in 5–15%, most commonly trisomy 21 (Down syndrome). Other congenital anomalies are present in approximately 18%, including gastrointestinal, cardiac, craniofacial abnormalities, cleft palate, and congenital deafness.
Diagnosis
Clinical Features
Most patients are diagnosed by 2 years of age, with presentation varying by age.
Neonatal presentation
Abdominal distension, failure to pass meconium within the first 48 hours of life, vomiting, enterocolitis characterized by abdominal pain, fever, foul-smelling and/or bloody diarrhea, vomiting progressing to sepsis and possible intestinal perforation, and sepsis.
Infancy
Chronic constipation, progressive abdominal distension, vomiting, failure to thrive, enterocolitis, and possible toxic megacolon.
Later childhood And Adulthood
Chronic constipation with obstruction, often refractory to standard treatment, rare overflow incontinence, abdominal distension, bloody foul-smelling diarrhea, malnutrition, and episodes of enterocolitis with systemic toxicity.
History
Frequent need for rectal stimulation or enemas to achieve bowel movements, narrow-caliber stools, encopresis and diarrhea are uncommon, and absence of typical triggers for functional constipation such as fissures, toilet training issues, or dietary factors.
Physical Examination
Possible palpable colon on the left, abdominal distension with signs of obstruction, findings consistent with malnutrition or failure to thrive, and an empty rectal vault on digital rectal examination.
Initial Evaluation
Plain abdominal radiographs commonly show distended small bowel and proximal colon (megacolon) with an empty rectum and a transition zone into a narrowed rectosigmoid segment. Neonates often demonstrate a distal obstructive pattern. In chronic constipation, imaging may show only fecal loading. In enterocolitis, bowel wall edema or pneumatosis intestinalis may be present.
Diagnostic Studies And Interpretation
Laboratory Studies
CBC, electrolytes, glucose, BUN, creatinine, urinalysis, and blood cultures if the patient appears toxic.
Imaging
Barium enema should be obtained after stabilization and is contraindicated if perforation or severe enterocolitis is suspected. Findings include a dilated proximal colon with a narrowed aganglionic distal segment, uncoordinated peristalsis, and a transition zone. A nondistensible rectum and delayed barium evacuation are classic findings. The transition zone may be absent in neonates or in infants who have undergone repeated rectal exams or enemas.
Procedures And Surgical Diagnosis
Rectal manometry may assist in diagnosis but is often abnormal in long-standing constipation; affected patients fail to demonstrate reflex relaxation of the internal anal sphincter with rectal balloon inflation. Definitive diagnosis requires a full-thickness rectal biopsy demonstrating absence of ganglion cells, which remains the diagnostic gold standard.
Differential Diagnosis
Neonates
Meconium ileus or meconium plug syndrome associated with cystic fibrosis, intestinal or anal atresia or hypoplasia, malrotation or duplication with volvulus, necrotizing enterocolitis, and sepsis.
Infants And Children
Functional constipation, toxic etiologies such as opiates or anticholinergics, infectious causes including botulism, acquired aganglionic colon, metabolic or endocrine disorders such as hypothyroidism, parathyroid or adrenal disease, electrolyte abnormalities, spinal cord defects, and abdominal masses.
Treatment
Initial Stabilization And Support
Airway, breathing, and circulation management with appropriate monitoring. Administer isotonic IV fluid bolus (20 mL/kg) for dehydration, shock, or sepsis.
Emergency Department Management
Infants should be treated as having bowel obstruction; nasogastric decompression is indicated if vomiting is present. Early consultation with a pediatric surgeon is essential. Broad-spectrum triple antibiotics are indicated for toxic patients or those with enterocolitis. Unstable patients may require emergent decompression with a loop colostomy. Stable patients may complete diagnostic evaluation as outpatients.
Definitive treatment consists of surgical resection of the aganglionic bowel with pull-through of normally innervated bowel to within 1 cm of the anal opening. Enterocolitis may occur before or after surgical intervention.
Medications
Ampicillin 50 mg/kg IV divided every 6 hours.
Gentamicin 2.5 mg/kg IV divided every 12–24 hours.
Metronidazole 7.5 mg/kg IV divided every 12–48 hours.
Follow-Up And Disposition
Admission Criteria
Neonates and infants with bowel obstruction, any patient with enterocolitis, and ill-appearing infants requiring NICU or PICU care with pediatric surgical support.
Discharge Criteria
Well-hydrated patients tolerating oral intake, typically older children presenting primarily with constipation, with reliable caregivers and close outpatient follow-up arranged.
Referral Considerations
Ongoing care should be coordinated with pediatric gastroenterology and pediatric surgery.
Key Clinical Insights And Common Pitfalls
Clinical presentation varies widely with age, ranging from neonatal obstruction to chronic constipation. The disease exists on a spectrum from mild constipation to life-threatening enterocolitis. Toxic patients require immediate stabilization, antibiotics, urgent imaging, and surgical consultation. Failure to recognize enterocolitis can result in rapid deterioration and death.
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Emergency And Acute Medicine – HIV And AIDS
Basics
Foundational Overview
Acquired immunodeficiency syndrome (AIDS) is defined by laboratory evidence of HIV infection with a CD4 count below 200 cells/mm³ or the presence of an AIDS-defining condition. These conditions include opportunistic infections (such as cryptosporidiosis), malignancies (including Kaposi sarcoma or invasive cervical cancer), and other HIV-related illnesses such as wasting syndrome or HIV-associated encephalopathy.
Opportunistic conditions correlate strongly with immune suppression:
At CD4 counts below 500 cells/mm³, patients are at risk for oroesophageal candidiasis, pneumococcal infections, oral hairy leukoplakia, and immune thrombocytopenic purpura.
At CD4 counts below 200 cells/mm³, common conditions include Pneumocystis jirovecii pneumonia (PCP), cryptococcal infection, disseminated tuberculosis, cryptosporidiosis, isosporiasis, toxoplasmosis, and histoplasmosis.
At CD4 counts below 50 cells/mm³, patients are vulnerable to central nervous system lymphoma, Mycobacterium avium complex (MAC), tuberculosis pericarditis or meningitis, cytomegalovirus (CMV) infection, and HIV-associated cholangiopathy, most commonly caused by Cryptosporidium parvum.
Diagnosis
Clinical Manifestations
Primary HIV infection typically occurs 2–6 weeks after exposure and may present with fever, malaise, a rash involving the face and trunk, flu-like symptoms with lymphadenopathy and hepatosplenomegaly, pharyngitis, and diarrhea. Up to 90% of patients may be asymptomatic during this stage.
Advanced HIV disease, usually defined by CD4 counts below 200 cells/mm³, commonly presents with fatigue, fevers, night sweats, weight loss or wasting, alopecia, chronic diarrhea, cough, dyspnea, hemoptysis, chronic low-grade headaches, altered mental status, seizures, dementia, neuropathy, painless visual loss, and various skin lesions.
History
Important risk factors include multiple sexual partners, unprotected intercourse with high-risk partners, men who have sex with men, intravenous drug use, blood transfusions prior to 1985, and lack of circumcision. Key historical elements include most recent and lowest recorded CD4 count, viral load, history of antiretroviral therapy and adherence, duration of HIV diagnosis, previous opportunistic infections, and prior hospitalizations or ICU admissions.
Initial Evaluation
HIV serologic testing is essential, recognizing a window period of up to 24 weeks between infection and seroconversion during which tests may be negative. HIV DNA amplification testing can detect infection within 1–2 weeks but is rarely available in the ED and requires careful follow-up.
Patients with respiratory symptoms require chest radiography, arterial blood gas analysis, sputum evaluation for Gram stain, acid-fast bacilli, and cultures, serum LDH levels, and blood cultures.
Cardiac symptoms warrant cardiac biomarkers, electrolytes, ECG, chest radiography, and blood cultures if endocarditis is suspected.
Neurologic symptoms require head CT with and without contrast and lumbar puncture with opening pressure and comprehensive CSF studies.
Gastrointestinal symptoms necessitate stool studies, urinalysis, pregnancy testing in women, pelvic examination when appropriate, liver enzymes, pancreatic enzymes, hepatitis serologies, and a low threshold for abdominal imaging or surgical consultation.
Fever of unknown origin requires broad infectious evaluation including bacterial, fungal, AFB, and MAC cultures.
Ocular complaints require slit-lamp examination with fluorescein staining.
Diagnostic Studies And Interpretation
Laboratory Testing
ELISA testing detects IgG antibodies against HIV with approximately 99% sensitivity and specificity but may be negative during the window period. Western blot testing confirms positive ELISA results by detecting antibodies to HIV proteins. Rapid HIV testing provides results within 5–20 minutes using oral swabs or blood samples but requires confirmatory testing.
Absolute lymphocyte count can estimate immune status: values above 2,000 cells/mm³ often correlate with CD4 counts above 200, while counts below 1,000 suggest advanced immunosuppression.
Imaging
Chest radiographs may show bilateral interstitial infiltrates in PCP, reticulonodular patterns in TB or fungal infections, hilar lymphadenopathy in TB or malignancy, lobar consolidation in bacterial pneumonia, or cavitary lesions in TB and necrotizing infections. A normal chest x-ray does not exclude PCP or TB.
Head CT may demonstrate multiple ring-enhancing lesions consistent with toxoplasmosis or CNS lymphoma, or nonenhancing subcortical lesions suggestive of progressive multifocal leukoencephalopathy.
Abdominal and pelvic CT imaging may reveal splenomegaly, intestinal perforation or obstruction, biliary disease, or pancreatitis related to infection, malignancy, or medications.
Differential Diagnosis
Pulmonary complaints may represent pulmonary embolism, pulmonary hypertension, TB, bacterial, viral, or fungal pneumonia, malignancy, or lymphocytic interstitial pneumonitis.
Neurologic symptoms raise concern for neurosyphilis, viral encephalitis, toxoplasmosis, CNS lymphoma, meningitis, stroke, metabolic encephalopathy, or progressive multifocal leukoencephalopathy.
Cardiac presentations include cardiomyopathy, myocarditis, pericarditis, endocarditis, acute coronary syndrome, or pericardial effusion.
Oral and esophageal symptoms may result from candidiasis, viral infections, bacterial disease, autoimmune conditions, or malignancy.
Chronic diarrhea, hepatomegaly, and renal dysfunction have broad infectious, metabolic, medication-related, and neoplastic etiologies in HIV-infected patients.
Treatment
Emergency Department Management
Patients appearing toxic or with rapidly progressive illness should receive empiric antibiotics in the ED. Initiation of antiretroviral therapy is recommended for patients with low CD4 counts, high viral loads, pregnancy, AIDS-defining illnesses, or HIV-associated nephropathy.
Highly active antiretroviral therapy (HAART) typically consists of triple therapy using combinations of non-nucleoside reverse transcriptase inhibitors, protease inhibitors, and nucleoside reverse transcriptase inhibitors.
Post-exposure prophylaxis should begin within 2 hours of exposure when possible and continue for 4 weeks, with two-drug regimens for most exposures and expanded three-drug regimens for high-risk cases.
Specific opportunistic infections require targeted therapy, including pyrimethamine-based regimens for toxoplasmosis, amphotericin B with flucytosine for cryptococcal meningitis, ganciclovir for CMV retinitis, fluconazole for esophageal candidiasis, clarithromycin-based therapy for MAC, trimethoprim-sulfamethoxazole for PCP with adjunctive steroids when hypoxemia is present, and plasmapheresis for acute HIV-related demyelinating neuropathy.
Medication-Related Considerations
Antiretroviral therapy is associated with numerous potential adverse effects including hypersensitivity reactions, pancreatitis, peripheral neuropathy, nephrolithiasis, hepatotoxicity, lactic acidosis, Stevens–Johnson syndrome, hemolytic anemia, neuropsychiatric effects, metabolic derangements, cardiomyopathy, and hematologic abnormalities.
Follow-Up And Disposition
Admission Criteria
Indications for hospitalization include unexplained fever with neurologic involvement, hypoxemia, suspected acute coronary syndrome, pericardial effusion, suspected bacterial pneumonia or TB, new neurologic deficits or seizures, hemodynamic instability, inability to ambulate or tolerate oral intake, and severe diarrhea with dehydration.
Discharge Criteria
Patients may be discharged if they can maintain oral intake, ambulate, perform self-care, and have reliable follow-up.
Referral Considerations
All patients should be referred to an HIV specialist for initiation and management of antiretroviral therapy. Screening for depression and psychiatric referral are essential to ensure treatment adherence. Patients with concerning symptoms should be referred for malignancy evaluation.
Key Clinical Insights And Common Pitfalls
Immune reconstitution inflammatory syndrome typically occurs within 8 weeks of initiating HAART. Occupational exposure carries a low but real risk of seroconversion. Patients on HAART have increased risk for metabolic disease and acute coronary syndromes. Exercise-induced desaturation may aid in diagnosing PCP when imaging is normal. HIV is an independent risk factor for COPDukar
COPD, pulmonary hypertension, stroke, venous thromboembolism, thrombotic thrombocytopenic purpura, osteoporosis, and osteonecrosis of the hip.
Basics
Foundational Overview
Acquired immunodeficiency syndrome (AIDS) is defined by laboratory evidence of HIV infection with a CD4 count below 200 cells/mm³ or the presence of an AIDS-defining condition. These conditions include opportunistic infections (such as cryptosporidiosis), malignancies (including Kaposi sarcoma or invasive cervical cancer), and other HIV-related illnesses such as wasting syndrome or HIV-associated encephalopathy.
Opportunistic conditions correlate strongly with immune suppression:
At CD4 counts below 500 cells/mm³, patients are at risk for oroesophageal candidiasis, pneumococcal infections, oral hairy leukoplakia, and immune thrombocytopenic purpura.
At CD4 counts below 200 cells/mm³, common conditions include Pneumocystis jirovecii pneumonia (PCP), cryptococcal infection, disseminated tuberculosis, cryptosporidiosis, isosporiasis, toxoplasmosis, and histoplasmosis.
At CD4 counts below 50 cells/mm³, patients are vulnerable to central nervous system lymphoma, Mycobacterium avium complex (MAC), tuberculosis pericarditis or meningitis, cytomegalovirus (CMV) infection, and HIV-associated cholangiopathy, most commonly caused by Cryptosporidium parvum.
Diagnosis
Clinical Manifestations
Primary HIV infection typically occurs 2–6 weeks after exposure and may present with fever, malaise, a rash involving the face and trunk, flu-like symptoms with lymphadenopathy and hepatosplenomegaly, pharyngitis, and diarrhea. Up to 90% of patients may be asymptomatic during this stage.
Advanced HIV disease, usually defined by CD4 counts below 200 cells/mm³, commonly presents with fatigue, fevers, night sweats, weight loss or wasting, alopecia, chronic diarrhea, cough, dyspnea, hemoptysis, chronic low-grade headaches, altered mental status, seizures, dementia, neuropathy, painless visual loss, and various skin lesions.
History
Important risk factors include multiple sexual partners, unprotected intercourse with high-risk partners, men who have sex with men, intravenous drug use, blood transfusions prior to 1985, and lack of circumcision. Key historical elements include most recent and lowest recorded CD4 count, viral load, history of antiretroviral therapy and adherence, duration of HIV diagnosis, previous opportunistic infections, and prior hospitalizations or ICU admissions.
Initial Evaluation
HIV serologic testing is essential, recognizing a window period of up to 24 weeks between infection and seroconversion during which tests may be negative. HIV DNA amplification testing can detect infection within 1–2 weeks but is rarely available in the ED and requires careful follow-up.
Patients with respiratory symptoms require chest radiography, arterial blood gas analysis, sputum evaluation for Gram stain, acid-fast bacilli, and cultures, serum LDH levels, and blood cultures.
Cardiac symptoms warrant cardiac biomarkers, electrolytes, ECG, chest radiography, and blood cultures if endocarditis is suspected.
Neurologic symptoms require head CT with and without contrast and lumbar puncture with opening pressure and comprehensive CSF studies.
Gastrointestinal symptoms necessitate stool studies, urinalysis, pregnancy testing in women, pelvic examination when appropriate, liver enzymes, pancreatic enzymes, hepatitis serologies, and a low threshold for abdominal imaging or surgical consultation.
Fever of unknown origin requires broad infectious evaluation including bacterial, fungal, AFB, and MAC cultures.
Ocular complaints require slit-lamp examination with fluorescein staining.
Diagnostic Studies And Interpretation
Laboratory Testing
ELISA testing detects IgG antibodies against HIV with approximately 99% sensitivity and specificity but may be negative during the window period. Western blot testing confirms positive ELISA results by detecting antibodies to HIV proteins. Rapid HIV testing provides results within 5–20 minutes using oral swabs or blood samples but requires confirmatory testing.
Absolute lymphocyte count can estimate immune status: values above 2,000 cells/mm³ often correlate with CD4 counts above 200, while counts below 1,000 suggest advanced immunosuppression.
Imaging
Chest radiographs may show bilateral interstitial infiltrates in PCP, reticulonodular patterns in TB or fungal infections, hilar lymphadenopathy in TB or malignancy, lobar consolidation in bacterial pneumonia, or cavitary lesions in TB and necrotizing infections. A normal chest x-ray does not exclude PCP or TB.
Head CT may demonstrate multiple ring-enhancing lesions consistent with toxoplasmosis or CNS lymphoma, or nonenhancing subcortical lesions suggestive of progressive multifocal leukoencephalopathy.
Abdominal and pelvic CT imaging may reveal splenomegaly, intestinal perforation or obstruction, biliary disease, or pancreatitis related to infection, malignancy, or medications.
Differential Diagnosis
Pulmonary complaints may represent pulmonary embolism, pulmonary hypertension, TB, bacterial, viral, or fungal pneumonia, malignancy, or lymphocytic interstitial pneumonitis.
Neurologic symptoms raise concern for neurosyphilis, viral encephalitis, toxoplasmosis, CNS lymphoma, meningitis, stroke, metabolic encephalopathy, or progressive multifocal leukoencephalopathy.
Cardiac presentations include cardiomyopathy, myocarditis, pericarditis, endocarditis, acute coronary syndrome, or pericardial effusion.
Oral and esophageal symptoms may result from candidiasis, viral infections, bacterial disease, autoimmune conditions, or malignancy.
Chronic diarrhea, hepatomegaly, and renal dysfunction have broad infectious, metabolic, medication-related, and neoplastic etiologies in HIV-infected patients.
Treatment
Emergency Department Management
Patients appearing toxic or with rapidly progressive illness should receive empiric antibiotics in the ED. Initiation of antiretroviral therapy is recommended for patients with low CD4 counts, high viral loads, pregnancy, AIDS-defining illnesses, or HIV-associated nephropathy.
Highly active antiretroviral therapy (HAART) typically consists of triple therapy using combinations of non-nucleoside reverse transcriptase inhibitors, protease inhibitors, and nucleoside reverse transcriptase inhibitors.
Post-exposure prophylaxis should begin within 2 hours of exposure when possible and continue for 4 weeks, with two-drug regimens for most exposures and expanded three-drug regimens for high-risk cases.
Specific opportunistic infections require targeted therapy, including pyrimethamine-based regimens for toxoplasmosis, amphotericin B with flucytosine for cryptococcal meningitis, ganciclovir for CMV retinitis, fluconazole for esophageal candidiasis, clarithromycin-based therapy for MAC, trimethoprim-sulfamethoxazole for PCP with adjunctive steroids when hypoxemia is present, and plasmapheresis for acute HIV-related demyelinating neuropathy.
Medication-Related Considerations
Antiretroviral therapy is associated with numerous potential adverse effects including hypersensitivity reactions, pancreatitis, peripheral neuropathy, nephrolithiasis, hepatotoxicity, lactic acidosis, Stevens–Johnson syndrome, hemolytic anemia, neuropsychiatric effects, metabolic derangements, cardiomyopathy, and hematologic abnormalities.
Follow-Up And Disposition
Admission Criteria
Indications for hospitalization include unexplained fever with neurologic involvement, hypoxemia, suspected acute coronary syndrome, pericardial effusion, suspected bacterial pneumonia or TB, new neurologic deficits or seizures, hemodynamic instability, inability to ambulate or tolerate oral intake, and severe diarrhea with dehydration.
Discharge Criteria
Patients may be discharged if they can maintain oral intake, ambulate, perform self-care, and have reliable follow-up.
Referral Considerations
All patients should be referred to an HIV specialist for initiation and management of antiretroviral therapy. Screening for depression and psychiatric referral are essential to ensure treatment adherence. Patients with concerning symptoms should be referred for malignancy evaluation.
Key Clinical Insights And Common Pitfalls
Immune reconstitution inflammatory syndrome typically occurs within 8 weeks of initiating HAART. Occupational exposure carries a low but real risk of seroconversion. Patients on HAART have increased risk for metabolic disease and acute coronary syndromes. Exercise-induced desaturation may aid in diagnosing PCP when imaging is normal. HIV is an independent risk factor for COPDukar
COPD, pulmonary hypertension, stroke, venous thromboembolism, thrombotic thrombocytopenic purpura, osteoporosis, and osteonecrosis of the hip.
- Published on
Emergency And Acute Medicine – Hordeolum And Chalazion
Basics
Clinical Overview
Hordeola and chalazia arise from inflammatory processes involving the eyelid glands along the lash margin. A hordeolum represents an acute obstruction of an eyelid gland that leads to inflammation and often abscess formation. A chalazion is the chronic consequence of retained, thickened glandular secretions, producing a granulomatous inflammatory response.
A hordeolum develops when outflow obstruction affects one or more eyelid glands. Secondary bacterial infection may occur, and progression to a localized abscess or, less commonly, periorbital cellulitis is possible.
A chalazion reflects chronic granulomatous inflammation of a meibomian gland. Blockage of the duct at the eyelid margin may cause glandular contents to leak into surrounding eyelid tissue, triggering a lipogranulomatous reaction. Chalazia are occasionally secondarily infected and may evolve from an incompletely resolved internal hordeolum.
Etiology And Risk Factors
Hordeola may become secondarily infected, most commonly with Staphylococcus species. Predisposing conditions include meibomian gland dysfunction, chronic blepharitis, rosacea, and a history of prior hordeola.
Diagnosis
Clinical Features
A hordeolum typically presents acutely as a red, tender, painful, swollen lesion along the eyelid margin. Lesions are usually solitary but may be multiple or recurrent. Inflammation is well localized, and presentation varies depending on the gland involved.
An external hordeolum (stye) originates from obstruction of superficial sebaceous or sweat glands with ducts between the eyelashes. It appears as an exquisitely tender lesion that often points anteriorly.
An internal hordeolum arises from obstruction of deeper sebaceous glands whose ducts open on the inner eyelid margin. It presents as a painful, palpable mass within the lid, may cause foreign body sensation or visual disturbance, and is often larger and more inflamed than external lesions. It may drain internally toward the conjunctiva or externally through the skin.
Hordeola are localized processes without systemic symptoms but may be complicated by conjunctivitis or periorbital cellulitis.
A chalazion presents as a firm, well-circumscribed, nontender or minimally tender eyelid nodule that is typically long-standing and noninflamed. Symptoms usually relate to its size and location, including cosmetic distortion, obstruction of the visual field, pressure on the globe, or corneal drying or injury from exposure. Chalazia are nonacute and nonemergent unless significant corneal compromise or globe pressure occurs.
History
Hordeolum is characterized by sudden onset of a well-localized, painful eyelid mass without systemic symptoms.
Physical Examination
Findings include focal tenderness and inflammation of an external or internal eyelid gland, with minimal surrounding edema. An abscess may point at the lash line, the palpebral conjunctiva, or externally through the skin.
Essential Evaluation
A complete ophthalmologic assessment should be performed, including slit-lamp examination and corneal evaluation. Patients should be assessed for associated cellulitis or systemic involvement.
For hordeola, identifying the gland of origin is important.
For chalazia, evaluation should focus on whether the lesion causes corneal exposure or injury.
Diagnostic Studies And Interpretation
Laboratory Testing
Cultures of expressed or draining material are rarely useful and typically do not alter management.
Differential Diagnosis
Blepharitis
Dacryocystitis
Dacryoadenitis
Pyogenic granuloma
Sebaceous cell carcinoma
Basal cell carcinoma
Squamous cell carcinoma
Management
Emergency Department Care
For hordeola, treatment focuses on relieving obstruction and preventing abscess formation. Warm compresses applied for 15 minutes, 4–6 times daily, are first-line therapy. Gentle massage of the lesion may help express obstructed material.
In rare severe cases, incision and drainage of an internal hordeolum may be required and is typically performed by an ophthalmologist. When drainage is toward the conjunctiva, a vertical incision is preferred to minimize meibomian gland injury and reduce the risk of corneal scarring. External skin incisions are rarely indicated; if required, a horizontal incision is used. In select severe external hordeola, removal of a single involved eyelash may be helpful.
Chalazia generally require no emergent intervention. Management is typically referral-based, with ophthalmologic options including incision and curettage or intralesional steroid injection. Lubricating eye drops may provide symptomatic relief.
Medications
Ophthalmic lubricating drops may be used as needed for comfort.
Follow-Up And Disposition
Discharge Criteria
Patients may be discharged if there is no evidence of secondary complications such as significant periorbital cellulitis with systemic symptoms.
Referral Considerations
Urgent ophthalmology consultation should be obtained if incision and drainage of an internal hordeolum is considered. Chalazia should be referred for definitive ophthalmologic management.
Follow-Up Recommendations
Ophthalmology follow-up within 1–2 days is recommended to assess response to conservative therapy. Most symptoms resolve completely within 1–2 weeks.
Key Points And Common Pitfalls
Conservative management with warm compresses and gentle massage is the standard of care for hordeola, with most cases resolving without further intervention.
Emergent incision and drainage is rarely necessary and carries risks including corneal injury, fistula formation, and cosmetic complications; ophthalmology consultation is preferred.
Chalazia do not require emergent treatment and are best managed with outpatient referral.
Basics
Clinical Overview
Hordeola and chalazia arise from inflammatory processes involving the eyelid glands along the lash margin. A hordeolum represents an acute obstruction of an eyelid gland that leads to inflammation and often abscess formation. A chalazion is the chronic consequence of retained, thickened glandular secretions, producing a granulomatous inflammatory response.
A hordeolum develops when outflow obstruction affects one or more eyelid glands. Secondary bacterial infection may occur, and progression to a localized abscess or, less commonly, periorbital cellulitis is possible.
A chalazion reflects chronic granulomatous inflammation of a meibomian gland. Blockage of the duct at the eyelid margin may cause glandular contents to leak into surrounding eyelid tissue, triggering a lipogranulomatous reaction. Chalazia are occasionally secondarily infected and may evolve from an incompletely resolved internal hordeolum.
Etiology And Risk Factors
Hordeola may become secondarily infected, most commonly with Staphylococcus species. Predisposing conditions include meibomian gland dysfunction, chronic blepharitis, rosacea, and a history of prior hordeola.
Diagnosis
Clinical Features
A hordeolum typically presents acutely as a red, tender, painful, swollen lesion along the eyelid margin. Lesions are usually solitary but may be multiple or recurrent. Inflammation is well localized, and presentation varies depending on the gland involved.
An external hordeolum (stye) originates from obstruction of superficial sebaceous or sweat glands with ducts between the eyelashes. It appears as an exquisitely tender lesion that often points anteriorly.
An internal hordeolum arises from obstruction of deeper sebaceous glands whose ducts open on the inner eyelid margin. It presents as a painful, palpable mass within the lid, may cause foreign body sensation or visual disturbance, and is often larger and more inflamed than external lesions. It may drain internally toward the conjunctiva or externally through the skin.
Hordeola are localized processes without systemic symptoms but may be complicated by conjunctivitis or periorbital cellulitis.
A chalazion presents as a firm, well-circumscribed, nontender or minimally tender eyelid nodule that is typically long-standing and noninflamed. Symptoms usually relate to its size and location, including cosmetic distortion, obstruction of the visual field, pressure on the globe, or corneal drying or injury from exposure. Chalazia are nonacute and nonemergent unless significant corneal compromise or globe pressure occurs.
History
Hordeolum is characterized by sudden onset of a well-localized, painful eyelid mass without systemic symptoms.
Physical Examination
Findings include focal tenderness and inflammation of an external or internal eyelid gland, with minimal surrounding edema. An abscess may point at the lash line, the palpebral conjunctiva, or externally through the skin.
Essential Evaluation
A complete ophthalmologic assessment should be performed, including slit-lamp examination and corneal evaluation. Patients should be assessed for associated cellulitis or systemic involvement.
For hordeola, identifying the gland of origin is important.
For chalazia, evaluation should focus on whether the lesion causes corneal exposure or injury.
Diagnostic Studies And Interpretation
Laboratory Testing
Cultures of expressed or draining material are rarely useful and typically do not alter management.
Differential Diagnosis
Blepharitis
Dacryocystitis
Dacryoadenitis
Pyogenic granuloma
Sebaceous cell carcinoma
Basal cell carcinoma
Squamous cell carcinoma
Management
Emergency Department Care
For hordeola, treatment focuses on relieving obstruction and preventing abscess formation. Warm compresses applied for 15 minutes, 4–6 times daily, are first-line therapy. Gentle massage of the lesion may help express obstructed material.
In rare severe cases, incision and drainage of an internal hordeolum may be required and is typically performed by an ophthalmologist. When drainage is toward the conjunctiva, a vertical incision is preferred to minimize meibomian gland injury and reduce the risk of corneal scarring. External skin incisions are rarely indicated; if required, a horizontal incision is used. In select severe external hordeola, removal of a single involved eyelash may be helpful.
Chalazia generally require no emergent intervention. Management is typically referral-based, with ophthalmologic options including incision and curettage or intralesional steroid injection. Lubricating eye drops may provide symptomatic relief.
Medications
Ophthalmic lubricating drops may be used as needed for comfort.
Follow-Up And Disposition
Discharge Criteria
Patients may be discharged if there is no evidence of secondary complications such as significant periorbital cellulitis with systemic symptoms.
Referral Considerations
Urgent ophthalmology consultation should be obtained if incision and drainage of an internal hordeolum is considered. Chalazia should be referred for definitive ophthalmologic management.
Follow-Up Recommendations
Ophthalmology follow-up within 1–2 days is recommended to assess response to conservative therapy. Most symptoms resolve completely within 1–2 weeks.
Key Points And Common Pitfalls
Conservative management with warm compresses and gentle massage is the standard of care for hordeola, with most cases resolving without further intervention.
Emergent incision and drainage is rarely necessary and carries risks including corneal injury, fistula formation, and cosmetic complications; ophthalmology consultation is preferred.
Chalazia do not require emergent treatment and are best managed with outpatient referral.
- Published on
Emergency And Acute Medicine – Horner’s Syndrome
Basics
Condition Summary
Horner’s syndrome results from unilateral interruption of the sympathetic pathway to the eye and face. Loss of sympathetic innervation produces a characteristic triad. Relaxation of the upper and lower eyelid retractors leads to ptosis (drooping of the eyelid). Disruption of pupillary dilator fibers causes miosis, with unopposed pupillary constriction. Loss of sympathetic input to facial sweat glands results in anhidrosis on the affected side.
Etiology And Causes
In approximately 40% of cases, no cause is identified. Neoplastic disease, particularly lung tumors or metastases to cervical lymph nodes, may interrupt preganglionic sympathetic fibers between the thoracic sympathetic trunk and the superior cervical ganglion.
Trauma, including penetrating neck injuries, may directly damage sympathetic fibers. Pneumothorax, especially tension pneumothorax, can cause traction on the sympathetic chain due to mediastinal shift.
Infiltration or infection of cervical lymph nodes, such as from sarcoidosis or tuberculosis, may also disrupt the pathway.
Vascular etiologies include migraine or cluster headaches and carotid artery dissection. Lateral medullary (Wallenberg) infarction may present with Horner’s syndrome accompanied by vertigo and ataxia, which can overshadow ocular findings. Cavernous sinus thrombosis may produce partial Horner-like features along with headache, eye pain, ocular motor palsies, chemosis, and proptosis.
Pediatric Considerations
Congenital or hereditary Horner’s syndrome may present with heterochromia iridis, characterized by a lighter (often blue) iris on the affected side and a darker iris on the unaffected side. Birth trauma can injure the sympathetic chain. New-onset Horner’s syndrome in a child warrants evaluation for an underlying tumor, particularly neuroblastoma.
Diagnosis
Clinical Features
Horner’s syndrome is defined by a classic triad: mild ptosis on the affected side, miosis with pupillary asymmetry of at least 1 mm, and ipsilateral facial anhidrosis. The clinical importance lies in its association with potentially serious underlying conditions rather than the ocular findings alone.
History
History should focus on conditions that predispose to Horner’s syndrome or its causes, including malignancy, vascular disease, and trauma. Minor trauma may precede carotid artery dissection. Cardiovascular risk factors and relevant exposures should be assessed. The presence of pain, particularly neck or facial pain, raises concern for carotid dissection.
Alert
Acute onset Horner’s syndrome associated with neck or facial pain should be presumed to be due to carotid artery dissection until proven otherwise, as approximately half of internal carotid dissections present with a painful Horner’s syndrome.
Physical Examination
A focused neurologic examination is essential to confirm Horner’s syndrome and identify additional neurologic deficits. The general examination should look for signs of associated conditions such as tumors, trauma, or pulmonary pathology.
Essential Evaluation
Assessment includes a thorough history and neurologic examination. A chest radiograph is recommended to screen for apical lung tumors or pneumothorax.
Diagnostic Studies And Interpretation
Provocative Testing
Pharmacologic confirmation can be achieved with ocular cocaine testing. One drop of 5% cocaine solution (2.5% in children) is instilled into each eye. Failure of the affected pupil to dilate compared with the unaffected pupil, resulting in increased anisocoria after approximately one hour, confirms a sympathetic denervation lesion.
Laboratory Testing
Laboratory studies are not useful for diagnosing Horner’s syndrome itself but may be indicated to evaluate suspected underlying conditions.
Imaging
Chest radiography is often indicated due to the association between Horner’s syndrome and intrathoracic pathology. CT or MRI of the head, neck, or chest should be guided by clinical findings.
When carotid artery dissection is suspected, CT angiography or MR angiography of the head and neck is appropriate, with the lesion expected on the same side as the Horner’s syndrome. If stroke is suspected, at minimum a noncontrast CT of the brain is required to exclude hemorrhage. Patients within the thrombolysis window should undergo emergent imaging per local stroke protocols.
Diagnostic Procedures
Ocular tonometry should be performed if acute glaucoma is a consideration.
Differential Diagnosis
Elevated intracranial pressure, typically associated with headache and altered consciousness
Physiologic anisocoria (pseudo–Horner’s syndrome), which is common and yields a negative cocaine test
Topical medications or exposures causing miosis
Migraine or cluster headache
Glaucoma, inflammatory eye disease, or ocular trauma
Management
Prehospital Considerations
Horner’s syndrome itself is benign, but associated life-threatening conditions must be rapidly identified. Increased intracranial pressure or tension pneumothorax requires immediate intervention. Patients with suspected acute stroke should be transported to a designated stroke center when feasible.
Initial Stabilization
If elevated intracranial pressure is suspected, initiate airway protection and intracranial pressure–lowering measures, including osmotic therapy. Tension pneumothorax requires immediate needle decompression followed by chest tube placement.
Emergency Department Care
Horner’s syndrome does not require direct treatment in the ED. Management is directed at identifying and treating the underlying cause.
Medications
Cocaine ophthalmic solution (5% in adults, 2.5% in children) is used diagnostically, with one drop placed in each eye.
Follow-Up And Disposition
Admission Criteria
Admission is not required for isolated Horner’s syndrome but may be necessary for associated conditions such as stroke, carotid dissection, malignancy, or infection.
Discharge Criteria
Stable patients with isolated Horner’s syndrome may be discharged with appropriate outpatient follow-up once emergent causes, particularly carotid dissection and stroke, have been reasonably excluded.
Follow-Up Recommendations
Ongoing evaluation often requires coordination with neurology and ophthalmology to identify the underlying etiology and guide further management.
Key Points And Common Pitfalls
The primary importance of Horner’s syndrome lies in recognizing its potential underlying causes. Failure to evaluate for serious etiologies such as carotid artery dissection, stroke, or malignancy is a critical pitfall.
Basics
Condition Summary
Horner’s syndrome results from unilateral interruption of the sympathetic pathway to the eye and face. Loss of sympathetic innervation produces a characteristic triad. Relaxation of the upper and lower eyelid retractors leads to ptosis (drooping of the eyelid). Disruption of pupillary dilator fibers causes miosis, with unopposed pupillary constriction. Loss of sympathetic input to facial sweat glands results in anhidrosis on the affected side.
Etiology And Causes
In approximately 40% of cases, no cause is identified. Neoplastic disease, particularly lung tumors or metastases to cervical lymph nodes, may interrupt preganglionic sympathetic fibers between the thoracic sympathetic trunk and the superior cervical ganglion.
Trauma, including penetrating neck injuries, may directly damage sympathetic fibers. Pneumothorax, especially tension pneumothorax, can cause traction on the sympathetic chain due to mediastinal shift.
Infiltration or infection of cervical lymph nodes, such as from sarcoidosis or tuberculosis, may also disrupt the pathway.
Vascular etiologies include migraine or cluster headaches and carotid artery dissection. Lateral medullary (Wallenberg) infarction may present with Horner’s syndrome accompanied by vertigo and ataxia, which can overshadow ocular findings. Cavernous sinus thrombosis may produce partial Horner-like features along with headache, eye pain, ocular motor palsies, chemosis, and proptosis.
Pediatric Considerations
Congenital or hereditary Horner’s syndrome may present with heterochromia iridis, characterized by a lighter (often blue) iris on the affected side and a darker iris on the unaffected side. Birth trauma can injure the sympathetic chain. New-onset Horner’s syndrome in a child warrants evaluation for an underlying tumor, particularly neuroblastoma.
Diagnosis
Clinical Features
Horner’s syndrome is defined by a classic triad: mild ptosis on the affected side, miosis with pupillary asymmetry of at least 1 mm, and ipsilateral facial anhidrosis. The clinical importance lies in its association with potentially serious underlying conditions rather than the ocular findings alone.
History
History should focus on conditions that predispose to Horner’s syndrome or its causes, including malignancy, vascular disease, and trauma. Minor trauma may precede carotid artery dissection. Cardiovascular risk factors and relevant exposures should be assessed. The presence of pain, particularly neck or facial pain, raises concern for carotid dissection.
Alert
Acute onset Horner’s syndrome associated with neck or facial pain should be presumed to be due to carotid artery dissection until proven otherwise, as approximately half of internal carotid dissections present with a painful Horner’s syndrome.
Physical Examination
A focused neurologic examination is essential to confirm Horner’s syndrome and identify additional neurologic deficits. The general examination should look for signs of associated conditions such as tumors, trauma, or pulmonary pathology.
Essential Evaluation
Assessment includes a thorough history and neurologic examination. A chest radiograph is recommended to screen for apical lung tumors or pneumothorax.
Diagnostic Studies And Interpretation
Provocative Testing
Pharmacologic confirmation can be achieved with ocular cocaine testing. One drop of 5% cocaine solution (2.5% in children) is instilled into each eye. Failure of the affected pupil to dilate compared with the unaffected pupil, resulting in increased anisocoria after approximately one hour, confirms a sympathetic denervation lesion.
Laboratory Testing
Laboratory studies are not useful for diagnosing Horner’s syndrome itself but may be indicated to evaluate suspected underlying conditions.
Imaging
Chest radiography is often indicated due to the association between Horner’s syndrome and intrathoracic pathology. CT or MRI of the head, neck, or chest should be guided by clinical findings.
When carotid artery dissection is suspected, CT angiography or MR angiography of the head and neck is appropriate, with the lesion expected on the same side as the Horner’s syndrome. If stroke is suspected, at minimum a noncontrast CT of the brain is required to exclude hemorrhage. Patients within the thrombolysis window should undergo emergent imaging per local stroke protocols.
Diagnostic Procedures
Ocular tonometry should be performed if acute glaucoma is a consideration.
Differential Diagnosis
Elevated intracranial pressure, typically associated with headache and altered consciousness
Physiologic anisocoria (pseudo–Horner’s syndrome), which is common and yields a negative cocaine test
Topical medications or exposures causing miosis
Migraine or cluster headache
Glaucoma, inflammatory eye disease, or ocular trauma
Management
Prehospital Considerations
Horner’s syndrome itself is benign, but associated life-threatening conditions must be rapidly identified. Increased intracranial pressure or tension pneumothorax requires immediate intervention. Patients with suspected acute stroke should be transported to a designated stroke center when feasible.
Initial Stabilization
If elevated intracranial pressure is suspected, initiate airway protection and intracranial pressure–lowering measures, including osmotic therapy. Tension pneumothorax requires immediate needle decompression followed by chest tube placement.
Emergency Department Care
Horner’s syndrome does not require direct treatment in the ED. Management is directed at identifying and treating the underlying cause.
Medications
Cocaine ophthalmic solution (5% in adults, 2.5% in children) is used diagnostically, with one drop placed in each eye.
Follow-Up And Disposition
Admission Criteria
Admission is not required for isolated Horner’s syndrome but may be necessary for associated conditions such as stroke, carotid dissection, malignancy, or infection.
Discharge Criteria
Stable patients with isolated Horner’s syndrome may be discharged with appropriate outpatient follow-up once emergent causes, particularly carotid dissection and stroke, have been reasonably excluded.
Follow-Up Recommendations
Ongoing evaluation often requires coordination with neurology and ophthalmology to identify the underlying etiology and guide further management.
Key Points And Common Pitfalls
The primary importance of Horner’s syndrome lies in recognizing its potential underlying causes. Failure to evaluate for serious etiologies such as carotid artery dissection, stroke, or malignancy is a critical pitfall.
- Published on
Infectious Diseases and Microbiology: Animal Bite and Clenched-Fist Injury–Related Infections
Basics
Description and Definition
Animal bites produce puncture wounds, scratches, or lacerations with variable tissue injury, while clenched-fist injuries and human bites result from tooth penetration and inoculation of oral flora into the skin.
Approach to the Patient
Immediate assessment focuses on identifying life- or limb-threatening injury, hemorrhage, and neurovascular compromise with a detailed neurologic and vascular examination of the affected area. Patients showing signs of shock require prompt hemodynamic stabilization, empiric antibiotics, and possible surgical consultation. It is critical to determine whether the bite involves a venomous species and to thoroughly explore wounds for deep structural injury involving tendons, vessels, nerves, joints, or organs, as well as retained foreign bodies such as teeth. Copious irrigation with sterile water or saline and meticulous debridement of devitalized tissue and debris are essential and often require local anesthesia. Wounds should be kept moist with topical antibacterial agents and covered to reduce microbial load. After adequate debridement and high-pressure irrigation, select wounds, including some on the hands and feet, may undergo primary closure, but most animal and human bite injuries should heal by secondary intention. Close follow-up is mandatory due to high infection risk. Imaging with radiography, CT, or MRI may be required to detect foreign bodies or deep injury. Bites to the hands and feet frequently warrant surgical evaluation because deep-space and tendon sheath infections can rapidly progress to sepsis and permanent damage. Tetanus and rabies prophylaxis must be addressed, and suspicious human bites should raise concern for child or domestic abuse.
Epidemiology
In the United States, approximately 40% of households own dogs and about one-third own cats. Children are the most common victims of animal bites and frequently sustain injuries to the head and neck. Around 2.5% of dog bites show clinical infection at the time of presentation.
Risk Factors
Severe outcomes are more likely in children due to exposure of the head, neck, and upper torso; in veterinarians and animal handlers; in immunocompromised individuals including those with HIV, malignancy, chemotherapy exposure, steroid use, asplenia, or liver disease; and in patients with diabetes mellitus who have impaired wound healing from vascular disease and neuropathy.
Etiology
Bite-related infections are typically polymicrobial, involving aerobic and anaerobic organisms derived from the biter’s oral flora and the victim’s skin flora, with methicillin-resistant Staphylococcus aureus commonly introduced from human skin. Dog bites are frequently associated with Capnocytophaga species and Pasteurella canis, while cat bites commonly yield Pasteurella multocida. Other zoonotic pathogens include Bartonella henselae, Francisella tularensis, and Leptospira species. Additional aerobic organisms include streptococci, staphylococci, Moraxella, and Neisseria, with anaerobes such as Fusobacterium, Bacteroides, Porphyromonas, and Prevotella contributing to mixed infections. Human bites often involve Streptococcus species, Staphylococcus aureus, Eikenella corrodens, Haemophilus influenzae, and anaerobes including Fusobacterium nucleatum, Prevotella, Porphyromonas, Peptococcus, and Peptostreptococcus. Aquatic animal bites may introduce Aeromonas, Vibrio species, Erysipelothrix, or Mycobacterium marinum. Rodents and rodent predators can transmit Streptobacillus moniliformis or Spirillum species, causing rat-bite fever.
Diagnosis
History
The history should clarify events surrounding the injury, characteristics of the biting animal including species, venom potential, vaccination status, and availability for rabies observation, as well as the patient’s immunization history, antibiotic allergies, liver disease, immunocompromised state, and other factors predisposing to severe infection.
Physical Examination
Assessment includes vital signs, a complete systemic examination, full exposure of the injured area, and secondary skin evaluation for occult trauma. Careful inspection determines wound depth and involvement of bone, joint, or tendon, with attention to tendon sheath pain, spreading erythema, lymphadenopathy, exudate, purulence, or fluctuance. A focused neurologic and vascular exam of the affected region is mandatory. Presentations range from isolated minor wounds to multiple severe injuries. Systemic toxicity, hemorrhage, and septic shock represent emergencies. Delayed complications include osteomyelitis, while meningitis, peritonitis, and endocarditis are rare manifestations of disseminated infection. Isolated ecchymosis or hematoma without skin break may indicate venom-related tissue reaction.
Diagnostic Tests and Interpretation
Laboratory Studies
Evaluation includes complete blood count, electrolytes, renal and liver function tests, and at least two sets of aerobic and anaerobic blood cultures obtained before antibiotics, with prolonged incubation for slow-growing oral flora. Gram stain and wound cultures may assist but are often nonspecific. Pasteurella species appear as gram-negative bacilli growing on blood or chocolate agar, and MRSA is commonly present from host skin contamination
.
Imaging
Plain radiographs assess for retained foreign bodies such as tooth fragments, while CT or MRI better define hemorrhage, abscess formation, tendon sheath involvement, and osteomyelitis.
Treatment
Medications
Tetanus and rabies prophylaxis must always be considered. Prophylactic antibiotics are recommended for most bites except superficial injuries, guided by the expected oral flora of the animal. First-line empiric therapy for human, dog, and cat bites is a beta-lactam/beta-lactamase inhibitor such as amoxicillin-clavulanate. Alternatives include combinations of trimethoprim-sulfamethoxazole, penicillin, fluoroquinolones, or doxycycline with metronidazole or clindamycin, noting that clindamycin and trimethoprim-sulfamethoxazole provide MRSA coverage. Intravenous therapy is required for systemic illness. Venomous snakebites require antivenom and ceftriaxone.
Ongoing Care and Follow-Up
Wounds require daily inspection and dressing changes, with a low threshold for urgent surgical intervention when deep penetration, foreign bodies, or tendon sheath involvement are suspected. Patients must be educated about warning signs of infection prior to discharge, and timely tetanus or rabies immunization may be lifesaving.
Basics
Description and Definition
Animal bites produce puncture wounds, scratches, or lacerations with variable tissue injury, while clenched-fist injuries and human bites result from tooth penetration and inoculation of oral flora into the skin.
Approach to the Patient
Immediate assessment focuses on identifying life- or limb-threatening injury, hemorrhage, and neurovascular compromise with a detailed neurologic and vascular examination of the affected area. Patients showing signs of shock require prompt hemodynamic stabilization, empiric antibiotics, and possible surgical consultation. It is critical to determine whether the bite involves a venomous species and to thoroughly explore wounds for deep structural injury involving tendons, vessels, nerves, joints, or organs, as well as retained foreign bodies such as teeth. Copious irrigation with sterile water or saline and meticulous debridement of devitalized tissue and debris are essential and often require local anesthesia. Wounds should be kept moist with topical antibacterial agents and covered to reduce microbial load. After adequate debridement and high-pressure irrigation, select wounds, including some on the hands and feet, may undergo primary closure, but most animal and human bite injuries should heal by secondary intention. Close follow-up is mandatory due to high infection risk. Imaging with radiography, CT, or MRI may be required to detect foreign bodies or deep injury. Bites to the hands and feet frequently warrant surgical evaluation because deep-space and tendon sheath infections can rapidly progress to sepsis and permanent damage. Tetanus and rabies prophylaxis must be addressed, and suspicious human bites should raise concern for child or domestic abuse.
Epidemiology
In the United States, approximately 40% of households own dogs and about one-third own cats. Children are the most common victims of animal bites and frequently sustain injuries to the head and neck. Around 2.5% of dog bites show clinical infection at the time of presentation.
Risk Factors
Severe outcomes are more likely in children due to exposure of the head, neck, and upper torso; in veterinarians and animal handlers; in immunocompromised individuals including those with HIV, malignancy, chemotherapy exposure, steroid use, asplenia, or liver disease; and in patients with diabetes mellitus who have impaired wound healing from vascular disease and neuropathy.
Etiology
Bite-related infections are typically polymicrobial, involving aerobic and anaerobic organisms derived from the biter’s oral flora and the victim’s skin flora, with methicillin-resistant Staphylococcus aureus commonly introduced from human skin. Dog bites are frequently associated with Capnocytophaga species and Pasteurella canis, while cat bites commonly yield Pasteurella multocida. Other zoonotic pathogens include Bartonella henselae, Francisella tularensis, and Leptospira species. Additional aerobic organisms include streptococci, staphylococci, Moraxella, and Neisseria, with anaerobes such as Fusobacterium, Bacteroides, Porphyromonas, and Prevotella contributing to mixed infections. Human bites often involve Streptococcus species, Staphylococcus aureus, Eikenella corrodens, Haemophilus influenzae, and anaerobes including Fusobacterium nucleatum, Prevotella, Porphyromonas, Peptococcus, and Peptostreptococcus. Aquatic animal bites may introduce Aeromonas, Vibrio species, Erysipelothrix, or Mycobacterium marinum. Rodents and rodent predators can transmit Streptobacillus moniliformis or Spirillum species, causing rat-bite fever.
Diagnosis
History
The history should clarify events surrounding the injury, characteristics of the biting animal including species, venom potential, vaccination status, and availability for rabies observation, as well as the patient’s immunization history, antibiotic allergies, liver disease, immunocompromised state, and other factors predisposing to severe infection.
Physical Examination
Assessment includes vital signs, a complete systemic examination, full exposure of the injured area, and secondary skin evaluation for occult trauma. Careful inspection determines wound depth and involvement of bone, joint, or tendon, with attention to tendon sheath pain, spreading erythema, lymphadenopathy, exudate, purulence, or fluctuance. A focused neurologic and vascular exam of the affected region is mandatory. Presentations range from isolated minor wounds to multiple severe injuries. Systemic toxicity, hemorrhage, and septic shock represent emergencies. Delayed complications include osteomyelitis, while meningitis, peritonitis, and endocarditis are rare manifestations of disseminated infection. Isolated ecchymosis or hematoma without skin break may indicate venom-related tissue reaction.
Diagnostic Tests and Interpretation
Laboratory Studies
Evaluation includes complete blood count, electrolytes, renal and liver function tests, and at least two sets of aerobic and anaerobic blood cultures obtained before antibiotics, with prolonged incubation for slow-growing oral flora. Gram stain and wound cultures may assist but are often nonspecific. Pasteurella species appear as gram-negative bacilli growing on blood or chocolate agar, and MRSA is commonly present from host skin contamination
.
Imaging
Plain radiographs assess for retained foreign bodies such as tooth fragments, while CT or MRI better define hemorrhage, abscess formation, tendon sheath involvement, and osteomyelitis.
Treatment
Medications
Tetanus and rabies prophylaxis must always be considered. Prophylactic antibiotics are recommended for most bites except superficial injuries, guided by the expected oral flora of the animal. First-line empiric therapy for human, dog, and cat bites is a beta-lactam/beta-lactamase inhibitor such as amoxicillin-clavulanate. Alternatives include combinations of trimethoprim-sulfamethoxazole, penicillin, fluoroquinolones, or doxycycline with metronidazole or clindamycin, noting that clindamycin and trimethoprim-sulfamethoxazole provide MRSA coverage. Intravenous therapy is required for systemic illness. Venomous snakebites require antivenom and ceftriaxone.
Ongoing Care and Follow-Up
Wounds require daily inspection and dressing changes, with a low threshold for urgent surgical intervention when deep penetration, foreign bodies, or tendon sheath involvement are suspected. Patients must be educated about warning signs of infection prior to discharge, and timely tetanus or rabies immunization may be lifesaving.
- Published on
Emergency And Acute Medicine – Humerus Fracture
Basics
Overview And Definitions
Humerus fractures include injuries to the proximal humerus and the humeral shaft. Proximal humeral fractures are commonly categorized as nondisplaced, displaced, or fracture–dislocations and account for approximately 5% of all fractures. Incidence increases with age, with a female-to-male ratio of 4:1, and the majority of patients are older than 60 years. These fractures represent the third most common osteoporotic fracture, following hip and distal radius fractures.
The Neer classification system is widely used for proximal humeral fractures and describes injuries based on the number and location of fracture fragments. Fractures are classified as 2-, 3-, or 4-part injuries involving the anatomic neck, surgical neck, greater tuberosity, or lesser tuberosity. Fracture–dislocations are also included in this system.
Humeral shaft fractures account for less than 3% of all fractures and may be spiral, oblique, or transverse in pattern. The AO classification categorizes these injuries as simple, wedge, or comminuted (complex) fractures.
Mechanisms And Causes
Proximal humeral fractures most commonly result from low-energy mechanisms, particularly falls, often onto an outstretched hand. Less frequently, they occur due to violent muscle contraction during seizures or electrical shock, or from higher-energy trauma.
Humeral shaft fractures are typically caused by high-energy direct trauma, either penetrating or blunt, or by bending forces. Less commonly, they result from falls or repetitive stress injuries, such as those seen in throwing athletes.
Diagnosis
Clinical Features
Patients usually present with pain, swelling, and localized tenderness over the humerus. There is often difficulty initiating active movement, and the arm may be held tightly against the chest. Shortening of the extremity, crepitus, ecchymosis, and signs of neurovascular compromise may be present.
History
Key historical elements include the mechanism of injury, patient age, fall risk, underlying malignancy, and associated injuries.
Physical Examination
A complete examination of the affected extremity is essential. Inspection should assess for deformity, shortening, swelling, and open wounds. Range of motion at the shoulder and elbow should be evaluated as tolerated. A detailed neurovascular examination is mandatory.
Essential Evaluation
Individual nerve function must be assessed, with special attention to the radial nerve, particularly in midshaft fractures. Median, ulnar, axillary (sensation over the lateral shoulder), and musculocutaneous nerves (sensation over the lateral forearm) should also be evaluated.
Vascular assessment includes palpation of radial, ulnar, and brachial pulses and confirmation of adequate capillary refill. Imaging is required to define the extent and type of injury.
Pediatric Considerations
Humerus fractures are most common in children younger than 3 years or older than 12 years. Neonatal fractures may occur due to birth trauma, especially in infants weighing more than 4.5 kg or in breech deliveries, and may present as pseudoparalysis.
In older children, mechanisms are similar to adults. The thicker periosteum in children often limits displacement of humeral shaft fractures. Proximal humeral Salter–Harris type I injuries should be suspected when radiographs are normal but significant pain persists, with Salter–Harris type II being most common. Nonaccidental trauma must be considered, particularly in children younger than 3 years, especially with suspicious fracture patterns.
Diagnostic Studies And Interpretation
Imaging
Plain radiographs are the initial imaging modality. Proximal humeral fractures require at least three views: anteroposterior, lateral, and axillary. The axillary view is critical for evaluating tuberosity displacement, glenoid involvement, and humeral head alignment.
Humeral shaft fractures require anteroposterior and lateral views of the entire humerus, including both the shoulder and elbow joints to rule out associated injuries.
CT scanning is useful in complex or comminuted proximal humeral fractures and in suspected fracture–dislocations, helping define fracture anatomy and surgical planning.
Differential Diagnosis
Acute hemorrhagic bursitis
Traumatic rotator cuff tear
Shoulder dislocation
Acromioclavicular joint separation
Calcific tendinitis
Contusion
Tendon rupture
Neurapraxia
Pathologic fracture
Management
Prehospital Care
Excessive movement of the injured arm should be avoided to prevent further neurovascular injury. Immobilization with a sling and swath is recommended, with rapid transport for patients exhibiting neurologic or vascular deficits.
Initial Stabilization
Primary and secondary trauma surveys should be performed to identify associated injuries. Immobilization helps reduce pain, prevent displacement, and minimize neurovascular injury. An axillary pad may improve comfort. Ice application helps limit swelling. Open fractures require sterile coverage, tetanus prophylaxis, and parenteral antibiotics.
Emergency Department Management
Adequate analgesia is essential, with narcotics administered orally, intramuscularly, or intravenously as first-line therapy.
Most proximal humeral fractures are single-part injuries and can be managed nonoperatively with sling and swath immobilization and early range-of-motion exercises. Displaced or multipart fractures should be described using the Neer classification. Fractures with more than 1 cm of displacement or more than 45 degrees of angulation are considered displaced and require orthopedic consultation.
Two-part fractures may often be managed nonoperatively after reduction, whereas three- and four-part fractures may require operative fixation or hemiarthroplasty, depending on patient age, comorbidities, and functional expectations. Emergent orthopedic consultation is indicated for open fractures, irreducible fracture–dislocations, or vascular compromise.
Most humeral shaft fractures can be managed nonoperatively without reduction. Up to 20 degrees of anterior angulation, 30 degrees of varus angulation, and 3 cm of shortening are generally well tolerated. Nondisplaced fractures may be treated with a coaptation splint, except for transverse fractures, which are better managed with a sling and swath. Displaced fractures may require a hanging cast under orthopedic guidance. Emergent consultation is required for neurovascular compromise, open fractures, segmental fractures, articular involvement, or a “floating elbow.”
Medications
Pain control is achieved primarily with narcotic analgesics. NSAIDs may be used as adjunctive therapy. Procedural sedation may be required for closed reductions.
Follow-Up And Disposition
Admission Criteria
Open fractures
Fractures with vascular compromise
Displaced fractures not amenable to closed management
Significant associated injuries requiring observation
Discharge Criteria
Nondisplaced fractures
Fractures successfully treated with closed reduction
Most isolated humeral shaft fractures
Selected complex proximal humeral fractures after orthopedic consultation
Referral Considerations
Most patients require outpatient orthopedic follow-up. Proximal humeral fractures classified as Neer type 2–4 should be reviewed with orthopedics for definitive planning. Displaced humeral shaft fractures require orthopedic management with functional bracing, casting, or surgical fixation.
Follow-Up Recommendations
Early follow-up is recommended to reassess neurovascular status, pain control, and fracture alignment. Stable proximal humeral fractures should be evaluated for early range-of-motion therapy to reduce the risk of adhesive capsulitis.
Key Points And Common Pitfalls
A thorough neurovascular examination is essential for all humeral fractures and should be repeated after manipulation. Radial nerve injury is the most common neurologic deficit associated with humeral shaft fractures and typically resolves spontaneously over months. Proximal humeral fractures involving the surgical neck or articular surface carry a risk of avascular necrosis. Multipart proximal humeral fractures often do not require admission but must have a clear orthopedic management plan due to the potential need for surgical intervention.
Basics
Overview And Definitions
Humerus fractures include injuries to the proximal humerus and the humeral shaft. Proximal humeral fractures are commonly categorized as nondisplaced, displaced, or fracture–dislocations and account for approximately 5% of all fractures. Incidence increases with age, with a female-to-male ratio of 4:1, and the majority of patients are older than 60 years. These fractures represent the third most common osteoporotic fracture, following hip and distal radius fractures.
The Neer classification system is widely used for proximal humeral fractures and describes injuries based on the number and location of fracture fragments. Fractures are classified as 2-, 3-, or 4-part injuries involving the anatomic neck, surgical neck, greater tuberosity, or lesser tuberosity. Fracture–dislocations are also included in this system.
Humeral shaft fractures account for less than 3% of all fractures and may be spiral, oblique, or transverse in pattern. The AO classification categorizes these injuries as simple, wedge, or comminuted (complex) fractures.
Mechanisms And Causes
Proximal humeral fractures most commonly result from low-energy mechanisms, particularly falls, often onto an outstretched hand. Less frequently, they occur due to violent muscle contraction during seizures or electrical shock, or from higher-energy trauma.
Humeral shaft fractures are typically caused by high-energy direct trauma, either penetrating or blunt, or by bending forces. Less commonly, they result from falls or repetitive stress injuries, such as those seen in throwing athletes.
Diagnosis
Clinical Features
Patients usually present with pain, swelling, and localized tenderness over the humerus. There is often difficulty initiating active movement, and the arm may be held tightly against the chest. Shortening of the extremity, crepitus, ecchymosis, and signs of neurovascular compromise may be present.
History
Key historical elements include the mechanism of injury, patient age, fall risk, underlying malignancy, and associated injuries.
Physical Examination
A complete examination of the affected extremity is essential. Inspection should assess for deformity, shortening, swelling, and open wounds. Range of motion at the shoulder and elbow should be evaluated as tolerated. A detailed neurovascular examination is mandatory.
Essential Evaluation
Individual nerve function must be assessed, with special attention to the radial nerve, particularly in midshaft fractures. Median, ulnar, axillary (sensation over the lateral shoulder), and musculocutaneous nerves (sensation over the lateral forearm) should also be evaluated.
Vascular assessment includes palpation of radial, ulnar, and brachial pulses and confirmation of adequate capillary refill. Imaging is required to define the extent and type of injury.
Pediatric Considerations
Humerus fractures are most common in children younger than 3 years or older than 12 years. Neonatal fractures may occur due to birth trauma, especially in infants weighing more than 4.5 kg or in breech deliveries, and may present as pseudoparalysis.
In older children, mechanisms are similar to adults. The thicker periosteum in children often limits displacement of humeral shaft fractures. Proximal humeral Salter–Harris type I injuries should be suspected when radiographs are normal but significant pain persists, with Salter–Harris type II being most common. Nonaccidental trauma must be considered, particularly in children younger than 3 years, especially with suspicious fracture patterns.
Diagnostic Studies And Interpretation
Imaging
Plain radiographs are the initial imaging modality. Proximal humeral fractures require at least three views: anteroposterior, lateral, and axillary. The axillary view is critical for evaluating tuberosity displacement, glenoid involvement, and humeral head alignment.
Humeral shaft fractures require anteroposterior and lateral views of the entire humerus, including both the shoulder and elbow joints to rule out associated injuries.
CT scanning is useful in complex or comminuted proximal humeral fractures and in suspected fracture–dislocations, helping define fracture anatomy and surgical planning.
Differential Diagnosis
Acute hemorrhagic bursitis
Traumatic rotator cuff tear
Shoulder dislocation
Acromioclavicular joint separation
Calcific tendinitis
Contusion
Tendon rupture
Neurapraxia
Pathologic fracture
Management
Prehospital Care
Excessive movement of the injured arm should be avoided to prevent further neurovascular injury. Immobilization with a sling and swath is recommended, with rapid transport for patients exhibiting neurologic or vascular deficits.
Initial Stabilization
Primary and secondary trauma surveys should be performed to identify associated injuries. Immobilization helps reduce pain, prevent displacement, and minimize neurovascular injury. An axillary pad may improve comfort. Ice application helps limit swelling. Open fractures require sterile coverage, tetanus prophylaxis, and parenteral antibiotics.
Emergency Department Management
Adequate analgesia is essential, with narcotics administered orally, intramuscularly, or intravenously as first-line therapy.
Most proximal humeral fractures are single-part injuries and can be managed nonoperatively with sling and swath immobilization and early range-of-motion exercises. Displaced or multipart fractures should be described using the Neer classification. Fractures with more than 1 cm of displacement or more than 45 degrees of angulation are considered displaced and require orthopedic consultation.
Two-part fractures may often be managed nonoperatively after reduction, whereas three- and four-part fractures may require operative fixation or hemiarthroplasty, depending on patient age, comorbidities, and functional expectations. Emergent orthopedic consultation is indicated for open fractures, irreducible fracture–dislocations, or vascular compromise.
Most humeral shaft fractures can be managed nonoperatively without reduction. Up to 20 degrees of anterior angulation, 30 degrees of varus angulation, and 3 cm of shortening are generally well tolerated. Nondisplaced fractures may be treated with a coaptation splint, except for transverse fractures, which are better managed with a sling and swath. Displaced fractures may require a hanging cast under orthopedic guidance. Emergent consultation is required for neurovascular compromise, open fractures, segmental fractures, articular involvement, or a “floating elbow.”
Medications
Pain control is achieved primarily with narcotic analgesics. NSAIDs may be used as adjunctive therapy. Procedural sedation may be required for closed reductions.
Follow-Up And Disposition
Admission Criteria
Open fractures
Fractures with vascular compromise
Displaced fractures not amenable to closed management
Significant associated injuries requiring observation
Discharge Criteria
Nondisplaced fractures
Fractures successfully treated with closed reduction
Most isolated humeral shaft fractures
Selected complex proximal humeral fractures after orthopedic consultation
Referral Considerations
Most patients require outpatient orthopedic follow-up. Proximal humeral fractures classified as Neer type 2–4 should be reviewed with orthopedics for definitive planning. Displaced humeral shaft fractures require orthopedic management with functional bracing, casting, or surgical fixation.
Follow-Up Recommendations
Early follow-up is recommended to reassess neurovascular status, pain control, and fracture alignment. Stable proximal humeral fractures should be evaluated for early range-of-motion therapy to reduce the risk of adhesive capsulitis.
Key Points And Common Pitfalls
A thorough neurovascular examination is essential for all humeral fractures and should be repeated after manipulation. Radial nerve injury is the most common neurologic deficit associated with humeral shaft fractures and typically resolves spontaneously over months. Proximal humeral fractures involving the surgical neck or articular surface carry a risk of avascular necrosis. Multipart proximal humeral fractures often do not require admission but must have a clear orthopedic management plan due to the potential need for surgical intervention.
- Published on
Infectious Diseases and Microbiology: Abdominal Pain and Fever
Basics
Description and Definition
This topic reviews conditions in which fever occurs together with abdominal pain.
Approach to the Patient
The initial priority is deciding whether the presentation represents a surgical emergency. Life-threatening diagnoses must be rapidly excluded, and clinicians should remember that pain referred from extra-abdominal sites can mimic primary abdominal disease. Severe intraabdominal infections may present with minimal or atypical findings, particularly in neonates, older adults, and immunocompromised patients. Rapid assessment of symptom onset, severity, and character is essential, along with immediate vital sign evaluation and a comprehensive physical examination. Beyond a careful abdominal exam, full systemic assessment is required, especially of the cardiopulmonary systems. Rectal examination should generally be performed, except in patients with severe neutropenia, in whom careful inspection is preferred.
Epidemiology
Appendicitis commonly presents to emergency departments with fever and abdominal pain. In the United States, most typhoid fever cases are acquired during travel, particularly to Mexico, India, and Pakistan. Travel to tropical regions raises concern for malaria, while travel to areas endemic for louse-borne relapsing fever such as Ethiopia, parts of South America, and East Asia suggests Borrelia recurrentis. HIV infection can produce fever and abdominal pain through multiple mechanisms and should be considered in individuals with risk factors or from high-prevalence regions such as sub-Saharan Africa and Southeast Asia, including those with intravenous drug exposure. Intestinal tuberculosis is associated with ingestion of unpasteurized dairy products, malnutrition, and HIV. Animal exposure may indicate leptospirosis, toxoplasmosis, brucellosis, or Q fever. Other vectors are linked to dengue fever, typhus, and psittacosis. Individuals with sickle cell disease or prior splenectomy are predisposed to salmonellosis. Melena, positive fecal occult blood tests, and weight loss should prompt consideration of solid tumors or lymphoma. Cardiovascular disease, the leading cause of mortality in Western countries, may frequently present with abdominal pain.
Etiology
Diffuse abdominal pain with fever suggests peritonitis, ileus or obstruction, mesenteric ischemia, ruptured aneurysm, or metabolic disorders. Infectious causes vary by location: right upper quadrant pain may result from acute cholecystitis including perforation, hepatitis, Fitz-Hugh–Curtis syndrome, pyelonephritis, pneumonia, or liver abscess; left upper quadrant pain from pyelonephritis, pneumonia, or splenic abscess; epigastric pain from diverticulitis, early appendicitis, primary or secondary peritonitis including tuberculous forms, acute gastroenteritis, pancreatitis, cholangitis, inflammatory bowel disease, Clostridioides difficile colitis, or mediastinitis; right lower quadrant pain from appendicitis, salpingitis, psoas abscess, mesenteric adenitis, pelvic inflammatory disease, or bowel perforation; left lower quadrant pain from diverticulitis, salpingitis, psoas abscess, mesenteric adenitis, pelvic infection, or bowel perforation. Noninfectious causes include acute porphyria, adrenal crisis, systemic inflammatory and granulomatous disorders, diabetic ketoacidosis, esophageal disease, familial Mediterranean fever, lead poisoning, intraabdominal or hematologic malignancy, mediastinal tumors, mesenteric ischemia or thrombosis, myocardial infarction, pancreatitis, pneumothorax complicating pneumonia, pulmonary embolism, ruptured ovarian follicle, and sickle cell crisis. Enteric fever presents with fever and abdominal pain and may include headache, hepatosplenomegaly, and a macular rash known as rose spots. Typhoid fever caused by Salmonella typhi is the classic example, but similar syndromes can result from Salmonella paratyphi and numerous bacterial, rickettsial, viral, fungal, and parasitic pathogens. Mesenteric adenitis often mimics appendicitis and is usually viral or due to Yersinia enterocolitica. Eosinophilia with abdominal cramps or diarrhea and fever suggests helminthic infection or intestinal lymphoma. Enterohemorrhagic Escherichia coli infections typically cause crampy pain before bloody diarrhea and are often afebrile. In patients with HIV, both typical causes seen in immunocompetent hosts and additional conditions such as typhlitis, bowel perforation with abscess, HIV-related cholangiopathy, hepatic abscesses, bacillary angiomatosis, pancreatitis, splenic infarction or abscess, gastrointestinal tuberculosis, cytomegalovirus disease, fungal and mycobacterial infections, parasitic enteritis, Giardia, Strongyloides, Kaposi sarcoma, and lymphoma must be considered.
Diagnosis
History
Assessment should include pain location, intensity, quality, radiation, aggravating and relieving factors, relation to meals, bowel habits, recent travel, dietary and animal exposures, and cardiovascular risk factors.
Physical Examination
Evaluation includes bowel sounds and abdominal bruits, localization and severity of tenderness, and palpation for hepatosplenomegaly. Signs of acute or chronic liver disease such as jaundice, scleral icterus, spider angiomata, clubbing, and ascites should be sought. The oropharynx and anus should be examined for lesions. Relative bradycardia supports enteric fever, which may also present with conjunctivitis, pharyngitis, or pulmonary findings. Acute diarrhea with sterile arthritis suggests Yersinia infection. Right lower quadrant rebound tenderness may reflect mesenteric adenitis, and only about half of appendicitis cases show classic migratory pain.
Diagnostic Tests and Interpretation
Laboratory Studies
Recommended tests include complete blood count with differential, electrolytes, renal function, liver enzymes and function tests, and calcium. Blood cultures should be obtained before empiric antibiotics, along with urine culture and electrocardiography. Blood, stool, and urine cultures are required in suspected enteric fever prior to therapy, with bone marrow cultures considered if blood cultures are negative and typhoid fever is suspected. Widal testing has limited diagnostic value outside Salmonella typhi. Leukopenia is common in typhoid fever. Eosinophilia warrants stool examination for ova and parasites. Fever is uncommon in giardiasis, occurring in a minority of cases, and diagnosis may require stool studies, small-bowel biopsy, or immunoassays. Malaria evaluation requires thick and thin blood smears every 24 hours for three sets, with rapid tests as adjuncts. Stool testing should be guided by context and include evaluation for C. difficile, ova and parasites, and bacterial cultures for major enteric pathogens. Most appendicitis cases demonstrate leukocytosis.
Imaging
Plain abdominal radiographs may reveal free air, loss of psoas shadow, or radiopaque calculi, but ultrasonography or computed tomography is often required. Ultrasound is the preferred initial test for suspected biliary or renal infection but is limited for deep structures and postoperative evaluation. CT imaging offers higher diagnostic accuracy, especially with contrast, though renal toxicity must be considered. Ultrasound is standard for initial assessment of biliary disease, while endoscopic ultrasonography provides very high accuracy for bile duct stones. Magnetic resonance cholangiography offers a noninvasive alternative for biliary imaging. Acute acalculous cholecystitis accounts for a minority of cases, and nuclear scanning is rarely first line but may be useful in selected situations. Endoscopic retrograde, percutaneous transhepatic, and intraoperative cholangiography are highly accurate for common bile duct stones but are invasive and carry complication risks.
Treatment
Medications
Empiric antimicrobial therapy is often required before a definitive diagnosis is established and should be tailored to the suspected infectious syndrome and travel history. Mesenteric adenitis is typically self-limited and may not require antibiotics, though trimethoprim-sulfamethoxazole, third-generation cephalosporins, or fluoroquinolones can be used when indicated. Mild to moderate community-acquired intraabdominal infections such as acute cholecystitis can be treated with a fluoroquinolone plus metronidazole or a beta-lactam/beta-lactamase inhibitor. Vancomycin is added when methicillin-resistant Staphylococcus aureus is suspected, while ampicillin is preferred for susceptible Enterococcus species. Severe community-acquired or health-care–associated intraabdominal infections require early broad-spectrum multidrug regimens targeting nosocomial organisms, often including antipseudomonal cephalosporins or carbapenems.
Ongoing Care and Follow-Up
Clinicians should remain alert for subtle or atypical presentations in neonates, infants, and older adults. Patients require close observation until fever resolves. Persistent unexplained fever and abdominal pain should prompt consideration of abdominal CT imaging when history, examination, and ultrasound are nondiagnostic.
Basics
Description and Definition
This topic reviews conditions in which fever occurs together with abdominal pain.
Approach to the Patient
The initial priority is deciding whether the presentation represents a surgical emergency. Life-threatening diagnoses must be rapidly excluded, and clinicians should remember that pain referred from extra-abdominal sites can mimic primary abdominal disease. Severe intraabdominal infections may present with minimal or atypical findings, particularly in neonates, older adults, and immunocompromised patients. Rapid assessment of symptom onset, severity, and character is essential, along with immediate vital sign evaluation and a comprehensive physical examination. Beyond a careful abdominal exam, full systemic assessment is required, especially of the cardiopulmonary systems. Rectal examination should generally be performed, except in patients with severe neutropenia, in whom careful inspection is preferred.
Epidemiology
Appendicitis commonly presents to emergency departments with fever and abdominal pain. In the United States, most typhoid fever cases are acquired during travel, particularly to Mexico, India, and Pakistan. Travel to tropical regions raises concern for malaria, while travel to areas endemic for louse-borne relapsing fever such as Ethiopia, parts of South America, and East Asia suggests Borrelia recurrentis. HIV infection can produce fever and abdominal pain through multiple mechanisms and should be considered in individuals with risk factors or from high-prevalence regions such as sub-Saharan Africa and Southeast Asia, including those with intravenous drug exposure. Intestinal tuberculosis is associated with ingestion of unpasteurized dairy products, malnutrition, and HIV. Animal exposure may indicate leptospirosis, toxoplasmosis, brucellosis, or Q fever. Other vectors are linked to dengue fever, typhus, and psittacosis. Individuals with sickle cell disease or prior splenectomy are predisposed to salmonellosis. Melena, positive fecal occult blood tests, and weight loss should prompt consideration of solid tumors or lymphoma. Cardiovascular disease, the leading cause of mortality in Western countries, may frequently present with abdominal pain.
Etiology
Diffuse abdominal pain with fever suggests peritonitis, ileus or obstruction, mesenteric ischemia, ruptured aneurysm, or metabolic disorders. Infectious causes vary by location: right upper quadrant pain may result from acute cholecystitis including perforation, hepatitis, Fitz-Hugh–Curtis syndrome, pyelonephritis, pneumonia, or liver abscess; left upper quadrant pain from pyelonephritis, pneumonia, or splenic abscess; epigastric pain from diverticulitis, early appendicitis, primary or secondary peritonitis including tuberculous forms, acute gastroenteritis, pancreatitis, cholangitis, inflammatory bowel disease, Clostridioides difficile colitis, or mediastinitis; right lower quadrant pain from appendicitis, salpingitis, psoas abscess, mesenteric adenitis, pelvic inflammatory disease, or bowel perforation; left lower quadrant pain from diverticulitis, salpingitis, psoas abscess, mesenteric adenitis, pelvic infection, or bowel perforation. Noninfectious causes include acute porphyria, adrenal crisis, systemic inflammatory and granulomatous disorders, diabetic ketoacidosis, esophageal disease, familial Mediterranean fever, lead poisoning, intraabdominal or hematologic malignancy, mediastinal tumors, mesenteric ischemia or thrombosis, myocardial infarction, pancreatitis, pneumothorax complicating pneumonia, pulmonary embolism, ruptured ovarian follicle, and sickle cell crisis. Enteric fever presents with fever and abdominal pain and may include headache, hepatosplenomegaly, and a macular rash known as rose spots. Typhoid fever caused by Salmonella typhi is the classic example, but similar syndromes can result from Salmonella paratyphi and numerous bacterial, rickettsial, viral, fungal, and parasitic pathogens. Mesenteric adenitis often mimics appendicitis and is usually viral or due to Yersinia enterocolitica. Eosinophilia with abdominal cramps or diarrhea and fever suggests helminthic infection or intestinal lymphoma. Enterohemorrhagic Escherichia coli infections typically cause crampy pain before bloody diarrhea and are often afebrile. In patients with HIV, both typical causes seen in immunocompetent hosts and additional conditions such as typhlitis, bowel perforation with abscess, HIV-related cholangiopathy, hepatic abscesses, bacillary angiomatosis, pancreatitis, splenic infarction or abscess, gastrointestinal tuberculosis, cytomegalovirus disease, fungal and mycobacterial infections, parasitic enteritis, Giardia, Strongyloides, Kaposi sarcoma, and lymphoma must be considered.
Diagnosis
History
Assessment should include pain location, intensity, quality, radiation, aggravating and relieving factors, relation to meals, bowel habits, recent travel, dietary and animal exposures, and cardiovascular risk factors.
Physical Examination
Evaluation includes bowel sounds and abdominal bruits, localization and severity of tenderness, and palpation for hepatosplenomegaly. Signs of acute or chronic liver disease such as jaundice, scleral icterus, spider angiomata, clubbing, and ascites should be sought. The oropharynx and anus should be examined for lesions. Relative bradycardia supports enteric fever, which may also present with conjunctivitis, pharyngitis, or pulmonary findings. Acute diarrhea with sterile arthritis suggests Yersinia infection. Right lower quadrant rebound tenderness may reflect mesenteric adenitis, and only about half of appendicitis cases show classic migratory pain.
Diagnostic Tests and Interpretation
Laboratory Studies
Recommended tests include complete blood count with differential, electrolytes, renal function, liver enzymes and function tests, and calcium. Blood cultures should be obtained before empiric antibiotics, along with urine culture and electrocardiography. Blood, stool, and urine cultures are required in suspected enteric fever prior to therapy, with bone marrow cultures considered if blood cultures are negative and typhoid fever is suspected. Widal testing has limited diagnostic value outside Salmonella typhi. Leukopenia is common in typhoid fever. Eosinophilia warrants stool examination for ova and parasites. Fever is uncommon in giardiasis, occurring in a minority of cases, and diagnosis may require stool studies, small-bowel biopsy, or immunoassays. Malaria evaluation requires thick and thin blood smears every 24 hours for three sets, with rapid tests as adjuncts. Stool testing should be guided by context and include evaluation for C. difficile, ova and parasites, and bacterial cultures for major enteric pathogens. Most appendicitis cases demonstrate leukocytosis.
Imaging
Plain abdominal radiographs may reveal free air, loss of psoas shadow, or radiopaque calculi, but ultrasonography or computed tomography is often required. Ultrasound is the preferred initial test for suspected biliary or renal infection but is limited for deep structures and postoperative evaluation. CT imaging offers higher diagnostic accuracy, especially with contrast, though renal toxicity must be considered. Ultrasound is standard for initial assessment of biliary disease, while endoscopic ultrasonography provides very high accuracy for bile duct stones. Magnetic resonance cholangiography offers a noninvasive alternative for biliary imaging. Acute acalculous cholecystitis accounts for a minority of cases, and nuclear scanning is rarely first line but may be useful in selected situations. Endoscopic retrograde, percutaneous transhepatic, and intraoperative cholangiography are highly accurate for common bile duct stones but are invasive and carry complication risks.
Treatment
Medications
Empiric antimicrobial therapy is often required before a definitive diagnosis is established and should be tailored to the suspected infectious syndrome and travel history. Mesenteric adenitis is typically self-limited and may not require antibiotics, though trimethoprim-sulfamethoxazole, third-generation cephalosporins, or fluoroquinolones can be used when indicated. Mild to moderate community-acquired intraabdominal infections such as acute cholecystitis can be treated with a fluoroquinolone plus metronidazole or a beta-lactam/beta-lactamase inhibitor. Vancomycin is added when methicillin-resistant Staphylococcus aureus is suspected, while ampicillin is preferred for susceptible Enterococcus species. Severe community-acquired or health-care–associated intraabdominal infections require early broad-spectrum multidrug regimens targeting nosocomial organisms, often including antipseudomonal cephalosporins or carbapenems.
Ongoing Care and Follow-Up
Clinicians should remain alert for subtle or atypical presentations in neonates, infants, and older adults. Patients require close observation until fever resolves. Persistent unexplained fever and abdominal pain should prompt consideration of abdominal CT imaging when history, examination, and ultrasound are nondiagnostic.
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Emergency And Acute Medicine – Hemoptysis
Basics And Description
Hemoptysis is the expectoration of blood originating from the tracheobronchial tree. The bronchial arteries are the source in approximately 90% of cases and are typically responsible for profuse bleeding. Pulmonary arteries account for about 5% of cases and usually cause smaller-volume bleeding, while nonbronchial systemic arteries account for the remaining 5%. Massive hemoptysis has been variably defined from 100 mL to 1 L in 24 hours; the most commonly accepted definition is greater than 300–600 mL in 24 hours, or more than 8 mL/kg/day in children. Mortality is significantly higher in massive hemoptysis, reaching approximately 38%, compared with about 4.5% in trivial to moderate hemoptysis. Malignancy and coagulopathy markedly increase mortality risk.
Etiology
Infectious causes are the most common and include acute or chronic bronchitis, pneumonia, necrotizing pneumonia or lung abscess, tuberculosis, viral infections, fungal infections, and parasitic diseases. Neoplastic causes include bronchogenic carcinoma, metastatic disease, carcinoid tumors, and small cell carcinoma. Pulmonary causes include bronchiectasis, pulmonary embolism or infarction, cystic fibrosis, bronchopleural fistula, and sarcoidosis. Cardiac causes include mitral stenosis, tricuspid endocarditis, and heart failure. Systemic diseases include Goodpasture syndrome, systemic lupus erythematosus, and vasculitides. Hematologic causes include coagulopathies, thrombocytopenia, platelet dysfunction, and disseminated intravascular coagulation. Vascular causes include pulmonary hypertension, arteriovenous malformations, pulmonary artery aneurysms, and aortobronchial fistulas. Drug-related causes include antiplatelet agents, anticoagulants, cocaine inhalation, and certain medications. Trauma, iatrogenic procedures, foreign-body aspiration, catamenial hemoptysis, amyloidosis, and idiopathic causes are additional considerations.
Clinical Presentation And Symptoms
Patients may present with cough productive of blood, chest pain, dyspnea, fever, weakness, fatigue, night sweats, and weight loss. Recurrent or chronic hemoptysis raises suspicion for bronchiectasis, arteriovenous malformations, or cystic fibrosis.
History And Physical Examination
History should assess smoking status, occupational or chemical exposures, travel history, medication use, anticoagulation, prior lung, renal, or valvular disease, and associated hematuria suggesting Goodpasture syndrome. Physical examination may reveal clubbing, ecchymoses, aphthous ulcers, nasal septal perforation, hematuria, or unilateral leg edema. Upper airway sources such as epistaxis or sinus disease should be excluded to rule out pseudohemoptysis. In children, careful HEENT evaluation is essential, and wheezing or crackles may suggest obstruction or infection.
Essential Workup
Differentiate true hemoptysis from pseudohemoptysis or gastrointestinal bleeding. Pulmonary bleeding is typically bright red, frothy, and mixed with sputum, whereas gastrointestinal bleeding is darker, associated with nausea or vomiting, and acidic. Estimation of bleeding volume and rate is critical to risk stratification.
Diagnostic Tests And Interpretation
Laboratory evaluation includes CBC, basic metabolic panel, coagulation studies, and urinalysis. Infectious workup may include blood cultures, sputum cultures, cytology, fungal studies, and acid-fast bacilli testing. Hypotensive or massive hemoptysis patients require type and cross-match and full metabolic evaluation. Imaging begins with chest radiography, which may be normal in up to 20% of cases. CT chest is the preferred study in stable patients and is the gold standard for diagnosing bronchiectasis and identifying malignancy or cavitary disease. CT angiography delineates bronchial and pulmonary arterial anatomy and can identify aneurysms or emboli. Bronchoscopy allows direct visualization, localization of bleeding, and therapeutic intervention but has limited yield for peripheral lesions.
Differential Diagnosis
Pseudohemoptysis from epistaxis, pharyngeal bleeding, or gastrointestinal hemorrhage must always be considered.
Initial Stabilization And Therapy
Airway protection and oxygenation are priorities. Suctioning should be readily available, and endotracheal intubation is indicated for airway compromise, severe hypoxemia, or massive bleeding. Large-bore IV access, continuous monitoring, and volume resuscitation are essential. In massive hemoptysis, asphyxiation is the primary cause of death rather than exsanguination.
Emergency Department Management
Treat underlying infection when suspected and correct hypoxemia and coagulopathy. In massive hemoptysis, position the patient upright or with the affected lung down to protect the nonbleeding lung. Bronchoscopy may be used for local control with vasoconstrictors, tamponade, or cautery. Temporary endobronchial tamponade may be achieved with balloon catheters or double-lumen tubes. Bronchial artery embolization is highly effective, with success rates approaching 98%, though rebleeding can occur. Surgical intervention is reserved for cases refractory to embolization or when structural lesions require resection.
Disposition And Follow-Up
ICU admission is required for massive hemoptysis, intubation, hemodynamic instability, hypoxemic respiratory failure, or airway compromise. General ward admission is appropriate for stable patients with identifiable causes requiring treatment. Discharge may be considered for patients with mild, self-limited hemoptysis who are hemodynamically stable, without coagulopathy or oxygen requirement, and who have reliable follow-up.
Follow-Up Recommendations
Patients should be counseled to stop smoking and avoid medications or supplements that increase bleeding risk. Immediate return to care is advised for worsening hemoptysis, dyspnea, chest pain, syncope, or dizziness.
Clinical Pearls And Common Errors
Early airway management is critical when deterioration is anticipated. In severe unilateral bleeding with hypoxemia, position the affected lung down. Bronchial artery embolization is highly effective and should be discussed early with interventional radiology.
Basics And Description
Hemoptysis is the expectoration of blood originating from the tracheobronchial tree. The bronchial arteries are the source in approximately 90% of cases and are typically responsible for profuse bleeding. Pulmonary arteries account for about 5% of cases and usually cause smaller-volume bleeding, while nonbronchial systemic arteries account for the remaining 5%. Massive hemoptysis has been variably defined from 100 mL to 1 L in 24 hours; the most commonly accepted definition is greater than 300–600 mL in 24 hours, or more than 8 mL/kg/day in children. Mortality is significantly higher in massive hemoptysis, reaching approximately 38%, compared with about 4.5% in trivial to moderate hemoptysis. Malignancy and coagulopathy markedly increase mortality risk.
Etiology
Infectious causes are the most common and include acute or chronic bronchitis, pneumonia, necrotizing pneumonia or lung abscess, tuberculosis, viral infections, fungal infections, and parasitic diseases. Neoplastic causes include bronchogenic carcinoma, metastatic disease, carcinoid tumors, and small cell carcinoma. Pulmonary causes include bronchiectasis, pulmonary embolism or infarction, cystic fibrosis, bronchopleural fistula, and sarcoidosis. Cardiac causes include mitral stenosis, tricuspid endocarditis, and heart failure. Systemic diseases include Goodpasture syndrome, systemic lupus erythematosus, and vasculitides. Hematologic causes include coagulopathies, thrombocytopenia, platelet dysfunction, and disseminated intravascular coagulation. Vascular causes include pulmonary hypertension, arteriovenous malformations, pulmonary artery aneurysms, and aortobronchial fistulas. Drug-related causes include antiplatelet agents, anticoagulants, cocaine inhalation, and certain medications. Trauma, iatrogenic procedures, foreign-body aspiration, catamenial hemoptysis, amyloidosis, and idiopathic causes are additional considerations.
Clinical Presentation And Symptoms
Patients may present with cough productive of blood, chest pain, dyspnea, fever, weakness, fatigue, night sweats, and weight loss. Recurrent or chronic hemoptysis raises suspicion for bronchiectasis, arteriovenous malformations, or cystic fibrosis.
History And Physical Examination
History should assess smoking status, occupational or chemical exposures, travel history, medication use, anticoagulation, prior lung, renal, or valvular disease, and associated hematuria suggesting Goodpasture syndrome. Physical examination may reveal clubbing, ecchymoses, aphthous ulcers, nasal septal perforation, hematuria, or unilateral leg edema. Upper airway sources such as epistaxis or sinus disease should be excluded to rule out pseudohemoptysis. In children, careful HEENT evaluation is essential, and wheezing or crackles may suggest obstruction or infection.
Essential Workup
Differentiate true hemoptysis from pseudohemoptysis or gastrointestinal bleeding. Pulmonary bleeding is typically bright red, frothy, and mixed with sputum, whereas gastrointestinal bleeding is darker, associated with nausea or vomiting, and acidic. Estimation of bleeding volume and rate is critical to risk stratification.
Diagnostic Tests And Interpretation
Laboratory evaluation includes CBC, basic metabolic panel, coagulation studies, and urinalysis. Infectious workup may include blood cultures, sputum cultures, cytology, fungal studies, and acid-fast bacilli testing. Hypotensive or massive hemoptysis patients require type and cross-match and full metabolic evaluation. Imaging begins with chest radiography, which may be normal in up to 20% of cases. CT chest is the preferred study in stable patients and is the gold standard for diagnosing bronchiectasis and identifying malignancy or cavitary disease. CT angiography delineates bronchial and pulmonary arterial anatomy and can identify aneurysms or emboli. Bronchoscopy allows direct visualization, localization of bleeding, and therapeutic intervention but has limited yield for peripheral lesions.
Differential Diagnosis
Pseudohemoptysis from epistaxis, pharyngeal bleeding, or gastrointestinal hemorrhage must always be considered.
Initial Stabilization And Therapy
Airway protection and oxygenation are priorities. Suctioning should be readily available, and endotracheal intubation is indicated for airway compromise, severe hypoxemia, or massive bleeding. Large-bore IV access, continuous monitoring, and volume resuscitation are essential. In massive hemoptysis, asphyxiation is the primary cause of death rather than exsanguination.
Emergency Department Management
Treat underlying infection when suspected and correct hypoxemia and coagulopathy. In massive hemoptysis, position the patient upright or with the affected lung down to protect the nonbleeding lung. Bronchoscopy may be used for local control with vasoconstrictors, tamponade, or cautery. Temporary endobronchial tamponade may be achieved with balloon catheters or double-lumen tubes. Bronchial artery embolization is highly effective, with success rates approaching 98%, though rebleeding can occur. Surgical intervention is reserved for cases refractory to embolization or when structural lesions require resection.
Disposition And Follow-Up
ICU admission is required for massive hemoptysis, intubation, hemodynamic instability, hypoxemic respiratory failure, or airway compromise. General ward admission is appropriate for stable patients with identifiable causes requiring treatment. Discharge may be considered for patients with mild, self-limited hemoptysis who are hemodynamically stable, without coagulopathy or oxygen requirement, and who have reliable follow-up.
Follow-Up Recommendations
Patients should be counseled to stop smoking and avoid medications or supplements that increase bleeding risk. Immediate return to care is advised for worsening hemoptysis, dyspnea, chest pain, syncope, or dizziness.
Clinical Pearls And Common Errors
Early airway management is critical when deterioration is anticipated. In severe unilateral bleeding with hypoxemia, position the affected lung down. Bronchial artery embolization is highly effective and should be discussed early with interventional radiology.
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Emergency And Acute Medicine – Hemorrhagic Fevers
Basics And Description
Hemorrhagic fever refers to a multisystem syndrome characterized by vasocapillary permeability, hemorrhage, and organ dysfunction. Viral hemorrhagic fevers (VHF) are caused by a distinct group of viruses and often begin with a nonspecific influenza-like illness. Hemorrhagic manifestations occur in a minority of patients and typically appear in later stages of disease.
Risk Factors
Travel to endemic regions
Exposure related to biologic warfare
Close contact with animals
Insect bites or ingestion
Pathophysiology
Viral hemorrhagic fevers cause endothelial injury leading to increased vascular permeability, hemorrhage, and progression to shock. The shock state is both hypovolemic and distributive and is often difficult to reverse. Rapid progression to hypotension indicates a very high mortality risk. Disseminated intravascular coagulation is commonly seen in Marburg and Crimean-Congo hemorrhagic fever but is less frequent in arenavirus infections. Dengue hemorrhagic fever is immune mediated and often results from secondary infection and is among the most common causes of VHF.
Etiology
Viral hemorrhagic fevers are caused by RNA viruses with zoonotic life cycles and short incubation periods of less than 10–21 days.
Filoviruses include Ebola and Marburg, with fruit bat reservoirs and transmission primarily in sub-Saharan Africa.
Arenaviruses include Lassa fever and South American hemorrhagic fevers, transmitted via aerosolized rodent excreta.
Flaviviruses include Dengue and Yellow fever, transmitted by mosquitoes, primarily in tropical regions.
Bunyaviridae include Rift Valley fever and Crimean-Congo hemorrhagic fever, transmitted by ticks or mosquitoes.
Hantaviridae include hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome, transmitted via aerosolized rodent excreta.
Alert
Viral hemorrhagic fevers represent a potential biowarfare threat. With the exception of dengue, most are transmissible via aerosols and body fluids. Some have very high morbidity and mortality, and many replicate efficiently in cell culture, allowing weaponization.
Diagnosis – Signs And Symptoms
Common symptoms include acute fever, malaise, headache, nausea, vomiting, flushing, diarrhea, abdominal pain, and myalgias.
Less common manifestations include gingival bleeding, conjunctival hemorrhage, petechiae, hematemesis, melena, epistaxis, and ecchymoses.
Hemorrhagic features usually appear after day three and may involve skin, IV sites, gums, lungs, gastrointestinal tract, or uterus. Diffuse alveolar hemorrhage and ARDS may occur, particularly in Ebola, Marburg, Lassa, Crimean-Congo hemorrhagic fever, and hantavirus infections.
Characteristic rashes include nonpruritic centripetal maculopapular eruptions in Ebola and Marburg, jaundice in Yellow fever, and blanching maculopapular truncal rash in Dengue.
Late-stage disease may progress to shock, seizures, coma, and death.
History And Physical Examination
History should assess recent travel, exposure to sick contacts, animal or insect exposure, and clustering of cases.
Strict protection of healthcare workers is essential, using universal blood and body fluid precautions.
Vital signs should be monitored closely, as narrowed pulse pressure may signal impending cardiovascular collapse.
Physical examination may reveal hemorrhage, rash, hepatomegaly, right upper quadrant tenderness, and abnormal lung findings.
Essential Workup
The primary goal is to distinguish VHF from other acute febrile illnesses, especially malaria, in returning travelers. Lung involvement suggests systemic disease and poorer prognosis. Consider the possibility of a biologic attack if multiple patients present with similar unusual findings.
Diagnostic Tests And Interpretation
Laboratory studies may show leukocytosis, leukopenia, thrombocytopenia, pancytopenia, or hemoconcentration. Elevated hematocrit suggests third spacing and impending shock. Renal and hepatic dysfunction are common. Coagulation studies may reveal DIC, particularly in Ebola, Marburg, and Crimean-Congo hemorrhagic fever.
Definitive diagnosis requires specialized biosafety level 4 laboratories using RT-PCR, viral isolation, or immunohistochemistry, coordinated through the CDC.
Imaging such as chest radiograph or CT may identify ARDS, pneumonia, or internal hemorrhage.
Differential Diagnosis
Malaria
Dengue fever
Rickettsial infections
Typhoid fever
Meningococcemia
Sepsis
Hemolytic uremic syndrome
Thrombotic thrombocytopenic purpura
Leukemia
Pit viper envenomation
Treatment – Prehospital And Initial Stabilization
Early recognition is critical due to increased globalization and imported cases. Suspected cases must be reported to the CDC immediately.
Patients should be isolated, and healthcare workers must use full protective equipment, including HEPA-filtered respirators during aerosol-generating procedures.
Emergency Department Management
Treatment is primarily supportive. Empiric antimalarial therapy should be initiated until malaria is excluded. Secondary infections should be treated aggressively.
Bleeding is usually mild; if severe, manage with blood products and clotting factors.
Fluid resuscitation must be cautious due to third spacing and risk of flash pulmonary edema. Colloids or blood products should be reserved for impending shock.
Ribavirin is effective against Lassa fever, South American hemorrhagic fever, Crimean-Congo hemorrhagic fever, and hantavirus infections but is ineffective against filoviruses.
Convalescent plasma may benefit South American hemorrhagic fever if administered early.
Medications
Ribavirin intravenous loading dose of 33 mg/kg, followed by 16 mg/kg every 6 hours for 4 days, then 8 mg/kg every 8 hours for 3 days.
Oral prophylaxis consists of 500 mg every 6 hours for 7 days.
Vaccines are available for Yellow fever, while others remain under development.
Disposition And Follow-Up
All suspected cases require admission with isolation precautions. ICU care is indicated for shock or multiorgan failure. Discharge is not appropriate when VHF is suspected.
Coordination with the CDC is mandatory for patient management and postexposure prophylaxis of contacts.
Clinical Pearls And Pitfalls
Use extreme caution with fluid resuscitation.
Hemoconcentration and pulmonary involvement are critical warning signs.
Always consider viral hemorrhagic fever in febrile patients returning from endemic regions.
Strict isolation and universal precautions are essential to prevent transmission.
Notify the CDC immediately for all suspected cases.
Basics And Description
Hemorrhagic fever refers to a multisystem syndrome characterized by vasocapillary permeability, hemorrhage, and organ dysfunction. Viral hemorrhagic fevers (VHF) are caused by a distinct group of viruses and often begin with a nonspecific influenza-like illness. Hemorrhagic manifestations occur in a minority of patients and typically appear in later stages of disease.
Risk Factors
Travel to endemic regions
Exposure related to biologic warfare
Close contact with animals
Insect bites or ingestion
Pathophysiology
Viral hemorrhagic fevers cause endothelial injury leading to increased vascular permeability, hemorrhage, and progression to shock. The shock state is both hypovolemic and distributive and is often difficult to reverse. Rapid progression to hypotension indicates a very high mortality risk. Disseminated intravascular coagulation is commonly seen in Marburg and Crimean-Congo hemorrhagic fever but is less frequent in arenavirus infections. Dengue hemorrhagic fever is immune mediated and often results from secondary infection and is among the most common causes of VHF.
Etiology
Viral hemorrhagic fevers are caused by RNA viruses with zoonotic life cycles and short incubation periods of less than 10–21 days.
Filoviruses include Ebola and Marburg, with fruit bat reservoirs and transmission primarily in sub-Saharan Africa.
Arenaviruses include Lassa fever and South American hemorrhagic fevers, transmitted via aerosolized rodent excreta.
Flaviviruses include Dengue and Yellow fever, transmitted by mosquitoes, primarily in tropical regions.
Bunyaviridae include Rift Valley fever and Crimean-Congo hemorrhagic fever, transmitted by ticks or mosquitoes.
Hantaviridae include hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome, transmitted via aerosolized rodent excreta.
Alert
Viral hemorrhagic fevers represent a potential biowarfare threat. With the exception of dengue, most are transmissible via aerosols and body fluids. Some have very high morbidity and mortality, and many replicate efficiently in cell culture, allowing weaponization.
Diagnosis – Signs And Symptoms
Common symptoms include acute fever, malaise, headache, nausea, vomiting, flushing, diarrhea, abdominal pain, and myalgias.
Less common manifestations include gingival bleeding, conjunctival hemorrhage, petechiae, hematemesis, melena, epistaxis, and ecchymoses.
Hemorrhagic features usually appear after day three and may involve skin, IV sites, gums, lungs, gastrointestinal tract, or uterus. Diffuse alveolar hemorrhage and ARDS may occur, particularly in Ebola, Marburg, Lassa, Crimean-Congo hemorrhagic fever, and hantavirus infections.
Characteristic rashes include nonpruritic centripetal maculopapular eruptions in Ebola and Marburg, jaundice in Yellow fever, and blanching maculopapular truncal rash in Dengue.
Late-stage disease may progress to shock, seizures, coma, and death.
History And Physical Examination
History should assess recent travel, exposure to sick contacts, animal or insect exposure, and clustering of cases.
Strict protection of healthcare workers is essential, using universal blood and body fluid precautions.
Vital signs should be monitored closely, as narrowed pulse pressure may signal impending cardiovascular collapse.
Physical examination may reveal hemorrhage, rash, hepatomegaly, right upper quadrant tenderness, and abnormal lung findings.
Essential Workup
The primary goal is to distinguish VHF from other acute febrile illnesses, especially malaria, in returning travelers. Lung involvement suggests systemic disease and poorer prognosis. Consider the possibility of a biologic attack if multiple patients present with similar unusual findings.
Diagnostic Tests And Interpretation
Laboratory studies may show leukocytosis, leukopenia, thrombocytopenia, pancytopenia, or hemoconcentration. Elevated hematocrit suggests third spacing and impending shock. Renal and hepatic dysfunction are common. Coagulation studies may reveal DIC, particularly in Ebola, Marburg, and Crimean-Congo hemorrhagic fever.
Definitive diagnosis requires specialized biosafety level 4 laboratories using RT-PCR, viral isolation, or immunohistochemistry, coordinated through the CDC.
Imaging such as chest radiograph or CT may identify ARDS, pneumonia, or internal hemorrhage.
Differential Diagnosis
Malaria
Dengue fever
Rickettsial infections
Typhoid fever
Meningococcemia
Sepsis
Hemolytic uremic syndrome
Thrombotic thrombocytopenic purpura
Leukemia
Pit viper envenomation
Treatment – Prehospital And Initial Stabilization
Early recognition is critical due to increased globalization and imported cases. Suspected cases must be reported to the CDC immediately.
Patients should be isolated, and healthcare workers must use full protective equipment, including HEPA-filtered respirators during aerosol-generating procedures.
Emergency Department Management
Treatment is primarily supportive. Empiric antimalarial therapy should be initiated until malaria is excluded. Secondary infections should be treated aggressively.
Bleeding is usually mild; if severe, manage with blood products and clotting factors.
Fluid resuscitation must be cautious due to third spacing and risk of flash pulmonary edema. Colloids or blood products should be reserved for impending shock.
Ribavirin is effective against Lassa fever, South American hemorrhagic fever, Crimean-Congo hemorrhagic fever, and hantavirus infections but is ineffective against filoviruses.
Convalescent plasma may benefit South American hemorrhagic fever if administered early.
Medications
Ribavirin intravenous loading dose of 33 mg/kg, followed by 16 mg/kg every 6 hours for 4 days, then 8 mg/kg every 8 hours for 3 days.
Oral prophylaxis consists of 500 mg every 6 hours for 7 days.
Vaccines are available for Yellow fever, while others remain under development.
Disposition And Follow-Up
All suspected cases require admission with isolation precautions. ICU care is indicated for shock or multiorgan failure. Discharge is not appropriate when VHF is suspected.
Coordination with the CDC is mandatory for patient management and postexposure prophylaxis of contacts.
Clinical Pearls And Pitfalls
Use extreme caution with fluid resuscitation.
Hemoconcentration and pulmonary involvement are critical warning signs.
Always consider viral hemorrhagic fever in febrile patients returning from endemic regions.
Strict isolation and universal precautions are essential to prevent transmission.
Notify the CDC immediately for all suspected cases.
