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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.
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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.
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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.
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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.
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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 Shock
Basics And Description
Hemorrhagic shock is the loss of effective circulating blood volume resulting in inadequate tissue and organ perfusion. Blood loss exceeds the body’s compensatory mechanisms, leading to hypoperfusion, impaired oxygen delivery, anaerobic metabolism, cellular injury, and death. It is the most common cause of shock following injury.
Compensated shock occurs when physiologic reserve maintains near-normal vital signs. Decompensated shock develops when blood loss overwhelms compensatory mechanisms, producing marked abnormalities in vital signs.
Estimated total blood volume is approximately 7% of ideal body weight (≈70 mL/kg), equivalent to about 4,900 mL in a 70-kg adult.
Etiology
Trauma, both penetrating and blunt, is the most common cause and includes abdominal injuries to the spleen or liver, chest injuries such as hemothorax or great vessel injury, and pelvic fractures with vascular disruption.
Nontraumatic causes include ruptured abdominal aortic aneurysm, mycotic aneurysm, arteriovenous malformations, gastrointestinal bleeding, ectopic pregnancy, postpartum hemorrhage, placenta previa, malignancy-related bleeding, retroperitoneal hemorrhage, severe epistaxis, hemoptysis, and vascular injuries.
Diagnosis – Signs And Symptoms
Class I hemorrhage involves up to 15% blood loss and presents with minimal changes in vital signs, mild anxiety, and normal urine output.
Class II hemorrhage (15–30%) causes tachycardia, tachypnea, narrowed pulse pressure, anxiety, and decreased urine output.
Class III hemorrhage (30–40%) results in hypotension, marked tachycardia and tachypnea, confusion, delayed capillary refill, and significant oliguria.
Class IV hemorrhage (>40%) presents with severe hypotension, extreme tachycardia, altered or absent consciousness, negligible urine output, and cold, pale skin.
Reliance on systolic blood pressure alone may delay recognition of shock.
Special Populations
Children may maintain normal vital signs longer due to greater physiologic reserve, but can deteriorate rapidly once decompensation occurs.
Pregnant patients require greater blood loss before maternal hypotension develops, yet fetal perfusion may be compromised early.
Older adults and patients with comorbid disease or medications such as beta-blockers may show blunted physiologic responses.
History And Physical Examination
Assessment focuses on mechanism of injury, medical history, medications, and risk factors. Physical examination includes careful evaluation of vital signs, mental status, skin perfusion, pulse pressure, abdominal and pelvic examination, and identification of potential bleeding sources.
Essential Workup
Immediate IV access for resuscitation and blood sampling is required. Type and cross-match should be obtained early.
Diagnostic Tests And Interpretation
Laboratory studies include CBC, coagulation profile, arterial blood gas, serum lactate, electrolytes, and pregnancy testing when indicated. Early hemoglobin and hematocrit values may remain normal despite significant blood loss.
Imaging may include chest radiograph for hemothorax, pelvic radiograph for occult fracture, focused abdominal sonography for trauma, endovaginal ultrasound in suspected ectopic pregnancy, and CT scanning once the patient is stable.
Procedures such as Foley catheter placement, nasogastric tube insertion, diagnostic peritoneal lavage, endoscopy, or angiography may be required based on suspected source.
Differential Diagnosis
Cardiac tamponade, tension pneumothorax, cardiogenic shock, sepsis, adrenal insufficiency, and neurogenic shock.
Treatment Principles
Management begins immediately upon recognition of shock while simultaneously identifying and controlling the source of bleeding. The goal is restoration of adequate perfusion with careful balance between resuscitation and risk of worsening hemorrhage.
Prehospital Care
Rapid assessment, early transport, IV access, and initial fluid resuscitation are standard. In penetrating trauma, delayed aggressive fluid resuscitation may reduce bleeding prior to definitive control.
Initial Stabilization And Therapy
Airway protection and supplemental 100% oxygen are provided as indicated. Circulation is supported with two large-bore IV lines or alternative access if necessary. Warmed isotonic crystalloid fluids are administered initially, followed by early blood transfusion in class III or IV shock. Type-specific blood is preferred, with type O blood used in life-threatening emergencies.
Emergency Department Management
Continuous monitoring, strict bed rest, NPO status, and aggressive hemorrhage control are essential. Response to initial resuscitation guides further management. Persistent instability requires immediate surgical or interventional radiology consultation. Massive transfusion protocols may be necessary, with close monitoring for coagulopathy and hypothermia.
Medications And Fluids
First-line therapy includes isotonic crystalloids and blood products. Additional products such as platelets, fresh frozen plasma, and cryoprecipitate are used based on clinical and laboratory findings.
Disposition
All patients with hemorrhagic shock require hospital admission, often to an intensive care or surgical service. Discharge from the emergency department is not appropriate.
Key Clinical Insights And Common Pitfalls
Severity of hemorrhage can be estimated through careful assessment of vital signs and physical findings.
Fluid resuscitation must balance restoration of perfusion with the risk of exacerbating uncontrolled bleeding.
Patient response to initial resuscitation is the most important guide for ongoing therapy and need for definitive intervention.
Basics And Description
Hemorrhagic shock is the loss of effective circulating blood volume resulting in inadequate tissue and organ perfusion. Blood loss exceeds the body’s compensatory mechanisms, leading to hypoperfusion, impaired oxygen delivery, anaerobic metabolism, cellular injury, and death. It is the most common cause of shock following injury.
Compensated shock occurs when physiologic reserve maintains near-normal vital signs. Decompensated shock develops when blood loss overwhelms compensatory mechanisms, producing marked abnormalities in vital signs.
Estimated total blood volume is approximately 7% of ideal body weight (≈70 mL/kg), equivalent to about 4,900 mL in a 70-kg adult.
Etiology
Trauma, both penetrating and blunt, is the most common cause and includes abdominal injuries to the spleen or liver, chest injuries such as hemothorax or great vessel injury, and pelvic fractures with vascular disruption.
Nontraumatic causes include ruptured abdominal aortic aneurysm, mycotic aneurysm, arteriovenous malformations, gastrointestinal bleeding, ectopic pregnancy, postpartum hemorrhage, placenta previa, malignancy-related bleeding, retroperitoneal hemorrhage, severe epistaxis, hemoptysis, and vascular injuries.
Diagnosis – Signs And Symptoms
Class I hemorrhage involves up to 15% blood loss and presents with minimal changes in vital signs, mild anxiety, and normal urine output.
Class II hemorrhage (15–30%) causes tachycardia, tachypnea, narrowed pulse pressure, anxiety, and decreased urine output.
Class III hemorrhage (30–40%) results in hypotension, marked tachycardia and tachypnea, confusion, delayed capillary refill, and significant oliguria.
Class IV hemorrhage (>40%) presents with severe hypotension, extreme tachycardia, altered or absent consciousness, negligible urine output, and cold, pale skin.
Reliance on systolic blood pressure alone may delay recognition of shock.
Special Populations
Children may maintain normal vital signs longer due to greater physiologic reserve, but can deteriorate rapidly once decompensation occurs.
Pregnant patients require greater blood loss before maternal hypotension develops, yet fetal perfusion may be compromised early.
Older adults and patients with comorbid disease or medications such as beta-blockers may show blunted physiologic responses.
History And Physical Examination
Assessment focuses on mechanism of injury, medical history, medications, and risk factors. Physical examination includes careful evaluation of vital signs, mental status, skin perfusion, pulse pressure, abdominal and pelvic examination, and identification of potential bleeding sources.
Essential Workup
Immediate IV access for resuscitation and blood sampling is required. Type and cross-match should be obtained early.
Diagnostic Tests And Interpretation
Laboratory studies include CBC, coagulation profile, arterial blood gas, serum lactate, electrolytes, and pregnancy testing when indicated. Early hemoglobin and hematocrit values may remain normal despite significant blood loss.
Imaging may include chest radiograph for hemothorax, pelvic radiograph for occult fracture, focused abdominal sonography for trauma, endovaginal ultrasound in suspected ectopic pregnancy, and CT scanning once the patient is stable.
Procedures such as Foley catheter placement, nasogastric tube insertion, diagnostic peritoneal lavage, endoscopy, or angiography may be required based on suspected source.
Differential Diagnosis
Cardiac tamponade, tension pneumothorax, cardiogenic shock, sepsis, adrenal insufficiency, and neurogenic shock.
Treatment Principles
Management begins immediately upon recognition of shock while simultaneously identifying and controlling the source of bleeding. The goal is restoration of adequate perfusion with careful balance between resuscitation and risk of worsening hemorrhage.
Prehospital Care
Rapid assessment, early transport, IV access, and initial fluid resuscitation are standard. In penetrating trauma, delayed aggressive fluid resuscitation may reduce bleeding prior to definitive control.
Initial Stabilization And Therapy
Airway protection and supplemental 100% oxygen are provided as indicated. Circulation is supported with two large-bore IV lines or alternative access if necessary. Warmed isotonic crystalloid fluids are administered initially, followed by early blood transfusion in class III or IV shock. Type-specific blood is preferred, with type O blood used in life-threatening emergencies.
Emergency Department Management
Continuous monitoring, strict bed rest, NPO status, and aggressive hemorrhage control are essential. Response to initial resuscitation guides further management. Persistent instability requires immediate surgical or interventional radiology consultation. Massive transfusion protocols may be necessary, with close monitoring for coagulopathy and hypothermia.
Medications And Fluids
First-line therapy includes isotonic crystalloids and blood products. Additional products such as platelets, fresh frozen plasma, and cryoprecipitate are used based on clinical and laboratory findings.
Disposition
All patients with hemorrhagic shock require hospital admission, often to an intensive care or surgical service. Discharge from the emergency department is not appropriate.
Key Clinical Insights And Common Pitfalls
Severity of hemorrhage can be estimated through careful assessment of vital signs and physical findings.
Fluid resuscitation must balance restoration of perfusion with the risk of exacerbating uncontrolled bleeding.
Patient response to initial resuscitation is the most important guide for ongoing therapy and need for definitive intervention.
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Emergency And Acute Medicine – Hemothorax
Basics And Description
Hemothorax is the accumulation of blood within the intrapleural space, most commonly following blunt or penetrating chest trauma, though nontraumatic causes exist. Bleeding usually results from disruption of chest wall tissues, pleura, or intrathoracic vessels, leading to decreased vital capacity, hypoxia, and respiratory compromise. Significant intravascular blood loss may cause hemodynamic instability and hemorrhagic shock. Massive hemothorax can increase intrathoracic pressure, impair venous return, and reduce cardiac output. In blunt trauma, hemothorax is rarely isolated and is frequently associated with pneumothorax, extrathoracic injuries, and pulmonary contusion. Large collections may release anticoagulant substances, promoting continued bleeding. Untreated hemothorax can progress to empyema or fibrothorax due to pleural adhesions and lung trapping.
Etiology
Traumatic causes include injury to major thoracic vessels such as intercostal arteries, internal mammary arteries, pulmonary vessels, the aorta, vena cava, and the heart. Lung parenchymal injuries may also cause bleeding, which often stops spontaneously because of low pulmonary pressures and high thromboplastin levels, and are frequently associated with pneumothorax. Nontraumatic or spontaneous hemothorax is rare and should prompt evaluation for coagulation disorders, malignancy, vascular catastrophes such as aortic dissection or ruptured aneurysm, pulmonary embolism with infarction, tuberculosis, bullous emphysema, pulmonary arteriovenous malformations, or lobar sequestration. Hemothorax may also occur from torn pleural adhesions during spontaneous pneumothorax or following tube thoracostomy.
Diagnosis – Signs And Symptoms
Small hemothoraces, generally less than 400 mL, may cause minimal or no changes in vital signs or physical examination. Large hemothoraces, typically exceeding 1,000 mL, present with restlessness, anxiety, pallor, pleuritic chest pain, hemoptysis, dyspnea, and air hunger. Signs of hemorrhagic shock appear when blood loss reaches or exceeds 30% of circulating volume, including tachycardia, tachypnea, and hypotension. In cases with slow or insidious onset, such as malignancy-related hemothorax, dyspnea is often the predominant symptom without acute hemodynamic compromise.
History
Important historical features include recent blunt or penetrating chest trauma, rib fractures, flail chest, or delayed onset of symptoms hours to days after injury. Delayed hemothorax may result from rupture of chest wall hematomas or intercostal vessel injury from rib fracture movement. Additional history includes known malignancy, metastatic disease, or recent thoracic procedures such as thoracentesis or chest tube placement.
Physical Examination
Vital signs may reveal hypoxia, tachypnea, tachycardia, or hypotension depending on severity. Jugular venous distention may be present with increased intrathoracic pressure, and tracheal deviation can occur in massive collections. Chest inspection may show asymmetric expansion, deformity, contusions, abrasions, or paradoxical movement. Palpation may elicit rib tenderness, crepitus, or subcutaneous emphysema, while percussion typically reveals dullness over the affected hemithorax. Auscultation demonstrates decreased or absent breath sounds, best appreciated in the upright patient.
Essential Workup
Chest radiography is the primary diagnostic study. In stable patients, an upright posteroanterior film is ideal and can detect pleural fluid volumes greater than 200–300 mL, seen as meniscus formation or blunting of the costophrenic angle. In supine trauma patients, up to 1,000 mL of blood may be missed, appearing only as diffuse haziness of the hemithorax. Associated injuries such as pneumothorax, rib fractures, pulmonary contusions, or mediastinal widening should be assessed.
Diagnostic Tests And Interpretation
Laboratory evaluation includes hematocrit monitoring for trends, type and cross-match, pulse oximetry, and arterial blood gas analysis when indicated. Pleural fluid hematocrit exceeding 50% of peripheral blood hematocrit confirms hemothorax. Ultrasound, particularly extended FAST, is highly sensitive for detecting intrapleural fluid in trained hands. Computed tomography is useful for identifying small hemothoraces not visible on chest radiographs and for evaluating associated injuries.
Differential Diagnosis
Hemopneumothorax, pneumothorax, pulmonary contusion, pleural effusion, and empyema or pneumonia.
Treatment – Prehospital Care
Initial management includes assessment of vital signs and oxygen saturation, supplemental oxygen, intravenous access, and fluid resuscitation for hypotension. Clinical differentiation between hemothorax and pneumothorax may be difficult; subcutaneous emphysema suggests pneumothorax, while dullness to percussion favors hemothorax. In unstable patients with suspected tension pneumothorax, needle thoracostomy should be performed immediately.
Initial Stabilization And Therapy
Airway, breathing, and circulation are prioritized. Endotracheal intubation is indicated for impending respiratory failure. High-flow oxygen, two large-bore intravenous lines, and rapid fluid resuscitation are initiated. If chest tube equipment is not immediately available in an unstable patient, needle thoracostomy should not be delayed. Patients should be positioned upright when possible.
Emergency Department Treatment And Procedures
Definitive management involves evacuation of blood from the pleural space via tube thoracostomy. A large-bore chest tube, typically 36–40 French, is inserted in the 4th or 5th intercostal space at the mid-axillary line, directed posteriorly and superiorly, and connected to underwater seal drainage with suction. Post-procedure chest radiography confirms placement and lung re-expansion. Autotransfusion should be considered when available. Indications for operative thoracotomy include initial chest tube output greater than 20 mL/kg in children or approximately 1,000 mL in adults, persistent bleeding exceeding 7 mL/kg/hr or 200 mL/hr for four hours, enlarging hemothorax, refractory hypotension, or clinical deterioration after initial response. Emergency department thoracotomy may be indicated in select cases of penetrating trauma with recent arrest or profound shock, and rarely in blunt trauma under specialized circumstances.
Medications
Local anesthetics are used for chest tube placement in awake patients. Procedural sedation and analgesia with agents such as fentanyl and midazolam may be administered in stable patients. Additional sedatives may be used as clinically appropriate.
Follow-Up And Disposition
Patients requiring tube thoracostomy should be admitted to a trauma, cardiothoracic, or surgical service experienced in chest tube management. Small, isolated hemothoraces detected incidentally may be observed for 4–6 hours and discharged if asymptomatic, normoxic, and without evidence of ongoing bleeding. Asymptomatic blunt chest trauma patients with normal initial radiographs do not require repeat imaging prior to discharge.
Key Clinical Insights And Common Pitfalls
The pleural cavity can hold more than 4 liters of blood, allowing massive hemorrhage without external bleeding. In supine patients, physical findings may be subtle due to posterior blood distribution. Hemothorax may be misread as pneumonia in the absence of trauma history. Concurrent diaphragmatic injury raises concern for intra-abdominal bleeding. Early preparation for autotransfusion is important, as the greatest blood loss often occurs at initial chest tube placement. Improper chest tube positioning, especially too anterior or superior, can impair drainage; all fenestrations must lie within the thoracic cavity. Prophylactic antibiotics with chest tube placement do not reduce pneumonia or empyema risk.
Basics And Description
Hemothorax is the accumulation of blood within the intrapleural space, most commonly following blunt or penetrating chest trauma, though nontraumatic causes exist. Bleeding usually results from disruption of chest wall tissues, pleura, or intrathoracic vessels, leading to decreased vital capacity, hypoxia, and respiratory compromise. Significant intravascular blood loss may cause hemodynamic instability and hemorrhagic shock. Massive hemothorax can increase intrathoracic pressure, impair venous return, and reduce cardiac output. In blunt trauma, hemothorax is rarely isolated and is frequently associated with pneumothorax, extrathoracic injuries, and pulmonary contusion. Large collections may release anticoagulant substances, promoting continued bleeding. Untreated hemothorax can progress to empyema or fibrothorax due to pleural adhesions and lung trapping.
Etiology
Traumatic causes include injury to major thoracic vessels such as intercostal arteries, internal mammary arteries, pulmonary vessels, the aorta, vena cava, and the heart. Lung parenchymal injuries may also cause bleeding, which often stops spontaneously because of low pulmonary pressures and high thromboplastin levels, and are frequently associated with pneumothorax. Nontraumatic or spontaneous hemothorax is rare and should prompt evaluation for coagulation disorders, malignancy, vascular catastrophes such as aortic dissection or ruptured aneurysm, pulmonary embolism with infarction, tuberculosis, bullous emphysema, pulmonary arteriovenous malformations, or lobar sequestration. Hemothorax may also occur from torn pleural adhesions during spontaneous pneumothorax or following tube thoracostomy.
Diagnosis – Signs And Symptoms
Small hemothoraces, generally less than 400 mL, may cause minimal or no changes in vital signs or physical examination. Large hemothoraces, typically exceeding 1,000 mL, present with restlessness, anxiety, pallor, pleuritic chest pain, hemoptysis, dyspnea, and air hunger. Signs of hemorrhagic shock appear when blood loss reaches or exceeds 30% of circulating volume, including tachycardia, tachypnea, and hypotension. In cases with slow or insidious onset, such as malignancy-related hemothorax, dyspnea is often the predominant symptom without acute hemodynamic compromise.
History
Important historical features include recent blunt or penetrating chest trauma, rib fractures, flail chest, or delayed onset of symptoms hours to days after injury. Delayed hemothorax may result from rupture of chest wall hematomas or intercostal vessel injury from rib fracture movement. Additional history includes known malignancy, metastatic disease, or recent thoracic procedures such as thoracentesis or chest tube placement.
Physical Examination
Vital signs may reveal hypoxia, tachypnea, tachycardia, or hypotension depending on severity. Jugular venous distention may be present with increased intrathoracic pressure, and tracheal deviation can occur in massive collections. Chest inspection may show asymmetric expansion, deformity, contusions, abrasions, or paradoxical movement. Palpation may elicit rib tenderness, crepitus, or subcutaneous emphysema, while percussion typically reveals dullness over the affected hemithorax. Auscultation demonstrates decreased or absent breath sounds, best appreciated in the upright patient.
Essential Workup
Chest radiography is the primary diagnostic study. In stable patients, an upright posteroanterior film is ideal and can detect pleural fluid volumes greater than 200–300 mL, seen as meniscus formation or blunting of the costophrenic angle. In supine trauma patients, up to 1,000 mL of blood may be missed, appearing only as diffuse haziness of the hemithorax. Associated injuries such as pneumothorax, rib fractures, pulmonary contusions, or mediastinal widening should be assessed.
Diagnostic Tests And Interpretation
Laboratory evaluation includes hematocrit monitoring for trends, type and cross-match, pulse oximetry, and arterial blood gas analysis when indicated. Pleural fluid hematocrit exceeding 50% of peripheral blood hematocrit confirms hemothorax. Ultrasound, particularly extended FAST, is highly sensitive for detecting intrapleural fluid in trained hands. Computed tomography is useful for identifying small hemothoraces not visible on chest radiographs and for evaluating associated injuries.
Differential Diagnosis
Hemopneumothorax, pneumothorax, pulmonary contusion, pleural effusion, and empyema or pneumonia.
Treatment – Prehospital Care
Initial management includes assessment of vital signs and oxygen saturation, supplemental oxygen, intravenous access, and fluid resuscitation for hypotension. Clinical differentiation between hemothorax and pneumothorax may be difficult; subcutaneous emphysema suggests pneumothorax, while dullness to percussion favors hemothorax. In unstable patients with suspected tension pneumothorax, needle thoracostomy should be performed immediately.
Initial Stabilization And Therapy
Airway, breathing, and circulation are prioritized. Endotracheal intubation is indicated for impending respiratory failure. High-flow oxygen, two large-bore intravenous lines, and rapid fluid resuscitation are initiated. If chest tube equipment is not immediately available in an unstable patient, needle thoracostomy should not be delayed. Patients should be positioned upright when possible.
Emergency Department Treatment And Procedures
Definitive management involves evacuation of blood from the pleural space via tube thoracostomy. A large-bore chest tube, typically 36–40 French, is inserted in the 4th or 5th intercostal space at the mid-axillary line, directed posteriorly and superiorly, and connected to underwater seal drainage with suction. Post-procedure chest radiography confirms placement and lung re-expansion. Autotransfusion should be considered when available. Indications for operative thoracotomy include initial chest tube output greater than 20 mL/kg in children or approximately 1,000 mL in adults, persistent bleeding exceeding 7 mL/kg/hr or 200 mL/hr for four hours, enlarging hemothorax, refractory hypotension, or clinical deterioration after initial response. Emergency department thoracotomy may be indicated in select cases of penetrating trauma with recent arrest or profound shock, and rarely in blunt trauma under specialized circumstances.
Medications
Local anesthetics are used for chest tube placement in awake patients. Procedural sedation and analgesia with agents such as fentanyl and midazolam may be administered in stable patients. Additional sedatives may be used as clinically appropriate.
Follow-Up And Disposition
Patients requiring tube thoracostomy should be admitted to a trauma, cardiothoracic, or surgical service experienced in chest tube management. Small, isolated hemothoraces detected incidentally may be observed for 4–6 hours and discharged if asymptomatic, normoxic, and without evidence of ongoing bleeding. Asymptomatic blunt chest trauma patients with normal initial radiographs do not require repeat imaging prior to discharge.
Key Clinical Insights And Common Pitfalls
The pleural cavity can hold more than 4 liters of blood, allowing massive hemorrhage without external bleeding. In supine patients, physical findings may be subtle due to posterior blood distribution. Hemothorax may be misread as pneumonia in the absence of trauma history. Concurrent diaphragmatic injury raises concern for intra-abdominal bleeding. Early preparation for autotransfusion is important, as the greatest blood loss often occurs at initial chest tube placement. Improper chest tube positioning, especially too anterior or superior, can impair drainage; all fenestrations must lie within the thoracic cavity. Prophylactic antibiotics with chest tube placement do not reduce pneumonia or empyema risk.
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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.
- Published on
Emergency And Acute Medicine – Hemorrhoid
Basics And Description
Hemorrhoids are normal venous sinusoids of the distal rectum and proximal anal canal that function as vascular cushions contributing to anal continence. These cushions consist of thick submucosa containing blood vessels, smooth muscle, and elastic connective tissue. An arteriovenous shunt system at the level of the internal hemorrhoids explains the typical presentation of bright red blood per rectum. Hemorrhoid disease develops when these normal structures become symptomatic. Hemorrhoids are generally painless unless thrombosed or strangulated. Pathologically, disease occurs when portions of the anal canal lining slide downward.
External hemorrhoids are located below the dentate line, covered by skin or anoderm, and drain into the internal iliac venous system. Internal hemorrhoids arise from submucosal vessels above the dentate line, drain into the portal venous system, and are typically found at the left lateral, right posterolateral, and right anterolateral positions. Internal hemorrhoids are classified by degree of prolapse: grade 1 causes painless bleeding without prolapse; grade 2 prolapses with bowel movements but reduces spontaneously; grade 3 prolapses with bowel movements and requires manual reduction; grade 4 is chronically prolapsed and not reducible.
Etiology
The exact cause of hemorrhoid disease is unclear. Gravitational forces and increased abdominal pressure contribute to distention of venous sinusoids. It is commonly associated with straining and irregular bowel habits, including hard, bulky stools or diarrhea, which cause tenesmus and excessive straining. These forces weaken submucosal support tissue, promoting prolapse of anal cushions. Additional contributing factors include higher resting anal pressures related to erect posture, hereditary absence of venous valves, and chronically elevated intra-abdominal pressure from conditions such as pregnancy, ascites, and portal hypertension.
Diagnosis – Signs And Symptoms
Patients most commonly present with painless rectal bleeding during or after defecation. Blood is typically bright red and may appear on toilet paper, coat the stool, or drip into the toilet bowl. Rectal discomfort or a sensation of pressure may occur. Severe pain suggests thrombosed external hemorrhoids or prolapsed internal hemorrhoids that have become strangulated. Pruritus ani is common, and anal fissures may coexist.
History
Key historical features include duration and severity of bleeding, association with pain, presence of new perianal masses, stool consistency, prior anorectal disease, changes in stool caliber, and use of anticoagulants.
Physical Examination
Examination begins with inspection of the perianal area by gently separating the buttocks. A discrete, dark blue, tender mass covered by skin is consistent with a thrombosed external hemorrhoid and may coexist with an internal component. A purplish, tender, mucosa-covered mass suggests a prolapsed and strangulated internal hemorrhoid, often accompanied by thrombosed external hemorrhoids. Asking the patient to bear down may reveal prolapse. Digital rectal examination is mandatory to exclude malignancy. Anoscopy allows direct visualization of the anal canal and identification of bleeding internal hemorrhoids.
Essential Workup
Diagnosis is primarily clinical and based on a detailed history and thorough anorectal examination.
Diagnostic Tests And Interpretation
Laboratory testing is not routinely required. A complete blood count is indicated if there is significant bleeding to assess hemoglobin and hematocrit. Platelet count and coagulation studies (PT, PTT, INR) should be obtained in patients on anticoagulation or with significant comorbid disease.
Differential Diagnosis
Rectal prolapse, anal fissure, perirectal abscess or fistula, condyloma acuminata, anorectal carcinoma, and melanoma.
Treatment – Prehospital Care
Establish intravenous access in cases of severe bleeding.
Initial Stabilization And Therapy
Apply direct digital pressure to control active bleeding when present.
Emergency Department Treatment And Procedures
Conservative therapy is the foundation of treatment for all patients. This includes warm sitz baths for 15 minutes three times daily and after bowel movements, a high-fiber diet targeting approximately 30 g/day, increased oral hydration, stool softeners, bulk-forming laxatives, and analgesia with NSAIDs or acetaminophen.
Thrombosed external hemorrhoids causing severe pain may be excised if symptoms are present for fewer than five days and the clot has not begun to resolve. The procedure is performed with the patient in the prone jackknife or left lateral decubitus position. After local anesthesia with lidocaine containing epinephrine, an elliptical incision is made to excise the clot and overlying skin. Hemostasis may require silver nitrate. A small piece of Gelfoam or gauze is applied, and the dressing is removed at the first sitz bath approximately six hours later.
Nonthrombosed prolapsed internal hemorrhoids may be manually reduced, sometimes requiring topical anesthesia or an anal sphincter block. Bleeding internal hemorrhoids may be treated with sclerotherapy using agents such as sodium morrhuate or hypertonic saline, or with rubber band ligation of one or two hemorrhoids, which should be avoided in immunocompromised patients. Nonstrangulated, nonreducible hemorrhoids are managed conservatively with surgical referral, whereas strangulated internal hemorrhoids require immediate surgical consultation.
Pregnancy-associated hemorrhoids are common in the third trimester and are managed conservatively. Certain topical agents should be avoided due to fetal risk.
Medications
Analgesics include acetaminophen with or without codeine and NSAIDs such as ibuprofen. Stool regulation is achieved with fiber supplements, psyllium, and docusate sodium. Topical therapies include lidocaine-based anorectal creams, hydrocortisone-containing preparations, and 0.2% nitroglycerin ointment applied locally to reduce sphincter spasm and pain. Caution is required with topical anesthetics due to systemic absorption.
Follow-Up And Disposition
Admission is indicated for strangulated grade 4 hemorrhoids requiring urgent surgery, severe anemia due to bleeding, or significant bleeding in patients on anticoagulation or with portal hypertension. Most patients can be discharged with outpatient management.
Issues For Referral
Surgical referral is indicated for grade 3 or 4 internal hemorrhoids, suspected malignancy, inflammatory bowel disease, coagulopathy, pregnancy, or immunocompromised status.
Follow-Up Recommendations
Patients with advanced hemorrhoids or concern for neoplasia should have colorectal surgery follow-up. Uncomplicated cases should follow up with primary care. All patients with bright red blood per rectum should be referred for gastrointestinal or colorectal evaluation to exclude malignancy.
Key Clinical Insights And Common Pitfalls
Hemorrhoids are a common but not exclusive cause of anorectal bleeding and pain. Failure to evaluate for alternative diagnoses, including malignancy, is a frequent pitfall.
Basics And Description
Hemorrhoids are normal venous sinusoids of the distal rectum and proximal anal canal that function as vascular cushions contributing to anal continence. These cushions consist of thick submucosa containing blood vessels, smooth muscle, and elastic connective tissue. An arteriovenous shunt system at the level of the internal hemorrhoids explains the typical presentation of bright red blood per rectum. Hemorrhoid disease develops when these normal structures become symptomatic. Hemorrhoids are generally painless unless thrombosed or strangulated. Pathologically, disease occurs when portions of the anal canal lining slide downward.
External hemorrhoids are located below the dentate line, covered by skin or anoderm, and drain into the internal iliac venous system. Internal hemorrhoids arise from submucosal vessels above the dentate line, drain into the portal venous system, and are typically found at the left lateral, right posterolateral, and right anterolateral positions. Internal hemorrhoids are classified by degree of prolapse: grade 1 causes painless bleeding without prolapse; grade 2 prolapses with bowel movements but reduces spontaneously; grade 3 prolapses with bowel movements and requires manual reduction; grade 4 is chronically prolapsed and not reducible.
Etiology
The exact cause of hemorrhoid disease is unclear. Gravitational forces and increased abdominal pressure contribute to distention of venous sinusoids. It is commonly associated with straining and irregular bowel habits, including hard, bulky stools or diarrhea, which cause tenesmus and excessive straining. These forces weaken submucosal support tissue, promoting prolapse of anal cushions. Additional contributing factors include higher resting anal pressures related to erect posture, hereditary absence of venous valves, and chronically elevated intra-abdominal pressure from conditions such as pregnancy, ascites, and portal hypertension.
Diagnosis – Signs And Symptoms
Patients most commonly present with painless rectal bleeding during or after defecation. Blood is typically bright red and may appear on toilet paper, coat the stool, or drip into the toilet bowl. Rectal discomfort or a sensation of pressure may occur. Severe pain suggests thrombosed external hemorrhoids or prolapsed internal hemorrhoids that have become strangulated. Pruritus ani is common, and anal fissures may coexist.
History
Key historical features include duration and severity of bleeding, association with pain, presence of new perianal masses, stool consistency, prior anorectal disease, changes in stool caliber, and use of anticoagulants.
Physical Examination
Examination begins with inspection of the perianal area by gently separating the buttocks. A discrete, dark blue, tender mass covered by skin is consistent with a thrombosed external hemorrhoid and may coexist with an internal component. A purplish, tender, mucosa-covered mass suggests a prolapsed and strangulated internal hemorrhoid, often accompanied by thrombosed external hemorrhoids. Asking the patient to bear down may reveal prolapse. Digital rectal examination is mandatory to exclude malignancy. Anoscopy allows direct visualization of the anal canal and identification of bleeding internal hemorrhoids.
Essential Workup
Diagnosis is primarily clinical and based on a detailed history and thorough anorectal examination.
Diagnostic Tests And Interpretation
Laboratory testing is not routinely required. A complete blood count is indicated if there is significant bleeding to assess hemoglobin and hematocrit. Platelet count and coagulation studies (PT, PTT, INR) should be obtained in patients on anticoagulation or with significant comorbid disease.
Differential Diagnosis
Rectal prolapse, anal fissure, perirectal abscess or fistula, condyloma acuminata, anorectal carcinoma, and melanoma.
Treatment – Prehospital Care
Establish intravenous access in cases of severe bleeding.
Initial Stabilization And Therapy
Apply direct digital pressure to control active bleeding when present.
Emergency Department Treatment And Procedures
Conservative therapy is the foundation of treatment for all patients. This includes warm sitz baths for 15 minutes three times daily and after bowel movements, a high-fiber diet targeting approximately 30 g/day, increased oral hydration, stool softeners, bulk-forming laxatives, and analgesia with NSAIDs or acetaminophen.
Thrombosed external hemorrhoids causing severe pain may be excised if symptoms are present for fewer than five days and the clot has not begun to resolve. The procedure is performed with the patient in the prone jackknife or left lateral decubitus position. After local anesthesia with lidocaine containing epinephrine, an elliptical incision is made to excise the clot and overlying skin. Hemostasis may require silver nitrate. A small piece of Gelfoam or gauze is applied, and the dressing is removed at the first sitz bath approximately six hours later.
Nonthrombosed prolapsed internal hemorrhoids may be manually reduced, sometimes requiring topical anesthesia or an anal sphincter block. Bleeding internal hemorrhoids may be treated with sclerotherapy using agents such as sodium morrhuate or hypertonic saline, or with rubber band ligation of one or two hemorrhoids, which should be avoided in immunocompromised patients. Nonstrangulated, nonreducible hemorrhoids are managed conservatively with surgical referral, whereas strangulated internal hemorrhoids require immediate surgical consultation.
Pregnancy-associated hemorrhoids are common in the third trimester and are managed conservatively. Certain topical agents should be avoided due to fetal risk.
Medications
Analgesics include acetaminophen with or without codeine and NSAIDs such as ibuprofen. Stool regulation is achieved with fiber supplements, psyllium, and docusate sodium. Topical therapies include lidocaine-based anorectal creams, hydrocortisone-containing preparations, and 0.2% nitroglycerin ointment applied locally to reduce sphincter spasm and pain. Caution is required with topical anesthetics due to systemic absorption.
Follow-Up And Disposition
Admission is indicated for strangulated grade 4 hemorrhoids requiring urgent surgery, severe anemia due to bleeding, or significant bleeding in patients on anticoagulation or with portal hypertension. Most patients can be discharged with outpatient management.
Issues For Referral
Surgical referral is indicated for grade 3 or 4 internal hemorrhoids, suspected malignancy, inflammatory bowel disease, coagulopathy, pregnancy, or immunocompromised status.
Follow-Up Recommendations
Patients with advanced hemorrhoids or concern for neoplasia should have colorectal surgery follow-up. Uncomplicated cases should follow up with primary care. All patients with bright red blood per rectum should be referred for gastrointestinal or colorectal evaluation to exclude malignancy.
Key Clinical Insights And Common Pitfalls
Hemorrhoids are a common but not exclusive cause of anorectal bleeding and pain. Failure to evaluate for alternative diagnoses, including malignancy, is a frequent pitfall.
