Emergency and Acute Medicine – Carbon Monoxide Poisoning


Foundational Overview
Carbon monoxide is a colorless, odorless, and nonirritating gas that causes toxicity by binding hemoglobin to form carboxyhemoglobin, thereby reducing oxygen-carrying capacity. It also acts as a direct cellular toxin and interferes with intracellular oxygen utilization, leading to tissue hypoxia despite normal arterial oxygen tension.


Mechanisms And Sources
Carbon monoxide exposure may be endogenous at low levels from normal metabolism but is most often due to incomplete combustion of carbon-based fuels. Common sources include internal combustion engines, furnaces, fireplaces, heaters, indoor grills, accidental fires, and tobacco smoke. Methylene chloride, found in paint removers and furniture strippers, is metabolized in vivo to carbon monoxide, with delayed peak carboxyhemoglobin levels due to prolonged half-life.


Clinical Presentation
Symptoms are often nonspecific and may vary by organ system. Neurologic manifestations include headache, dizziness, ataxia, confusion, syncope, seizures, and coma. Gastrointestinal symptoms include nausea and vomiting. Cardiovascular findings may include chest pain and palpitations, while respiratory symptoms include dyspnea. Visual disturbances such as decreased acuity may occur.


Examination Findings
Neurologic examination may reveal acute encephalopathy, seizures, or coma. Cardiovascular findings include tachycardia, dysrhythmias, premature ventricular contractions, and myocardial ischemia or infarction. Respiratory findings include tachypnea and noncardiogenic pulmonary edema. Additional findings may include retinal hemorrhage, respiratory alkalosis, rhabdomyolysis, and lactic acidosis.


Initial Evaluation Strategy
A high index of suspicion is critical, as symptoms may be mild or vague. History should assess for similar symptoms in household members, malfunctioning heating systems, use of space heaters or ovens for heat, and illness in pets. Arterial blood gas typically shows normal PaO₂ with low measured oxygen saturation and may reveal metabolic acidosis in severe cases. Carboxyhemoglobin levels should be measured early but may underestimate severity if time has elapsed since exposure; normal levels are 0–3%, up to 10% in smokers.


Diagnostic Interpretation
Pulse oximetry is unreliable because it cannot differentiate oxyhemoglobin from carboxyhemoglobin and may appear falsely normal. Laboratory studies may reveal metabolic acidosis with elevated anion gap. Cardiac enzymes should be obtained when ischemia is suspected, and pregnancy testing is indicated when relevant. ECG may show dysrhythmias or nonspecific ST-T changes. Chest radiography may demonstrate pulmonary edema, and head CT may show bilateral globus pallidus lesions in unclear cases.


Conditions To Exclude
Alternative diagnoses include viral syndromes, meningitis or encephalitis, intracranial hemorrhage, gastroenteritis, migraine or tension headache, ethanol intoxication, sedative–hypnotic overdose, cyanide poisoning, salicylate toxicity, and toxic alcohol exposure.


Prehospital Care
Immediate administration of 100% oxygen is essential.


Early Emergency Management
Initial priorities include airway, breathing, and circulation, establishment of IV access, continuous cardiac monitoring, and delivery of 100% oxygen.


Definitive Emergency Treatment
Administer 100% normobaric oxygen via face mask or endotracheal tube until carboxyhemoglobin levels fall below 10%. The half-life of carboxyhemoglobin is approximately 300 minutes in room air, 90 minutes with 100% oxygen, and 20 minutes at 3 atmospheres in hyperbaric conditions. Hyperbaric oxygen therapy may reduce delayed neurologic sequelae and significantly shortens carboxyhemoglobin half-life, though its use remains controversial. Potential complications include barotrauma, pneumothorax, seizures, decompression sickness, and pulmonary edema. Consultation with a hyperbaric specialist is advised for altered mental status, focal neurologic deficits, seizures, cardiovascular instability, persistent metabolic acidosis, carboxyhemoglobin levels above 25%, or pregnancy with levels above 10%.


Pregnancy-Specific Considerations
Fetal hemoglobin has a higher affinity for carbon monoxide, resulting in fetal carboxyhemoglobin levels that exceed maternal levels by 10–15% and delayed fetal clearance, increasing risk of fetal hypoxia.


Disposition Planning
Admission is warranted for persistent symptoms after four hours of oxygen therapy, myocardial ischemia, seizures, syncope, metabolic acidosis, or hemodynamic instability. Discharge may be considered if the patient is asymptomatic after four hours of observation and none of the above criteria are present, with psychiatric clearance when exposure was intentional.


Follow-Up Guidance
Local fire authorities should be notified in cases of residential exposure to ensure environmental safety.


Key Clinical Insights
Carbon monoxide poisoning should be suspected in patients presenting with headache during heater use or when multiple individuals in the same environment develop similar symptoms. Early administration of 100% oxygen is critical, and timely transfer for hyperbaric therapy should be considered when indicated.

Emergency and Acute Medicine – Central Retinal Vein Occlusion


Overview
Central retinal vein occlusion (CRVO) is characterized by decreased visual acuity due to venous outflow obstruction of the retina. Vision loss is typically acute, unilateral, and painless. The condition results from impaired venous drainage leading to retinal hemorrhage, edema, and ischemia.


Pathophysiologic Types
Ischemic CRVO accounts for approximately 20–25% of cases and represents complete venous obstruction. Blocked venous return causes capillary backflow, extensive hemorrhage, macular edema, and retinal ischemia. Thrombosis is promoted by limited space at the lamina cribrosa, slow blood flow, vessel wall changes, adjacent arteriosclerotic arterial compression, and increased blood viscosity.
Nonischemic CRVO represents partial or incomplete occlusion and is generally milder with better visual prognosis.


Clinical Features
Patients present with acute, painless, unilateral loss of vision. In nonischemic CRVO, vision loss may be intermittent or incomplete. Visual acuity is often severely reduced, commonly worse than 20/200. An afferent pupillary defect may be present. Fundoscopic examination reveals dilated and tortuous retinal veins, widespread retinal hemorrhages involving all four quadrants in central involvement, optic disc edema, and cotton wool spots. Extensive hemorrhage produces the classic “blood and thunder” appearance.


Essential Assessment
Measure blood pressure. Perform visual acuity testing, visual field assessment, fundoscopy, and tonometry. Normal intraocular pressure ranges from 10–21 mm Hg.


Diagnostic Evaluation
Laboratory studies include CBC, PT/PTT, ESR, ANA, and serum protein electrophoresis to assess for systemic or hyperviscosity conditions. Fluorescein angiography, performed by ophthalmology, differentiates ischemic from nonischemic CRVO by identifying areas of capillary nonperfusion. Gonioscopy is used to evaluate for iris or angle neovascularization.


Differential Considerations
Amaurosis fugax or TIA, cavernous sinus thrombosis, diabetic or hypertensive retinopathy, hyperviscosity syndromes (sickle cell disease, polycythemia, leukemia, multiple myeloma), ocular ischemia syndrome, papilledema, retinal artery occlusion, retinal detachment, temporal arteritis, vitreous hemorrhage, severe anemia with thrombocytopenia, and functional vision loss.


Initial Management Principles
There are no prehospital eye-specific interventions. In the ED, address elevated intraocular pressure if present and manage underlying systemic conditions. The cornerstone of management is early recognition and urgent ophthalmologic referral.


Emergency Department Management
No therapy has proven definitive benefit in the ED setting. In consultation with ophthalmology, attempted therapies may include aspirin, anti-inflammatory agents, systemic corticosteroids, systemic anticoagulation, fibrinolytics (controversial), or laser chorioretinal anastomosis.


Definitive and Ophthalmologic Therapies
Ophthalmologists may use intravitreal corticosteroids such as triamcinolone or antivascular endothelial growth factor agents such as bevacizumab. Panretinal photocoagulation is often performed if neovascularization develops.


Disposition and Follow-Up
Admission depends on ophthalmologic assessment and need for intervention. Patients may be discharged if immediate ophthalmology follow-up is ensured. If ophthalmologic care is unavailable, initiate management of associated conditions and transfer to a facility with specialty services. Long-term follow-up is essential, particularly for ischemic CRVO, to detect neovascularization and secondary glaucoma. Patients require full medical evaluation for underlying vascular disease and comorbidity management.


Clinical Insights and Pitfalls
Elevated intraocular pressure from edema or neovascularization can worsen ischemia and lead to permanent vision loss if untreated. Bilateral CRVO or CRVO in young patients should prompt evaluation for hyperviscosity syndromes and systemic disease.

Emergency and Acute Medicine – Central Retinal Artery Occlusion


Overview
Central retinal artery occlusion (CRAO) is an obstruction of the central retinal artery resulting in sudden, painless, monocular vision loss. It typically affects adults aged 50–70 years and is often described as a “stroke of the eye.” The ophthalmic artery is the first branch of the carotid artery. Risk factors include hypertension, atherosclerosis, carotid artery disease, valvular heart disease, coronary artery disease, vasculitis, lupus, sickle cell disease, and trauma. Incidence is approximately 1–10 per 100,000. Irreversible retinal injury can occur within 90 minutes.


Causative Mechanisms
Embolic causes are most common and include cholesterol or platelet emboli from carotid atherosclerosis, carotid stenosis, valvular heart disease, atrial myxoma, or arterial dissection. Thrombotic causes result from rupture of an atherosclerotic plaque or hypercoagulable states such as sickle cell disease. Inflammatory causes include giant cell arteritis, lupus, and systemic vasculitis. Arterial spasm may be migraine-related. Reduced ocular perfusion may occur with severe hypotension, acute angle-closure glaucoma, or retrobulbar hemorrhage.


Clinical Presentation
Patients present with sudden, painless, unilateral vision loss. Some report prior transient episodes of visual loss lasting seconds to minutes (amaurosis fugax). Visual acuity is markedly reduced. An afferent pupillary defect is usually present. Fundoscopy may reveal emboli within retinal vessels appearing as yellow-white glistening plaques, ischemic retinal edema within 15–20 minutes, and a classic cherry-red spot at the fovea. Retinal arteries may appear empty or show segmented “box-carring.” Within 1–2 hours, the infarcted retina becomes opaque. Partial visual field deficits suggest branch retinal artery involvement.


Essential Evaluation
Immediate assessment includes visual acuity, visual fields, fundoscopic examination, intraocular pressure measurement, and urgent ophthalmology consultation.


Diagnostic Studies
Laboratory evaluation targets underlying causes and includes CBC with platelets, PT/PTT, electrolytes, renal function, glucose, ESR and CRP (especially in patients >55 years for giant cell arteritis), ANA, RF, RPR, hemoglobin electrophoresis, and serum protein electrophoresis. Imaging focuses on embolic sources and includes carotid Doppler ultrasound and echocardiography. Fluorescein angiography or electroretinography may confirm diagnosis.


Differential Considerations
Acute angle-closure glaucoma, central retinal vein occlusion, giant cell arteritis, optic neuritis, and retinal detachment.


Emergency Management Principles
This is a true ophthalmologic emergency. Treatment must begin immediately to attempt retinal salvage. Goals include embolus displacement or dissolution, vasodilation to improve retinal perfusion, and reduction of intraocular pressure to enhance the perfusion gradient.


Emergency Department Interventions
Initiate immediate ocular (global) massage with the patient supine: apply firm pressure on the closed eyelid for 15 seconds, release for 15 seconds, and repeat for five cycles. Administer 100% oxygen via nonrebreather mask and consider hyperbaric oxygen if within 24 hours of onset. Carbogen inhalation may be used if available. Reduce intraocular pressure with IV acetazolamide and topical timolol. Administer aspirin and IV heparin to prevent clot propagation. Obtain emergent ophthalmology consultation for possible anterior chamber paracentesis and consideration of intra-arterial fibrinolysis. If inflammatory arteritis is suspected, begin high-dose systemic corticosteroids immediately.


Medications
First-line options include acetazolamide 500 mg IV or PO, timolol maleate 0.5% ophthalmic drops, IV heparin (80 U/kg bolus then 18 U/kg/hr infusion), and carbogen inhalation. Second-line or adjunctive therapies include aspirin 325 mg PO, methylprednisolone 250 mg IV for suspected arteritis, mannitol, and sublingual nitroglycerin.


Disposition and Follow-Up
Most acute cases require admission for urgent evaluation of embolic, thrombotic, or inflammatory sources. Chronic or remote occlusions without active disease may be evaluated outpatient. All suspected cases require immediate ophthalmology involvement. Carotid imaging is recommended in most patients.


Clinical Insights and Pitfalls
Transient monocular vision loss (amaurosis fugax) is a warning sign for CRAO and systemic stroke and requires urgent evaluation. CRAO is a medical and ophthalmologic emergency with a very narrow therapeutic window. Thorough documentation of visual acuity and fundoscopic findings is essential.

Emergency and Acute Medicine – Cellulitis


Core Concepts
Cellulitis is an acute, spreading infection of the skin and subcutaneous tissues with erythema, warmth, pain, tenderness, and progressive expansion. Extension into deeper layers may evolve into necrotizing soft-tissue infection. Predisposing factors include lymphedema, tinea pedis, open wounds, pre-existing lesions such as furuncles, prior trauma or surgery, retained foreign body, vascular or immune compromise, and injection drug use.


Likely Causes
Uncomplicated cellulitis is most often due to group A streptococci or Staphylococcus aureus, including community-associated MRSA (CA-MRSA). CA-MRSA risk is higher with prior MRSA infection, close contact with MRSA cases, daycare exposure, children, soldiers, incarcerated persons, contact-sport athletes, IV drug users, and men who have sex with men; CA-MRSA prevalence is high enough that empiric coverage is often appropriate, especially in nonresponding cases. Hospital-acquired MRSA is associated with recent hospitalization or long-term care, surgery, vascular devices, dialysis, recent antibiotic exposure, and injection drug use and is resistant to many antibiotics. After lymphatic disruption, nongroup A β-hemolytic streptococci (groups C, B, G) are more common. Diabetic cellulitis may be polymicrobial with streptococci, S. aureus, gram-negatives, and anaerobes, especially with ulcers. Special patterns include periorbital cellulitis (staph and strep), buccal cellulitis (historically Hib, plus anaerobic oral flora with intraoral lacerations or dental abscess), and less common exposures such as Pasteurella (cat/dog bites), Eikenella (human bites), Pseudomonas (hot-tub folliculitis; puncture wounds), Aeromonas (freshwater), Vibrio (seawater/raw seafood), Erysipelothrix (raw fish/meat handlers), clostridia, and anthrax. Pediatric patterns include facial cellulitis (strep pneumo and Hib—declining with vaccination), perianal cellulitis (group A strep), and neonatal cases (group B strep).


Clinical Features
Typical findings include pain, warmth, erythema, edema/induration, fever/chills, tender regional nodes, lymphangitis, and sometimes superficial vesicles. A concurrent subcutaneous abscess can coexist, and a deep abscess should be suspected if there is treatment failure. Buccal/odontogenic cellulitis may progress with fever, neck swelling, dysphagia, and deep-space spread. Pediatric facial cellulitis can be rapidly progressive, usually unilateral with URTI symptoms, and carries risk of cavernous sinus thrombosis and optic nerve injury. Perianal cellulitis presents with pruritic erythema extending outward from the anus, pain with defecation, and sometimes blood-streaked stools. Bedside clues: staphylococcal infection tends to have focal pustule/abscess with fluctuance or drainage and a slower course, while streptococcal infection often has sharper borders, lymphangitis, lymphedema association, and may include nausea from toxin effects.


Key Assessment
Cellulitis is primarily a clinical diagnosis; the exam should look for a portal of entry or deeper infection and assess for airway risk in deep facial/neck involvement.


Testing Strategy
Routine WBC is usually unnecessary. Aspirate/punch biopsy for Gram stain and culture is most useful in treatment failures and in admitted patients to identify resistant organisms such as MRSA. Blood cultures are typically negative in uncomplicated disease but may help in lymphedema-associated infections, buccal or periorbital cellulitis, water-exposure cases, or systemic symptoms with fever/chills. Plain radiographs can detect foreign bodies, subcutaneous gas, or suggest abscess; early osteomyelitis is not reliably seen. Ultrasound helps identify abscess when exam is equivocal and may show “cobblestoning” of the subcutaneous tissue in cellulitis. CT/MRI can help evaluate for necrotizing fasciitis.


Conditions to Differentiate
Important alternatives include necrotizing fasciitis, lymphangitis/lymphadenitis, thrombophlebitis or DVT, insect bite/allergy, gout/pseudogout, ruptured Baker cyst, herpetic whitlow, neoplasm, phytophotodermatitis, erythema migrans, and for facial disease, angioedema, conjunctivitis, or contusion. Pediatric perianal differentials include Candida intertrigo, psoriasis, pinworms, abuse, behavioral causes, and inflammatory bowel disease.


Emergency Management
Airway compromise is a concern with deep facial or neck extension. General approach: account for local resistance patterns and include CA-MRSA coverage when appropriate (notably uncomplicated cellulitis in many settings, periorbital disease, and diabetics). Typical outpatient duration is 7–10 days, with cool compresses, analgesia, elevation, and treatment of tinea pedis when present.


Antibiotic Approach by Scenario
Simple cellulitis outpatient: oral cephalexin plus TMP-SMX for CA-MRSA coverage; alternatives for β-lactam include dicloxacillin, macrolide, or levofloxacin; alternatives to TMP-SMX include clindamycin or doxycycline. Inpatient: IV nafcillin (or equivalent) plus IV vancomycin. Post-lymphatic disruption cellulitis: treat like simple cellulitis. Diabetic cellulitis outpatient: amoxicillin/clavulanate plus TMP-SMX or clindamycin; inpatient: IV ampicillin/sulbactam or imipenem-cilastatin plus IV vancomycin. Adult periorbital cellulitis outpatient: dicloxacillin or azithromycin plus TMP-SMX; inpatient: IV vancomycin. Adult buccal cellulitis outpatient: amoxicillin/clavulanate; inpatient: IV ceftriaxone; odontogenic cases require drainage and anaerobe coverage such as clindamycin. Pediatric facial cellulitis: IV ceftriaxone. Perianal cellulitis: oral penicillin VK outpatient or IV penicillin G inpatient. Bite wounds: amoxicillin/clavulanate. Foot puncture wounds: ciprofloxacin or IV ceftazidime. MRSA: hospital-acquired—IV vancomycin or linezolid; CA-MRSA—TMP-SMX, clindamycin, or doxycycline orally, and vancomycin or clindamycin IV.


Medication Options
Common regimens include amoxicillin/clavulanate, ampicillin/sulbactam, azithromycin, ceftazidime, ceftriaxone, cephalexin, ciprofloxacin, clindamycin, dicloxacillin, doxycycline, imipenem-cilastatin, levofloxacin, linezolid, nafcillin, penicillin VK, aqueous penicillin G, TMP-SMX, and vancomycin with pediatric adjustments and therapeutic monitoring where appropriate.


Disposition Criteria
Admit patients who appear toxic, have tissue necrosis, immunosuppression, significant comorbid illness, inability to tolerate oral meds, unreliable follow-up, or high-risk anatomy. Discharge is reasonable for mild infection in a nontoxic patient who can take oral therapy, has no immunosuppression or major comorbidities, no hand/face involvement, and has reliable follow-up within 24–48 hours.


Follow-Up Guidance
Reassess within 24–48 hours, sooner if fever worsens, lymphangitis develops, or erythema expands. Mark the edge of erythema prior to discharge to track progression.


Clinical Traps
Strep and staph remain the most common causes, and CA-MRSA is common enough that empiric coverage is often required. Clinicians are not reliably accurate at identifying MRSA by appearance alone. Deep abscess can be mistaken for cellulitis; use clinical suspicion and ultrasound to avoid missed abscess.

Emergency and Acute Medicine – Cavernous Sinus Thrombosis


Overview
Cavernous sinus thrombosis is thrombosis within a major intracranial venous drainage pathway and is most often infectious in origin. Infection commonly spreads from facial, odontogenic, or paranasal sinus sources, with hematogenous or contiguous extension. Less frequently, thrombosis occurs in the setting of hypercoagulable states. The cavernous sinus lies superolateral to the sphenoid sinus and surrounds the sella; cranial nerves III, IV, V1, and V2 course within its lateral wall, while cranial nerve VI and the internal carotid artery run medially. Although the cavernous sinus is most often involved, the transverse and superior sagittal sinuses may also be affected.


Pathophysiologic Mechanisms
Infection spreads hematogenously from facial, otic, or neck sources or directly from infected sinus cavities, most commonly sphenoid and ethmoid sinuses. Bacterial proliferation triggers inflammation and coagulation, leading to venous thrombosis. Resulting venous congestion affects adjacent neurovascular structures, producing ophthalmoplegia from involvement of cranial nerves III, IV, or VI, pupillary abnormalities from cranial nerve III dysfunction, and sensory deficits of the forehead or cheek from cranial nerves V1 and V2.


Causative Factors
Septic thrombosis is most common, with Staphylococcus aureus responsible for approximately 70% of cases; Streptococcus pneumoniae, gram-negative organisms, and anaerobes are also implicated. Fungal causes such as Aspergillus and Rhizopus are less frequent. Aseptic causes include granulomatous disease such as tuberculosis, inflammatory disorders, mass effect from skull-base tumors or aneurysms, and hypercoagulable states.


Clinical Presentation
Headache is present in the majority of patients, often accompanied by fever, ocular or retrobulbar pain, facial swelling, visual disturbances, facial dysesthesia, and lethargy or altered mental status. Early physical findings include periorbital edema and chemosis with retinal venous congestion, followed by ptosis, proptosis, and ophthalmoplegia. Cranial nerve deficits are common, particularly lateral gaze palsy from cranial nerve VI involvement and sensory changes in V1 or V2 distributions. Advanced disease may present with meningismus, seizures, coma, or septic shock.


Risk-Oriented History
High-risk features include recent facial trauma, ENT or neurosurgical procedures, manipulation of central facial furuncles, diabetes, or immunocompromised states such as HIV infection, chronic steroid use, or malignancy. Pediatric patients may present with nonspecific symptoms including fever, vomiting, lethargy, or signs of increased intracranial pressure, particularly following otitis or pharyngitis; neonatal cases are especially challenging to diagnose.


Initial Clinical Assessment
Diagnosis is primarily clinical, suggested by venous congestion, ocular findings, unilateral symptoms that rapidly progress to bilateral involvement, and overall toxic appearance. Laboratory studies are supportive but nonspecific, and early imaging findings may be subtle.


Diagnostic Evaluation
Laboratory testing may show leukocytosis, bandemia, and elevated ESR or D-dimer, but lacks sensitivity and specificity. Cerebrospinal fluid analysis may demonstrate parameningeal inflammation or meningitis. Noncontrast CT imaging can be normal early but may later show increased density, filling defects with contrast, dilation of the superior ophthalmic vein, intracranial hemorrhage, or signs of raised intracranial pressure. MRI with MR venography is the diagnostic modality of choice, allowing direct visualization of thrombus and venous structures at all stages of disease.


Alternative Diagnoses
Consider meningitis or encephalitis, intracranial abscess, orbital or periorbital cellulitis, carotid artery aneurysm or fistula, pseudotumor cerebri, acute angle-closure glaucoma, intracranial hemorrhage, and Tolosa–Hunt syndrome.


Emergency Stabilization
Patients may be critically ill and unstable. Immediate assessment and stabilization of airway, breathing, and circulation are essential, with early intubation for airway protection when mental status is impaired and aggressive fluid resuscitation for hemodynamic instability.


Definitive Emergency Management
Initiate broad-spectrum intravenous antibiotics promptly to cover gram-positive organisms including MRSA, gram-negative organisms, and anaerobes, typically using vancomycin or nafcillin combined with a third-generation cephalosporin and metronidazole or clindamycin when indicated. Anticoagulation with heparin may limit clot propagation and improve outcomes, though its use remains controversial and requires exclusion of intracranial hemorrhage prior to initiation. Endovascular thrombolysis may be considered in refractory, severe cases. Systemic corticosteroids may be beneficial in selected patients, particularly with pituitary involvement or inflammatory etiologies. Surgical consultation is required for drainage of the primary infectious source, such as sinus or dental abscesses, and intracranial pressure should be managed aggressively when elevated.


Disposition and Follow-Up
All patients with cavernous sinus thrombosis require hospital admission to a monitored setting, often the intensive care unit. Neurology and neurosurgical consultation are mandatory, and discharge from the emergency department is not appropriate.


Complications and Clinical Cautions
Potential complications include permanent visual impairment, persistent cranial nerve palsies, meningitis, intracranial abscess, seizures, pituitary necrosis with endocrine insufficiency, septic emboli, sepsis, and shock. Mortality remains significant. Maintain a high index of suspicion in patients with recent ENT infections, refractory headache, ocular findings, or hypercoagulable risk factors, as early CT imaging may be misleadingly normal and MRI/MRV should be pursued promptly.

Emergency and Acute Medicine – Carpal Fractures


Overview
Carpal fractures involve the most frequently injured region of the upper extremity. The scaphoid accounts for approximately 68% of cases, followed by the triquetrum at about 18%. These injuries often coexist with other wrist trauma, including scaphocapitate syndrome (capitate fracture with scaphoid fracture), perilunate dislocations, hamate fractures with fourth and fifth carpometacarpal injuries, and concurrent distal radius fractures.


Mechanisms of Injury
Typical mechanisms include a fall on an outstretched hand with wrist hyperextension or hyperflexion, direct blows, axial loading, and repetitive or chronic use injuries. Hyperflexion commonly results in dorsal avulsion fractures, while hyperextension leads to volar avulsion fractures. Hook of hamate fractures are classically associated with forceful swinging motions, such as with racquets or golf clubs.


Clinical Features
Patients usually report a fall or direct impact. Examination reveals pain, swelling, and reduced wrist motion. Careful palpation of individual carpal bones is possible with proper wrist positioning. Scaphoid fractures often present with snuffbox tenderness, which is sensitive but nonspecific; specificity improves with wrist pronation and ulnar deviation. Axial thumb compression may elicit pain but lacks specificity. Palmar tenderness over the scaphoid tubercle at the distal wrist crease with wrist extension is more specific.


Initial Assessment Priorities
A complete examination of the entire upper extremity and shoulder girdle is required to identify associated injuries. A thorough neurovascular assessment is essential, particularly for hamate fractures, which may involve ulnar nerve or artery injury.


Diagnostic Evaluation
Standard imaging includes anteroposterior, lateral, and oblique views of the wrist and hand. Dedicated views, such as scaphoid views, should be obtained when suspicion remains high. CT scanning provides superior fracture detection, while MRI is useful for identifying occult fractures and ligamentous injuries.


Conditions to Differentiate
Consider metacarpal base fractures, distal radius or ulna fractures, lunate dislocation, perilunate dislocation, and in children, distal radius epiphyseal injuries, as pediatric wrist trauma rarely represents a simple sprain.


Early Management
In the prehospital or early ED setting, protect open wounds, elevate the limb, apply ice, remove constricting jewelry, and immobilize the wrist with padded splints. As with all trauma, assess for life-threatening injuries first.


Definitive Emergency Care
Most isolated carpal fractures are initially treated with immobilization aimed at maintaining alignment. Thumb spica splints are used for scaphoid and trapezium fractures. Sugar-tong splints are appropriate for capitate and lunate fractures, maintaining the wrist in neutral position. Volar splints are suitable for triquetrum, pisiform, trapezoid, and hamate fractures with slight wrist extension. Suspected fractures, especially scaphoid injuries, should be splinted even if initial radiographs are negative. Open fractures require immediate irrigation, IV antibiotics targeting Staphylococcus aureus with additional gram-negative coverage for severe soft tissue injury, tetanus prophylaxis, neurovascular monitoring, and urgent orthopedic consultation.


Pain Control
Analgesia includes NSAIDs, mild oral narcotics, or other oral analgesics. Proper immobilization often provides significant pain relief.


Disposition Planning
Open fractures and unstable or displaced injuries requiring operative intervention warrant admission. Closed, nondisplaced fractures adequately immobilized may be discharged with orthopedic follow-up in 7–10 days.


Follow-Up Strategy
All confirmed fractures require orthopedic referral for casting and definitive care. Missed injuries or inadequate immobilization can result in nonunion, avascular necrosis, chronic pain, and disability. Persistent pain despite negative initial imaging should prompt repeat radiographs or advanced imaging after 7–10 days.


Clinical Pearls and Pitfalls
Carpal fractures are frequently occult on initial imaging and easily missed. All clinically suspected fractures should be immobilized. While most scaphoid fractures occur in isolation, other carpal fractures are commonly associated with additional wrist or hand injuries. Long-term outcomes depend heavily on early recognition, proper splinting in a functional position, and timely orthopedic follow-up.

Emergency and Acute Medicine – Peripartum Cardiomyopathy


Core Definition
Peripartum cardiomyopathy is a dilated cardiomyopathy that develops during the final month of pregnancy or within the first 5 months after delivery. Diagnosis requires all of the following: onset of heart failure in the defined peripartum period, no identifiable alternative cause, no preexisting cardiac disease, and objective echocardiographic evidence of systolic dysfunction. Incidence is approximately 3–5 per 10,000 live births. About half of cases recover spontaneously. Reported mortality ranges from 18% to 56%. Thromboembolic complications are more common than in other cardiomyopathies.


Risk Profile and Prognostic Indicators
Risk is increased in women older than 30 years, multiparity, multiple gestations, prolonged tocolytic therapy exceeding 4 weeks, obesity, preeclampsia, and African American race. Poor prognosis is associated with low left ventricular ejection fraction at 6 months postpartum, symptom onset more than 2 weeks after delivery, age over 30 years, African American descent, and multiparity.


Proposed Pathophysiology
The exact cause remains uncertain. Leading theories include viral myocarditis facilitated by pregnancy-related immunosuppression, autoimmune reaction to maternal or fetal antigens, maladaptive response to pregnancy-related hemodynamic stress, stress-induced cytokine activation, prolonged tocolysis, and nutritional deficiencies such as selenium deficiency.


Clinical Presentation
Common symptoms include dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough, dizziness, chest discomfort, fatigue, anorexia, and arrhythmias. History should focus on timing of symptom onset, persistent unexplained cough, excessive weight gain greater than 2–4 lb per week, prior cardiac disease, and complications in previous pregnancies. Examination findings may include jugular venous distention, gallop rhythm, mitral regurgitation murmur, loud P2, pulmonary rales, rapid-onset peripheral edema, hepatomegaly, and hepatojugular reflux.


Essential Evaluation
Chest radiography may show pulmonary venous congestion, cardiomegaly (difficult to interpret in pregnancy), and pleural effusions. Electrocardiography is nonspecific but may demonstrate left ventricular hypertrophy, left atrial enlargement, T-wave changes, ventricular ectopy (≈40%), or atrial fibrillation (≈20%).


Diagnostic Data Interpretation
Laboratory studies typically show normal electrolytes and renal function. Mild postpartum anemia may worsen dyspnea and fatigue. BNP is useful in differentiating cardiac from pulmonary causes of dyspnea; levels >100 pg/mL strongly support heart failure, while ≤50 pg/mL has a high negative predictive value. Chest imaging may demonstrate progressive pulmonary edema patterns from cephalization to interstitial and alveolar edema, sometimes mimicking pneumonia. Echocardiography confirms diagnosis by showing global ventricular dilation, wall thinning, and reduced systolic function. Diagnostic criteria include ejection fraction <45%, fractional shortening <30%, and indexed lv end-diastolic dimension>2.72 cm/m², with exclusion of valvular disease and tamponade. Endomyocardial biopsy is reserved for suspected myocarditis or consideration of immunosuppressive therapy.


Conditions to Exclude
Alternative causes of dilated cardiomyopathy include ischemia, infarction, valvular disease, chronic hypertension, familial cardiomyopathy, alcohol or drug toxicity, metabolic disorders, thyroid disease, infections, autoimmune disease, neuromuscular disorders, and mitochondrial disease. Other causes of dyspnea or edema include pulmonary embolism, pneumonia, asthma, anemia, hyperthyroidism, constrictive pericarditis, tamponade, nephrotic syndrome, and cirrhosis.


Initial and Emergency Management
Differentiate pulmonary edema from reactive airway disease early. Rapid assessment of airway, breathing, and circulation is essential. Provide supplemental oxygen, consider noninvasive ventilation, and address preload and afterload carefully.


Antepartum management includes nitrates, hydralazine, IV diuretics, amlodipine, digoxin for rate control, cautious use of carvedilol when stable, low-molecular-weight heparin when EF <35%, fetal monitoring, and invasive monitoring if unstable.


Postpartum therapy allows addition of ACE inhibitors or ARBs. Anticoagulation is frequently recommended due to high thromboembolic risk. Heparin is preferred during pregnancy; warfarin is avoided until postpartum. Refractory or severe cases may require inotropes, vasopressors, vasodilators, mechanical circulatory support, or extracorporeal membrane oxygenation. Immunosuppressive therapy may be considered if no improvement occurs after 2 weeks of optimal medical therapy, though evidence remains mixed.


Disposition Decisions
All symptomatic patients with new-onset peripartum cardiomyopathy require admission. ICU care is indicated for pulmonary edema, cardiogenic shock, or ischemia. Discharge may be considered only in carefully selected patients with mild dysfunction, established disease, rapid symptom resolution, no ischemia, and reliable close follow-up.


Follow-Up Guidance
Cardiology follow-up is mandatory. Patients should maintain adequate hydration, restrict dietary sodium, avoid alcohol, use compression stockings if needed, monitor daily weights, and seek care for rapid weight gain, worsening dyspnea, syncope, or palpitations.


Clinical Pearls and Pitfalls
Thromboembolism risk is high in pregnancy-associated cardiomyopathy. Early recognition and coordinated management with cardiology and obstetrics significantly improve outcomes.