Emergency And Acute Medicine – Decompression Sickness


Core Description
Decompression sickness is a multisystem disease caused by the formation of inert gas bubbles, primarily nitrogen, that escape from solution into body tissues and fluids during or after a reduction in ambient pressure.


Etiology And Pathophysiology
Decompression sickness occurs when nitrogen that has dissolved in body tissues under increased ambient pressure comes out of solution too rapidly during ascent. As ambient pressure increases, the partial pressure of inspired nitrogen rises, leading to progressive nitrogen absorption into tissues, particularly with longer exposure times. When ascent occurs too quickly, the pressure gradient overwhelms the body’s ability to eliminate nitrogen gradually. Tissues become supersaturated, and gas bubbles form.
According to Henry’s law, the amount of gas dissolved in a liquid is directly proportional to the partial pressure of that gas. Increased partial pressure results in greater gas dissolution, while decreased partial pressure causes gas to come out of solution. Nitrogen bubbles act as foreign bodies, triggering inflammatory and coagulation pathways, increasing vascular permeability, reducing intravascular volume, and causing hemoconcentration.
Clinical manifestations depend on bubble location. Bubbles may obstruct blood flow or lymphatics, leading to ischemia, infarction, or lymphedema, or they may cause mechanical tissue distention resulting in pain.


Risk Factors
Dive-related factors include greater depth, longer bottom time, multiple dives within a day, rapid ascent, and cold water exposure. Human factors include obesity, dehydration, pulmonary disease, and intercurrent illness. Proper use of dive tables or computers reduces but does not eliminate risk. Predive vigorous exercise may reduce risk. Approximately 50% of patients develop symptoms within 1 hour and 90% within 6 hours. Air travel after diving can precipitate decompression sickness because of reduced cabin pressure.


Clinical Presentation


Cutaneous Manifestations
Skin findings include scarlatiniform, erysipeloid, or mottled rashes. Cutis marmorata, a mottled appearance, often indicates more severe disease. A peau d’orange appearance may occur due to lymphatic obstruction.


Musculoskeletal Manifestations (The Bends)
Patients experience dull, deep muscular or joint pain, most commonly affecting the elbows and shoulders. Pain is typically not worsened by movement and is not reproducible with palpation.


Gastrointestinal Manifestations
Symptoms include nausea, vomiting, and abdominal pain.


Pulmonary Manifestations (The Chokes)
Pulmonary symptoms result from obstruction of pulmonary vasculature by gas bubbles and include acute respiratory distress, substernal chest pain or pressure, cough, dyspnea, and hypoxia.


Central Nervous System Manifestations
Neurologic symptoms include weakness, fatigue, numbness, paresthesias, agitation, headache, dizziness, vertigo, seizures, bladder or bowel incontinence, lethargy, and visual disturbances. The spinal cord, particularly the lower thoracic and lumbar regions, is most commonly affected.


Inner Ear Manifestations (The Staggers)
Vestibular involvement causes dizziness, vertigo, tinnitus, and nausea. These symptoms resemble inner ear barotrauma but carry a worse prognosis.


History And Physical Examination
A detailed dive history is essential, including depth, duration, ascent profile, surface intervals, and timing of symptom onset. Physical examination should be comprehensive, with particular attention to a detailed neurologic assessment to identify subtle or evolving deficits.


Essential Evaluation
Diagnosis is primarily clinical and based on recognition of risk factors and characteristic presentations. Neurologic findings should be carefully documented, including improvement or progression. Definitive diagnosis may be supported by a trial of pressure, as rapid symptom relief during recompression in a hyperbaric chamber is often diagnostic.


Diagnostic Testing And Interpretation
Laboratory studies may show elevated hematocrit due to hemoconcentration. Electrolytes, renal function, glucose, and urinalysis should be obtained, with increased urine specific gravity suggesting volume depletion. Arterial blood gas analysis and pulse oximetry are used to monitor oxygenation.
Imaging may include chest radiography to assess for pulmonary barotrauma or noncardiogenic pulmonary edema. Extremity radiographs may help exclude traumatic causes of pain. Head CT is indicated for altered mental status or focal neurologic deficits.


Differential Diagnosis
Consider musculoskeletal injury unrelated to bubble formation, inner or middle ear barotrauma, arterial gas embolism, cerebrovascular accident, and trauma.


Prehospital Management
Early recognition is critical, as postdive extremity pain may be misattributed to muscle strain and neurologic symptoms may be minimized by patients. If air evacuation is required, altitude should be limited to less than 1,000 feet or a pressurized aircraft should be used. In-water recompression is controversial, technically difficult, and requires extensive support.


Initial Stabilization
Airway, breathing, and circulation should be managed promptly. Administer 100% normobaric oxygen via mask or endotracheal tube to enhance nitrogen elimination, reduce bubble size, and improve tissue oxygenation. Maintain the patient in a supine position to minimize cerebral involvement. Early recompression in a hyperbaric chamber is essential.


Emergency Department Management
Administer intravenous 0.9% normal saline to correct dehydration and maintain urine output of 1–2 mL/kg/hour. Dehydration is common due to pressure-induced diuresis, exertion, dry compressed air breathing, and capillary leak. Adequate hydration promotes nitrogen elimination.
Arrange urgent hyperbaric oxygen recompression therapy and transfer to the nearest facility. Insert a prophylactic chest tube for known pneumothorax to prevent tension pneumothorax during recompression. Inflate endotracheal and Foley catheter balloons with saline or water to prevent compression-related damage.
Provide analgesics and antiemetics as needed. Diazepam may be used for severe vertigo. Adjunctive NSAIDs or heliox may reduce the number of recompression treatments required. Consultation with Divers Alert Network is recommended for expert guidance and referral.


Disposition And Follow-Up
All patients with suspected or confirmed decompression sickness should be referred for hyperbaric therapy. Stable patients with mild symptoms may be discharged after treatment. Patients should avoid air travel after treatment, as reduced ambient pressure may worsen symptoms.


Follow-Up Recommendations
Ensure hyperbaric medicine follow-up and reinforce diving safety counseling.


Key Clinical Lessons And Common Errors
Musculoskeletal decompression sickness can be difficult to distinguish from benign musculoskeletal pain. Significant fatigue alone may represent decompression sickness. Even mild or resolving symptoms warrant hyperbaric recompression therapy. Do not delay recompression for laboratory testing or imaging when decompression sickness is the likely diagnosis. In-water recompression should be avoided.

Emergency and Acute Medicine – Caustic Ingestion


Core Concept
Caustic ingestion causes chemical injury to tissues through acid or alkali exposure. Alkalis dissociate in water to form hydroxyl (OH⁻) ions, producing liquefaction necrosis that primarily damages the esophagus, though gastric injury can occur. Injury progresses from superficial hyperemia and mucosal edema to blistering, ulceration, full-thickness necrosis, perforation, and late fibrosis with esophageal strictures. Alkalis typically do not cause systemic toxicity.
Acids dissociate to form hydrogen (H⁺) ions, leading to coagulation necrosis with eschar formation. Due to rapid esophageal transit, acids mainly injure the stomach, producing edema, inflammation, hemorrhage, necrosis, perforation, and late gastric outlet obstruction. Acids are well absorbed and may cause hemolysis and systemic metabolic acidosis.


Etiologic Sources
Injuries result from direct chemical exposure to acids or alkalis, commonly found in household and industrial products. These include ammonia hydroxide, sodium hydroxide (drain and oven cleaners), sodium hypochlorite (bleach), sulfuric acid (car batteries), hydrochloric acid (toilet cleaners), hydrofluoric acid (glass etching and microchip industries), phenol, formaldehyde, iodine, detergents containing borates or phosphates, rust removers, and button batteries.


Clinical Manifestations
Oropharyngeal findings may include pain, erythema, burns, erosions, ulcers, drooling, hoarseness, stridor, or aphonia; absence of visible lesions does not exclude severe visceral injury. Pulmonary involvement presents with cough, tachypnea, or aspiration pneumonitis. Gastrointestinal symptoms include chest or abdominal pain, dysphagia, odynophagia, emesis or hematemesis, melena, and signs of perforation or peritonitis. Cardiovascular findings include tachycardia and hypotension. Acid ingestion may cause hemolysis. Dermal exposure causes chemical burns, and ocular exposure ranges from conjunctival injection to full-thickness corneal injury. Metabolic acidosis may be present, particularly with acid ingestion.


Essential Initial Assessment
A clear history or signs of exposure are critical. Normal oropharyngeal examination does not rule out esophageal or gastric injury.


Diagnostic Evaluation
Laboratory testing includes CBC, electrolytes, BUN, creatinine, glucose, and arterial blood gas analysis. Blood cultures are indicated if mediastinitis or peritonitis is suspected. Type and cross-match should be obtained when bleeding is a concern. Chest and abdominal radiographs assess for perforation. Esophagogastroduodenoscopy is indicated in symptomatic patients to assess injury severity and should be performed within 12–24 hours, provided the airway is secure and there is no severe pharyngeal injury or respiratory distress. Acute contrast studies are not recommended but may be used later to evaluate strictures.


Key Alternative Diagnoses
Other chemical burns, foreign body ingestion, and upper airway infection or angioedema should be considered.


Prehospital Care
For oral exposure with mild symptoms, rinse the mouth with water or milk if the patient can swallow, has no vomiting, airway compromise, or significant abdominal pain. Copious irrigation is required for ocular or dermal exposure.


Emergency Stabilization
Airway protection is paramount; perform early intubation if respiratory compromise is present, avoiding blind nasotracheal intubation. Treat hypotension with isotonic IV fluids.


Emergency Department Management
Immediate irrigation of skin or eyes with water or normal saline should continue until physiologic pH is achieved, recognizing that alkali exposures require more prolonged irrigation. Induced emesis, activated charcoal, gastric lavage, and neutralizing agents are contraindicated. Limited dilution with water or milk may be considered within 30 minutes of ingestion if there is no airway compromise or suspected perforation; excessive volumes should be avoided. Keep patients NPO after oral exposure. Administer antiemetics and IV acid suppression for symptom control. Initiate broad-spectrum antibiotics if mediastinitis, peritonitis, or corticosteroid therapy is planned. Corticosteroid use to prevent esophageal strictures remains controversial and should be decided collaboratively; antibiotics are required if steroids are used. Surgical consultation is mandatory for suspected perforation or full-thickness necrosis. Hydrofluoric acid exposures require calcium therapy, including topical, intradermal, or intra-arterial calcium gluconate depending on severity and location.


Medications
Supportive medications may include ondansetron for nausea, IV proton pump inhibitors or H2 blockers for symptom relief, and corticosteroids only with multidisciplinary agreement. Calcium gluconate is essential for hydrofluoric acid injuries.


Disposition
All symptomatic patients and all nonaccidental ingestions require hospital admission. Asymptomatic patients with accidental ingestion who can swallow without difficulty and have no concerning findings may be discharged with instructions.


Follow-Up
Psychiatric evaluation is required for intentional ingestions.


Clinical Pearls
Early dilution with water or milk within 30 minutes may limit injury in select patients. Copious irrigation is essential for dermal and ocular exposures, particularly with alkalis. The absence of oral burns does not exclude severe internal injury.

Emergency and Acute Medicine – Cardiogenic Shock


Core Concept
Cardiogenic shock is defined by sustained hypotension and systemic hypoperfusion resulting from primary cardiac pump failure despite adequate intravascular volume and left ventricular filling pressures. It remains the leading cause of in-hospital mortality in patients with acute myocardial infarction (AMI). Approximately 5–8% of patients with STEMI develop cardiogenic shock. Pathophysiology includes severe LV dysfunction (often ≥40% infarction), infarction superimposed on chronic LV disease, reinfarction, mechanical complications (acute mitral regurgitation, ventricular septal rupture, free wall rupture with tamponade), and right ventricular infarction. A systemic inflammatory response with excess nitric oxide may worsen vasodilation and myocardial depression. Early β-blocker, ACE inhibitor, or aggressive diuretic use may contribute to shock development in vulnerable patients.


Underlying Causes
Acute myocardial infarction
Sepsis
Myocarditis
Myocardial contusion
Valvular heart disease
Dilated or ischemic cardiomyopathy
Left atrial myxoma
Drug toxicity (β-blockers, calcium channel blockers, anthracyclines)


Clinical Presentation
Airway and breathing findings include early tachypnea and labored respirations progressing to respiratory failure, diffuse crackles or wheezing, and hypoxia. Circulatory findings include systolic blood pressure <90 mm hg or a ≥30 drop from baseline, tachycardia, weak pulses, oliguria (<20 ml />r), cyanosis, pallor, diaphoresis, altered mental status, and hypothermia. Jugular venous distention is common. Cardiac findings may include ischemic chest pain, apical systolic murmur (acute MR), gallop rhythm (S3 indicating severe LV dysfunction; S4 common in AMI with sinus rhythm), or a systolic click suggesting papillary muscle or chordal rupture. GI symptoms include epigastric pain, nausea, and vomiting. Neurologic findings include obtundation or confusion. History should be obtained rapidly from patient, family, or EMS, focusing on cardiac risk factors and medication use. Physical exam emphasizes differentiation from distributive or hypovolemic shock; cool extremities with elevated JVP favor cardiogenic shock.


Initial Evaluation Priorities
Diagnostic studies help define the extent of myocardial injury and identify candidates for urgent catheterization or surgery.


Key Diagnostics
Electrocardiogram may show ST-elevation MI, NSTEMI patterns, dysrhythmias, or LV hypertrophy; a normal ECG does not exclude AMI. Laboratory tests include troponin, CK/CK-MB, BNP (diagnostic and prognostic), electrolytes, renal function (acute kidney injury strongly predicts mortality), CBC, and relevant drug levels (e.g., digoxin). Chest radiograph may demonstrate pulmonary edema, pleural effusions, cardiomegaly, pneumonia, pneumothorax, or pericardial effusion. Emergent transthoracic echocardiography with Doppler is critical to assess LV function, wall-motion abnormalities, acute MR or septal defects, RV size and function (RV infarction vs pulmonary embolism), and pericardial tamponade.


Important Differentials
Obstructive shock: tension pneumothorax, cardiac tamponade, pulmonary embolism, air embolism, esophageal rupture
Distributive shock: sepsis, anaphylaxis, adrenal crisis, neurogenic shock
Hypovolemic shock: hemorrhage, dehydration, GI losses, burns


Prehospital Management
Immediate airway, oxygen, IV access, and monitoring. Consider cautious fluid bolus if lungs are clear. Administer aspirin. Use nitroglycerin or morphine for ischemic pain only if hypotension is absent. Transport AMI patients to centers with 24-hour revascularization capability.


Early Stabilization in the ED
Secure airway and provide ventilatory support as needed; etomidate is preferred for induction due to minimal hemodynamic effect. Establish two large-bore IV lines and continuous cardiac monitoring. Administer a cautious fluid challenge (100–250 mL NS) if no pulmonary congestion. Insert Foley catheter for urine output monitoring.


Definitive Emergency Management
For AMI, initiate aspirin and heparin, consider thrombolysis if PCI or CABG unavailable, and use GP IIb/IIIa inhibitors when appropriate prior to PCI. Norepinephrine is the first-line vasopressor for hypotension; dopamine may be used if norepinephrine is unavailable. In normotensive patients with low cardiac output, dobutamine may be added, sometimes combined with nitroprusside in acute MR. Milrinone may be considered as adjunctive in selected cases. Pulmonary edema in normotensive patients may be treated with nitroglycerin infusion or diuretics. Early cardiology consultation is essential; intra-aortic balloon pump support can improve survival in experienced centers. Early revascularization is the single most effective life-saving intervention.


Common Medications
Dobutamine 3–5 μg/kg/min IV, titrate as needed
Dopamine 3–5 μg/kg/min IV, titrate as needed
Norepinephrine starting at 2 μg/min IV, titrate to MAP
Nitroglycerin 10–20 μg/min IV (non-PVC tubing)
Milrinone loading 50 μg/kg, then 0.375–0.75 μg/kg/min IV
Furosemide 40–80 mg IV (if appropriate)
Nitroprusside 0.3 μg/kg/min IV, titrate cautiously


Disposition
All patients with cardiogenic shock require admission to an intensive care unit.


Clinical Takeaways
Cardiogenic shock is the most common cause of death in hospitalized AMI patients. Early identification of preshock states, rapid hemodynamic support, and prompt revascularization dramatically improve outcomes.

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 – 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 – 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.