Emergency and Acute Medicine – Burns


Overview And Definitions
Burns are acute injuries to skin and underlying tissues resulting from thermal, chemical, electrical, radiation, or mechanical energy transfer. Severity is determined by burn depth, total body surface area (TBSA) involved, anatomic location, and associated inhalation or systemic injury.


Etiology And Mechanisms
Burns are broadly classified into seven categories. Scald injuries result from hot liquids, grease, or steam. Contact burns arise from exposure to hot or cold surfaces. Thermal burns are caused by fire or open flames. Radiation burns occur from ionizing or nonionizing exposure. Chemical burns result from acids, alkalis, or other corrosive substances. Electrical burns occur from low- or high-voltage exposure and may cause deep tissue injury with minimal skin findings. Friction burns include road rash and rope burns.


Clinical Presentation And Associated Findings
Most burns demonstrate visible skin injury. Inhalation injury should be suspected with facial burns, pharyngeal erythema, singed nasal hair or eyelashes, carbonaceous sputum, and changes in respiratory mechanics such as wheezing, coughing, or tachypnea. Electrical and chemical burns may appear deceptively minor externally, sometimes showing only entry or exit wounds.
History should include an AMPLE assessment, burn source and environment, possibility of explosion, medical history, medications, allergies, and tetanus status. Carbon monoxide poisoning is the most common cause of death in fires and renders pulse oximetry unreliable. Cyanide poisoning should be considered when synthetic materials such as wool, nylon, silk, or polyurethane are involved.
Physical examination prioritizes airway assessment, followed by a full trauma survey. Evaluate the face, oropharynx, and nares for inhalation injury, assess the cervical spine when mechanism is concerning, examine the eyes for corneal burns, and estimate burn depth and surface area. In children, specific burn patterns may raise concern for nonaccidental injury.


Assessment Of Burn Severity
Burn size is expressed as a percentage of TBSA. In adults, the rule of nines estimates surface area: head and neck 9%, each arm 9%, each leg 18%, anterior trunk 18%, posterior trunk 18%, and perineum or palm 1%. In infants and children, the head accounts for a larger percentage and the legs for less.
The Lund and Browder chart provides age-adjusted estimates and is more accurate. The palm method, where the patient’s palm and fingers equal approximately 1% TBSA, is useful for scattered burns.
Depth classification includes superficial (first-degree) burns involving only the epidermis with erythema and pain, healing without scarring. Partial-thickness (second-degree) burns involve the dermis and may be superficial or deep. Superficial partial-thickness burns are pink, moist, painful, and heal within weeks with minimal scarring. Deep partial-thickness burns have pale dermis, reduced sensation, and often result in scarring or contractures. Full-thickness (third-degree) burns extend through the dermis, producing leathery, insensate skin and requiring surgical management. Fourth-degree burns involve deeper structures such as fascia, muscle, or bone and cause significant disability.


Diagnostic Evaluation
Severe burns require laboratory evaluation including CBC, electrolytes, renal function, glucose, coagulation studies, type and crossmatch, and pregnancy testing when appropriate. Arterial blood gas with carboxyhemoglobin level is indicated for suspected inhalation injury. Cyanide levels may be obtained selectively. Imaging may include chest radiography. Bronchoscopy is useful to evaluate inhalation injury, and ECG monitoring is important in electrical burns and in older patients.


Prehospital And Initial Management
Immediate care focuses on stopping the burning process, removing contaminated clothing or jewelry, keeping the patient warm, and cooling burned areas when appropriate. Airway protection with early oxygen administration is essential, with prompt intubation for respiratory compromise. Early IV access and fluid resuscitation are critical in burns exceeding 20% TBSA. Adequate analgesia should be provided, wounds covered with clean materials, and patients transported promptly to a burn center when indicated.


Emergency Department Management
Airway control remains the top priority, with early intubation for upper airway involvement or circumferential neck burns. Provide supplemental oxygen, IV access, continuous monitoring, analgesia, and assessment for associated injuries.
Fluid resuscitation for partial- and full-thickness burns greater than 20% TBSA is guided by the Parkland formula in adults: 4 mL/kg/%TBSA using lactated Ringer solution, with half administered in the first 8 hours and the remainder over the next 16 hours. Urine output goals are 0.5 mL/kg/hr in adults and 1 mL/kg/hr in children.
Escharotomy is indicated for circumferential burns causing vascular or respiratory compromise. Wound care includes topical antibiotics, nonadherent dressings, and avoidance of prophylactic systemic antibiotics. Transfer to a burn center should not be delayed for wound care. Minor burns may be managed as outpatients with careful cleansing, blister management, topical therapy, and daily dressing changes.


Special Populations
Children require modified fluid resuscitation, with the Galveston formula providing more accurate estimates. They are at higher risk of hypothermia and hypoglycemia and require close monitoring. Nonaccidental trauma must be considered.
In pregnancy, maternal and fetal risks are significant, fluid needs may be higher, and early obstetric consultation and fetal monitoring are recommended.


Disposition And Follow-Up
Admission is required for moderate to severe burns, suspected abuse, inability to manage wounds, or need for specialized care. Burn center referral is indicated for extensive burns, involvement of critical areas, electrical or chemical burns, inhalation injury, or significant comorbidities.
Patients with minor, noncritical burns may be discharged if reliable, with close follow-up arranged within 1–2 days to reassess wound status, pain control, and infection.


Clinical Insights And Common Errors
Early airway protection and aggressive fluid resuscitation are critical determinants of outcome. Delayed recognition of inhalation injury can be fatal. Adequate pain control should never be deferred. Children require vigilant monitoring for hypoglycemia and hypothermia, and fluid needs must be reassessed frequently.

Emergency and Acute Medicine – Bundle Branch Blocks


Overview And Definitions
Bundle branch blocks (BBBs) result from impaired intraventricular conduction through the right or left bundle branches. In complete BBB, conduction is absent or markedly delayed in one bundle while the other conducts normally, causing the affected ventricle to depolarize via slower muscle-to-muscle transmission. This produces a widened, disorganized QRS complex ≥120 msec.
Incomplete BBB represents delayed but not fully blocked conduction, with QRS duration between 100 and 120 msec.
Right bundle branch block (RBBB) reflects delayed right ventricular depolarization, whereas left bundle branch block (LBBB) reflects delayed left ventricular depolarization. LBBB may result from delay in the main left bundle or both left fascicles and leads to early right septal activation with loss of normal septal Q waves on ECG.


Anatomic And Conduction Considerations
The left bundle divides into two fascicles. The left anterior fascicle conducts impulses inferiorly, anteriorly, and to the right; its blockage alters frontal plane axis. The left posterior fascicle activates the midseptum and inferior–posterior walls; isolated block is rare.
Bifascicular block refers to RBBB combined with either left anterior or left posterior fascicular block.


Etiology And Pathophysiology
Common causes include myocardial infarction, cardiomyopathy, chronic hypertension, valvular heart disease, age-related fibrosis of the Purkinje system, and postoperative changes after cardiac surgery. Congenital heart disease such as atrial septal defect may be associated. Exercise-induced BBBs can occur.
Certain diseases and conditions are notable, including Brugada syndrome (typically presenting with RBBB pattern and associated with sudden cardiac death) and Chagas disease, particularly in Central and South America.
Medications may contribute, including β-blockers, calcium channel blockers, tricyclic antidepressants, class Ia and Ic antiarrhythmics, and digoxin.


Clinical Presentation
Many patients are asymptomatic. RBBB may be associated with a split S2 that persists with expiration, while LBBB produces a paradoxical or reversed split S2. When symptoms occur, they may include syncope or presyncope, chest pain, or manifestations related to the underlying cardiac disease.


Initial Evaluation And Essential Workup
A 12-lead ECG is central to diagnosis. Careful clinical assessment is required to identify ischemia, syncope, or associated dysrhythmias.


Electrocardiographic Features
RBBB shows a QRS duration ≥0.12 sec when complete and 0.10–0.12 sec when incomplete, with rsrʹ, rsRʹ, or rSRʹ (“M-shaped”) complexes in V1–V2 and a wide, deep S wave in V5–V6. Brugada syndrome presents with RBBB morphology plus ST-segment elevation in V1–V3.
LBBB is characterized by broad, slurred R waves in leads V5–V6, I, and aVL; small or absent R waves with deep S waves in V1–V2; and absence of normal septal Q waves in V5–V6 and I.
Left anterior fascicular block shows a QRS <120 msec with left-axis deviation (approximately −45° to −90°), deep s waves in ii, iii, and avf, qr complexes i avl.< />pan>
Left posterior fascicular block shows QRS <120 msec with right-axis deviation (≥120°), rs complexes in i and avl, qr ii, iii, avf, after excluding other causes of deviation.< />pan>


Diagnostic Testing
Laboratory testing may include electrolytes when metabolic disturbances are suspected and cardiac enzymes if ischemia is a concern. Chest radiography can reveal cardiomegaly or congestive heart failure. Electrophysiologic testing may be indicated in patients with unexplained syncope and structural heart disease as part of inpatient evaluation.


Differential Diagnosis
Consider ventricular tachycardia, myocardial infarction, ventricular hypertrophy, hyperkalemia, and drug-induced conduction abnormalities. In patients with LBBB, myocardial infarction assessment relies on criteria such as the Sgarbossa criteria, including concordant ST elevation or depression and excessive discordant ST elevation.


Management In The Emergency Setting
Isolated bundle branch block itself does not require specific therapy. Management focuses on treating associated conditions such as ischemia, heart failure, or syncope. Continuous monitoring is important, as BBBs can complicate rhythm interpretation and mimic ventricular tachycardia or ischemia.
Patients with symptomatic bifascicular block or high-grade atrioventricular block should have transcutaneous pacing pads applied, with sedation and analgesia as needed. Transvenous pacing is indicated for bifascicular block with type II second-degree or third-degree AV block, or for alternating LBBB and RBBB. New BBB with symptoms suggestive of myocardial infarction warrants urgent reperfusion therapy or catheterization.


Disposition And Follow-Up
Admission is required for patients with suspected myocardial ischemia, syncope, dysrhythmias, or BBB associated with high-grade AV block. Asymptomatic patients or those with incidental findings may be discharged with appropriate counseling. Referral to a cardiologist is recommended to evaluate for underlying cardiac disease.


Clinical Pearls And Pitfalls
New conduction abnormalities should always prompt consideration of myocardial ischemia. Specific ECG criteria help identify infarction in the presence of bundle branch block. Careful rhythm interpretation is essential to avoid misdiagnosing ventricular tachycardia or missing acute ischemia.

Emergency and Acute Medicine – Brugada Syndrome


Overview And Definitions
Brugada syndrome is an inherited cardiac channelopathy caused by mutations in cardiac sodium (Na⁺) channels, occurring in the absence of structural heart disease. It carries a very high risk of sudden cardiac death, typically due to ventricular fibrillation. Two-year mortality approaches 30% without intervention. The condition accounts for 40–60% of cases previously labeled idiopathic ventricular fibrillation. It is more prevalent in men, particularly those of Southeast Asian descent, but can affect all ages, sexes, and races.


Etiology And Pathophysiology
Brugada syndrome is inherited in an autosomal dominant pattern in approximately 50% of cases, with variable penetrance. More than 70 sodium channel mutations have been identified, most involving the SCN5A gene, which accounts for roughly 20% of cases. The abnormal sodium current predisposes to malignant ventricular dysrhythmias, especially under triggering conditions such as fever, metabolic derangements, or drug exposure.


Clinical Presentation
Patients most commonly present with syncope, near-syncope, palpitations, or sudden cardiac arrest due to polymorphic ventricular tachycardia or ventricular fibrillation. Episodes often occur at rest or during sleep. A history may reveal nocturnal agonal respirations, fever-associated symptoms, cocaine use, or exposure to tricyclic antidepressants or psychotropic drugs. Family history is critical and may include unexplained drowning, early or sudden cardiac death, or known Brugada syndrome in relatives. Physical examination is usually normal but should focus on excluding alternative causes of syncope or dysrhythmia.


Diagnostic Evaluation
A 12-lead ECG is essential. Toxicology screening and careful history and family assessment are required. Laboratory studies should evaluate electrolytes, metabolic abnormalities, and ischemia when appropriate.


Electrocardiographic Findings
Diagnosis is based on characteristic ECG patterns in the right precordial leads (V1–V3), often with right bundle branch block or incomplete right bundle branch block morphology and ST-segment elevation.
Type 1 (coved pattern) shows ≥2 mm ST elevation with a downsloping, concave ST segment and a negative symmetric T wave, without QRS duration mismatch between V1 and V6.
Type 2 (saddleback pattern) shows an r′ ≥2 mm followed by convex ST elevation and a QRS duration mismatch between V1 and V6. ST elevation may be limited to V1 and rarely extends to V3.


Additional Testing
Laboratory testing includes serum chemistries, cardiac biomarkers if ischemia is suspected, CBC in syncope evaluation, and D-dimer when pulmonary embolism is considered. Chest radiography assesses cardiomegaly, and CT angiography is used selectively. Electrophysiology testing with sodium channel blocker challenge may unmask diagnostic ECG changes. Implantable cardioverter-defibrillator (ICD) placement dramatically reduces mortality.


Differential Diagnosis
Consider other causes of syncope and dysrhythmia, including vasovagal syncope, hypovolemia, pregnancy, atrial and ventricular tachyarrhythmias, Wolff–Parkinson–White syndrome, long QT syndromes, high-grade AV block, symptomatic bradycardia, and drug overdose (especially TCAs). ECG mimics include isolated RBBB, athletic heart changes, septal hypertrophy, pectus excavatum, arrhythmogenic right ventricular cardiomyopathy, STEMI, myocarditis, pericarditis, electrolyte disorders, and pulmonary embolism.


Management And Emergency Care
Initial management follows standard airway, breathing, and circulation principles, with full ACLS protocols for arrest or unstable dysrhythmias. Continuous cardiac monitoring is required. Cardiology consultation for electrophysiology evaluation is essential. Electrolyte and metabolic abnormalities should be corrected promptly. Antiarrhythmic medications are generally ineffective. Management of asymptomatic patients remains controversial, though EP evaluation is recommended.


Disposition And Follow-Up
Patients with concerning ECG findings, unexplained syncope, ongoing dysrhythmias, or inability to obtain urgent cardiology follow-up should be admitted. Discharge may be considered only if the patient is asymptomatic, hemodynamically stable, and cleared by cardiology, including appropriate ICD interrogation if present. All patients with suspected or confirmed Brugada syndrome require electrophysiology follow-up.


Key Clinical Insights And Diagnostic Traps
Maintain suspicion for Brugada syndrome in cases of unexplained syncope or sudden cardiac death, particularly with a relevant family history. The ECG pattern—RBBB or incomplete RBBB with ST elevation isolated to V1–V3—is central to diagnosis, but several mimics exist. Fever, systemic illness, or drugs may unmask the Brugada pattern. Early cardiology involvement is critical, as ICD implantation is the only proven therapy that nearly eliminates the risk of sudden cardiac death.

Emergency and Acute Medicine – Acute Bronchitis


Overview And Definitions
Acute bronchitis is an inflammatory condition of the bronchial airways characterized by mucosal hyperemia, edema, and excess mucus production. Impairment of ciliary function and local immune defenses leads to airway obstruction caused by edema, secretions, and bronchial smooth muscle spasm. The condition is usually self-limited and most often follows an upper respiratory tract infection.


Etiology And Pathophysiology
Acute bronchitis is predominantly viral in origin. Common pathogens include parainfluenza, influenza A and B, respiratory syncytial virus, human metapneumovirus, adenovirus, coronavirus, rhinovirus, echovirus, coxsackievirus, and, less commonly, measles and herpes viruses, which may cause severe disease. Certain organisms are associated with more prolonged or severe illness, including Mycoplasma pneumoniae, Chlamydia pneumoniae, and Bordetella pertussis. Pertussis incidence is increasing even among immunized individuals due to waning immunity. Bacterial causes are otherwise uncommon except in patients with chronic lung disease.


Clinical Presentation
Patients often describe a prodrome of malaise, chills, myalgias, coryza, and sore throat, followed by cough that is initially dry and later becomes mucoid or mucopurulent. Mild dyspnea and chest discomfort or burning related to coughing are common. Symptoms typically improve after 3–5 days, though cough and fatigue may persist for 1–3 weeks. Physical examination may reveal low-grade fever, tachypnea, rhonchi or wheezing, and occasional crackles. Mild hemoptysis can occur.


Diagnostic Evaluation
Diagnosis is primarily clinical. Routine laboratory testing is generally unnecessary. Influenza A and B testing may be useful when results would alter management or reporting. Pertussis should be considered in patients with cough lasting 14 days or longer, especially with paroxysms, post-tussive vomiting, inspiratory whoop, or known outbreak exposure. Chest radiography is not routinely indicated but should be obtained in patients with hypoxia, dyspnea, chest pain, tachycardia, tachypnea, fever ≥38°C, focal lung findings, advanced age, or significant comorbid disease. Imaging typically shows no consolidation in uncomplicated bronchitis.


Differential Diagnosis
Important alternatives include pneumonia, reactive airway disease or asthma, aspiration, acute sinusitis, and, in chronic cases, gastroesophageal reflux disease, chronic bronchitis, bronchiectasis, ACE inhibitor–related cough, malignancy, heart failure, sarcoidosis, and psychogenic cough.


Management And Emergency Care
Treatment is supportive. Oxygen is administered for hypoxia, and fluids are given if dehydration is present. Bronchodilators may benefit patients with wheezing or evidence of airflow obstruction. Antitussives and antipyretics can be used for symptomatic relief. Antiviral therapy such as oseltamivir or zanamivir may be considered for early influenza-related illness, and amantadine may be used selectively during influenza A outbreaks, accounting for resistance patterns. Antibiotics are generally not recommended, even with purulent sputum, due to minimal benefit and risks of resistance and adverse effects. They may be considered if fever recurs after initial improvement or if pertussis is confirmed. Smoking cessation should be encouraged but does not alone justify antibiotic use.


Disposition And Follow-Up
Most patients can be safely discharged if there is no significant respiratory compromise. Admission is reserved for those with hypoxia, significant cardiopulmonary disease, severe illness, or diagnostic uncertainty. Patients should be advised that cough may persist for several weeks and instructed to return for worsening symptoms, new dyspnea, or lack of improvement after 2–3 weeks. Routine follow-up is unnecessary if symptoms resolve.


Key Clinical Insights And Common Errors
High fever, hypoxia, or focal pulmonary findings should prompt evaluation for pneumonia. Acute bronchitis is most often viral, and unnecessary antibiotic use is a frequent error. Immunocompromised patients may develop more severe disease and warrant closer monitoring and coordination with their primary physician.

Emergency and Acute Medicine – Bronchiolitis


Overview and Definitions
Bronchiolitis is a lower respiratory tract infection characterized by airway inflammation, bronchoconstriction, wheezing, tachypnea, and varying degrees of respiratory distress, typically preceded by an upper respiratory prodrome.


Etiology and Pathophysiology
Respiratory syncytial virus is responsible for approximately 85–90% of cases. Other causative viruses include influenza, parainfluenza, and adenovirus. Disease incidence peaks during winter months. Viral infection leads to mucosal edema, increased mucus production, and small airway obstruction, resulting in impaired ventilation and increased work of breathing.


Clinical Presentation
Bronchiolitis primarily affects children younger than 2 years, most commonly infants under 1 year. Initial symptoms include nasal congestion with marked rhinorrhea, followed by cough that may be associated with posttussive vomiting. Wheezing, crackles, and rhonchi are common on auscultation. Respiratory distress manifests as tachypnea, nasal flaring, retractions, and grunting, often worsening over 1–3 days. Fever is usually low-grade (<39.5°c). hypoxemia is typically mild, and cyanosis rare. decreased oral intake common, though frank dehydration uncommon. apnea may occur, particularly in premature or very young infants. high-risk children receive monthly intramuscular palivizumab during rsv season to reduce infection risk.< />pan>


Essential Evaluation
Diagnosis is clinical. Assessment focuses on respiratory effort, oxygenation, and hydration status. Pulse oximetry is useful for confirming oxygenation and trending disease progression. Identification of the viral cause may assist with inpatient cohorting but rarely alters acute management.


Diagnostic Tests and Interpretation
Most patients require no laboratory testing beyond pulse oximetry. Nasopharyngeal aspirates or washes for viral studies may be considered in critically ill children, febrile infants under 3 months, those with atypical features, suspected alternative diagnoses (e.g., pertussis or chlamydia), significant comorbidities (chronic lung or cardiac disease), or prematurity. Chest radiographs typically show hyperinflation, peribronchial thickening, atelectasis, or variable infiltrates; atelectasis in young infants suggests more severe disease. Imaging is not routinely indicated and is reserved for atypical presentations, lack of improvement after 2–3 weeks, concern for alternative diagnoses, or impending respiratory failure. Septic evaluation may be required in febrile neonates, and urine testing should be considered in febrile infants 1–3 months old.


Differential Diagnosis
Asthma or recurrent virus-induced wheezing, pertussis (paroxysmal cough without wheeze between spells), bacterial pneumonia (toxic appearance, focal consolidation), foreign body aspiration (sudden onset, often afebrile), and congestive heart failure (feeding difficulty, failure to thrive).


Prehospital Care
Young infants have limited respiratory reserve and may deteriorate rapidly. Continuous cardiorespiratory monitoring and oxygen supplementation are indicated when saturations fall below 90–92% or distress is severe. Vigilance for apnea is critical, especially in infants under 7 weeks, weight <4 kg, or with marked tachypnea comorbidities. bag-mask ventilation may be required for recurrent apneas.< />pan>


Initial Stabilization in the ED
Management follows pediatric advanced life support principles with attention to airway, ventilation, and hydration. Early intubation is indicated for recurrent apnea or impending respiratory failure.


Emergency Department Management
Supplemental oxygen is provided for hypoxemia. Parenteral hydration is used when oral intake is inadequate or respiratory distress is significant. Most children do not benefit from routine pharmacotherapy. Bronchodilators may be trialed in moderate to severe disease, continued only if a clear reduction in work of breathing is observed. Corticosteroids alone generally do not alter outcomes; however, combined nebulized epinephrine with oral dexamethasone may reduce admissions in moderate to severe cases, likely due to synergistic effects. Antibiotics are not indicated unless there is evidence of bacterial infection. Ribavirin has no role in ED management.


Medications
Therapeutic trials may include nebulized albuterol or levalbuterol, nebulized epinephrine, and dexamethasone in selected patients. Most children require no medications, and bronchodilators after discharge are ineffective unless clear benefit was demonstrated prior to discharge.


Disposition
Admission is indicated for hypoxemia requiring oxygen, inability to maintain hydration, significant or persistent respiratory distress, apnea, severe comorbidities, failure to improve after therapy, or unreliable home monitoring. Discharge may be considered when feeding is adequate, oxygenation is acceptable on room air, respiratory distress has resolved, and close follow-up is assured.


Follow-Up Care
Because bronchiolitis often worsens early in its course, close outpatient follow-up within 24 hours is essential. Caregivers should be counseled regarding signs of worsening respiratory distress, dehydration, and apnea. Symptoms may persist for 2–3 weeks, and small, frequent feeds are recommended.


Key Clinical Insights and Common Errors
Infants with bronchiolitis frequently present with a combination of respiratory distress, hypoxia, dehydration, and apnea. Underestimating the potential for rapid deterioration is a common error; vigilant monitoring and early supportive care are critical to preventing adverse outcomes.

Emergency and Acute Medicine – Bradyarrhythmias


Overview and Definitions
Bradyarrhythmias are defined as a ventricular heart rate <60 beats />in. Sinus bradycardia may be a normal physiologic variant, whereas all other bradyarrhythmias are considered pathologic. Patients may be asymptomatic or present with hypotension, altered mental status, fatigue, nausea, syncope, or cardiac arrest. Management depends on ECG findings and the patient’s clinical stability rather than heart rate alone.


Etiology and Pathophysiology
Bradyarrhythmias may be idiopathic or secondary to intrinsic or extrinsic causes. Idiopathic causes include healthy, well-conditioned athletes. Intrinsic cardiac causes include sinus node dysfunction (e.g., sick sinus syndrome with brady–tachy variants), atrioventricular (AV) block with junctional or ventricular escape rhythms, infiltrative diseases (amyloidosis, sarcoidosis, hemochromatosis), collagen vascular diseases (SLE, scleroderma, rheumatoid arthritis), congenital or acquired anatomic abnormalities (postsurgical, post-transplant, postradiation), muscular disorders (myotonic dystrophy), and myocardial contusion from trauma.
Extrinsic causes include myocardial ischemia or infarction (RCA infarction → sinus bradycardia; LAD infarction → high-grade AV block), acidemia, medications and toxins (β-blockers, calcium channel blockers, digoxin, clonidine, antiarrhythmics, lithium, organophosphates), electrolyte abnormalities (hypo-/hyperkalemia, hypoglycemia, hypo-/hypercalcemia, hypermagnesemia), hypoxia, hypothermia, hypotension or severe hypertension, endocrine disorders (hypothyroidism), infections (Lyme disease, Chagas disease, diphtheria, endocarditis, myocarditis), and neurologic conditions (increased intracranial pressure, increased vagal tone, carotid sinus hypersensitivity, spinal cord injury). Vagal triggers include micturition, defecation, coughing, vomiting, ocular pressure, and other Valsalva maneuvers.


Special Populations
In children, hypoxia is the most common cause of bradycardia. During pregnancy, maternal SLE may result in congenital complete heart block.


Clinical Presentation
Many patients are asymptomatic. Symptomatic presentations include lightheadedness, confusion, fatigue, decreased level of consciousness, dyspnea, cyanosis, pallor, chest pain or pressure, diaphoresis, hypotension, syncope, hypothermia, or cardiac arrest.


History and Physical Examination
Key historical elements include recent medication changes, urine output patterns suggesting electrolyte disturbances, trauma (intracranial injury or myocardial contusion), and activity at symptom onset suggesting increased vagal tone. Physical examination focuses on respiratory status, perfusion and pulses, rhythm regularity, mental status with full neurologic assessment, body habitus, skin/hair/nails, and temperature.


Essential Evaluation
Immediate evaluation includes ECG with continuous cardiac monitoring, pulse oximetry, blood pressure monitoring, and bedside glucose and electrolyte assessment.


Diagnostic Tests and Interpretation
Laboratory testing may include serum glucose, electrolytes, BUN/creatinine, cardiac enzymes, digoxin level, thyroid function tests, rheumatologic markers (ANA, RF), Lyme titers, and iron studies. Imaging includes chest radiograph and CT head for altered mental status.
ECG findings define the rhythm: sinus bradycardia with normal P–QRS relationship; sinoatrial block; sinus arrest; AV block (first degree, Mobitz I, Mobitz II, complete heart block); junctional rhythm; and idioventricular rhythm with wide QRS complexes.


Differential Diagnosis
Normal physiologic bradycardia, cardiac ischemia, medication or toxin effects, pacemaker malfunction, hypoxia, hypothermia, electrolyte disturbances, renal failure, hypothyroidism, infection, rheumatologic disease, neuromuscular disease, increased intracranial pressure, and myocardial contusion.


Prehospital Management
Treat the patient rather than the heart rate. Provide oxygen for all patients. In hypothermia, rewarm gently and avoid pacing; administer magnesium as indicated. Use atropine or epinephrine only for hypotension or altered mental status. Initiate transcutaneous pacing if other measures fail.


Initial Stabilization in the ED
Address ABCs, administer oxygen, apply pacing pads, establish IV access, and begin continuous cardiac monitoring.


Emergency Department Management
Asymptomatic bradycardia requires monitoring and evaluation. Symptomatic or unstable bradycardia is treated with oxygen, atropine for symptomatic sinus bradycardia and low-grade AV block, epinephrine, and pacing. High-grade AV block typically requires pacing. Definitive care targets the underlying cause.


Medications
Atropine, epinephrine, calcium gluconate, dextrose, digoxin immune Fab, glucagon, insulin, and pacing are used based on etiology and stability. First-line therapy includes atropine, epinephrine, and pacing; second-line therapy addresses the specific cause.


Disposition
ICU admission is required for hemodynamic instability, Mobitz II or complete heart block, pacing or vasopressor needs, or acute ischemia. Telemetry admission is appropriate for stable cases. Asymptomatic sinus bradycardia may be discharged.


Follow-Up and Referral
All patients except those with isolated asymptomatic sinus bradycardia require cardiology follow-up. Specialty referral is indicated for underlying systemic causes.


Key Clinical Insights and Common Errors
Sinus bradycardia without symptoms is the only potentially normal bradyarrhythmia; all others warrant evaluation or follow-up. Ensure oxygenation, IV access, ECG, and continuous monitoring in all cases. Pediatric bradycardia is most often due to hypoxia. Pacing pads should be readily available for symptomatic patients. Definitive management hinges on identifying and correcting the underlying cause rather than focusing solely on heart rate.

Emergency and Acute Medicine – Bowel Obstruction (Small and Large)


Overview And Definitions
Bowel obstruction is interruption of normal intestinal transit from mechanical or functional (nonmechanical) causes. Small-bowel obstruction (SBO) accounts for about 20% of acute surgical admissions. Adhesions are the leading cause (≈60%), followed by neoplasms, hernias, strictures (e.g., inflammatory bowel disease), trauma-related bowel wall hematoma, and miscellaneous causes such as ascaris infection. Large-bowel obstruction (LBO) occurs primarily in older adults and is most commonly due to carcinoma (≈60%), diverticular disease (≈20%), volvulus (≈5%), colitis (ischemic or radiation), Crohn’s disease, foreign bodies, and functional obstruction. Functional, nonmechanical etiologies include paralytic ileus (e.g., electrolyte derangements, injury) and pseudo-obstruction (Ogilvie syndrome), which represents about 11%.


Etiology And Pathophysiology
Obstruction causes proximal intestinal dilation from swallowed air and accumulated GI secretions, increasing intraluminal pressure. Retrograde peristalsis produces vomiting. Progressive bowel edema and ongoing secretions worsen distention and lead to third spacing into the lumen. Strangulated obstruction can cause bowel wall ischemia, promoting aerobic and anaerobic bacterial overgrowth with methane and hydrogen production. This can progress to peritonitis, sepsis, and death. Mortality is essentially 100% for untreated strangulated obstruction, drops to ~8% with surgery within 36 hours, and rises to ~25% if surgery is delayed beyond 36 hours.


Clinical Presentation
Key historical clues include prior abdominal surgery, malignancy, hernias, prior colonoscopy, and significant family history. Pain is often intermittent early, but becomes constant with strangulation; symptoms may be vague in elderly or altered patients. Vomiting varies with level of obstruction—bilious emesis with proximal obstruction and feculent emesis with distal obstruction. Patients may report obstipation, constipation, diarrhea, stool caliber changes, and weight loss.


Vital signs may show tachycardia and hypotension from volume depletion, fever with strangulation or perforation, and hypothermia with sepsis. Abdominal examination often reveals distention and variable, frequently diffuse tenderness. Bowel sounds may be hyperactive and high-pitched early, becoming hypoactive late. Pain out of proportion to exam should raise concern for ischemic or gangrenous bowel. Peritoneal signs suggest strangulation or perforation. Evaluate for ventral, inguinal, and femoral hernias. Digital rectal exam may reveal a rectal mass or blood (gross or occult).


Geriatric Considerations
Abdominal pain in older adults may be vague. Nausea, vomiting, and abdominal pain can also occur with acute myocardial infarction; however, abdominal distention, obstipation, and colicky pain support a GI source.


Pediatric Considerations
Intussusception is the leading cause of obstruction in infants, most commonly between 3 and 12 months. Other causes include incarcerated inguinal or umbilical hernia and malrotation with volvulus, which can occur as early as 3–7 days of life. The “double bubble” sign on plain radiograph suggests partial duodenal obstruction (air in stomach and proximal duodenum). Pyloric stenosis presents with progressive, projectile, nonbilious postprandial vomiting, typically at 2–5 weeks of age, with a male predominance (≈5:1). Additional pediatric causes include duodenal atresia, Hirschsprung disease, and imperforate anus.


Essential Evaluation
A careful history and physical examination are central.


Diagnostic Tests And Interpretation
Laboratory studies commonly include CBC (leukocytosis is common), electrolytes/BUN/creatinine/glucose (hypokalemia, hypochloremic metabolic alkalosis, prerenal azotemia), lactate, amylase/lipase, liver enzymes/function tests to exclude hepatobiliary pathology, stool heme testing, urinalysis, type and crossmatch, PT/PTT, and ECG in patients at risk for coronary disease.


Imaging begins with upright chest radiograph to assess for pulmonary pathology and free air under the diaphragm. Abdominal radiographs (supine and upright) have ~75% sensitivity and ~53% specificity. Findings include dilated bowel loops (normal small bowel <3 cm), cecal dilation>13 cm suggesting perforation risk, air–fluid levels, and the “string of pearls” sign when small bowel is nearly fluid-filled. Plain films are less helpful for detecting strangulation. CT abdomen is highly sensitive (≈90% for SBO; ≈91% for LBO), identifies neoplasms and stages malignancy, localizes the transition point, and is more useful than plain films for early strangulation when IV contrast is used; CT has reduced the need for contrast enemas. MRI can approach CT sensitivity but availability varies. Ultrasound is more sensitive and specific than plain films for SBO but generally less accurate than CT. Upper GI studies, barium enemas, and endoscopy may be used when carcinoma or a mass is suspected, though their use has declined due to CT and they may be difficult in severely ill patients.


Differential Diagnosis
Paralytic ileus, pseudo-obstruction (Ogilvie), perforated ulcer, pancreatitis, cholecystitis, colitis, and mesenteric ischemia.


Prehospital Care
Establish IV access for patients with dehydration, vomiting, or significant abdominal pain.


Initial Stabilization And ED Management
Prioritize ABCs. Provide isotonic IV fluid resuscitation with 0.9% normal saline or lactated Ringer’s, especially for volume depletion and suspected strangulation or perforation (adults: 1 L bolus; pediatrics: 20 mL/kg bolus). Correct electrolyte abnormalities, particularly hypokalemia. Place a nasogastric tube for decompression, insert a Foley catheter for urine output monitoring, and obtain early surgical consultation. Administer antibiotics when strangulation or perforation is suspected, ensuring coverage for gram-negative aerobes and anaerobes. Provide analgesics and antiemetics. Address underlying causes when appropriate (e.g., steroids for inflammatory bowel disease or radiation enteritis).


Medications
For suspected ischemia/strangulation, options include combination therapy with metronidazole (1 g IV then 500 mg IV q6h; pediatrics 7.5-30 mg/kg/day divided q6-8h) plus ciprofloxacin 400 mg IV q12h or ceftriaxone 1-2 g IV q24h (pediatrics 25-75 mg/kg/day IV up to 2 g divided q12-24h). Single-agent broad-spectrum regimens include piperacillin-tazobactam 3.375 g IV q4-6h (pediatrics 150-400 mg/kg/day divided q6-8h), ampicillin-sulbactam 1.5-3 g IV q6h (pediatrics 100-400 mg/kg/day divided q6h), meropenem 1 g IV q8h (pediatrics 60-120 mg/kg/day divided q8h), or imipenem-cilastatin 250-1,000 mg IV q6-8h (pediatrics 50-100 mg/kg/day divided q6-12h). Analgesia may include morphine 2-10 mg per dose (pediatrics 0.1-0.2 mg/kg IV/IM/SC q2-4h) q2-6h PRN. Antiemetics include ondansetron 4 mg IV (pediatrics 0.1 mg/kg IV divided q8h) q4-8h PRN or promethazine 12.5-25 mg (pediatrics >2 years: 0.25–1 mg/kg/day IV/IM/PR divided q4–6h PRN) q4h.


Disposition
All suspected or confirmed bowel obstructions require admission with early surgical consultation. Discharge is appropriate only when labs and imaging are normal, symptoms resolve, and obstruction is no longer suspected.


Follow-Up Recommendations
Discharged patients should have normal laboratory and radiologic studies, a timely re-evaluation appointment, and clear return precautions outlining symptoms that require immediate ED return.


Clinical Insights And Common Errors
Patients with vomiting should be carefully examined for incarcerated hernias. Strangulated obstruction can be missed when symptoms are subtle, particularly in very young, very old, or altered patients. Another frequent error is inadequate correction of fluid deficits and electrolyte abnormalities.

Emergency and Acute Medicine – Botulism


Overview And Definitions
Botulism is a rare but highly lethal neuroparalytic illness in the United States, with fewer than 200 cases annually, yet it carries major bioterrorism significance. It is caused by a heat-labile polypeptide exotoxin produced by Clostridium botulinum, recognized as the most potent toxin known. The toxin irreversibly inhibits acetylcholine release at presynaptic cholinergic nerve terminals, resulting in flaccid paralysis. Neurologic recovery depends on axonal sprouting and formation of new synapses, accounting for the prolonged and often incomplete recovery. Symptom onset typically occurs within 12–72 hours but may be delayed up to one week, and death may occur within 24 hours of symptom onset. Mortality approaches 60–70% without treatment and decreases to 3–10% with aggressive supportive care. The principal clinical forms include food-borne, wound, and infantile botulism, with toxin absorption occurring through mucosal surfaces or nonintact skin.


Food-borne botulism results from ingestion of preformed toxin, most commonly associated with improperly canned or stored foods. Conditions required include contamination with spores, anaerobic conditions allowing germination, sufficient time for toxin production, inadequate heating, and ingestion by a susceptible host. Wound botulism presents after traumatic contamination of wounds, often without GI symptoms, and is frequently associated with intravenous drug use. Adult intestinal toxemia botulism occurs in individuals with altered gut flora due to structural abnormalities, immunocompromise, or prolonged antibiotic exposure and may recur. Inhalational botulism is rare but poses a significant bioterrorism risk. Iatrogenic botulism from cosmetic or therapeutic use is exceedingly uncommon.


Pediatric Considerations
Infantile botulism accounts for 50–76% of reported cases, with 90% occurring in infants younger than six months. It follows ingestion of C. botulinum spores that germinate within the immature gut, often associated with soil or dust exposure and weaning from breast milk. Presentation begins with constipation, followed by bulbar weakness and progressive descending flaccid paralysis. Honey is a known source of spores and should not be given to children under one year of age.


Etiology And Pathophysiology
Clostridium botulinum is a large, spore-forming, obligate anaerobic gram-positive bacillus ubiquitous in the environment. Seven antigenically distinct toxins (A–G) exist, with types A, B, E, and rarely F responsible for most human disease.


Clinical Features
Diagnosis is primarily clinical. Patients with classic food-borne botulism present with early bulbar palsies, including diplopia, dysphagia, dysarthria, and dysphonia, followed by symmetric descending paralysis. Sensation remains intact, and mentation is preserved. Progressive respiratory muscle weakness leads to ventilatory failure. Autonomic dysfunction is common and includes dry mouth, blurred vision, orthostatic hypotension, constipation, and urinary retention. Fever is typically absent. Wound botulism may be associated with fever. Infantile botulism presents with constipation, poor feeding, hypotonia, weak cry, lethargy, and respiratory compromise. Inhalational botulism mirrors food-borne disease but lacks gastrointestinal symptoms.


Evaluation And Diagnostic Testing
The diagnosis should prompt immediate notification of state health authorities or the CDC. Laboratory evaluation includes CBC, electrolytes, renal function, glucose, and arterial blood gas analysis to assess respiratory compromise. Confirmatory testing is performed via mouse bioassay on blood, stool, gastric contents, or suspected food sources, with results available in 6–96 hours. CSF analysis is normal, aiding distinction from Guillain–Barré syndrome. Neuroimaging is typically normal. Electrophysiologic studies show normal nerve conduction with reduced evoked muscle action potentials.


Differential Diagnosis
Consider myasthenia gravis, Lambert–Eaton syndrome, Guillain–Barré syndrome, tick paralysis, hypokalemic periodic paralysis, magnesium intoxication, diphtheritic neuropathy, poliomyelitis, and rare basilar stroke syndromes. In infants, sepsis, dehydration, metabolic disorders, and spinal muscular atrophy must be excluded.


Management Principles
Respiratory failure is the leading cause of death, making early airway protection and mechanical ventilation the cornerstone of management. Antitoxin therapy must be administered immediately once botulism is suspected, without waiting for laboratory confirmation. Wound botulism requires surgical débridement. Antibiotics are not effective for intestinal botulism and may worsen symptoms by increasing toxin release but may be used for secondary wound infections. Standard precautions are sufficient, as person-to-person transmission does not occur.


Pharmacologic Therapy
Infant botulism is treated with human-derived botulism immune globulin (BabyBIG®), which significantly reduces hospital stay. Adults require heptavalent botulinum antitoxin obtained through the CDC under emergency use protocols. Antibiotics are reserved for secondary infections. Vaccination with toxoid is limited to laboratory personnel.


Disposition And Follow-Up
All suspected cases require admission, with ICU care for any respiratory compromise. Discharge is appropriate only after prolonged, progressive neurologic recovery. Long-term follow-up often includes rehabilitation for persistent weakness, which may last up to one year, and psychological support for patients and families.


Clinical Insights And Common Errors
Botulism represents a public health emergency requiring rapid coordination with health authorities. Outbreaks involving multiple patients should heighten suspicion, as few alternative diagnoses present in clusters. Antitoxin halts disease progression but does not reverse established paralysis, emphasizing the importance of early administration before overt respiratory failure develops. Bulbar weakness may be misinterpreted as altered mental status, delaying diagnosis, and early respiratory insufficiency may be clinically subtle.

Emergency and Acute Medicine – Boerhaave Syndrome


Overview and Definitions
Boerhaave syndrome refers to a spontaneous rupture of the esophagus caused by a sudden rise in intra-abdominal pressure combined with negative intrathoracic pressure. This results in a full-thickness, transmural longitudinal tear. The absence of a serosal layer in the esophagus makes it particularly vulnerable to perforation and rapid mediastinal contamination. Preexisting mucosal injury, such as esophagitis, further weakens the wall. Most ruptures occur along the left posterolateral aspect of the distal third of the esophagus. This condition carries very high morbidity and mortality, the highest among gastrointestinal perforations. Overall mortality approaches 20%, and delays beyond 24 hours may double mortality. Cervical perforations have the lowest mortality, followed by abdominal and thoracic ruptures.


Etiology
The most frequent precipitant is forceful vomiting or retching. Other associated triggers include heavy lifting, seizures, childbirth, blunt trauma, induced emesis, caustic ingestion, and laughing. Risk is increased in patients with Barrett ulcer, HIV/AIDS, pill esophagitis, and chronic alcohol use. The condition predominantly affects middle-aged men. Notably, iatrogenic causes account for over half of all esophageal perforations overall.
Pediatric note: Rare; reported in neonates. Always consider caustic ingestion.


Clinical Features
Symptoms are often nonspecific, contributing to diagnostic delay. The most common presentation is acute chest or epigastric pain following vomiting or retching.
Mackler triad—vomiting, chest pain, and subcutaneous emphysema—is classic but uncommon. Chest pain is typically retrosternal and pleuritic, radiates to the back or left shoulder, worsens with swallowing, and may be associated with odynophagia. Swallowing can provoke coughing. A history of heavy alcohol intake is frequently present.
Alert: Subtle or vague symptoms are common and worsen prognosis if diagnosis is delayed.


Physical Examination
Findings may include dyspnea, diaphoresis, tachypnea, fever, and shock in severe cases. Subcutaneous emphysema of the neck or chest wall and mediastinal crepitus (Hamman crunch) may be present. Pleural effusions, usually left-sided, are common. Untreated cases progress to mediastinitis and abscess formation. Hemorrhage is uncommon.


Essential Evaluation
Obtain upright chest radiographs (PA and lateral if tolerated) to assess for pneumomediastinum, subcutaneous emphysema, pleural effusion, pneumothorax, widened mediastinum, hydropneumothorax, empyema, free intraperitoneal air, and the Naclerio V sign.
A contrast esophagram is key to identifying the perforation and guiding management. Contrast choice remains debated: water-soluble agents are less irritating if leaked but less sensitive and dangerous if aspirated, while barium is more sensitive but more irritating to the mediastinum. If the initial study is negative and suspicion remains high, repeat imaging is warranted.


Diagnostic Tests and Interpretation
Laboratory studies include CBC, PT/PTT/INR, and blood cultures. Pleural fluid analysis may show low pH (<6), elevated amylase, and undigested food particles. ecg is useful to exclude cardiac causes.< />pan>
CT chest is sensitive for detecting mediastinal air, periesophageal fluid, and pleural involvement, though it does not localize the tear. Endoscopy is controversial due to risk of worsening the perforation.


Differential Diagnosis
Myocardial infarction, aortic dissection, pneumothorax, pneumonia, pulmonary embolism, pericarditis, pancreatitis, cholecystitis, intestinal obstruction, mesenteric ischemia, lung abscess, ruptured viscus, and benign spontaneous pneumomediastinum.


Management
Prehospital: Secure the airway if needed. Establish two large-bore IV lines and treat hypotension with 0.9% normal saline. Avoid opiates prior to ED arrival when possible.
Initial stabilization: Follow ABCs. Administer 100% oxygen or intubate if airway compromise is present. Give 20 mL/kg crystalloid bolus and initiate dopamine if hypotension persists. Consider central access for unstable patients.
ED care: Keep patient NPO, carefully place a nasogastric tube for decompression, insert a urinary catheter, expedite diagnostic evaluation, and obtain immediate surgical consultation. Definitive treatment is usually surgical repair; endoscopic stenting or conservative management may be considered in selected patients with contained perforations. Begin broad-spectrum IV antibiotics targeting oral and gastrointestinal flora.


Medications
Ampicillin/sulbactam 3 g IV q6h; Gentamicin 2 mg/kg loading dose then 1.7 mg/kg q8h or 5–7 mg/kg daily; Imipenem/cilastatin 250–500 mg IV q6h; Dopamine 2–20 μg/kg/min IV as needed.


Disposition
All patients require admission to a surgical ICU. Cervical perforations may be managed with drainage alone, whereas thoracic and abdominal perforations require operative repair. There is no role for ED discharge.


Consultation and Follow-Up
Immediate involvement of thoracic or general surgery is mandatory. Ongoing management and follow-up are dictated by the surgical team.


Key Clinical Insights And Common Errors
Early chest radiographs may appear normal. Left-sided pleural involvement typically indicates distal esophageal rupture, whereas right-sided involvement suggests a proximal tear. A negative initial esophagram does not exclude injury—repeat imaging in decubitus positions if suspicion remains high. Delays in diagnosis and intervention markedly increase mortality; rapid recognition and early surgical consultation are essential.

Emergency and Acute Medicine – Blow-Out Fracture


Overview and Definitions
A blow-out fracture is an orbital floor fracture without orbital rim involvement. It follows sudden blunt trauma to the globe—classically from a projectile larger than half the size of a fist—with force transmitted through the noncompressible globe to the weakest point: the orbital floor. Because the orbital floor forms the roof of the maxillary and ethmoid sinuses, fracture can create communication between these spaces, causing orbital emphysema. The orbit contains fat that stabilizes the globe; fracture may allow herniation of orbital fat into the maxillary/ethmoid sinuses, producing enophthalmos from increased orbital volume and sinus congestion, with possible fluid collection from edema/bleeding. The infraorbital nerve runs in a bony canal ~3 mm below the floor; injury can cause hypoesthesia of the ipsilateral cheek and upper lip. To differentiate swelling-related numbness from nerve injury, test sensation on the ipsilateral gingiva (infraorbital distribution). The inferior rectus and inferior oblique course along the floor; restriction may occur from entrapment, contusion, or cranial nerve dysfunction—typically diplopia on upward gaze and impaired elevation on exam. The medial rectus lies above the ethmoid sinus and is less often entrapped; when involved, it causes diplopia on ipsilateral lateral gaze.


Etiology
Occurs when a projectile strikes the globe and the transmitted force fractures the orbital floor. Common projectiles include paintball, handball, racquetball, baseball, rock, or possibly a fist (larger projectiles may be blocked by the orbital rim). Blow-out fractures are also seen after MVCs, the most common cause of maxillofacial trauma.


Pediatric Considerations
Children more often have orbital roof fractures with associated CNS injuries. Orbital floor fractures are unlikely before age 7 because the floor is less weak prior to sinus pneumatization. However, children can sustain fractures with unrecognized rectus entrapment—the “white-eyed” fracture—often presenting with nausea, vomiting, headache, and irritability that mimic head injury and distract from the ocular diagnosis.


Clinical Features
Typical findings include periorbital tenderness, swelling, and ecchymosis. Ocular motility issues include restricted upward gaze (inferior rectus entrapment) and restricted ipsilateral lateral gaze (medial rectus entrapment). Infraorbital hypoesthesia may extend to the upper lip. Enophthalmos may be present from fat displacement. Periorbital emphysema can occur from sinus communication. Epistaxis is possible. Visual acuity is typically normal; decreased acuity suggests more extensive injury. There is no orbital rim step-off (by definition).


Associated Severe Injuries and Complications
Ocular injuries may include ruptured globe (up to 30%; ophthalmologic emergency), retrobulbar hemorrhage, and emphysematous optic nerve compression. Cervical spine and intracranial injuries may coexist. Common associated ocular findings: subconjunctival hemorrhage, corneal abrasion/laceration, hyphema, traumatic mydriasis, traumatic iridocyclitis (uveitis). Less common: iridodialysis, retinal detachment, vitreous hemorrhage, optic nerve injury. Associated fractures include nasal bone, zygomatic arch, and Le Fort fractures. Late complications include sinusitis, orbital infection, permanent extraocular movement restriction, and enophthalmos.


History and Physical Examination
History often includes being struck in the eye by a projectile. Perform a thorough ophthalmologic exam and palpate orbital bones for step-off, but avoid pressure on the globe until rupture is excluded. Desmarres lid retractors may be needed with significant lid swelling. Document pupillary responses and visual acuity (use handheld methods; Rosenbaum card is useful). Assess extraocular movements for disconjugate gaze/diplopia. Test sensation in the infraorbital nerve distribution (including ipsilateral gingiva). Examine lids/adnexa for emphysema. Perform slit-lamp and fundoscopic exams for associated injuries. Complete a full exam for other injuries and neurologic impairment.


Diagnostic Testing and Imaging
Labs: pre-op labs if indicated; pregnancy test prior to radiography when appropriate.
Imaging: If CT is unavailable/contraindicated, plain radiographs can help: facial films, Waters view and exaggerated Waters—classic “teardrop sign” (herniated orbital contents into ipsilateral maxillary sinus), maxillary sinus opacification/air–fluid level (less specific), visible floor fracture, and orbital lucency consistent with emphysema. CT is preferred to define anatomy; obtain axial and coronal 1.5-mm cuts. True coronal acquisition is preferred, but reconstructed coronals are acceptable if positioning is not possible.
Procedure: Forced duction test helps distinguish entrapment from nerve dysfunction—apply topical anesthesia to the conjunctiva on the opposite side and pull the globe away from the suspected entrapment; restricted mobility = positive, indicating physical entrapment.
Pediatrics: Orbital CT is the study of choice; plain films are less helpful. Early identification of entrapment is critical because delayed diagnosis worsens long-term outcomes; early surgical intervention can significantly improve results.


Differential Diagnosis
Cranial nerve palsy, orbital cellulitis, periorbital cellulitis, periorbital contusion/ecchymosis, retrobulbar hemorrhage, ruptured globe.


Management
Prehospital: If globe injury is possible, place a metal protective eye shield and keep patient supine.
Initial stabilization: Evaluate for intracranial/cervical spine injuries, rule out ruptured globe, and check visual acuity (decrease suggests more extensive injury).
ED care (after globe rupture excluded): Apply cool compresses for 24–48 hr to reduce swelling and potentially minimize/reverse herniation and avoid surgery. Instruct to avoid Valsalva and nose blowing to prevent compressive orbital emphysema. Provide prophylactic antibiotics, nasal decongestants if not contraindicated, analgesia, and tetanus prophylaxis.


Medications
Prophylactic antibiotics (to reduce risk of sinusitis/orbital cellulitis): Cephalexin 250 mg q6h for 10 days.
Systemic corticosteroids (advocated by some to hasten edema resorption and better assess entrapment/orbital damage): Prednisone 60–80 mg/day, start within 48 hr, continue 5 days.
Nasal decongestant: Phenylephrine nasal spray BID for 2–4 days (if not contraindicated).


Disposition and Follow-Up
Admission is rare; ~85% resolve without surgery. Consult facial trauma in the ED and consider admission/urgent management if: ≥50% floor fracture, diplopia or entrapment (especially in children), or enophthalmos >2 mm. Most patients can be observed 10–14 days until swelling resolves, then follow up with facial trauma surgeon to decide on surgical repair.


Follow-Up Advice
Symptoms should gradually improve. Return to the ED for increasing swelling, tenderness, redness, or pain, and for any visual disturbance, vision loss, or increasing eye pain.


Clinical Insights and Common Errors
Be extremely vigilant with pupillary responses and visual acuity—abnormalities may be the earliest sign of serious complications such as globe rupture or optic nerve injury from emphysematous/retrobulbar compression. Carefully assess for muscle entrapment in all patients, especially children, to avoid missing white-eyed fractures and long-term sequelae. Watch for the oculocardiac (Aschner) reflex—bradycardia triggered by extraocular muscle traction or globe compression—more common in children; treat by removing the stimulus, and atropine may be required in some cases.