Emergency And Acute Medicine – Cyanide Poisoning


Overview
Cyanide toxicity occurs through inhalation or gastrointestinal absorption. Cyanide is an intracellular toxin that disrupts aerobic metabolism by inhibiting oxidative phosphorylation, resulting in impaired oxygen utilization and reduced ATP production. Detoxification primarily occurs via the hepatic mitochondrial enzyme rhodanese, which combines cyanide with sulfur in an irreversible reaction to form the less toxic, water-soluble thiocyanate. Cyanide can also bind hemoglobin to form reversible cyanhemoglobin or bind hydroxocobalamin to form nontoxic cyanocobalamin. Effective detoxification depends on adequate sulfur availability, particularly thiosulfate.


Causes And Sources
Cyanide exposure most commonly occurs during fires as a combustion by-product of natural and synthetic materials. Industrial sources include metal plating, microchip and plastic manufacturing, chemical synthesis, pesticides, and solvents such as artificial nail remover and metal polishes. Cyanide may also be produced during nitroprusside metabolism and by certain bacterial infections. Dietary sources include amygdalin-containing plants such as apricot pits, peach pits, apple seeds, pear seeds, and cassava. Jewelry making is another recognized exposure risk.


Clinical Features
The heart and brain are the most sensitive organs and are typically affected first. Neurologic manifestations include headache, confusion, syncope, seizures, and coma. Cardiovascular findings include dyspnea, chest pain, rapid progression to cardiorespiratory collapse, and death. Gastrointestinal symptoms such as nausea and vomiting may occur. Oral exposure can be caustic, with as little as 50 mg causing death. Inhalational exposure to 50 ppm may cause anxiety, palpitations, dyspnea, and headache, while concentrations of 100–135 ppm can be lethal in less than one hour.


Initial Evaluation
A history suggestive of smoke inhalation, industrial exposure, or intentional ingestion should raise suspicion. Classic findings such as the odor of bitter almonds or bright red retinal vessels are often absent. Key clinical clues include abrupt onset or rapid deterioration, severe lactic acidosis, and elevated venous oxygen saturation due to impaired cellular oxygen utilization, resulting in arterialized venous blood gases.


Diagnostic Studies
Laboratory evaluation typically includes complete blood count, metabolic panel, liver profile, creatine phosphokinase, carboxyhemoglobin, and methemoglobin levels. Cyanide levels are usually send-out tests and not available in real time; levels above 0.5–1 mg/L are toxic, and levels of 2.5–3 mg/L are often fatal. Blood gas analysis may show elevated mixed venous oxygen saturation, reduced arteriovenous oxygen difference, and markedly elevated lactate levels greater than 8 mmol/L, which serve as a useful surrogate marker when exposure history is consistent. Chest radiography may assist in evaluating concurrent inhalation injury.


Conditions To Differentiate
The differential diagnosis includes carbon monoxide poisoning, hydrogen sulfide exposure, methemoglobinemia, sulfhemoglobinemia, inert gas asphyxiation, and other causes of high anion gap metabolic acidosis.


Prehospital Management
Immediate removal from the source of exposure is critical, while preventing secondary contamination of rescuers. Contaminated clothing should be removed and bagged, and liquid exposures require thorough washing with soap and water. Vapor exposures may resolve with simple removal from the environment.


Emergency Stabilization
Initial management follows standard airway, breathing, and circulation principles. Administer 100% oxygen regardless of measured oxygen tension, as it acts synergistically with antidotes. Gastric lavage and activated charcoal may be considered for recent oral ingestion if no contraindications exist. Dermal exposures require standard decontamination measures.


Definitive Treatment
Hydroxocobalamin is the preferred first-line antidote for patients with significant toxicity, including persistent high anion gap metabolic acidosis, hyperlactatemia, seizures, syncope, dysrhythmias, or hypotension. It binds cyanide to form cyanocobalamin, which is renally excreted. Advantages include the absence of methemoglobinemia and hypotension. Limitations include cost, drug incompatibilities within IV lines, and interference with certain laboratory assays.


An alternative is the traditional cyanide antidote kit, which includes amyl nitrite, sodium nitrite, and sodium thiosulfate. Nitrites induce methemoglobinemia to sequester cyanide away from mitochondria, while sodium thiosulfate enhances enzymatic detoxification via rhodanese. Nitrites should not be used empirically and require caution due to the risk of excessive methemoglobinemia and hypotension. Hyperbaric oxygen therapy may be considered as adjunctive treatment to maximize tissue oxygenation.


Medication Summary
First-line therapy is hydroxocobalamin administered intravenously at weight-based dosing, with repeat dosing if necessary. Activated charcoal may be used for recent ingestions. Second-line therapy involves the cyanide antidote kit, including carefully dosed nitrites and sodium thiosulfate. Special dosing considerations apply in pediatric patients, pregnancy, and those with hepatic or renal impairment.


Disposition And Follow-Up
All symptomatic patients require intensive care unit admission. Asymptomatic patients may be discharged after at least four hours of observation if no symptoms develop, as survival beyond this period is usually associated with full recovery. Psychiatric evaluation is indicated for intentional exposures.


Key Clinical Insights And Common Errors
In patients presenting with hypotension, seizures, altered mental status, severe lactic acidosis, and high anion gap metabolic acidosis, cyanide poisoning should be strongly considered and treated empirically. Serum lactate is a valuable surrogate marker when exposure history is suggestive. Victims of smoke inhalation may have combined cyanide toxicity, carbon monoxide poisoning, and methemoglobinemia. When carbon monoxide levels are markedly elevated, concomitant cyanide exposure should be suspected. To avoid worsening oxygen delivery, initial treatment should prioritize hydroxocobalamin or sodium thiosulfate without nitrites when methemoglobinemia would be harmful.

Emergency and Acute Medicine – Corneal Abrasion


Definition and General Description
A corneal abrasion is defined as any tear, defect, or disruption of the corneal epithelium. It is a common ocular injury that may result from direct trauma, spontaneous epithelial breakdown, foreign body exposure, or contact lens use. Because the cornea is densely innervated, even small epithelial defects can cause significant pain and visual disturbance.


Etiology and Mechanisms of Injury
Traumatic corneal abrasions are most frequently caused by fingernails, tree branches, hairbrushes or combs, sand or small stones, snow, pens or pencils, toys, chemical exposures, airbag deployment, pepper spray, paper or cardboard, makeup applicators, and animal paws. Foreign body–related abrasions may occur from materials such as wood, glass, metal, rust, plastic, fiberglass, or vegetable matter, including foreign bodies trapped beneath the eyelid. Contact lens–related abrasions are associated with overwear, improper lens fit, or inadequate lens hygiene. Spontaneous corneal abrasions usually occur in patients with a history of prior corneal trauma or those with an underlying defect of the corneal epithelium, such as recurrent corneal erosion syndrome.


Clinical Presentation
Patients typically present with severe ocular pain accompanied by a gritty or scratchy sensation, excessive tearing, blepharospasm, and a persistent foreign body sensation. Photophobia is common and may be pronounced if traumatic iritis is present. Additional symptoms include conjunctival injection, blurred or diminished vision, and headache.


The history should specifically address any direct trauma to the eye, known or suspected foreign body exposure, contact lens use, previous corneal abrasions, prior ocular or periocular surgery, pre-existing visual impairment, and the timing of symptom onset. Associated injuries or symptoms should be assessed, as well as any treatment attempted before presentation. Inquiry about occupational or recreational eye protection, systemic diseases such as diabetes or autoimmune disorders, and tetanus immunization status is also important.


Pediatric Considerations
In children, the presentation may differ significantly from adults. Excessive crying may be the primary manifestation. In infants younger than 12 months, there is often no clear history of eye trauma, and corneal abrasion may present as an inconsolable crying infant. In neonates and infants aged 1–12 weeks, corneal abrasions may be incidental findings and not the cause of irritability. Children older than 12 months are more likely to have a history of minor eye trauma and demonstrate more obvious ocular signs.


Physical Examination and Diagnostic Evaluation
If clinically indicated, the initial evaluation should include assessment for other life-threatening injuries following standard primary survey principles. A focused but complete eye examination is essential and should aim to exclude penetrating injury or infection. This includes gross inspection of the eye, assessment of visual acuity, and a penlight examination to evaluate conjunctival injection, pupil shape and reactivity, and the presence of corneal opacity or infiltrate. The upper eyelids should be everted to assess for retained foreign bodies. Slit-lamp examination allows evaluation of the anterior chamber for inflammation, detection of corneal laceration or penetrating trauma, and identification of infiltrates. Fluorescein staining is used to confirm the diagnosis and determine the size and location of the epithelial defect.


In pediatric patients, handheld slit lamps and Wood lamps can be particularly helpful in facilitating examination.


Differential Diagnosis
The differential diagnosis includes viral or bacterial conjunctivitis, corneal ulcer, acute glaucoma, herpes zoster ophthalmicus, infectious or ultraviolet keratitis, recurrent corneal erosion syndrome, and uveitis. More serious ocular injuries must also be considered, including corneal laceration or perforation, hyphema, iris prolapse, and lens disruption.


Initial Management and Emergency Department Care
Initial therapy includes instillation of a topical anesthetic, such as proparacaine or tetracaine, to facilitate examination. In the emergency department, superficial foreign bodies should be removed when present. A residual rust ring does not require emergent removal and can be addressed within 24–48 hours. Pain control may be achieved with oral NSAIDs, acetaminophen, or oral opioids when necessary.


Topical NSAIDs such as diclofenac or ketorolac have demonstrated effectiveness for pain control, although there are rare reports of adverse effects; these agents should be avoided in patients with pre-existing ocular surface disease or those who have recently undergone eye surgery. Cycloplegic agents may be used selectively to relieve ciliary spasm, including cyclopentolate, tropicamide, or homatropine.


Topical antibiotics are commonly prescribed despite limited evidence, primarily to prevent secondary infection. Ointments are preferred over drops due to their lubricating properties. Antibiotics should be discontinued once the patient has been symptom free for 24 hours. Contact lens wearers require antipseudomonal coverage, such as ciprofloxacin. Eye patching does not improve healing or pain control, particularly within the first 24 hours, and is not recommended for small abrasions. Patching should never be used in contact lens wearers or in injuries with high infection risk, such as those involving organic matter. The role of patching in large abrasions greater than 10 mm remains unclear.


Contact lenses should not be worn until the abrasion has fully healed and the eye has felt normal for at least one week without medication. In cases of severe pain, a bandage contact lens may be considered, provided there is no evidence of infection and close daily follow-up is ensured. Routine tetanus prophylaxis is not required, but immunization should be updated if the abrasion is caused by or contaminated with dirt or organic material. Emergent ophthalmology consultation is required for suspected intraocular foreign bodies, penetrating globe injuries, or the presence of corneal infiltrates, white spots, or opacities.


Medications
Commonly used medications include topical ciprofloxacin 0.35% drops four times daily, erythromycin 0.5% ointment four times daily, gentamicin drops or ointment, sulfacetamide drops or ointment, and tobramycin drops or ointment. Cycloplegics such as cyclopentolate, tropicamide, or homatropine may be used as indicated. Topical NSAIDs include diclofenac 0.1% or ketorolac 0.5% drops four times daily. Proparacaine should be used only once in the emergency department and not prescribed for outpatient use.


Disposition and Follow-Up
Hospital admission is reserved for patients with associated injuries requiring inpatient care. All uncomplicated corneal abrasions may be discharged from the emergency department. Although no definitive studies define optimal follow-up, standard practice recommends follow-up for all corneal abrasions to ensure complete healing without infection or scarring. Contact lens wearers, patients with patched eyes, or those with bandage contact lenses should be re-evaluated by ophthalmology within 24 hours. Central or large abrasions also warrant ophthalmologic follow-up within 24 hours, while smaller peripheral abrasions may be rechecked within 48–72 hours.


Essential Clinical Cautions and Common Errors
Clinicians must always carefully evaluate for penetrating globe injuries and signs of infection. Patients should never be discharged with topical anesthetics, as these agents are toxic to the corneal epithelium and delay healing, despite limited evidence suggesting dilute formulations may be safe. Mydriatic agents should not be used in patients with a history of glaucoma. Contact lens use should not be resumed until the patient has been evaluated and cleared by ophthalmology.

Emergency And Acute Medicine – Cyanosis


Overview
Cyanosis is an abnormal bluish discoloration of the skin or mucous membranes caused by increased concentrations of deoxygenated hemoglobin or abnormal hemoglobin derivatives within capillary blood. Clinically significant levels include deoxygenated hemoglobin greater than 5 g/dL, methemoglobin greater than 1.5 g/dL, or sulfhemoglobin greater than 0.5 g/dL. The absolute amount of deoxygenated hemoglobin determines the blue coloration, not the oxyhemoglobin concentration. Cyanosis is more apparent in patients with polycythemia and may be difficult to detect in anemic patients. Skin thickness and pigmentation influence visibility. Cyanosis may be central, reflecting systemic hypoxemia or abnormal hemoglobin, or peripheral, reflecting increased oxygen extraction or impaired blood flow.


Pathophysiologic Types
Central cyanosis results from hypoxemia, right-to-left cardiac shunting, or abnormal hemoglobin species. Peripheral cyanosis occurs when tissues extract excessive oxygen due to hypoperfusion, vasoconstriction from cold exposure, or arterial or venous insufficiency. Acrocyanosis is a painless, symmetric bluish discoloration of distal extremities with an unclear underlying mechanism.


Causes
Central causes include impaired pulmonary function from hypoventilation, ventilation–perfusion mismatch, or diffusion defects; intracardiac or intrapulmonary shunts; high-altitude exposure; and abnormal hemoglobins. Peripheral causes include shock, cold exposure, arterial insufficiency, venous insufficiency, Raynaud phenomenon, and acrocyanosis. Abnormal hemoglobin states include congenital or acquired methemoglobinemia and sulfhemoglobinemia, often related to medications, chemicals, or genetic enzyme deficiencies.


Pediatric Considerations
In children, cyanosis may reflect cyanotic congenital heart disease such as tetralogy of Fallot, transposition of the great vessels, truncus arteriosus, pulmonary or tricuspid atresia, Ebstein anomaly, total anomalous pulmonary venous return, or duct-dependent lesions. Respiratory causes include upper and lower airway obstruction, bronchiolitis, pneumonia, pulmonary edema, or foreign body aspiration. Neurologic causes such as breath-holding spells should also be considered.


Clinical Presentation
Patients exhibit a bluish discoloration of skin or mucous membranes that typically blanches with pressure. Methemoglobinemia may produce chocolate-brown blood or slate-gray discoloration. History should establish onset, progression, associated symptoms such as dyspnea or altered mental status, medication use, and possible occupational or chemical exposures. Physical examination focuses on respiratory distress, hemodynamic stability, distribution of discoloration, cardiac and pulmonary findings, presence of clubbing, and peripheral perfusion.


Initial Assessment
Airway and ventilation assessment is the first priority. Hypoxemia from cardiac or pulmonary causes is most common and should be addressed immediately. Abnormal hemoglobin states should be considered when cyanosis persists despite adequate oxygenation.


Diagnostic Evaluation
Pulse oximetry may be misleading in abnormal hemoglobin states, hypoperfusion, or pigmented skin. Arterial blood gas analysis assesses oxygen tension and saturation; cyanosis with a normal PaO₂ suggests methemoglobinemia. Chocolate-colored blood supports this diagnosis, which should be confirmed by measuring methemoglobin levels. Laboratory studies include complete blood count and basic chemistries. Imaging such as chest radiography and targeted neck films helps evaluate pulmonary, cardiac, or airway pathology. Echocardiography is useful when shunt or structural heart disease is suspected.


Conditions To Differentiate
Noncyanotic causes of skin discoloration that do not blanch include drug-induced pigmentation, heavy metal deposition, metabolic disorders, tattoos, and rare conditions such as chromhidrosis.


Emergency Management
Prehospital and emergency care focuses on securing the airway, providing 100% oxygen via a nonrebreather mask, correcting ventilation problems, and supporting circulation. Bronchodilators, racemic epinephrine, diuretics, or prostaglandin E1 may be required depending on the underlying cause. Methylene blue is indicated for symptomatic methemoglobinemia with levels above 30%, except in patients with glucose-6-phosphate dehydrogenase deficiency.


Disposition
Most patients with cyanosis require hospital admission, and any instability mandates intensive care. Discharge may be considered only when a reversible cause has been identified, treated, and resolved, with stable oxygenation and close follow-up arranged.


Practical Insights And Common Diagnostic Errors
Always presume hypoxemia first and rapidly evaluate airway and breathing. Cyanosis that does not improve with high-flow oxygen or is associated with chocolate-colored blood should prompt evaluation for methemoglobinemia. Failure to recognize abnormal hemoglobin states is a frequent cause of delayed diagnosis.

Emergency And Acute Medicine – Cystic Fibrosis


Foundational Overview
Cystic fibrosis is caused by a defect in the cystic fibrosis transmembrane conductance regulator (CFTR). CFTR functions as an ATP-regulated chloride channel that modulates chloride and sodium transport across epithelial cell surfaces. Dysfunction leads to abnormal electrolyte movement in exocrine glands and secretory epithelia. The result is thick, viscous secretions, impaired mucociliary clearance, recurrent pulmonary infections, and progressive obstructive lung disease. Exocrine pancreatic insufficiency causes malabsorption, while chronic sinus disease is common.


Cystic fibrosis occurs in approximately 1 in 3,600 live births in the White population, 1 in 29,000 in African American individuals, and 1 in 6,500 in Hispanic individuals. About 30% of cases are detected through newborn screening, and 75% are diagnosed within the first two years of life. Approximately 30,000 children and young adults in the United States live with cystic fibrosis. Median life expectancy in the U.S. is about 40 years, with 40% of patients older than 18 years. Roughly 10 million Americans are asymptomatic carriers. Sixteen percent of lung transplants in the U.S. are performed for cystic fibrosis–related lung disease.


Predisposing Factors
Cystic fibrosis is an autosomal recessive genetic disorder involving the CFTR gene on the long arm of chromosome 7. Numerous mutations exist, resulting in variable phenotypes. Classic disease is most commonly associated with homozygous ΔF508 mutations. Cystic fibrosis remains the most common lethal genetic disease in the United States.


Infectious Contributors And Pathogenesis
Patients are predisposed to chronic and recurrent pulmonary infections, often involving multidrug-resistant organisms. Common pathogens include methicillin-sensitive and methicillin-resistant Staphylococcus aureus, Pseudomonas aeruginosa (with prevalence increasing with age and chronic infection in more than 70% of adults), Haemophilus influenzae, Stenotrophomonas maltophilia, and Achromobacter xylosoxidans.
Burkholderia cepacia occurs in approximately 3% of patients and is associated with rapid clinical deterioration. Nontuberculous mycobacteria, including Mycobacterium avium complex and Mycobacterium abscessus, and fungal pathogens such as Aspergillus are also encountered.


Clinical Manifestations
General findings include failure to thrive, recurrent respiratory infections, anasarca in infancy, and a characteristic salty taste of the skin.


Head and neck involvement includes nasal polyps, severe headaches from sinusitis, and recurrent otitis media.


Pulmonary features include persistent cough that progresses from dry to productive, recurrent bronchiolitis or pneumonitis in the first year of life, wheezing, hemoptysis, pneumonia, chronic bronchitis, bronchiectasis, respiratory distress, pneumothorax, and pneumomediastinum. Pulmonary complications are the most common cause of hospitalization.


Cardiac complications include congestive heart failure, cor pulmonale, and pulmonary hypertension.


Gastrointestinal manifestations include abdominal pain, meconium ileus, distal intestinal obstructive syndrome (DIOS, also called meconium ileus equivalent), gastroesophageal reflux, cholelithiasis, pancreatitis, pancreatic insufficiency, ileocecal intussusception, foul-smelling fatty stools, jaundice or cirrhosis, rectal prolapse, hematemesis, and small-intestinal bacterial overgrowth.


Musculoskeletal and systemic findings include bone pain, edema or joint effusions, decreased cortical bone thickness, and recurrent venous thrombosis. Cardiorespiratory failure is the leading cause of death.


Essential Diagnostic Evaluation
Initial confirmation relies on sweat chloride testing. DNA analysis is indicated if sweat testing is equivocal. Nasal potential difference testing is reserved for cases where DNA analysis is inconclusive.


Diagnostic Studies And Interpretation
The sweat chloride test is diagnostic when chloride concentration exceeds 60 mEq/L in the presence of classic symptoms. Stool studies may demonstrate decreased elastase, trypsin, or chymotrypsin, and increased fat on 72-hour fecal fat testing. Immunoreactive trypsin (IRT) screening identifies increased risk but may yield false positives or negatives.


DNA analysis detects approximately 90% of cystic fibrosis chromosomes and is positive when two abnormal CFTR genes are present. Genotyping alone cannot establish the diagnosis, as more than 1,300 CFTR mutations exist and modifying mutations may attenuate disease severity.


Laboratory evaluation may reveal thrombocytopenia, hyponatremic hypochloremic metabolic alkalosis, hyperglycemia or new-onset diabetes in adolescents and adults (with ketoacidosis being rare), and abnormal liver function tests or prolonged prothrombin time in the setting of liver disease or bleeding. Arterial blood gases may show hypoxemia and metabolic alkalosis. Sputum cultures often reveal chronic pseudomonal colonization.


Specialized studies include nasal potential difference testing, which is complex and time-consuming, and semen analysis demonstrating azoospermia in affected males.


Imaging findings on chest radiography include hyperaeration, peribronchial thickening, atelectasis, hilar lymphadenopathy, pneumothorax, pneumomediastinum, bronchiectasis, and blebs. Chest CT better defines bronchiectasis and bleb disease. Abdominal imaging is indicated for pain, vomiting, or distention to evaluate for DIOS or intussusception. Barium enema is used when intussusception is suspected. Routine sinus radiographs are of limited value, as they are almost always abnormal; CT imaging is required for operative planning.


Bronchoalveolar lavage may demonstrate neutrophilic inflammation but is unnecessary when pulmonary disease is clinically evident.


Conditions To Exclude
Respiratory alternatives include asthma, recurrent pneumonia, bronchiectasis from other causes, pertussis, immunodeficiency, foreign body aspiration, alpha-1 antitrypsin deficiency, and ciliary dyskinesia.
Gastrointestinal mimics include chronic diarrhea, gastroenteritis, and milk allergy.
Other causes of elevated sweat electrolytes include fucosidosis, glycogen storage disease type I, mucopolysaccharidoses, hypothyroidism, vasopressin-resistant diabetes insipidus, adrenal insufficiency, familial cholestasis or hypoparathyroidism, malnutrition, ectodermal dysplasia, atopic dermatitis, and prostaglandin E1 infusion.


Emergency And Acute Care Management
Prehospital considerations include transcutaneous pacing for unstable type II second-degree or third-degree heart block. Atropine should be avoided in type II second-degree block due to risk of progression to complete heart block.


Emergency department priorities focus on stabilization of airway, breathing, and circulation, with correction of fluid, electrolyte, glucose, and respiratory abnormalities. Bronchodilators and steroids are used for wheezing. Small pneumothoraces under 5–10% may be observed, while larger ones require thoracostomy. Early consultation with the patient’s cystic fibrosis specialist is essential.


Right-sided heart failure is treated with diuretics. Hemoptysis requires evaluation of coagulation status and transfusion as indicated. Ventilatory support may be necessary in severe respiratory failure.


DIOS often requires surgical intervention. Hematemesis is managed with packed red blood cells, correction of coagulopathy, and early endoscopic consultation. Intussusception is treated with air or barium enema, with surgery if unsuccessful. Rectal prolapse is manually reduced, with surgical consultation as needed.


Respiratory care includes aggressive pulmonary toilet, chest physiotherapy, mucus-thinning inhaled agents, and antibiotics tailored to culture and sensitivity results. Treatment regimens vary based on organism profile, including coverage for MSSA, MRSA, Pseudomonas aeruginosa, Burkholderia cepacia, and Haemophilus influenzae. Ciprofloxacin may replace aminoglycosides when organisms are sensitive.


Disease-specific therapies include CFTR modulators such as ivacaftor to improve protein function, nebulized hypertonic saline to restore airway surface liquid, and dornase alfa to reduce mucus viscosity. Adjunctive strategies include high-dose ibuprofen for anti-inflammatory effects, inhaled antibiotics, nutritional optimization, exercise programs, and consideration of lung transplantation in advanced disease.


Pharmacologic Therapy
Antibiotic regimens include aminoglycosides, antipseudomonal penicillins, cephalosporins, carbapenems, vancomycin, and trimethoprim–sulfamethoxazole, dosed carefully due to altered pharmacokinetics in undernourished patients. Close monitoring of drug levels, particularly with aminoglycosides, is essential.


Disposition And Follow-Up
Hospital admission is required for pulmonary exacerbations with significant decline from baseline, hypoxemia, resistant organisms, or failure of outpatient therapy, as well as pneumothorax, hemoptysis, hematemesis, intussusception, unexplained abdominal pain, bowel obstruction, or hyperglycemia.


Discharge requires close follow-up to review culture sensitivities and adjust therapy. Patients should avoid excessive heat exposure and may require oral salt supplementation during periods of heavy sweating.


Care Coordination And Long-Term Planning
All patients should be followed by a specialized cystic fibrosis pulmonary center. Acute exacerbations warrant early consultation. Long-term care requires a multidisciplinary team approach incorporating airway clearance, antibiotics, nutritional support, pancreatic enzyme replacement, and exercise programs.


Key Clinical Insights And Common Pitfalls
In cystic fibrosis patients with acute respiratory distress, pneumothorax must always be considered and promptly evaluated with chest imaging. In those presenting with abdominal pain or vomiting, distal intestinal obstructive syndrome and intussusception should remain high on the differential.

Emergency And Acute Medicine – Implantable Defibrillators


Basics And Description
An implantable cardioverter-defibrillator (ICD) is a small, battery-powered cardiac device implanted subcutaneously in patients at risk for sudden cardiac arrest due to malignant arrhythmias. One or more leads are positioned via venous access to the heart, typically endocardial in the right atrium and right ventricle, or epicardial via the coronary sinus to the left ventricle. The ICD detects atrial and ventricular arrhythmias and delivers electrical shocks between the generator (“can”) and coils in the right ventricle and superior vena cava/right atrial junction to restore sinus rhythm. Implantation technique is similar to pacemaker placement. Newer subcutaneous ICDs (S-ICD) avoid endocardial leads, reducing the risk of bloodstream infection. Approximately 450,000 sudden cardiac deaths occur annually in the United States, with over 100,000 ICDs implanted each year. ICDs reduce mortality more effectively than antiarrhythmic drugs in patients with left ventricular dysfunction, particularly when ejection fraction is below 35%, with an absolute mortality reduction of about 7% in the first two years. Benefit is demonstrated in ischemic and nonischemic dilated cardiomyopathy and hypertrophic cardiomyopathy.


Complications And Device Outcomes
Immediate postimplant complications include pneumothorax, vascular perforation, and acute lead dislodgement. Appropriate shocks occur in approximately 5% of patients annually for primary prevention and 20% annually for secondary prevention. Electrical storm is defined as two or more appropriate shocks within 24 hours. Inappropriate shocks occur in 10–20% of recipients and are commonly due to oversensing or misclassification of supraventricular tachycardia. Device infection occurs in 1–12% of patients, with acute infections (1–30 days) most often due to staphylococcal species and later infections commonly due to Staphylococcus epidermidis or gram-negative organisms. Mortality ranges from 31–66% if an infected device is not removed. Pocket hematomas should not be aspirated. Vascular occlusion related to leads may occur.


Etiology
Electrical storm may result from decompensated heart failure, acute ischemia, metabolic disturbances, drug-induced proarrhythmia, thyrotoxicosis, fever in dilated cardiomyopathy, genetic channelopathies (including Brugada syndrome, long QT syndrome, catecholaminergic polymorphic ventricular tachycardia, and arrhythmogenic right ventricular cardiomyopathy), postcardiac surgery states, or ICD-induced pacing phenomena. Inappropriate shocks may result from oversensing of cardiac or noncardiac signals, electromagnetic interference, lead fracture, loose set screws, or header circuitry problems, as well as misclassification of atrial fibrillation, atrial flutter, sinus tachycardia, or other supraventricular tachycardias. Device- and site-related issues include wound infection, pocket hematoma, and venous thrombosis from lead-related venous obstruction.


Clinical Presentation
Patients who feel unwell before a shock and improved afterward likely received appropriate therapy. Patients who feel well before and after a shock likely experienced inappropriate therapy. Persistent symptoms before and after a shock suggest ongoing arrhythmia or ischemia. Appropriate shocks may be associated with syncope, near syncope, dizziness, dyspnea, palpitations, chest discomfort, or diaphoresis. Inappropriate shocks may occur with palpitations from supraventricular tachycardia or may be asymptomatic in lead-related malfunction. Device infection presents with fever, chills, malaise, hypotension, new murmur, or local wound findings such as erythema, warmth, purulent drainage, skin erosion, or fluctuance. Vascular complications present with unilateral upper-extremity swelling or superficial venous distention.


Evaluation And Workup
Following ICD therapy, device interrogation is essential to determine whether shocks were appropriate and to identify lead malfunction. A 12-lead ECG may show transient ST changes or enzyme elevation after shock delivery that do not necessarily represent myocardial injury. Chest radiography can identify lead fracture or dislodgement. Upper-extremity swelling suggests venous thrombosis. Laboratory evaluation includes cardiac enzymes when ischemia is suspected, complete blood count and blood cultures for infection, and coagulation studies when thrombosis is suspected. MRI is absolutely contraindicated. Magnet application inhibits tachyarrhythmia therapies but does not affect bradycardia pacing.


Differential Diagnosis
Consider appropriate ICD therapy for ventricular tachycardia or fibrillation, inappropriate therapy due to supraventricular tachycardia or device malfunction, phantom shocks perceived during sleep, acute coronary syndrome, heart failure exacerbation, and systemic infection.


Management And Treatment
Initial management follows standard advanced cardiac life support protocols with continuous monitoring. Electrical storm may require intravenous antiarrhythmic therapy such as amiodarone. Inappropriate shocks are managed by treating the underlying supraventricular arrhythmia with beta blockers or calcium channel blockers and inhibiting ICD therapies with magnet placement if needed. Device infections require prompt blood cultures and broad-spectrum antibiotics, with early consultation for device removal. External defibrillation is safe but should not be delivered directly over the ICD generator.


Medications
Common agents include intravenous amiodarone for ventricular arrhythmias, beta blockers or diltiazem for rate control, and antibiotics such as cefazolin or vancomycin for suspected device infection. Anticoagulation with warfarin is indicated for documented venous thrombosis.


Disposition And Follow-Up
Admission is required for patients with ongoing ischemia, heart failure, multiple ICD shocks, suspected infection, expanding pocket hematoma, need for lead revision, or upper-extremity thrombosis. Stable patients with a single appropriate shock and no evidence of ischemia or heart failure may be discharged with electrophysiology follow-up. Device-related complications require surgical or electrophysiology consultation prior to discharge.


Key Clinical Lessons And Common Errors
Aspiration of an ICD pocket should be avoided. External defibrillation pads should not be placed directly over the device, as this may shunt energy away from the myocardium. Prompt differentiation between appropriate and inappropriate shocks guides management and disposition.

Emergency And Acute Medicine – Deep Vein Thrombosis


Core Description
A constant balance exists between intravascular clot formation and clot dissolution. Thrombosis develops when clot formation overwhelms fibrinolysis. Venous clots may be superficial (above the fascia) or deep; the latter constitutes deep vein thrombosis (DVT). Pulmonary embolism (PE) and DVT represent two ends of the same disease spectrum known as venous thromboembolism (VTE). DVT may involve upper or lower extremities and may be distal or proximal relative to the popliteal vein. The incidence is approximately 2 first-time VTE events per 1,000 person-years, increases with age, and is common among hospitalized medical and surgical patients. Diagnosis is more accurate with active surveillance rather than clinical suspicion alone.


Pediatric Considerations
DVT is uncommon in children. When present, evaluation for underlying hypercoagulable conditions is essential. Upper-extremity DVT in children is frequently associated with central venous catheters.


Etiology And Risk Factors
Thrombus formation is influenced by multiple interacting factors. Hypercoagulable states include malignancy, myeloproliferative disorders, nephrotic syndrome, sepsis, inflammatory conditions such as ulcerative colitis, increased estrogen states including pregnancy and exogenous hormones, antiphospholipid syndrome, inherited thrombophilias (protein C, protein S, antithrombin III deficiencies, factor V Leiden, prothrombin gene mutation), and autoimmune conditions.
Venous stasis occurs with prolonged bed rest, immobilization (casts), long-distance travel, paralysis from neurologic disease, congestive heart failure, and obesity.
Vascular injury or anatomic abnormalities include trauma, surgery, central venous lines (particularly for upper-extremity DVT), and May–Thurner syndrome.
Additional contributors include advanced age, certain medications (hydralazine, procainamide, phenothiazines), tobacco use, prior DVT or PE, and genetic predisposition. There is no universal consensus on which VTE patients require testing for inherited thrombophilias.


Pregnancy And Geriatric Considerations
Pregnancy increases DVT risk, particularly during the third trimester and up to two weeks postpartum. Advanced age independently increases DVT and PE risk, and presentations may be atypical in older adults.


Clinical Features
Typical findings include unilateral leg swelling, with a circumference difference greater than 1 cm considered significant, warmth, erythema, pain, tenderness, and sometimes a palpable cord. Superficial thrombophlebitis may present as a visible, tender, cord-like structure. Upper-extremity DVT causes arm swelling, warmth, and tenderness.
Severe presentations include phlegmasia cerulea dolens, characterized by a cold, tender, swollen, cyanotic limb with secondary arterial insufficiency and venous gangrene, and phlegmasia alba dolens, presenting with a cold, tender, pale limb due to arterial compromise.


Essential Evaluation
Assessment of pretest probability is central to DVT evaluation. Careful history and physical examination interpreted within the patient’s risk-factor profile guide diagnostic decisions, as individual signs and symptoms lack sufficient predictive value. Consider evaluation for occult malignancy when clinically appropriate, as VTE may be its initial manifestation.


Diagnostic Testing And Interpretation
D-dimer testing detects fibrin degradation products and is useful only when negative, allowing exclusion of DVT in low-risk patients. A positive result is nonspecific and mandates further imaging. ELISA-based D-dimer assays are the most validated, particularly when combined with pretest probability assessment.
Compression ultrasonography is the first-line diagnostic modality. Normal veins compress fully, whereas thrombosed veins do not. Duplex ultrasonography, combining B-mode imaging with Doppler, has sensitivity in the high 90% range. In high-risk patients with an initial negative ultrasound, repeat imaging or contrast venography is recommended.
Contrast venography, once the gold standard, is now rarely used because of invasiveness and associated complications. Other modalities such as radionuclide venography and impedance plethysmography are infrequently used.


Differential Diagnosis
Consider superficial thrombophlebitis, cellulitis, muscle or ligament tears, ruptured Baker cyst, bilateral edema from cardiac, hepatic, or renal disease, venous insufficiency, drug-induced edema, unilateral edema from abdominal masses or lymphedema, and postphlebitic syndrome.


Initial Stabilization
In cases of phlegmasia alba or cerulea dolens, establish IV access, administer supplemental oxygen, and obtain urgent vascular or surgical consultation.


Emergency Department Management
Systemic anticoagulation is the cornerstone of therapy in patients without contraindications, as PE develops in approximately 50% of untreated DVT. Options include unfractionated heparin, low-molecular-weight heparin (LMWH), fondaparinux, or adjusted-dose subcutaneous heparin. Carefully selected patients may be managed as outpatients.
Warfarin should be initiated only after heparin therapy to avoid transient hypercoagulability. Current evidence is insufficient to universally recommend newer oral anticoagulants in this setting.
Inferior vena cava filters are indicated when anticoagulation is contraindicated or when thromboembolism occurs despite adequate anticoagulation. Filters may also be considered in select high-risk scenarios, though randomized trials show no superiority over anticoagulation alone. Filters can also be placed in the superior vena cava for upper-extremity DVT.
Thrombolysis is rarely indicated because of increased bleeding risk but may be considered in select cases, particularly catheter-directed therapy for upper-extremity DVT. Thrombectomy may be appropriate for extensive disease after vascular consultation. Septic thrombophlebitis requires antibiotics and may necessitate surgical intervention.


Medication Management
Anticoagulation is continued until the INR is therapeutic for two consecutive days. Typical regimens include unfractionated heparin with a bolus followed by infusion titrated to aPTT, LMWH such as enoxaparin or tinzaparin, and warfarin initiated at standard dosing with INR monitoring. Treatment duration is generally at least three months and individualized thereafter.


Disposition And Follow-Up
Admission is indicated for patients unable to receive outpatient anticoagulation, those with concomitant PE, high bleeding risk, phlegmasia, or serious comorbidities.
Outpatient management is appropriate for reliable patients without serious comorbid disease who can administer LMWH and adhere to follow-up.
Vascular surgery consultation is warranted if arterial insufficiency is suspected or when considering vena cava filter placement.


Follow-Up Recommendations
Patients managed as outpatients require close monitoring of hematocrit, platelet count, and INR within several days. Repeat imaging is recommended when clinical suspicion remains high despite an initial negative ultrasound.


Key Clinical Lessons And Common Errors
A negative Homans sign does not exclude DVT. Always assess pretest probability using clinical judgment or validated tools such as the Wells score. In high-risk patients, proceed directly to imaging rather than relying on D-dimer testing. In moderate-risk patients with negative initial studies, arrange repeat evaluation within one week.

Emergency And Acute Medicine – Dacryocystitis And Dacryoadenitis


Core Description
Dacryoadenitis and dacryocystitis are inflammatory disorders of the lacrimal system. Dacryoadenitis refers to inflammation or infection of the lacrimal gland, which produces tears. Dacryocystitis is a suppurative infection of the lacrimal drainage system, specifically the lacrimal sac, usually occurring in the setting of ductal obstruction. Dacryoadenitis may be inflammatory or infectious and can result from contiguous spread or systemic disease, whereas dacryocystitis is almost always infectious due to tear stasis within an obstructed duct.


Epidemiology
Dacryoadenitis is uncommon and is more frequently seen on the left side. Acquired cases are rare. Dacryocystitis is more common, most often affecting adult females older than 30 years, though it may also present in infants.


Etiology Of Dacryoadenitis
Dacryoadenitis is most commonly associated with systemic inflammatory and autoimmune conditions, including Sjögren syndrome, sarcoidosis, Crohn disease, and lacrimal gland tumors. Infectious causes may be primary or secondary to contiguous spread from bacterial conjunctivitis or periorbital cellulitis. Acute suppurative dacryoadenitis in adults is most often caused by Staphylococcus aureus, streptococci, Chlamydia trachomatis, and Neisseria gonorrhoeae. Chronic dacryoadenitis is more commonly related to nasal flora rather than ocular organisms.


Pediatric Considerations In Dacryoadenitis
In children, viral causes predominate, including mumps, measles, Epstein–Barr virus, cytomegalovirus, coxsackievirus, and varicella-zoster virus. A slowly enlarging lacrimal gland mass in children may represent a dermoid cyst rather than infection.


Etiology Of Dacryocystitis
Under normal conditions, tears drain through the lacrimal duct into the lacrimal sac and then into the middle turbinate and sinuses via a pumping mechanism. Dacryocystitis develops when the duct becomes partially or completely obstructed. In adults, chronic inflammation related to ethmoid sinusitis is a common underlying cause, though trauma, dacryoliths, nasal or sinus surgery, or any local obstructive process may contribute. Obstruction leads to tear stasis, bacterial overgrowth, and infection. The infection may be recurrent or chronic. Sinus flora predominate over ocular flora, with Staphylococcus aureus being the most common organism. Complications include draining fistulae, recurrent conjunctivitis, abscess formation, and orbital cellulitis.


Pediatric Considerations In Dacryocystitis
Congenital dacryocystitis typically presents in infancy due to dacryocystoceles and carries high morbidity and mortality, often from systemic spread of infection. The most common pathogen in this population is Streptococcus pneumoniae.


Clinical Presentation
Both dacryoadenitis and dacryocystitis usually present with unilateral eye pain, redness, and swelling.


Dacryoadenitis Symptoms And Signs
Patients may develop acute or indolent swelling and erythema of the upper eyelid, with maximal tenderness in the temporal portion beneath the orbital rim, producing an S-shaped eyelid. A palpable mass may be present. Associated findings include conjunctival injection, discharge, chemosis, variable tear production, ipsilateral preauricular lymphadenopathy, and surrounding cellulitis. Systemic toxicity may occur. Visual acuity, slit-lamp examination, and funduscopic findings are typically normal, though globe displacement may cause visual distortion. Chronic dacryoadenitis presents as a slowly progressive, painless swelling.
Alert: Rapidly assess for possible spread from gonococcal conjunctivitis, as morbidity is high, visual loss is likely, systemic illness is common, and treatment differs significantly.


Dacryocystitis Symptoms And Signs
Dacryocystitis presents as an acutely inflamed, localized mass inferior and medial to the inner canthus. Epiphora is the hallmark symptom due to tear outflow obstruction. Applying pressure to the mass may express purulent material from the punctum, which is diagnostically helpful. Lower eyelid cellulitis may occur. Fever is usually low grade, and patients rarely appear toxic.


Essential Evaluation
A complete ocular examination is required, including visual acuity, extraocular movements, slit-lamp examination, funduscopic examination, eyelid eversion, and nasal inspection.
Pediatric Alert: Carefully assess for extension to orbital cellulitis or meningitis.


Diagnostic Testing And Interpretation
Purulent material should be sent for Gram stain, culture, and sensitivity testing. Chocolate agar should be used if gonococcal infection is suspected. CBC and blood cultures may be obtained when systemic infection is suspected. CT imaging of the orbit and sinuses is indicated to assess for deep tissue involvement, recurrent dacryoadenitis, or suspected orbital extension, particularly in children or high-risk patients.


Differential Diagnosis
For dacryoadenitis, consider autoimmune disease, lacrimal gland tumors, hordeolum, periorbital or orbital cellulitis, severe blepharitis, insect bites, and traumatic injury.
For dacryocystitis, consider insect bites, trauma, acute ethmoid sinusitis, periorbital cellulitis, and acute conjunctivitis.


Emergency Department Management
Early recognition and treatment are essential to prevent local extension and systemic infection. Topical antibiotics may be used to prevent secondary conjunctivitis.


Management Of Dacryoadenitis
Supportive care includes cool compresses and nonsteroidal analgesics. Viral causes are typically self-limited. Bacterial infections require antibiotics, with oral agents such as cephalexin or amoxicillin/clavulanate for mild cases and intravenous therapy such as cefazolin or ticarcillin/clavulanate for severe infections. Administer tetanus toxoid when indicated. Incision and drainage are rarely required and should be performed only in severe cases with ophthalmology or facial surgery consultation.
In children, use cool compresses and analgesics; if the cause is unclear, treat empirically with antibiotics as in adults.


Management Of Dacryocystitis
Drainage of the infected lacrimal sac is essential. Warm compresses and gentle massage may relieve obstruction. Intranasal vasoconstrictors can facilitate drainage. Incision and drainage should be avoided in the ED when possible, as it increases the risk of fistula formation. Duct instrumentation is contraindicated in the acute setting due to risk of permanent scarring and stenosis. Use topical ophthalmic antibiotics to prevent conjunctivitis and systemic antibiotics to treat infection and prevent spread. Administer intravenous antibiotics for febrile or severe infections. Provide adequate analgesia.


Pediatric Management Considerations
Newborns typically respond to massage and topical antibiotics in approximately 95% of cases. Failure to resolve within the first year may require ophthalmologic probing. Children younger than 4 years with dacryocystitis are at increased risk for Haemophilus influenzae infection if not fully immunized. Afebrile, well-appearing children with reliable caregivers may be treated with oral cefaclor or amoxicillin/clavulanate, while acutely ill children require intravenous cefuroxime due to the high risk of bacteremia, septicemia, and meningitis.


Pharmacologic Therapy
Recommended agents include amoxicillin/clavulanate, cefaclor, cefazolin, cefuroxime, cephalexin, erythromycin ophthalmic ointment, trimethoprim–polymyxin ophthalmic ointment, and ticarcillin/clavulanate, dosed appropriately for adults and children. Intranasal tetracaine and phenylephrine may be used to facilitate drainage.


Disposition And Follow-Up
Hospital admission is indicated for febrile or toxic adults, immunocompromised patients, extensive cellulitis, suspected deep tissue or meningeal spread, and high-risk pediatric cases, including unimmunized children or those without reliable follow-up. Prompt ophthalmology referral is required for all cases. Patients with dacryocystitis require confirmation of complete drainage and assessment for definitive intervention to prevent recurrence before discharge.


Key Clinical Lessons And Common Errors
In any patient with a red eye and eyelid swelling, the lacrimal system must be carefully examined. Skin incision and drainage of dacryocystitis should be avoided whenever possible to prevent fistula formation; intranasal vasoconstrictors are preferred to facilitate drainage.

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.