- Published on
Emergency and Acute Medicine – Cough
Physiologic Basis and Clinical Overview
Cough is a sudden, forceful, spasmodic contraction of the thoracic cavity that results in the rapid expulsion of air from the lungs, typically producing a characteristic sound. The cough mechanism begins with a deep inspiration followed by closure of the glottis, contraction of expiratory muscles, and a marked rise in intrapulmonary pressure. When the glottis opens, air is expelled at high velocity, facilitating the clearance of secretions and foreign material. Vibration of the vocal cords in conjunction with the tracheobronchial walls, lung parenchyma, and airway secretions produces the audible cough.
Cough serves as a vital protective defense mechanism for clearing the airway and may occur voluntarily or involuntarily. Involuntary coughing is mediated through vagal afferent nerves, while voluntary coughing is under cortical control, allowing suppression or intentional initiation. Because of this cortical influence, placebo effects can significantly impact cough frequency and severity. The reflex arc involves activation of respiratory tissue receptors, transmission through afferent neurons to the central cough center, and efferent signaling to the respiratory muscles. Mechanical receptors located in the larynx, trachea, and carina respond to touch and displacement, whereas chemical receptors in the larynx and bronchi respond to gases, fumes, mucus, edema, pus, and thermal stimuli.
Severe or persistent coughing may result in complications including epistaxis, subconjunctival hemorrhage, syncope, pneumothorax, pneumomediastinum, emesis, hernia formation, rectal prolapse, urinary or fecal incontinence, seizures, encephalitis, intracranial hemorrhage, spinal epidural hemorrhage, digital clubbing, and pruriginous rash.
Etiology and Duration-Based Classification
Acute cough, defined as lasting less than three weeks, is most commonly caused by pneumonia, acute bronchitis, sinusitis, pertussis, tuberculosis, upper respiratory tract infections, cough-variant asthma, COPD exacerbations, bronchiectasis, pulmonary embolism, left ventricular failure, airway obstruction from food or pills, gastroesophageal reflux disease, allergies, and bronchospasm.
Subacute cough, lasting three to eight weeks, is often postinfectious in origin and may be associated with pertussis, bronchitis, bacterial sinusitis, asthma, GERD, or pulmonary embolism.
Chronic cough, persisting for more than eight weeks, is commonly due to postnasal drip, asthma, GERD, chronic bronchitis, tuberculosis, bronchiectasis, eosinophilic bronchitis, ACE inhibitor use, bronchogenic carcinoma, carcinomatosis, sarcoidosis, left ventricular failure, aspiration syndromes, or psychogenic and habitual causes.
Pediatric Considerations
In children, the most frequent causes of cough include asthma, viral respiratory illness, acute bronchitis, pneumonia, sinusitis, and GERD. Less common causes include tracheobronchomalacia, mediastinal tumors, acyanotic congenital heart disease such as ventricular septal defect or patent ductus arteriosus, pulmonary stenosis, tetralogy of Fallot, retained airway foreign bodies, chronic milk aspiration, and environmental exposures. Evaluation should incorporate neonatal history, feeding patterns, growth and developmental milestones, allergy history, eczema, and sleep disorders. Chest radiography is indicated when foreign body ingestion or aspiration is suspected.
Clinical Features
Cough may be productive or nonproductive. Frothy sputum suggests pulmonary edema, while mucopurulent sputum is often associated with bacterial pneumonia or bronchitis but may also occur in viral infections. Rust-colored sputum suggests pneumococcal pneumonia, and “currant jelly” sputum is characteristic of Klebsiella pneumoniae. Hemoptysis may occur in a variety of conditions. Post-tussive syncope or emesis and paroxysmal coughing are suggestive of pertussis. Associated symptoms include shortness of breath, chest pain, fever, chills, night sweats, and wheezing. GERD-related cough may be accompanied by heartburn, dysphagia, regurgitation, belching, or early satiety. Weight loss, poor appetite, and fatigue raise concern for malignancy.
History should focus on cough duration to classify it as acute, subacute, or chronic, sputum characteristics including hemoptysis, and the presence of post-tussive emesis or syncope. Gastrointestinal symptoms may suggest GERD, while weight loss and night sweats in chronic cough raise suspicion for tuberculosis.
Physical Examination
Vital signs should be carefully assessed. Lung examination may reveal absent or decreased breath sounds suggesting reduced airflow or hyperinflation, crackles indicating alveolar opening, rhonchi from large airway obstruction, wheezes from narrowed airways, or stridor indicating upper airway obstruction. Signs of respiratory distress include use of accessory muscles and abdominal breathing.
Essential Diagnostic Approach
A comprehensive medical history should include cough duration, associated symptoms, exposure to sick contacts, smoking history, ACE inhibitor use, immunocompromised status including HIV, and potential tuberculosis exposure. Electrocardiography is indicated in patients with cardiac disease, chest pain, abnormal vital signs, or absence of infectious symptoms.
Laboratory studies should be guided by clinical presentation and may include a complete blood count with differential, sputum Gram stain and culture, acid-fast bacilli testing, CD4 count, pertussis serology, D-dimer testing, and influenza testing in high-risk or hospitalized patients.
Chest radiography is indicated for immunocompromised patients and in otherwise healthy patients with acute cough and sputum production when accompanied by tachycardia, tachypnea, fever above 38°C, focal lung findings, ill appearance, change in chronic cough pattern, or persistence of cough after discontinuation of an ACE inhibitor. Chest CT is reserved for abnormal radiographs or evaluation for pulmonary embolism. Peak flow testing may assist in asthma evaluation, while bronchoscopy is indicated for unexplained masses on imaging, hemoptysis, or suspected malignancy.
Differential Diagnosis
The differential diagnosis mirrors the etiologic categories described above and should be guided by duration, associated symptoms, and patient risk factors.
Emergency Department Management
Initial evaluation requires assessment of airway, breathing, and circulation. Treatment is directed at the underlying cause. Respiratory infections may require antibiotics, antivirals for influenza, decongestants, or antitussives. Asthma exacerbations are treated with inhaled beta-agonists and corticosteroids. GERD-related cough is managed with H2 blockers, proton pump inhibitors, and antacids. Suspected pertussis requires macrolide therapy and five days of isolation. Exacerbations of chronic bronchitis are treated with inhaled beta-agonists and steroids. Malignancy-related cough is managed with supportive care.
Pharmacologic Therapy
Antibiotic selection should target the suspected pathogen. Antiviral therapy includes oseltamivir at standard adult and pediatric dosing. Antitussives such as codeine, dextromethorphan, and hydrocodone may be used judiciously. Bronchodilators include inhaled albuterol and ipratropium. Decongestants such as chlorpheniramine and phenylpropanolamine may be used when indicated. Mucolytics such as guaifenesin aid secretion clearance. Corticosteroids may include intranasal dexamethasone or systemic methylprednisolone or prednisone, depending on severity and etiology.
Disposition and Follow-Up
Hospital admission is warranted for patients with hypoxemia, critical illness, suspected tuberculosis with radiographic findings, immunocompromised patients with fever, or those at risk for sepsis or bacteremia. Patients may be discharged if oxygenation is at baseline, oral medications are tolerated, and a safe home environment is assured. Close outpatient follow-up with a primary care physician is recommended.
Patient Guidance and Preventive Measures
Patients should be advised to stop smoking and avoid exposure to tobacco smoke, asbestos, and other respiratory irritants. Dietary modifications for GERD include avoiding caffeine-containing beverages, refraining from eating at least four hours before bedtime, and elevating the head during sleep. Immediate medical attention is required for chest pain, hemoptysis, shortness of breath, or syncope.
Key Clinical Insights and Common Errors
For patients whose clinical presentation is consistent with GERD-related cough, empiric treatment is recommended before pursuing diagnostic testing. In cases of presumed acute bronchitis, routine antibiotic therapy is not supported by evidence and should be avoided.
Physiologic Basis and Clinical Overview
Cough is a sudden, forceful, spasmodic contraction of the thoracic cavity that results in the rapid expulsion of air from the lungs, typically producing a characteristic sound. The cough mechanism begins with a deep inspiration followed by closure of the glottis, contraction of expiratory muscles, and a marked rise in intrapulmonary pressure. When the glottis opens, air is expelled at high velocity, facilitating the clearance of secretions and foreign material. Vibration of the vocal cords in conjunction with the tracheobronchial walls, lung parenchyma, and airway secretions produces the audible cough.
Cough serves as a vital protective defense mechanism for clearing the airway and may occur voluntarily or involuntarily. Involuntary coughing is mediated through vagal afferent nerves, while voluntary coughing is under cortical control, allowing suppression or intentional initiation. Because of this cortical influence, placebo effects can significantly impact cough frequency and severity. The reflex arc involves activation of respiratory tissue receptors, transmission through afferent neurons to the central cough center, and efferent signaling to the respiratory muscles. Mechanical receptors located in the larynx, trachea, and carina respond to touch and displacement, whereas chemical receptors in the larynx and bronchi respond to gases, fumes, mucus, edema, pus, and thermal stimuli.
Severe or persistent coughing may result in complications including epistaxis, subconjunctival hemorrhage, syncope, pneumothorax, pneumomediastinum, emesis, hernia formation, rectal prolapse, urinary or fecal incontinence, seizures, encephalitis, intracranial hemorrhage, spinal epidural hemorrhage, digital clubbing, and pruriginous rash.
Etiology and Duration-Based Classification
Acute cough, defined as lasting less than three weeks, is most commonly caused by pneumonia, acute bronchitis, sinusitis, pertussis, tuberculosis, upper respiratory tract infections, cough-variant asthma, COPD exacerbations, bronchiectasis, pulmonary embolism, left ventricular failure, airway obstruction from food or pills, gastroesophageal reflux disease, allergies, and bronchospasm.
Subacute cough, lasting three to eight weeks, is often postinfectious in origin and may be associated with pertussis, bronchitis, bacterial sinusitis, asthma, GERD, or pulmonary embolism.
Chronic cough, persisting for more than eight weeks, is commonly due to postnasal drip, asthma, GERD, chronic bronchitis, tuberculosis, bronchiectasis, eosinophilic bronchitis, ACE inhibitor use, bronchogenic carcinoma, carcinomatosis, sarcoidosis, left ventricular failure, aspiration syndromes, or psychogenic and habitual causes.
Pediatric Considerations
In children, the most frequent causes of cough include asthma, viral respiratory illness, acute bronchitis, pneumonia, sinusitis, and GERD. Less common causes include tracheobronchomalacia, mediastinal tumors, acyanotic congenital heart disease such as ventricular septal defect or patent ductus arteriosus, pulmonary stenosis, tetralogy of Fallot, retained airway foreign bodies, chronic milk aspiration, and environmental exposures. Evaluation should incorporate neonatal history, feeding patterns, growth and developmental milestones, allergy history, eczema, and sleep disorders. Chest radiography is indicated when foreign body ingestion or aspiration is suspected.
Clinical Features
Cough may be productive or nonproductive. Frothy sputum suggests pulmonary edema, while mucopurulent sputum is often associated with bacterial pneumonia or bronchitis but may also occur in viral infections. Rust-colored sputum suggests pneumococcal pneumonia, and “currant jelly” sputum is characteristic of Klebsiella pneumoniae. Hemoptysis may occur in a variety of conditions. Post-tussive syncope or emesis and paroxysmal coughing are suggestive of pertussis. Associated symptoms include shortness of breath, chest pain, fever, chills, night sweats, and wheezing. GERD-related cough may be accompanied by heartburn, dysphagia, regurgitation, belching, or early satiety. Weight loss, poor appetite, and fatigue raise concern for malignancy.
History should focus on cough duration to classify it as acute, subacute, or chronic, sputum characteristics including hemoptysis, and the presence of post-tussive emesis or syncope. Gastrointestinal symptoms may suggest GERD, while weight loss and night sweats in chronic cough raise suspicion for tuberculosis.
Physical Examination
Vital signs should be carefully assessed. Lung examination may reveal absent or decreased breath sounds suggesting reduced airflow or hyperinflation, crackles indicating alveolar opening, rhonchi from large airway obstruction, wheezes from narrowed airways, or stridor indicating upper airway obstruction. Signs of respiratory distress include use of accessory muscles and abdominal breathing.
Essential Diagnostic Approach
A comprehensive medical history should include cough duration, associated symptoms, exposure to sick contacts, smoking history, ACE inhibitor use, immunocompromised status including HIV, and potential tuberculosis exposure. Electrocardiography is indicated in patients with cardiac disease, chest pain, abnormal vital signs, or absence of infectious symptoms.
Laboratory studies should be guided by clinical presentation and may include a complete blood count with differential, sputum Gram stain and culture, acid-fast bacilli testing, CD4 count, pertussis serology, D-dimer testing, and influenza testing in high-risk or hospitalized patients.
Chest radiography is indicated for immunocompromised patients and in otherwise healthy patients with acute cough and sputum production when accompanied by tachycardia, tachypnea, fever above 38°C, focal lung findings, ill appearance, change in chronic cough pattern, or persistence of cough after discontinuation of an ACE inhibitor. Chest CT is reserved for abnormal radiographs or evaluation for pulmonary embolism. Peak flow testing may assist in asthma evaluation, while bronchoscopy is indicated for unexplained masses on imaging, hemoptysis, or suspected malignancy.
Differential Diagnosis
The differential diagnosis mirrors the etiologic categories described above and should be guided by duration, associated symptoms, and patient risk factors.
Emergency Department Management
Initial evaluation requires assessment of airway, breathing, and circulation. Treatment is directed at the underlying cause. Respiratory infections may require antibiotics, antivirals for influenza, decongestants, or antitussives. Asthma exacerbations are treated with inhaled beta-agonists and corticosteroids. GERD-related cough is managed with H2 blockers, proton pump inhibitors, and antacids. Suspected pertussis requires macrolide therapy and five days of isolation. Exacerbations of chronic bronchitis are treated with inhaled beta-agonists and steroids. Malignancy-related cough is managed with supportive care.
Pharmacologic Therapy
Antibiotic selection should target the suspected pathogen. Antiviral therapy includes oseltamivir at standard adult and pediatric dosing. Antitussives such as codeine, dextromethorphan, and hydrocodone may be used judiciously. Bronchodilators include inhaled albuterol and ipratropium. Decongestants such as chlorpheniramine and phenylpropanolamine may be used when indicated. Mucolytics such as guaifenesin aid secretion clearance. Corticosteroids may include intranasal dexamethasone or systemic methylprednisolone or prednisone, depending on severity and etiology.
Disposition and Follow-Up
Hospital admission is warranted for patients with hypoxemia, critical illness, suspected tuberculosis with radiographic findings, immunocompromised patients with fever, or those at risk for sepsis or bacteremia. Patients may be discharged if oxygenation is at baseline, oral medications are tolerated, and a safe home environment is assured. Close outpatient follow-up with a primary care physician is recommended.
Patient Guidance and Preventive Measures
Patients should be advised to stop smoking and avoid exposure to tobacco smoke, asbestos, and other respiratory irritants. Dietary modifications for GERD include avoiding caffeine-containing beverages, refraining from eating at least four hours before bedtime, and elevating the head during sleep. Immediate medical attention is required for chest pain, hemoptysis, shortness of breath, or syncope.
Key Clinical Insights and Common Errors
For patients whose clinical presentation is consistent with GERD-related cough, empiric treatment is recommended before pursuing diagnostic testing. In cases of presumed acute bronchitis, routine antibiotic therapy is not supported by evidence and should be avoided.
- Published on
Emergency And Acute Medicine – Croup
Description
Croup is a viral infection of the upper respiratory tract that most commonly affects children between 6 months and 3 years of age. It typically presents as laryngotracheitis or laryngotracheobronchitis with inspiratory stridor caused by extrathoracic airway obstruction. Expiratory wheezing suggests lower airway involvement. The disease results from inflammatory edema of the subglottic region, the narrowest portion of the pediatric airway, and may progress to respiratory failure in severe cases.
Etiology
The most common causative organisms are parainfluenza virus types 1, 2, and 3. Other causes include human coronavirus NL63, influenza A and B, adenovirus, respiratory syncytial virus, measles, Mycoplasma pneumoniae, and herpes simplex virus.
Clinical Presentation
Children usually develop a nonspecific upper respiratory prodrome with or without fever. Important historical features include duration of illness, prior tracheal intubation, risk of foreign body aspiration, previous episodes of croup, history of wheezing, and immunization status, particularly against Haemophilus influenzae type b, diphtheria, pertussis, tetanus, and influenza.
On examination, children are often not toxic appearing and typically prefer to sit upright. Cyanosis is uncommon and suggests severe disease when present. Clinicians should assess the quality of cry or voice, mental status, hydration, presence of drooling or trismus, neck mobility, stridor at rest, and work of breathing.
Severity can be graded using the Westley croup score, which incorporates stridor, retractions, air entry, cyanosis, and level of consciousness.
Diagnostic Evaluation
Continuous pulse oximetry is recommended. Routine laboratory testing is not indicated. Imaging is generally unnecessary but, when obtained for atypical presentations, anteroposterior and lateral neck radiographs may show the classic “steeple sign” reflecting subglottic narrowing. Imaging should never delay airway management in patients with suspected epiglottitis or bacterial tracheitis, and children must be closely monitored if imaging is performed.
Differential Diagnosis
Infectious causes include bacterial tracheitis, epiglottitis, retropharyngeal or parapharyngeal abscess, peritonsillar abscess, and diphtheria. Noninfectious causes include foreign body aspiration, angioedema, congenital airway abnormalities such as laryngomalacia or tracheomalacia, acquired subglottic stenosis, vocal cord paralysis, airway burns, hemangioma, laryngeal papillomatosis, and vocal cord dysfunction in adolescents.
Initial Management
Children should be allowed to maintain their position of comfort, and interventions that may increase distress, such as IV access or intramuscular injections, should be deferred when possible. In cases of severe respiratory distress, immediate nebulized epinephrine should be administered.
Emergency Department Management
Nebulized racemic epinephrine or L-epinephrine is indicated for stridor at rest or significant respiratory distress and is effective in reducing airway edema. Supplemental oxygen may be provided via blow-by if hypoxia is suspected. Dexamethasone significantly improves outcomes by reducing the need for intubation, hospital admission, and return visits, and is effective even in mild cases. If there is an incomplete response to epinephrine, heliox may be considered to reduce work of breathing.
For patients with impending or established respiratory failure, tracheal intubation should be performed by the most experienced provider available using an uncuffed endotracheal tube 0.5–1 mm smaller than standard size. If epiglottitis or foreign body aspiration is suspected, airway management should ideally occur in the operating room with surgical backup available.
Medications
Racemic epinephrine 2.25% is administered as 0.25–0.5 mL nebulized in normal saline. L-epinephrine 1:1,000 may be given as 5 mL nebulized. Dexamethasone is given as a single dose of 0.6 mg/kg, up to a maximum of 10 mg, via oral, intravenous, or intramuscular routes. Heliox may be administered as a 70:30 helium–oxygen mixture. Antibiotics are not indicated.
Disposition And Follow-Up
Hospital admission is recommended for young infants, children with pre-existing airway disease, persistent or recurrent stridor at rest despite treatment, or those requiring repeated epinephrine treatments. Pediatric intensive care admission is indicated for severe obstruction, frequent need for epinephrine or heliox, or need for intubation.
Children may be discharged if they have normal oxygenation on room air, no stridor at rest after observation for at least 2–3 hours, and reliable caregivers with access to follow-up care.
Referral Considerations
Evaluation by specialists is warranted for children with suspected anatomic airway abnormalities, recurrent episodes, prior intubation, or infants younger than one year with unexplained stridor.
Follow-Up Guidance
Most children with uncomplicated croup do not require routine follow-up. Caregivers should be instructed to seek medical attention if stridor persists, worsens, or recurs.
Key Teaching Points And Common Errors
Stridor in young infants warrants careful evaluation due to a higher likelihood of congenital airway abnormalities. Early epiglottitis or bacterial tracheitis may closely mimic croup and should be considered when symptoms are atypical or severe.
Description
Croup is a viral infection of the upper respiratory tract that most commonly affects children between 6 months and 3 years of age. It typically presents as laryngotracheitis or laryngotracheobronchitis with inspiratory stridor caused by extrathoracic airway obstruction. Expiratory wheezing suggests lower airway involvement. The disease results from inflammatory edema of the subglottic region, the narrowest portion of the pediatric airway, and may progress to respiratory failure in severe cases.
Etiology
The most common causative organisms are parainfluenza virus types 1, 2, and 3. Other causes include human coronavirus NL63, influenza A and B, adenovirus, respiratory syncytial virus, measles, Mycoplasma pneumoniae, and herpes simplex virus.
Clinical Presentation
Children usually develop a nonspecific upper respiratory prodrome with or without fever. Important historical features include duration of illness, prior tracheal intubation, risk of foreign body aspiration, previous episodes of croup, history of wheezing, and immunization status, particularly against Haemophilus influenzae type b, diphtheria, pertussis, tetanus, and influenza.
On examination, children are often not toxic appearing and typically prefer to sit upright. Cyanosis is uncommon and suggests severe disease when present. Clinicians should assess the quality of cry or voice, mental status, hydration, presence of drooling or trismus, neck mobility, stridor at rest, and work of breathing.
Severity can be graded using the Westley croup score, which incorporates stridor, retractions, air entry, cyanosis, and level of consciousness.
Diagnostic Evaluation
Continuous pulse oximetry is recommended. Routine laboratory testing is not indicated. Imaging is generally unnecessary but, when obtained for atypical presentations, anteroposterior and lateral neck radiographs may show the classic “steeple sign” reflecting subglottic narrowing. Imaging should never delay airway management in patients with suspected epiglottitis or bacterial tracheitis, and children must be closely monitored if imaging is performed.
Differential Diagnosis
Infectious causes include bacterial tracheitis, epiglottitis, retropharyngeal or parapharyngeal abscess, peritonsillar abscess, and diphtheria. Noninfectious causes include foreign body aspiration, angioedema, congenital airway abnormalities such as laryngomalacia or tracheomalacia, acquired subglottic stenosis, vocal cord paralysis, airway burns, hemangioma, laryngeal papillomatosis, and vocal cord dysfunction in adolescents.
Initial Management
Children should be allowed to maintain their position of comfort, and interventions that may increase distress, such as IV access or intramuscular injections, should be deferred when possible. In cases of severe respiratory distress, immediate nebulized epinephrine should be administered.
Emergency Department Management
Nebulized racemic epinephrine or L-epinephrine is indicated for stridor at rest or significant respiratory distress and is effective in reducing airway edema. Supplemental oxygen may be provided via blow-by if hypoxia is suspected. Dexamethasone significantly improves outcomes by reducing the need for intubation, hospital admission, and return visits, and is effective even in mild cases. If there is an incomplete response to epinephrine, heliox may be considered to reduce work of breathing.
For patients with impending or established respiratory failure, tracheal intubation should be performed by the most experienced provider available using an uncuffed endotracheal tube 0.5–1 mm smaller than standard size. If epiglottitis or foreign body aspiration is suspected, airway management should ideally occur in the operating room with surgical backup available.
Medications
Racemic epinephrine 2.25% is administered as 0.25–0.5 mL nebulized in normal saline. L-epinephrine 1:1,000 may be given as 5 mL nebulized. Dexamethasone is given as a single dose of 0.6 mg/kg, up to a maximum of 10 mg, via oral, intravenous, or intramuscular routes. Heliox may be administered as a 70:30 helium–oxygen mixture. Antibiotics are not indicated.
Disposition And Follow-Up
Hospital admission is recommended for young infants, children with pre-existing airway disease, persistent or recurrent stridor at rest despite treatment, or those requiring repeated epinephrine treatments. Pediatric intensive care admission is indicated for severe obstruction, frequent need for epinephrine or heliox, or need for intubation.
Children may be discharged if they have normal oxygenation on room air, no stridor at rest after observation for at least 2–3 hours, and reliable caregivers with access to follow-up care.
Referral Considerations
Evaluation by specialists is warranted for children with suspected anatomic airway abnormalities, recurrent episodes, prior intubation, or infants younger than one year with unexplained stridor.
Follow-Up Guidance
Most children with uncomplicated croup do not require routine follow-up. Caregivers should be instructed to seek medical attention if stridor persists, worsens, or recurs.
Key Teaching Points And Common Errors
Stridor in young infants warrants careful evaluation due to a higher likelihood of congenital airway abnormalities. Early epiglottitis or bacterial tracheitis may closely mimic croup and should be considered when symptoms are atypical or severe.
- Published on
Emergency And Acute Medicine – Cushing Syndrome
Overview
Cushing disease refers specifically to excess adrenocorticotropic hormone (ACTH) production from a pituitary adenoma. Cushing syndrome describes the clinical state resulting from prolonged exposure to excessive glucocorticoids, regardless of the source.
Predisposing Factors
Genetic associations include multiple endocrine neoplasia type I and Carney complex, which is characterized by pigmented lentigines, atrial myxomas, and germ-cell tumors associated with Cushing disease.
Underlying Causes
The most common cause is exogenous glucocorticoid administration, whether therapeutic or surreptitious. Endogenous causes include ACTH-secreting pituitary adenomas, adrenal cortisol overproduction from adenoma, carcinoma, or micronodular disease, and ectopic ACTH production. Tumors associated with ectopic ACTH secretion include small cell lung carcinoma (most common), uterine cervical carcinoma, pancreatic islet cell tumors associated with MEN I, medullary thyroid carcinoma, pheochromocytoma, ganglioneuroma, melanoma, prostate carcinoma, and carcinoid tumors arising from the lung, pancreas, gastrointestinal tract, thymus, or ovary.
Clinical Recognition
The most critical emergency consideration is recognizing the risk of addisonian (adrenal) crisis during periods of physiologic stress. While Cushing syndrome itself is not usually an emergency diagnosis, early identification in the emergency setting may prevent significant morbidity and mortality.
In children, suspicion should be raised when obesity progresses in the absence of normal linear growth. During pregnancy, Cushing syndrome is rare but has been associated with severe preeclampsia and HELLP syndrome.
History And Physical Findings
Patients may have a prior diagnosis of Cushing disease or a history of corticosteroid use. Changes in weight, facial appearance, hirsutism, or psychiatric symptoms are important historical clues.
On examination, characteristic findings include moon facies, a dorsocervical fat pad (buffalo hump), central obesity with thin extremities, and supraclavicular fat deposition. These features are particularly concerning in stressed patients because of the risk of adrenal crisis.
Cardiovascular manifestations include uncontrolled hypertension. Neurologic findings may include stroke, pseudotumor cerebri (especially with exogenous steroid use), or spinal lipomatosis causing cord or nerve root compression. Gastrointestinal complications include peptic ulcer disease, gastrointestinal hemorrhage, pancreatitis, and fatty liver. Psychiatric manifestations are common and include mood disorders, depression, memory impairment, euphoria, and toxic psychosis.
Musculoskeletal findings include proximal muscle weakness, pathologic fractures, osteoporosis, and avascular necrosis of the humeral or femoral heads. Endocrine effects include glucose intolerance, hyperlipidemia, amenorrhea, hirsutism, or male-pattern balding in females. Hematologic changes include neutrophilia with lymphopenia and eosinopenia, increasing susceptibility to opportunistic infections. Ophthalmologic complications include cataracts and glaucoma, particularly with exogenous steroid use. Dermatologic features include wide purple striae, hyperpigmentation of the buccal mucosa due to excess ACTH, facial plethora, thin skin, poor wound healing, easy bruising, acne, and hyperhidrosis.
Essential Emergency Evaluation
Definitive diagnosis cannot be established in the emergency department. The priority is identifying patients at risk for addisonian crisis and managing concurrent life-threatening conditions such as myocardial infarction, stroke, sepsis, pathologic fractures, uncontrolled diabetes, or psychiatric emergencies requiring admission.
Diagnostic Studies
Laboratory evaluation may reveal hypokalemia with metabolic alkalosis, diminished glucose tolerance, overt diabetes, glycosuria, leukocytosis, and eosinopenia. Electrocardiography is useful to evaluate for myocardial ischemia, and chest radiography may identify tumors producing ectopic ACTH. Plain radiographs may be indicated if pathologic fractures are suspected and may show delayed bone age.
Definitive outpatient testing includes pituitary MRI, adrenal CT imaging, and dexamethasone suppression testing. Low-dose dexamethasone testing is used as a screening tool, though false positives are common. High-dose dexamethasone suppression testing may be required to confirm endogenous Cushing syndrome.
Alternative Diagnoses To Consider
Conditions that may mimic Cushing syndrome include alcohol-induced pseudo-Cushing syndrome, obesity, psychiatric disorders such as depression or panic disorder, and physiologic states including chronic stress, late pregnancy, and chronic strenuous exercise.
Emergency Management
Patients with iatrogenic Cushing syndrome may develop acute addisonian crisis during stress. These patients can also exhibit severe behavioral disturbances. The leading causes of death in untreated Cushing syndrome are infection, stroke, and myocardial infarction.
Initial management focuses on preventing adrenal crisis and treating associated complications. This includes intravenous fluids, glucose control, blood pressure management, appropriate cultures and antibiotics for suspected infection, and prompt treatment of cardiovascular or neurologic emergencies. Stress-dose steroids with hydrocortisone should be administered in patients with suspected adrenal crisis.
Medications that reduce cortisol production are rarely initiated in the emergency setting and should only be started under endocrinology guidance in patients with severe symptoms awaiting definitive therapy.
Definitive Therapy
Management depends on etiology. Exogenous steroid exposure requires gradual tapering when feasible, along with calcium, vitamin D, and estrogen supplementation if appropriate. Pituitary-dependent disease is treated with transsphenoidal surgery, with radiation reserved for refractory cases. Adrenal tumors require surgical resection, with medical therapy for unresectable metastatic disease. Ectopic ACTH-producing tumors are treated with surgical resection when possible and medical therapy otherwise.
Medications
Hydrocortisone is indicated only in adrenal crisis and is given intravenously. Additional agents such as ketoconazole, metyrapone, aminoglutethimide, mifepristone, mitotane, cyproheptadine, bromocriptine, pasireotide, or spironolactone may be used for symptomatic control under specialist supervision.
Disposition And Follow-Up
Hospital admission is required for patients with complications such as myocardial infarction, stroke, sepsis, pathologic fracture, uncontrolled diabetes, psychiatric emergencies, or impending adrenal crisis. Stable patients without these features may be discharged with close follow-up.
Referral And Long-Term Care
All patients with suspected Cushing syndrome require referral for definitive evaluation. Conditions secondary to hypercortisolism should be addressed concurrently.
Practical Insights And Common Pitfalls
Maintain a high index of suspicion in physiologically stressed patients with characteristic body habitus, especially those with supraclavicular fat pads. Early recognition is essential to prevent addisonian crisis and associated morbidity.
Overview
Cushing disease refers specifically to excess adrenocorticotropic hormone (ACTH) production from a pituitary adenoma. Cushing syndrome describes the clinical state resulting from prolonged exposure to excessive glucocorticoids, regardless of the source.
Predisposing Factors
Genetic associations include multiple endocrine neoplasia type I and Carney complex, which is characterized by pigmented lentigines, atrial myxomas, and germ-cell tumors associated with Cushing disease.
Underlying Causes
The most common cause is exogenous glucocorticoid administration, whether therapeutic or surreptitious. Endogenous causes include ACTH-secreting pituitary adenomas, adrenal cortisol overproduction from adenoma, carcinoma, or micronodular disease, and ectopic ACTH production. Tumors associated with ectopic ACTH secretion include small cell lung carcinoma (most common), uterine cervical carcinoma, pancreatic islet cell tumors associated with MEN I, medullary thyroid carcinoma, pheochromocytoma, ganglioneuroma, melanoma, prostate carcinoma, and carcinoid tumors arising from the lung, pancreas, gastrointestinal tract, thymus, or ovary.
Clinical Recognition
The most critical emergency consideration is recognizing the risk of addisonian (adrenal) crisis during periods of physiologic stress. While Cushing syndrome itself is not usually an emergency diagnosis, early identification in the emergency setting may prevent significant morbidity and mortality.
In children, suspicion should be raised when obesity progresses in the absence of normal linear growth. During pregnancy, Cushing syndrome is rare but has been associated with severe preeclampsia and HELLP syndrome.
History And Physical Findings
Patients may have a prior diagnosis of Cushing disease or a history of corticosteroid use. Changes in weight, facial appearance, hirsutism, or psychiatric symptoms are important historical clues.
On examination, characteristic findings include moon facies, a dorsocervical fat pad (buffalo hump), central obesity with thin extremities, and supraclavicular fat deposition. These features are particularly concerning in stressed patients because of the risk of adrenal crisis.
Cardiovascular manifestations include uncontrolled hypertension. Neurologic findings may include stroke, pseudotumor cerebri (especially with exogenous steroid use), or spinal lipomatosis causing cord or nerve root compression. Gastrointestinal complications include peptic ulcer disease, gastrointestinal hemorrhage, pancreatitis, and fatty liver. Psychiatric manifestations are common and include mood disorders, depression, memory impairment, euphoria, and toxic psychosis.
Musculoskeletal findings include proximal muscle weakness, pathologic fractures, osteoporosis, and avascular necrosis of the humeral or femoral heads. Endocrine effects include glucose intolerance, hyperlipidemia, amenorrhea, hirsutism, or male-pattern balding in females. Hematologic changes include neutrophilia with lymphopenia and eosinopenia, increasing susceptibility to opportunistic infections. Ophthalmologic complications include cataracts and glaucoma, particularly with exogenous steroid use. Dermatologic features include wide purple striae, hyperpigmentation of the buccal mucosa due to excess ACTH, facial plethora, thin skin, poor wound healing, easy bruising, acne, and hyperhidrosis.
Essential Emergency Evaluation
Definitive diagnosis cannot be established in the emergency department. The priority is identifying patients at risk for addisonian crisis and managing concurrent life-threatening conditions such as myocardial infarction, stroke, sepsis, pathologic fractures, uncontrolled diabetes, or psychiatric emergencies requiring admission.
Diagnostic Studies
Laboratory evaluation may reveal hypokalemia with metabolic alkalosis, diminished glucose tolerance, overt diabetes, glycosuria, leukocytosis, and eosinopenia. Electrocardiography is useful to evaluate for myocardial ischemia, and chest radiography may identify tumors producing ectopic ACTH. Plain radiographs may be indicated if pathologic fractures are suspected and may show delayed bone age.
Definitive outpatient testing includes pituitary MRI, adrenal CT imaging, and dexamethasone suppression testing. Low-dose dexamethasone testing is used as a screening tool, though false positives are common. High-dose dexamethasone suppression testing may be required to confirm endogenous Cushing syndrome.
Alternative Diagnoses To Consider
Conditions that may mimic Cushing syndrome include alcohol-induced pseudo-Cushing syndrome, obesity, psychiatric disorders such as depression or panic disorder, and physiologic states including chronic stress, late pregnancy, and chronic strenuous exercise.
Emergency Management
Patients with iatrogenic Cushing syndrome may develop acute addisonian crisis during stress. These patients can also exhibit severe behavioral disturbances. The leading causes of death in untreated Cushing syndrome are infection, stroke, and myocardial infarction.
Initial management focuses on preventing adrenal crisis and treating associated complications. This includes intravenous fluids, glucose control, blood pressure management, appropriate cultures and antibiotics for suspected infection, and prompt treatment of cardiovascular or neurologic emergencies. Stress-dose steroids with hydrocortisone should be administered in patients with suspected adrenal crisis.
Medications that reduce cortisol production are rarely initiated in the emergency setting and should only be started under endocrinology guidance in patients with severe symptoms awaiting definitive therapy.
Definitive Therapy
Management depends on etiology. Exogenous steroid exposure requires gradual tapering when feasible, along with calcium, vitamin D, and estrogen supplementation if appropriate. Pituitary-dependent disease is treated with transsphenoidal surgery, with radiation reserved for refractory cases. Adrenal tumors require surgical resection, with medical therapy for unresectable metastatic disease. Ectopic ACTH-producing tumors are treated with surgical resection when possible and medical therapy otherwise.
Medications
Hydrocortisone is indicated only in adrenal crisis and is given intravenously. Additional agents such as ketoconazole, metyrapone, aminoglutethimide, mifepristone, mitotane, cyproheptadine, bromocriptine, pasireotide, or spironolactone may be used for symptomatic control under specialist supervision.
Disposition And Follow-Up
Hospital admission is required for patients with complications such as myocardial infarction, stroke, sepsis, pathologic fracture, uncontrolled diabetes, psychiatric emergencies, or impending adrenal crisis. Stable patients without these features may be discharged with close follow-up.
Referral And Long-Term Care
All patients with suspected Cushing syndrome require referral for definitive evaluation. Conditions secondary to hypercortisolism should be addressed concurrently.
Practical Insights And Common Pitfalls
Maintain a high index of suspicion in physiologically stressed patients with characteristic body habitus, especially those with supraclavicular fat pads. Early recognition is essential to prevent addisonian crisis and associated morbidity.
- Published on
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.
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.
- Published on
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.
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.
- Published on
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.
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.
- Published on
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.
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.
- Published on
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.
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.
- Published on
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.
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.
- Published on
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.
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.
