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Emergency And Acute Medicine – Pneumonia in Adults
Pneumonia in adults is an acute infection of the lung parenchyma and is the seventh leading cause of death and the leading infectious cause of mortality in the United States. Mortality is highest in elderly patients and those with chronic heart, lung, liver, or kidney disease, diabetes mellitus, alcoholism, malignancy, asplenia, immunosuppression, or recent antimicrobial use. Pneumonia is classified by source as community-acquired (CAP), healthcare-associated (HCAP), hospital-acquired (HAP), or ventilator-associated (VAP), and by presentation as typical or atypical. Complications include bacteremia, sepsis, lung abscess, empyema, and respiratory failure.
The most common cause of community-acquired pneumonia is Streptococcus pneumoniae. Other typical CAP pathogens include Haemophilus influenzae, Klebsiella pneumoniae, Moraxella catarrhalis, Streptococcus pyogenes, and Staphylococcus aureus. Atypical CAP pathogens include Mycoplasma pneumoniae, Chlamydophila pneumoniae, Legionella pneumophila, and respiratory viruses. Healthcare- and hospital-associated pneumonias are more commonly caused by gram-negative organisms such as Pseudomonas and Stenotrophomonas, as well as methicillin-resistant Staphylococcus aureus (MRSA). Immunocompromised patients are at risk for organisms such as Mycobacterium tuberculosis and Pneumocystis jirovecii. Aspiration pneumonia may involve chemical pneumonitis with or without oral and gastric anaerobes.
Typical pneumonia presents with acute onset of fever, chills, rigors, productive cough, dyspnea, and pleuritic chest pain. Atypical pneumonia has a more subacute onset with a viral prodrome, nonproductive cough, low-grade fever, headache, myalgias, and malaise, often without pleuritic pain or rigors. On examination, patients may demonstrate tachypnea, tachycardia, hypoxia, and fever. Lung findings can include dullness to percussion, increased tactile fremitus, egophony, rales, rhonchi, or decreased breath sounds, although pneumonia may be present without classic consolidation findings. Elderly patients frequently present atypically, sometimes with confusion or functional decline as the primary symptom.
Diagnosis is based on clinical findings supported by imaging. Laboratory evaluation generally includes a complete blood count and serum chemistry panel. Blood and sputum cultures are typically reserved for ICU patients. Urine antigen testing for S. pneumoniae and Legionella may be helpful in select cases. Lactate levels may assist in identifying sepsis. Chest radiography is the primary imaging modality and may demonstrate consolidation, air bronchograms, interstitial infiltrates, pleural effusion, empyema, or cavitation. Radiographic findings are nonspecific for particular pathogens. Imaging may be deferred in young, healthy patients treated empirically as outpatients, and a negative radiograph does not exclude pneumonia if clinical suspicion is high.
Initial management includes supplemental oxygen, IV access, fluid resuscitation when indicated, cardiac monitoring, bronchodilators if bronchospasm is present, and airway management in cases of severe respiratory distress. Empiric antibiotic therapy should follow established guidelines. Previously healthy outpatients may receive azithromycin or doxycycline. Patients with significant comorbidities should receive a β-lactam plus macrolide combination or a respiratory fluoroquinolone alone. Inpatients not requiring ICU care may receive a β-lactam plus macrolide or a respiratory fluoroquinolone. ICU patients should receive a β-lactam plus either a macrolide or respiratory fluoroquinolone, with additional coverage for Pseudomonas or MRSA when risk factors are present. Aspiration pneumonia may require anaerobic coverage such as clindamycin or metronidazole. Prompt antibiotic administration is critical in ill-appearing patients.
Disposition decisions are guided by clinical judgment and validated tools such as the CURB-65 score and the Pneumonia Severity Index. CURB-65 evaluates confusion, elevated BUN, respiratory rate ≥30, hypotension, and age ≥65. Scores of 0–1 generally support outpatient management, while higher scores favor admission and possible ICU care. Admission is also indicated for unstable vital signs, hypoxia, significant comorbidities, failure of outpatient therapy, or inability to ensure follow-up. Discharge may be appropriate for patients younger than 65 without comorbidities, with normal vital signs and reliable follow-up within 72 hours.
Clinicians must avoid delays in antibiotic initiation in critically ill patients and remain vigilant for pneumonia in those presenting with presumed exacerbations of chronic lung disease. Tuberculosis and HIV risk factors should always be assessed. Elderly and immunocompromised patients may lack classic symptoms, making a high index of suspicion essential for timely diagnosis and management.
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Emergency And Acute Medicine – Pneumocystis Pneumonia
Pneumocystis pneumonia, commonly referred to as PCP, is caused by Pneumocystis jirovecii and remains the most common opportunistic infection in patients with HIV, particularly when the CD4 count is less than 200 cells/mm³. Although previously known as Pneumocystis carinii pneumonia, the organism is now classified as a fungus. Transmission is believed to occur via the respiratory aerosol route. Organisms colonize the respiratory tract, cysts rupture, and trophozoites proliferate within the alveoli, producing a characteristic foamy exudate that interferes with gas exchange. Most cases likely represent reactivation of latent infection, although person-to-person transmission has been suggested. PCP also occurs in patients with impaired cellular immunity due to cancer, chronic corticosteroid therapy, organ transplantation, or malnutrition. In children, infection tends to be more severe.
The clinical presentation is typically subacute. Up to 7% of patients may initially be asymptomatic. Patients often report fever, nonproductive or minimally productive cough, and progressive dyspnea. In HIV-positive patients, symptoms may develop gradually over weeks to months, whereas in non–HIV immunocompromised hosts the course may progress over days. Dyspnea on exertion with exercise-induced oxygen desaturation is common. Associated symptoms include chills, fatigue, weight loss, and chest discomfort. Patients receiving inhaled pentamidine prophylaxis may present with milder pulmonary symptoms but have a higher incidence of pneumothorax and extrapulmonary disease. On examination, tachypnea and tachycardia are common, and lung auscultation may reveal crackles or rhonchi, although findings can be minimal relative to the degree of hypoxemia.
Essential evaluation includes complete blood count, electrolytes, arterial blood gas, lactate dehydrogenase (LDH), blood cultures, and chest imaging. Arterial blood gas analysis should be obtained in all suspected cases to calculate the alveolar–arterial gradient, which is usually elevated. Adjunctive corticosteroids are indicated when the A–a gradient exceeds 35 mm Hg or the PaO₂ is less than 70 mm Hg. LDH is often elevated in HIV-associated PCP and higher levels may correlate with worse prognosis, though it is nonspecific. Chest radiography classically demonstrates bilateral interstitial or diffuse alveolar infiltrates. However, up to 25% of patients may have a normal radiograph early in the disease. Atypical findings include lobar infiltrates, cysts, pneumothoraces, pleural effusions, or nodular infiltrates. High-resolution CT is highly sensitive and typically shows patchy ground-glass opacities.
Definitive diagnosis requires identification of Pneumocystis organisms in respiratory specimens. Induced sputum examination has high specificity but variable sensitivity depending on specimen quality and laboratory expertise, and it is less sensitive in non–HIV patients or those on pentamidine prophylaxis. Bronchoalveolar lavage is recommended when induced sputum is nondiagnostic and clinical suspicion remains high, with sensitivity approaching 80–100%.
Initial management follows airway, breathing, and circulation principles. Supplemental oxygen should be administered, escalating from nasal cannula to nonrebreather mask as needed. Endotracheal intubation is required for refractory hypoxemia or hypercapnic respiratory failure. Intravenous fluids should be given for hypotension or dehydration. Empiric antimicrobial therapy should be initiated promptly when PCP is suspected. Intravenous trimethoprim–sulfamethoxazole is the first-line therapy and should be continued for 21 days. Intravenous pentamidine is an alternative for patients intolerant of first-line therapy. Oral therapy may be appropriate in mild cases. Alternative regimens include trimethoprim–dapsone, clindamycin–primaquine, or atovaquone. Adjunctive corticosteroids must be started within the first 72 hours in patients with significant hypoxemia to reduce mortality and the risk of respiratory failure. Suspected PCP patients should be isolated from other immunocompromised individuals.
Admission is indicated for moderate to severe disease, defined by hypoxemia or elevated A–a gradient, inability to tolerate oral medications, or unreliable follow-up. Intensive monitoring is required for patients with respiratory compromise. Selected patients with mild disease, stable oxygenation, and reliable follow-up may be managed as outpatients. Close follow-up with an infectious disease specialist is essential.
PCP should always be considered in immunocompromised patients presenting with dyspnea and diffuse infiltrates, particularly those with HIV or suspected undiagnosed HIV infection. Well-appearing patients with unexpectedly low oxygen saturation are at higher risk for rapid deterioration. Clinicians must also consider coexisting infections such as tuberculosis or atypical bacterial pneumonia in this population.
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Emergency And Acute Medicine – Pleural Effusion
Pleural effusion is the abnormal accumulation of fluid within the pleural space. Under normal conditions, the pleural cavity contains approximately 0.1–0.2 mL/kg of clear, low-protein fluid that facilitates lung movement within the thorax. Fluid balance is governed by hydrostatic and oncotic forces, with formation primarily from the parietal pleura and reabsorption through the visceral pleura and lymphatics. Disruption of these forces or lymphatic drainage results in fluid accumulation.
Effusions are classified as transudative or exudative. Transudative effusions are low in protein and cells and result from increased hydrostatic pressure or decreased oncotic pressure without primary pleural disease. Common causes include congestive heart failure, cirrhosis with ascites, nephrotic syndrome, peritoneal dialysis, pulmonary embolism, and hypoalbuminemia. Exudative effusions contain higher protein and cellular content and result from pleural inflammation or impaired lymphatic drainage. Causes include pneumonia, tuberculosis, malignancy, mesothelioma, metastatic disease, pulmonary embolism, pancreatitis, subdiaphragmatic abscess, esophageal rupture, rheumatologic disease, trauma, hemothorax, chylothorax, and certain medications.
Small effusions are often asymptomatic. Larger effusions may cause dyspnea, pleuritic chest pain, cough, tachypnea, and hypoxia. Physical examination may reveal decreased breath sounds, decreased tactile fremitus, dullness to percussion, increased egophony above the fluid level, and occasionally a pleural friction rub. Evaluation should also focus on identifying the underlying cause such as heart failure, infection, or malignancy.
Initial workup includes cardiac monitoring, pulse oximetry, laboratory studies including complete blood count and metabolic panel, and chest imaging. Upright chest radiography typically shows blunting of the costophrenic angle and requires approximately 200–250 mL of fluid for detection. Lateral decubitus films or bedside ultrasound can detect as little as 5–10 mL of fluid and help differentiate free-flowing from loculated effusions. Ultrasound improves safety and reduces pneumothorax risk during thoracentesis. CT of the chest with intravenous contrast is the most sensitive imaging modality and is useful for identifying loculated collections and underlying pulmonary or pleural pathology. Pulmonary embolism should always be considered in cases of unexplained effusion.
Thoracentesis is indicated for new effusions in ill patients or for symptomatic relief of dyspnea due to large effusions. Fluid analysis distinguishes transudative from exudative effusions using Light criteria. An effusion is exudative if one or more of the following are present: pleural fluid protein to serum protein ratio greater than 0.5, pleural fluid LDH to serum LDH ratio greater than 0.6, or pleural fluid LDH greater than two-thirds the upper limit of normal serum LDH. Exudative effusions require further analysis including cell count, Gram stain, culture, cytology, pH, glucose, and other tests guided by clinical suspicion. A pleural fluid hematocrit greater than half of serum hematocrit defines hemothorax. A pH less than 7 or glucose less than 60 mg/dL suggests complicated parapneumonic effusion or empyema.
Therapeutic thoracentesis should avoid removal of more than 1,500 mL to reduce the risk of re-expansion pulmonary edema. Indications for tube thoracostomy include empyema, complicated parapneumonic effusion with low pH or glucose, positive Gram stain or culture, loculated effusion, or hemothorax. Post-procedure chest radiography is recommended to evaluate for pneumothorax.
Emergency management includes airway, breathing, and circulation stabilization with supplemental oxygen and intravenous access. Emergent thoracentesis is required for significant respiratory compromise. Treatment is directed at the underlying cause. Heart failure–related effusions require diuresis. Parapneumonic effusions require antibiotics. Pulmonary embolism requires anticoagulation, and the presence of bloody effusion is not a contraindication. Rheumatologic effusions may respond to anti-inflammatory therapy. Loculated effusions may require intrapleural fibrinolytics or surgical intervention.
Admission is indicated for respiratory compromise, unknown etiology, empyema, suspected parapneumonic effusion, or complications of thoracentesis. Intensive care is required for severe respiratory or hemodynamic instability. Discharge may be considered when the cause is identified, respiratory status is stable, and appropriate follow-up is arranged.
The most common causes of pleural effusion are congestive heart failure, pneumonia, and malignancy. Failure to recognize life-threatening causes such as pulmonary embolism, esophageal rupture, or hemothorax can result in significant morbidity and mortality. Bedside ultrasound is invaluable in diagnosis and procedural guidance and should be used whenever available.
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Emergency And Acute Medicine – Plant Poisoning
Plant exposure is one of the most common reasons for contacting a poison center, and the majority of cases involve unintentional ingestion in children younger than 6 years. Accurate identification of the ingested plant is critical whenever possible, as toxicity varies widely depending on species and toxin class. Plants may produce toxicity through anticholinergic compounds, cardiac glycosides, nicotine-like alkaloids, cyanogenic compounds, calcium oxalate crystals, pyrrolizidine alkaloids, sodium channel activators, or toxalbumins.
Plants with anticholinergic properties such as jimson weed and deadly nightshade act as competitive antagonists at muscarinic receptors and produce the classic toxidrome of dry, warm, flushed skin, urinary retention, absent bowel sounds, and agitated delirium. Plants containing cardiac glycosides such as foxglove and oleander inhibit the sodium–potassium ATPase pump and cause digoxin-like toxicity, including gastrointestinal symptoms, bradycardia, tachydysrhythmias, and hyperkalemia. Nicotine-like alkaloid–containing plants such as tobacco and poison hemlock stimulate nicotinic receptors, leading to hypertension and tachycardia early, followed by bradycardia, muscle weakness, and respiratory failure in severe cases.
Cyanogenic plants such as apricot, cherry, and cassava are metabolized to cyanide and interfere with cellular respiration, causing abdominal pain, altered mental status, lactic acidosis, seizures, cardiovascular collapse, and multiorgan failure. Calcium oxalate–containing plants such as dumb cane and philodendron release microscopic crystals that cause immediate burning pain, oral swelling, and potential airway compromise; ocular exposure results in keratoconjunctivitis. Pyrrolizidine alkaloid–containing plants may cause acute hepatitis and, with chronic exposure, hepatic veno-occlusive disease. Sodium channel–activating plants such as aconite and rhododendron may produce gastrointestinal symptoms, bradycardia with atrioventricular block, tachydysrhythmias, seizures, and cardiovascular instability. Toxalbumin-containing plants such as castor bean interfere with ribosomal function and can cause severe systemic toxicity depending on route and dose.
In pediatric patients, lip, tongue, and oropharyngeal irritation is common, especially with calcium oxalate plants, and airway compromise is a concern. Children often ingest concentrated plant parts such as seeds or berries, which increases toxicity risk. Even small amounts of certain plants, such as yellow oleander leaves or jimson weed seeds, may be life-threatening.
Diagnosis is primarily clinical and depends on history, plant identification, and toxidrome recognition. Laboratory evaluation may include electrolytes, renal function, glucose, liver function tests, and blood gas analysis for acid–base status. Digoxin levels should be obtained in suspected cardiac glycoside poisoning. Lactate measurement is useful in suspected cyanogenic toxicity. Electrocardiography is essential in patients with suspected cardiotoxic plant ingestion.
Prehospital care focuses on airway, breathing, and circulation. Syrup of ipecac is not recommended. Plant material should be collected in a paper bag for identification.
Emergency department management is largely supportive. Airway protection and cardiac monitoring are priorities. Intravenous fluids should be administered for dehydration or hypotension, with vasopressors initiated if fluid resuscitation fails. Anticholinergic agitation is treated with benzodiazepines, and physostigmine may be considered for severe delirium. Cardiac glycoside toxicity with significant bradycardia, tachydysrhythmias, or hyperkalemia warrants digoxin-specific antibody fragments. Cyanogenic toxicity with severe lactic acidosis or hemodynamic instability should be treated with hydroxocobalamin or a cyanide antidote kit. Atropine is indicated for bradycardia associated with sodium channel–active plant toxins. Calcium oxalate exposures are managed with irrigation, analgesia, and airway monitoring. Toxalbumin and pyrrolizidine alkaloid exposures require supportive care and specialist consultation.
Patients require admission if they develop dysrhythmias, refractory hypotension, altered mental status, intractable vomiting, metabolic acidosis, or evidence of end-organ damage. Children should be admitted with a lower threshold due to smaller lethal doses and less specific symptoms. Patients may be discharged if they return to baseline mental status, tolerate oral intake, demonstrate stable cardiac function, and have no anticipated delayed toxicity.
Death from unintentional plant ingestion is rare, but intentional ingestion, misuse of herbal preparations, or consumption of highly toxic species can be fatal. Early recognition of toxidromes and consultation with poison control or a medical toxicologist are essential to optimize outcomes.
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KembaraXtra -Medicine- Emergency and Acute Medicine – Peripheral Neuropathy
Peripheral neuropathy is a broad term describing disorders of peripheral nerves that may involve motor, sensory, or autonomic fibers. Patients commonly present with muscle weakness, atrophy, pain, numbness, or a combination of these symptoms. The condition may be acute or chronic, symmetric or asymmetric, and distal or proximal in distribution.
Etiology varies widely and depends on the clinical presentation. Causes include metabolic disorders, endocrine disease, nutritional deficiencies, toxins, medications, autoimmune conditions, infections, hereditary disorders, trauma, and neoplastic processes. Diabetes mellitus is the most common cause of symmetric peripheral neuropathy. Acute demyelinating processes such as Guillain–Barré syndrome must be considered in rapidly progressive cases.
Sensory nerve dysfunction presents with numbness, tingling, paresthesias, dysesthesias, or burning pain. Large-fiber neuropathy leads to decreased vibration and position sense, whereas small-fiber neuropathy affects pain and temperature sensation. Deep tendon reflexes are often reduced due to impairment of the sensory afferent limb. Symptoms typically follow a stocking-glove distribution in symmetric polyneuropathy.
Motor nerve involvement causes weakness, usually distal greater than proximal. Fasciculations may occur, and chronic disease can lead to muscle atrophy and diminished tone. Reflexes may be reduced or absent due to impaired motor efferent conduction.
Autonomic dysfunction may manifest as orthostatic hypotension, constipation, urinary retention, erectile dysfunction, or other signs of impaired autonomic regulation.
History should focus on duration of symptoms, pattern of involvement (symmetric versus asymmetric), distribution (distal versus proximal), and whether symptoms are sensory, motor, or mixed. Medication exposure, toxin exposure, systemic disease, recent infections, and family history should be reviewed.
Physical examination requires a thorough neurologic assessment, including strength testing, reflex evaluation, and detailed sensory examination. Sensory loss in a stocking-glove pattern supports a length-dependent polyneuropathy. Early absence of reflexes, particularly in an acute presentation, should raise concern for demyelinating neuropathy such as Guillain–Barré syndrome, which can progress to respiratory failure.
Essential evaluation depends on acuity and severity. In acute or rapidly progressive weakness, early neurology consultation is critical. Laboratory studies may include a basic metabolic panel, complete blood count, liver function tests, urinalysis, thyroid-stimulating hormone, and targeted testing such as HIV or vitamin B12 levels based on clinical suspicion. Electrocardiogram and imaging such as chest radiograph or head CT may be obtained when indicated by associated symptoms.
Electromyography and nerve conduction studies are typically arranged by neurology to characterize axonal versus demyelinating patterns. Lumbar puncture may be required when Guillain–Barré syndrome is suspected.
Differential diagnosis depends on distribution. Focal neuropathies are often due to entrapment syndromes such as carpal tunnel, ulnar tunnel, tarsal tunnel, or peroneal nerve compression. Multifocal neuropathy (mononeuropathy multiplex) may result from diabetes, vasculitis, connective tissue disease, sarcoidosis, leprosy, malignancy, or HIV infection. Symmetric polyneuropathy commonly results from diabetes, hypothyroidism, nutritional deficiency, alcohol use, medication toxicity, critical illness, electrolyte disturbances, toxins, or Guillain–Barré syndrome. Myelopathy may mimic peripheral neuropathy and should be suspected in patients with back pain, saddle anesthesia, or lower extremity weakness.
Initial management in the emergency setting focuses on airway protection in severe cases, especially when Guillain–Barré syndrome is suspected. Monitoring for respiratory compromise is essential. Offending toxins or medications should be discontinued, and underlying systemic conditions should be treated.
Pain control may include opioids when necessary. Neuropathic pain can be managed with agents such as gabapentin, titrated gradually to effect. Carbamazepine may be used for specific neuropathic syndromes such as trigeminal neuralgia. Intravenous immunoglobulin is indicated for Guillain–Barré syndrome.
Admission is required for patients with respiratory distress, acute gait disturbance, rapidly progressive weakness, or intractable pain. Stable patients without respiratory compromise or significant functional impairment may be discharged with appropriate outpatient follow-up.
Failure to recognize Guillain–Barré syndrome is a critical pitfall, as delayed diagnosis can lead to respiratory failure and significant morbidity. Early identification and appropriate monitoring are essential in patients with acute, progressive peripheral neuropathy.
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KembaraXtra -Medicine- Emergency and Acute Medicine – Pericarditis
Pericarditis is inflammation, infection, or infiltration of the pericardial sac surrounding the heart. A pericardial effusion may or may not be present. Acute pericarditis has a rapid onset and may be complicated by cardiac tamponade if significant fluid accumulates. Constrictive pericarditis results from chronic inflammation leading to thickening, fibrosis, and adherence of the pericardium to the myocardium, impairing diastolic filling.
The most common cause is idiopathic, presumed viral in many cases. Viral etiologies include coxsackievirus, echovirus, adenovirus, Epstein–Barr virus, cytomegalovirus, hepatitis B, HIV, and others. Bacterial causes include tuberculosis, staphylococcal and streptococcal species, Haemophilus, Salmonella, and Legionella. Fungal, parasitic, neoplastic, uremic, autoimmune, post–myocardial infarction (Dressler syndrome), radiation, trauma, postpericardiotomy, aortic dissection, myxedema, pancreatitis, inflammatory bowel disease, amyloidosis, and drug-induced causes are also recognized.
Chest pain is the hallmark symptom. It is typically sharp, pleuritic, and substernal, worsened by lying supine or coughing, and improved by sitting up or leaning forward. Pain may radiate to the trapezius ridge due to phrenic nerve irritation. Associated symptoms include fever, mild dyspnea, cough, hoarseness, nausea, and anorexia. A history of recent viral illness, autoimmune disease, malignancy, or prior pericarditis episodes is common.
On examination, tachycardia and tachypnea may be present. A pericardial friction rub is highly specific and best heard at the lower left sternal border, often accentuated when the patient leans forward. The classic rub is triphasic, with presystolic, systolic, and early diastolic components, though any combination may be heard. If a significant effusion develops, features of cardiac tamponade may appear, including hypotension, jugular venous distention, and muffled heart sounds. Pulsus paradoxus may be present. Constrictive pericarditis produces signs of right- and left-sided heart failure such as peripheral edema, ascites, hepatic congestion, and pulmonary edema.
Electrocardiography typically demonstrates four classic stages. Stage 1 shows diffuse concave ST elevation with PR depression, except in aVR and V1. Stage 2 reveals normalization of ST and PR segments with T-wave flattening. Stage 3 shows diffuse T-wave inversion. Stage 4 reflects normalization of T waves. Electrical alternans suggests a significant effusion. Cardiac enzymes may be mildly elevated in myopericarditis but are useful to distinguish from acute myocardial infarction.
Laboratory studies may show leukocytosis and elevated inflammatory markers such as ESR and C-reactive protein. Chest radiograph is usually normal unless more than 250 mL of fluid has accumulated, in which case cardiomegaly may be visible. Echocardiography is the diagnostic modality of choice for detecting pericardial effusion and can identify even small fluid collections. CT scanning can detect pericardial thickening or calcifications, particularly in constrictive pericarditis. Pericardiocentesis is reserved for diagnostic clarification or therapeutic relief in tamponade.
Initial management follows standard airway, breathing, and circulation principles. Emergent pericardiocentesis is indicated in hemodynamically unstable patients with tamponade. Most cases of idiopathic or viral pericarditis are treated with nonsteroidal anti-inflammatory drugs. Ibuprofen or aspirin are commonly used and may be tapered gradually to reduce recurrence. Colchicine is recommended in combination with NSAIDs to decrease recurrence rates and may be continued for approximately three months. Corticosteroids are reserved for refractory cases, autoimmune causes, or when NSAIDs are contraindicated, as they are associated with higher recurrence rates. Bacterial pericarditis requires urgent IV antibiotics and drainage. Uremic pericarditis requires intensified dialysis. Neoplastic pericarditis is managed in conjunction with oncology.
Patients with hemodynamic instability, cardiac tamponade, malignant arrhythmias, large effusions, anticoagulation use, high fever, immunosuppression, trauma, malignancy, or suspected bacterial etiology require hospital admission, often to a monitored or intensive care setting. Stable patients with mild symptoms and no high-risk features may be managed as outpatients with close follow-up.
The classic presentation includes a recent viral illness followed by sharp, positional chest pain and a friction rub. Distinguishing pericarditis from acute myocardial infarction and other causes of chest pain is critical. NSAIDs remain the cornerstone of therapy, and most patients improve within two weeks with appropriate treatment.
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KembaraXtra -Medicine- Emergency and Acute Medicine – Periorbital and Orbital Cellulitis
Periorbital (preseptal) cellulitis and orbital cellulitis are infections involving the tissues around the eye, distinguished by their anatomic relationship to the orbital septum. The orbital septum is a connective tissue extension of the orbital periosteum that separates superficial eyelid structures from the deeper orbital contents. Periorbital cellulitis is confined to tissues anterior to this septum, whereas orbital cellulitis involves structures deep to it. This distinction is critical because orbital cellulitis is a true medical emergency with risk of permanent vision loss and life-threatening complications.
Periorbital cellulitis most commonly occurs as a complication of upper respiratory tract infection or sinusitis, where inflammatory edema leads to vascular and lymphatic congestion. It may also arise from local eyelid infections such as blepharitis, hordeolum, or dacryocystitis, or from surrounding skin disruptions including insect bites, minor trauma, impetigo, or dermatologic conditions. The septum typically acts as a barrier to deeper spread, although it may be incomplete.
Orbital cellulitis usually results from extension of infection from adjacent structures, most commonly ethmoid sinusitis penetrating the thin lamina papyracea. Other causes include dental abscess, retained orbital foreign body, puncture wounds, orbital fractures, postoperative infections, and hematogenous spread through valveless orbital veins. Rarely, it results from direct progression of periorbital cellulitis. Common pathogens include Streptococcus pneumoniae, Streptococcus viridans, Streptococcus pyogenes, Streptococcus anginosus, and Staphylococcus aureus. Anaerobes, Bacteroides species, and gram-negative organisms may also be involved.
All forms of orbital cellulitis carry significant morbidity and mortality risk. Complications include permanent visual loss, subperiosteal abscess, cavernous sinus thrombosis, and central nervous system infections. Fungal orbital cellulitis, particularly cerebrorhino-orbital phycomycosis (CROP), is rare but highly lethal, especially in immunocompromised patients and those with diabetic ketoacidosis. It often begins in the paranasal sinuses and invades blood vessels, causing thrombosis and tissue necrosis. Bloody nasal discharge and necrosis of the palate or nasal mucosa may be present.
In children, routine Hib and pneumococcal vaccinations have reduced incidence, but infection still occurs. Periorbital cellulitis is approximately five times more common and usually affects children younger than five years, whereas orbital cellulitis is more common in children older than five.
Both conditions present with unilateral red, swollen eyelids, and swelling may be severe in either. The key differences lie in systemic toxicity and ocular involvement. Orbital cellulitis is often preceded by sinusitis (60–90% of cases), dental infection, trauma, or recent surgery. Patients may report eye pain, visual changes, decreased color vision, diplopia, restricted or painful extraocular movements, and headache. Fever above 39°C and a toxic appearance are common. On examination, findings may include proptosis, conjunctival injection, chemosis, afferent pupillary defect, decreased visual acuity, ophthalmoplegia, and signs of meningismus.
Periorbital cellulitis typically follows local skin injury or superficial infection and presents more subacutely with low-grade fever and minimal systemic symptoms. Visual acuity and extraocular movements remain normal, and there are no signs of deep orbital involvement.
A complete eye examination is essential in all cases. This includes assessment of visual acuity, extraocular movements, pupillary response, fundoscopic examination, intraocular pressure measurement, and a thorough neurologic exam.
Laboratory studies are supportive but not diagnostic. A white blood cell count below 15,000 is more typical of periorbital cellulitis, whereas higher counts may suggest orbital involvement. Blood cultures and cultures of purulent material may be obtained, particularly if bacteremia is suspected. When gonorrhea is considered, appropriate culture media should be used.
Contrast-enhanced CT of the orbits is indicated when there are central nervous system signs, visual disturbances, proptosis, painful or restricted extraocular movements, ophthalmoplegia, bilateral edema, lack of improvement within 24 hours, or clinical deterioration. CT helps define the extent of infection, detect sinusitis, orbital emphysema, subperiosteal abscess, foreign bodies, and cavernous sinus thrombosis. Lumbar puncture may be necessary in toxic patients with meningismus to exclude CNS involvement.
Treatment depends on severity and depth of infection. Periorbital cellulitis in stable patients typically responds to oral antibiotics such as amoxicillin-clavulanate, cephalexin, clindamycin, or dicloxacillin. Parenteral antibiotics are indicated for toxic appearance, suspected bacteremia, or inability to tolerate oral therapy. Close follow-up within 24–48 hours is essential.
Orbital cellulitis requires hospital admission and immediate intravenous antibiotics. Early ophthalmology consultation is mandatory, and ENT consultation should be considered when sinusitis is the source. Empiric therapy commonly includes IV ceftriaxone or other broad-spectrum coverage, with vancomycin added if MRSA is suspected. Metronidazole may be included when anaerobic infection is likely. Surgical intervention may be required for abscess drainage, sinus decompression, or optic nerve decompression. In suspected fungal infection, high-dose IV amphotericin B and urgent surgical debridement are required.
Patients with periorbital cellulitis may be discharged if they have no systemic toxicity, no orbital findings, can tolerate oral antibiotics, and have reliable follow-up. Admission is required for orbital cellulitis, systemic toxicity, visual impairment, inability to arrange follow-up, progression on oral therapy, or high-risk conditions.
Any patient presenting with a red, swollen eye must be carefully evaluated for orbital cellulitis. A detailed history should include recent sinusitis, trauma, dental infection, surgery, immunocompromised state, or recent diabetic ketoacidosis. Clinicians must carefully assess for systemic toxicity, visual changes, pain with eye movement, and neurologic symptoms to avoid missing this potentially vision- and life-threatening condition.
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Emergency and Acute Medicine – Periodontal Abscess
A periodontal abscess is a localized collection of pus within the supporting structures of the teeth, including the periodontal ligament and alveolar bone. It typically develops as a complication of progressive periodontal disease, where bone loss leads to the formation of periodontal pockets. Food particles and debris accumulate within these pockets. Coronal epithelial tissues may reattach to the tooth surface while bacteria and debris remain trapped, impairing drainage. This environment promotes secondary infection and abscess formation.
Although primarily localized, periodontal abscesses can lead to serious complications if untreated. These include osteomyelitis, dentocutaneous fistula, cavernous sinus thrombosis, Ludwig angina, maxillary sinusitis, mediastinitis, tooth loss, and sepsis. In children, periodontal abscesses are rare; periapical abscesses are more common and typically originate in the pulp, often associated with dental caries.
The infection is usually polymicrobial. Common pathogens include anaerobic gram-negative rods, Peptostreptococci, viridans group streptococci, and Neisseria species.
Diagnosis is clinical. Patients typically present with localized dental pain, facial swelling, malaise, and sometimes fever. On examination, there may be focal gingival swelling or fluctuance, tenderness to palpation, increased tooth mobility, and possible lymphadenopathy. A parulis—a pimple-like lesion on the gingiva—may be present in chronic abscesses, representing the end of a draining sinus tract. Pus may be expressed from the sinus tract. Heat sensitivity may occur. Trismus is generally absent unless infection has spread to the muscles of mastication.
Imaging and laboratory studies are not routinely required for diagnosis. However, panoramic, periapical, or occlusal radiographs may help confirm the diagnosis and determine the extent of disease. Bedside ultrasound can assist in identifying fluid collections. CT imaging may be indicated if there is concern for extension into adjacent structures. Anaerobic cultures may be considered in complicated cases or in immunocompromised patients. Electric pulp testing, performed by a dental specialist during follow-up, helps assess tooth viability.
The differential diagnosis includes periapical abscess, maxillary sinusitis, aphthous ulcers, oral herpes, salivary gland tumors, mumps, sialadenitis, localized adenopathy, facial cellulitis, acute otitis media, and peritonsillar abscess. In children, periapical abscess is more likely. For asymptomatic parulis, fibroma, pyogenic granuloma, peripheral ossifying granuloma, or Kaposi sarcoma should be considered.
Prehospital management rarely involves airway emergencies. However, if signs of airway compromise are present, airway equipment should be available, the patient transported upright, and supplemental oxygen provided. Initial stabilization in the emergency setting includes assessment of airway patency and securing the airway if there is respiratory distress, inability to manage secretions, or significant oropharyngeal swelling.
Emergency department management focuses on analgesia and drainage. NSAIDs or opioids may be used for pain control. Incision and drainage are performed under local anesthesia, typically using 2% lidocaine with epinephrine. A small stab incision is made toward the alveolar bone, followed by blunt dissection and irrigation with saline. If the cavity is large, a small iodoform gauze or Penrose drain may be placed for 24–48 hours and secured to prevent aspiration.
Antibiotics are indicated when the abscess is extensive or when systemic signs are present. Penicillin VK is considered first-line therapy. For penicillin-allergic patients, azithromycin, erythromycin, or clindamycin may be used. Clindamycin is also appropriate for patients who fail penicillin therapy. Ampicillin/sulbactam may be required for severe infections. Warm salt water rinses are recommended hourly while awake for 24–48 hours.
Admission is required for severe infections, complications such as cavernous sinus thrombosis or osteomyelitis, airway compromise, Ludwig angina, systemic toxicity, immunocompromised patients, treatment failure, or inability to manage the condition at home. Uncomplicated cases may be discharged with close dental follow-up within 24–48 hours.
Dental follow-up is essential for definitive care, including assessment of tooth viability, possible extraction, root canal therapy, and removal of drains. Without proper dental evaluation, symptoms may recur and long-term tooth preservation may be compromised. Maxillary sinusitis may be misdiagnosed if a thorough oral examination is not performed, underscoring the importance of careful assessment and timely referral.
A periodontal abscess is a localized collection of pus within the supporting structures of the teeth, including the periodontal ligament and alveolar bone. It typically develops as a complication of progressive periodontal disease, where bone loss leads to the formation of periodontal pockets. Food particles and debris accumulate within these pockets. Coronal epithelial tissues may reattach to the tooth surface while bacteria and debris remain trapped, impairing drainage. This environment promotes secondary infection and abscess formation.
Although primarily localized, periodontal abscesses can lead to serious complications if untreated. These include osteomyelitis, dentocutaneous fistula, cavernous sinus thrombosis, Ludwig angina, maxillary sinusitis, mediastinitis, tooth loss, and sepsis. In children, periodontal abscesses are rare; periapical abscesses are more common and typically originate in the pulp, often associated with dental caries.
The infection is usually polymicrobial. Common pathogens include anaerobic gram-negative rods, Peptostreptococci, viridans group streptococci, and Neisseria species.
Diagnosis is clinical. Patients typically present with localized dental pain, facial swelling, malaise, and sometimes fever. On examination, there may be focal gingival swelling or fluctuance, tenderness to palpation, increased tooth mobility, and possible lymphadenopathy. A parulis—a pimple-like lesion on the gingiva—may be present in chronic abscesses, representing the end of a draining sinus tract. Pus may be expressed from the sinus tract. Heat sensitivity may occur. Trismus is generally absent unless infection has spread to the muscles of mastication.
Imaging and laboratory studies are not routinely required for diagnosis. However, panoramic, periapical, or occlusal radiographs may help confirm the diagnosis and determine the extent of disease. Bedside ultrasound can assist in identifying fluid collections. CT imaging may be indicated if there is concern for extension into adjacent structures. Anaerobic cultures may be considered in complicated cases or in immunocompromised patients. Electric pulp testing, performed by a dental specialist during follow-up, helps assess tooth viability.
The differential diagnosis includes periapical abscess, maxillary sinusitis, aphthous ulcers, oral herpes, salivary gland tumors, mumps, sialadenitis, localized adenopathy, facial cellulitis, acute otitis media, and peritonsillar abscess. In children, periapical abscess is more likely. For asymptomatic parulis, fibroma, pyogenic granuloma, peripheral ossifying granuloma, or Kaposi sarcoma should be considered.
Prehospital management rarely involves airway emergencies. However, if signs of airway compromise are present, airway equipment should be available, the patient transported upright, and supplemental oxygen provided. Initial stabilization in the emergency setting includes assessment of airway patency and securing the airway if there is respiratory distress, inability to manage secretions, or significant oropharyngeal swelling.
Emergency department management focuses on analgesia and drainage. NSAIDs or opioids may be used for pain control. Incision and drainage are performed under local anesthesia, typically using 2% lidocaine with epinephrine. A small stab incision is made toward the alveolar bone, followed by blunt dissection and irrigation with saline. If the cavity is large, a small iodoform gauze or Penrose drain may be placed for 24–48 hours and secured to prevent aspiration.
Antibiotics are indicated when the abscess is extensive or when systemic signs are present. Penicillin VK is considered first-line therapy. For penicillin-allergic patients, azithromycin, erythromycin, or clindamycin may be used. Clindamycin is also appropriate for patients who fail penicillin therapy. Ampicillin/sulbactam may be required for severe infections. Warm salt water rinses are recommended hourly while awake for 24–48 hours.
Admission is required for severe infections, complications such as cavernous sinus thrombosis or osteomyelitis, airway compromise, Ludwig angina, systemic toxicity, immunocompromised patients, treatment failure, or inability to manage the condition at home. Uncomplicated cases may be discharged with close dental follow-up within 24–48 hours.
Dental follow-up is essential for definitive care, including assessment of tooth viability, possible extraction, root canal therapy, and removal of drains. Without proper dental evaluation, symptoms may recur and long-term tooth preservation may be compromised. Maxillary sinusitis may be misdiagnosed if a thorough oral examination is not performed, underscoring the importance of careful assessment and timely referral.
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Emergency and Acute Medicine – Periodic Paralysis
Periodic paralysis is a disorder of skeletal muscle ion channel function that results in episodic flaccid weakness of the extremities. It is usually inherited and is triggered by abnormalities in serum potassium levels or thyrotoxicosis. Primary forms are familial and typically autosomal dominant mutations affecting skeletal muscle sodium, calcium, or potassium channels. Secondary forms include thyrotoxic, hypokalemic, and hyperkalemic variants.
Hypokalemic periodic paralysis is the most common form, with a prevalence of approximately 1 in 100,000, and about one-third of cases arise from new autosomal dominant mutations. Hyperkalemic periodic paralysis is less common, with a prevalence of 1 in 200,000, and most individuals with the mutation develop symptoms. Thyrotoxic periodic paralysis occurs in approximately 2% of patients with thyrotoxicosis, is more common in Asian populations, and is clinically similar to hypokalemic periodic paralysis. Andersen–Tawil syndrome is a rare subtype associated with periodic paralysis and cardiac arrhythmias.
The disorder results from mutations in skeletal muscle ion channel genes. Mutations in SCN4A affect sodium channels and are associated with both hypokalemic and hyperkalemic forms. Mutations in CACNA1S affect calcium channels and are linked to hypokalemic periodic paralysis. Andersen–Tawil syndrome is associated with mutations in the KCNJ2 gene. Age of onset varies: hypokalemic and Andersen–Tawil forms typically begin in the first or second decade, hyperkalemic in the first decade, and thyrotoxic periodic paralysis usually presents in the second to fifth decades.
Patients present with intermittent episodes of symmetrical muscle weakness, typically affecting the legs more than the arms. Attacks often have rapid onset and may recur, with some patients experiencing persistent mild weakness between episodes. Triggers include carbohydrate-rich meals, rest after strenuous exercise, illness, lack of sleep, medications such as insulin or β-agonists, cold exposure, menstruation, pregnancy, and thyroid dysfunction. Hypokalemic attacks may last from one hour to several days, hyperkalemic attacks usually last 15 minutes to 4 hours, and thyrotoxic attacks resemble hypokalemic episodes in duration.
On examination, patients are alert with intact sensation and normal sphincter tone. Weakness is symmetrical, reflexes are reduced or absent, and proximal muscles are often more affected. In thyrotoxic periodic paralysis, findings may include tachycardia, warm moist skin, goiter, or exophthalmos. Andersen–Tawil syndrome may present with dysmorphic features such as short stature, low-set ears, broad nasal base, and micrognathia, along with cardiac arrhythmias. Severe hypokalemia may rarely involve respiratory muscles.
Essential evaluation includes serum electrolytes and electrocardiography. In hypokalemic periodic paralysis, potassium is low or normal during attacks, and ECG may show sinus bradycardia, flattened T waves, or ST depression. In hyperkalemic periodic paralysis, potassium is normal or elevated and ECG may rarely show peaked T waves. In thyrotoxic periodic paralysis, potassium is decreased during attacks, and thyroid studies reveal suppressed TSH with elevated T4. ECG may show tachyarrhythmias, conduction abnormalities, or widened QRS complexes. Andersen–Tawil syndrome is associated with prolonged QT interval and ventricular arrhythmias. Imaging is not required in the emergency setting.
Management is primarily supportive with airway, breathing, and circulation stabilization, oxygen, IV access, and monitoring. In hypokalemic periodic paralysis, oral potassium replacement is preferred, typically 40 mEq, with cautious IV replacement if needed. Overcorrection must be avoided. In hyperkalemic periodic paralysis, many attacks resolve spontaneously, but IV calcium gluconate may help terminate an episode. In thyrotoxic periodic paralysis, treatment includes potassium replacement and management of thyrotoxicosis, often with a nonselective β-blocker for tachycardia. Andersen–Tawil syndrome requires careful potassium management and monitoring for arrhythmias. Patients with hypokalemic periodic paralysis should avoid volatile anesthetics and depolarizing neuromuscular blockers, as these may trigger attacks or malignant hyperthermia.
Admission is recommended for patients with severe electrolyte abnormalities, persistent weakness, cardiac arrhythmias, respiratory compromise, or Andersen–Tawil syndrome due to the risk of sudden cardiac death. Patients with resolved symptoms and no cardiopulmonary compromise may be discharged with referral to neurology, and endocrinology in cases of thyrotoxic periodic paralysis. Genetic counseling is appropriate in primary forms due to the 50% inheritance risk.
Early recognition and appropriate correction of electrolyte abnormalities are critical. Andersen–Tawil patients and those with persistent symptoms should be admitted. Caution with anesthetic agents is essential in all forms of periodic paralysis.
Periodic paralysis is a disorder of skeletal muscle ion channel function that results in episodic flaccid weakness of the extremities. It is usually inherited and is triggered by abnormalities in serum potassium levels or thyrotoxicosis. Primary forms are familial and typically autosomal dominant mutations affecting skeletal muscle sodium, calcium, or potassium channels. Secondary forms include thyrotoxic, hypokalemic, and hyperkalemic variants.
Hypokalemic periodic paralysis is the most common form, with a prevalence of approximately 1 in 100,000, and about one-third of cases arise from new autosomal dominant mutations. Hyperkalemic periodic paralysis is less common, with a prevalence of 1 in 200,000, and most individuals with the mutation develop symptoms. Thyrotoxic periodic paralysis occurs in approximately 2% of patients with thyrotoxicosis, is more common in Asian populations, and is clinically similar to hypokalemic periodic paralysis. Andersen–Tawil syndrome is a rare subtype associated with periodic paralysis and cardiac arrhythmias.
The disorder results from mutations in skeletal muscle ion channel genes. Mutations in SCN4A affect sodium channels and are associated with both hypokalemic and hyperkalemic forms. Mutations in CACNA1S affect calcium channels and are linked to hypokalemic periodic paralysis. Andersen–Tawil syndrome is associated with mutations in the KCNJ2 gene. Age of onset varies: hypokalemic and Andersen–Tawil forms typically begin in the first or second decade, hyperkalemic in the first decade, and thyrotoxic periodic paralysis usually presents in the second to fifth decades.
Patients present with intermittent episodes of symmetrical muscle weakness, typically affecting the legs more than the arms. Attacks often have rapid onset and may recur, with some patients experiencing persistent mild weakness between episodes. Triggers include carbohydrate-rich meals, rest after strenuous exercise, illness, lack of sleep, medications such as insulin or β-agonists, cold exposure, menstruation, pregnancy, and thyroid dysfunction. Hypokalemic attacks may last from one hour to several days, hyperkalemic attacks usually last 15 minutes to 4 hours, and thyrotoxic attacks resemble hypokalemic episodes in duration.
On examination, patients are alert with intact sensation and normal sphincter tone. Weakness is symmetrical, reflexes are reduced or absent, and proximal muscles are often more affected. In thyrotoxic periodic paralysis, findings may include tachycardia, warm moist skin, goiter, or exophthalmos. Andersen–Tawil syndrome may present with dysmorphic features such as short stature, low-set ears, broad nasal base, and micrognathia, along with cardiac arrhythmias. Severe hypokalemia may rarely involve respiratory muscles.
Essential evaluation includes serum electrolytes and electrocardiography. In hypokalemic periodic paralysis, potassium is low or normal during attacks, and ECG may show sinus bradycardia, flattened T waves, or ST depression. In hyperkalemic periodic paralysis, potassium is normal or elevated and ECG may rarely show peaked T waves. In thyrotoxic periodic paralysis, potassium is decreased during attacks, and thyroid studies reveal suppressed TSH with elevated T4. ECG may show tachyarrhythmias, conduction abnormalities, or widened QRS complexes. Andersen–Tawil syndrome is associated with prolonged QT interval and ventricular arrhythmias. Imaging is not required in the emergency setting.
Management is primarily supportive with airway, breathing, and circulation stabilization, oxygen, IV access, and monitoring. In hypokalemic periodic paralysis, oral potassium replacement is preferred, typically 40 mEq, with cautious IV replacement if needed. Overcorrection must be avoided. In hyperkalemic periodic paralysis, many attacks resolve spontaneously, but IV calcium gluconate may help terminate an episode. In thyrotoxic periodic paralysis, treatment includes potassium replacement and management of thyrotoxicosis, often with a nonselective β-blocker for tachycardia. Andersen–Tawil syndrome requires careful potassium management and monitoring for arrhythmias. Patients with hypokalemic periodic paralysis should avoid volatile anesthetics and depolarizing neuromuscular blockers, as these may trigger attacks or malignant hyperthermia.
Admission is recommended for patients with severe electrolyte abnormalities, persistent weakness, cardiac arrhythmias, respiratory compromise, or Andersen–Tawil syndrome due to the risk of sudden cardiac death. Patients with resolved symptoms and no cardiopulmonary compromise may be discharged with referral to neurology, and endocrinology in cases of thyrotoxic periodic paralysis. Genetic counseling is appropriate in primary forms due to the 50% inheritance risk.
Early recognition and appropriate correction of electrolyte abnormalities are critical. Andersen–Tawil patients and those with persistent symptoms should be admitted. Caution with anesthetic agents is essential in all forms of periodic paralysis.
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KembaraXtra -Medicine- Emergency and Acute Medicine – Perilunate Dislocation
Perilunate dislocation is a serious high-energy wrist injury in which the lunate remains aligned with the distal radius, while the distal carpal bones—most notably the capitate—are displaced dorsally in approximately 95% of cases and volarly in about 5%. It is an unstable injury that requires early surgical treatment because it carries a high risk of long-term complications, particularly post-traumatic arthritis. The scaphoid is frequently fractured in association with perilunate dislocations.
The usual mechanism of injury is wrist hyperextension combined with ulnar deviation. These injuries typically result from significant trauma such as falls from height, motor vehicle accidents, industrial accidents, or sporting injuries. Because of the force involved, concomitant upper extremity injuries are common and must always be assessed.
Patients typically present with severe wrist pain, marked swelling, and diffuse tenderness. There may be decreased range of motion and sometimes visible deformity. Paresthesias in the median nerve distribution are common due to swelling and compression within the carpal tunnel. A careful history often reveals a high-energy injury. On examination, the wrist is swollen and painful with limited motion. Sensory changes in the median nerve distribution may be present, and neurovascular status—including capillary refill and 2-point discrimination—must be carefully assessed and documented. Skin integrity should be evaluated, as open injuries can occur. Importantly, this diagnosis is frequently missed on initial evaluation.
Radiographs of the wrist are essential and must include AP, lateral, and oblique views. The true lateral view is most diagnostic. Normally, the radius, lunate, and capitate should align in a straight line on the lateral film. In perilunate dislocation, the lunate remains aligned with the radius, but the capitate is displaced dorsally (most commonly) or volarly. CT or MRI is generally not required in the emergency department but may be used for preoperative planning.
The differential diagnosis includes lunate dislocation, lunate fracture, scapholunate dissociation, distal radius fracture, and other ligamentous wrist injuries. In pediatric patients, nonaccidental trauma should be considered.
Management begins with assessment for more serious associated injuries, followed by immobilization, elevation, ice application, and adequate pain control. Closed reduction should be attempted emergently. Traction is applied for approximately 10 minutes using finger traps with counterweights, followed by manual traction. The injury is briefly recreated with wrist extension while volar pressure is applied over the lunate, and then slow wrist flexion is performed to relocate the distal carpal bones. After reduction, the wrist should be immobilized in a sugar-tong splint in neutral position, post-reduction radiographs obtained, and neurovascular status reassessed. Procedural sedation is often required.
Definitive treatment requires operative fixation with ligament repair to restore stability and minimize long-term complications. All patients should have urgent hand surgery consultation.
Patients should be admitted if the injury is open, irreducible, associated with neurovascular compromise, or part of multiple trauma. Closed injuries with successful reduction and intact neurovascular status may be discharged with reliable orthopedic follow-up within 2–3 days, though all cases ultimately require surgical evaluation.
Complications are common even with appropriate treatment and include median nerve injury, tendon problems, wrist instability, complex regional pain syndrome, decreased grip strength, and post-traumatic arthritis. Up to 25% of these injuries are missed at initial presentation. Delayed diagnosis significantly worsens outcomes and may necessitate salvage procedures.
