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KembaraXtra -Medicine- Emergency and Acute Medicine – Perforated Viscus
A perforated viscus is a full-thickness disruption of a hollow abdominal organ that allows gastrointestinal contents to spill into the peritoneal cavity. This results in chemical and bacterial peritonitis, leading rapidly to systemic inflammatory response and potential septic shock. Perforation may occur from ulceration, inflammation, obstruction, ischemia, trauma, or iatrogenic injury. It is a surgical emergency requiring rapid recognition and intervention.
The most common cause is perforated peptic ulcer disease, frequently associated with NSAID use or Helicobacter pylori infection. Other causes include small bowel ischemia, inflammatory bowel disease, neoplasms, foreign bodies, diverticular disease, appendicitis, penetrating or blunt abdominal trauma, endoscopic procedures, and radiation enteritis or proctitis. In pediatric patients, trauma is the most common cause, particularly in neonates after difficult delivery, nonaccidental trauma, motor vehicle collisions, or falls. The jejunum is a common rupture site in children.
Patients typically present with sudden, severe abdominal pain that is initially localized but rapidly becomes diffuse as peritonitis develops. Examination reveals rigidity, guarding, rebound tenderness, and absent bowel sounds. Systemic findings may include fever, tachycardia, tachypnea, and hypotension. In advanced cases, patients may present in hypovolemic or septic shock. Elderly patients often have atypical presentations with less pronounced pain, minimal guarding, absence of leukocytosis, altered mental status, hypothermia, or blunted tachycardia due to medications or comorbidities.
The essential initial study is an upright chest radiograph to detect pneumoperitoneum. After the patient has been upright for 5–10 minutes, as little as 1–2 mL of free air may be visualized under the diaphragm. Sensitivity ranges from 50% to 85%. A left lateral decubitus abdominal radiograph may be more sensitive than a supine film. The double wall (Rigler) sign, in which both the mucosal and serosal surfaces of bowel are visible, suggests free intraperitoneal air. Abdominal CT is highly sensitive for detecting small amounts of free air and is indicated when clinical suspicion remains high despite normal plain films.
Laboratory evaluation includes CBC, electrolytes, renal function, glucose, liver function tests, coagulation profile, urinalysis, lipase, arterial blood gas, and lactate. Leukocytosis and elevated lactate support the diagnosis but are not required. Type and cross-match should be performed in unstable patients. ECG may be necessary to exclude cardiac causes of abdominal pain. In pregnant patients, ectopic pregnancy must be excluded.
Management begins with aggressive resuscitation following trauma and sepsis principles. Hypotension and tachycardia are treated with rapid infusion of 0.9% normal saline, typically 500 mL to 1 L boluses in adults, repeated as needed. Pediatric patients receive 20 mL/kg boluses. Vasopressors may be required if fluids are insufficient. Nasogastric decompression and Foley catheter placement are recommended. Broad-spectrum intravenous antibiotics must be administered promptly to cover enteric gram-negative bacilli, gram-positive cocci, and anaerobes. Appropriate regimens include a carbapenem, piperacillin–tazobactam, or a third- or fourth-generation cephalosporin combined with metronidazole. Analgesia should be provided without delaying surgical consultation.
Immediate surgical consultation is mandatory for all suspected or confirmed cases. Imaging should not delay operative intervention in unstable patients. Discharge is not appropriate, as perforated viscus is a surgical emergency requiring admission and definitive management. Early recognition, prompt antibiotic therapy, aggressive resuscitation, and urgent surgical intervention are critical to reducing morbidity and mortality.
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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 – 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.
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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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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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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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Infectious Diseases and Microbiology: Postoperative Fever
Basics
Description
Postoperative fever is defined as a body temperature above 38°C (100.4°F) occurring after an invasive procedure. It is classified by timing: immediate (during surgery or within hours), acute (within the first postoperative week), subacute (1–4 weeks after surgery), and delayed (more than one month postoperatively). Most cases result from the inflammatory response to surgery and resolve spontaneously, but fever may signal a serious complication. Evaluation requires careful history, physical examination, and appropriate laboratory and imaging studies, including cultures and Gram stains when indicated. Early postoperative fever is frequently noninfectious; however, fever persisting beyond 96 hours is more likely infectious. Consider that patients may have been incubating community-acquired infection preoperatively. New or persistent fever beyond four days strongly suggests ongoing pathology or a new complication. Surgical wounds, catheter insertion sites, and all dressings must be inspected, and recent interventions such as blood transfusions reviewed.
Epidemiology
Drug fever is the most common noninfectious cause of postoperative fever, most often linked to antimicrobials and heparin. Pneumonia is a common cause after cardiac surgery and occurs in more than 5% of such patients. Sternal wound infections after cardiothoracic surgery occur in up to 5%, typically around postoperative day seven. Postoperative aspergillosis after cardiothoracic procedures carries very high mortality. Fever alone is a poor predictor of infection, with low sensitivity. Postsurgical mediastinitis has high mortality. In obstetrics and gynecology, bacterial vaginosis may increase postoperative infection risk.
General Prevention
Aggressive pulmonary hygiene, including incentive spirometry and mobilization, reduces pulmonary complications such as atelectasis.
Etiology
Common infectious causes include urinary tract infection, pneumonia, sinusitis, suppurative thrombophlebitis, catheter-related infections, and Clostridioides difficile–associated diarrhea. Noninfectious causes include deep venous thrombosis, pulmonary embolism, subarachnoid hemorrhage, gout, and fat embolism. Surgical site infections are uncommon within the first 1–3 days except for aggressive pathogens such as group A streptococci or clostridia, which can present early. Atelectasis is frequently blamed but likely coincidental rather than causal. Other serious causes include transplant rejection. Drug-induced fever is most often associated with beta-lactams, antiepileptics, and heparin. Inflammatory states such as acute myocardial infarction, pancreatitis, or acute respiratory distress syndrome may produce fever without infection. Endocrine emergencies such as adrenal insufficiency or thyrotoxicosis may also present with fever.
Diagnosis
Physical Examination
Drug fever lacks specific features and usually develops days after medication exposure; rash and eosinophilia are uncommon. Malignant hyperthermia typically occurs intraoperatively but may be delayed up to 24 hours and is associated with agents such as succinylcholine or volatile anesthetics. Neuroleptic malignant syndrome is associated with antipsychotics, particularly haloperidol. Withdrawal syndromes from alcohol, opioids, barbiturates, or benzodiazepines may cause fever hours to days after admission, and prior substance use history may not be readily available.
Diagnostic Tests and Interpretation
Laboratory Studies
Urinalysis and urine culture are recommended in patients with indwelling catheters longer than 72 hours. Procalcitonin has uncertain value in distinguishing bacterial causes of postoperative fever.
Imaging
Duplex ultrasonography with Doppler should be considered for new extremity swelling suggestive of deep venous thrombosis. Routine chest radiography is not required within the first 72 postoperative hours if fever is the only indication.
Diagnostic Procedures/Other
Wound swab cultures are rarely useful unless there is clear clinical evidence of infection. Suspected deep intraabdominal abscess may require imaging and, if inconclusive, surgical exploration.
Treatment
Medications
Antibiotics are generally not indicated for early postoperative fever without evidence of infection. Critically ill patients or those with hemodynamic instability should receive empiric broad-spectrum antibiotics after thorough evaluation, but therapy should be discontinued after 48 hours if no infectious source is identified. Atelectasis management includes coughing exercises, incentive spirometry, chest physiotherapy, beta-2 agonists, intermittent positive-pressure breathing, and nebulization. Empiric antifungal therapy is not recommended initially.
Ongoing Care and Follow-Up
Drug fever is diagnosed by exclusion when other causes are ruled out. Surgical wounds and invasive device sites must be repeatedly examined for signs of infection.
Complications
Postoperative infections increase morbidity and mortality, may lead to sepsis, impair wound healing, and cause respiratory failure and other serious outcomes.
Basics
Description
Postoperative fever is defined as a body temperature above 38°C (100.4°F) occurring after an invasive procedure. It is classified by timing: immediate (during surgery or within hours), acute (within the first postoperative week), subacute (1–4 weeks after surgery), and delayed (more than one month postoperatively). Most cases result from the inflammatory response to surgery and resolve spontaneously, but fever may signal a serious complication. Evaluation requires careful history, physical examination, and appropriate laboratory and imaging studies, including cultures and Gram stains when indicated. Early postoperative fever is frequently noninfectious; however, fever persisting beyond 96 hours is more likely infectious. Consider that patients may have been incubating community-acquired infection preoperatively. New or persistent fever beyond four days strongly suggests ongoing pathology or a new complication. Surgical wounds, catheter insertion sites, and all dressings must be inspected, and recent interventions such as blood transfusions reviewed.
Epidemiology
Drug fever is the most common noninfectious cause of postoperative fever, most often linked to antimicrobials and heparin. Pneumonia is a common cause after cardiac surgery and occurs in more than 5% of such patients. Sternal wound infections after cardiothoracic surgery occur in up to 5%, typically around postoperative day seven. Postoperative aspergillosis after cardiothoracic procedures carries very high mortality. Fever alone is a poor predictor of infection, with low sensitivity. Postsurgical mediastinitis has high mortality. In obstetrics and gynecology, bacterial vaginosis may increase postoperative infection risk.
General Prevention
Aggressive pulmonary hygiene, including incentive spirometry and mobilization, reduces pulmonary complications such as atelectasis.
Etiology
Common infectious causes include urinary tract infection, pneumonia, sinusitis, suppurative thrombophlebitis, catheter-related infections, and Clostridioides difficile–associated diarrhea. Noninfectious causes include deep venous thrombosis, pulmonary embolism, subarachnoid hemorrhage, gout, and fat embolism. Surgical site infections are uncommon within the first 1–3 days except for aggressive pathogens such as group A streptococci or clostridia, which can present early. Atelectasis is frequently blamed but likely coincidental rather than causal. Other serious causes include transplant rejection. Drug-induced fever is most often associated with beta-lactams, antiepileptics, and heparin. Inflammatory states such as acute myocardial infarction, pancreatitis, or acute respiratory distress syndrome may produce fever without infection. Endocrine emergencies such as adrenal insufficiency or thyrotoxicosis may also present with fever.
Diagnosis
Physical Examination
Drug fever lacks specific features and usually develops days after medication exposure; rash and eosinophilia are uncommon. Malignant hyperthermia typically occurs intraoperatively but may be delayed up to 24 hours and is associated with agents such as succinylcholine or volatile anesthetics. Neuroleptic malignant syndrome is associated with antipsychotics, particularly haloperidol. Withdrawal syndromes from alcohol, opioids, barbiturates, or benzodiazepines may cause fever hours to days after admission, and prior substance use history may not be readily available.
Diagnostic Tests and Interpretation
Laboratory Studies
Urinalysis and urine culture are recommended in patients with indwelling catheters longer than 72 hours. Procalcitonin has uncertain value in distinguishing bacterial causes of postoperative fever.
Imaging
Duplex ultrasonography with Doppler should be considered for new extremity swelling suggestive of deep venous thrombosis. Routine chest radiography is not required within the first 72 postoperative hours if fever is the only indication.
Diagnostic Procedures/Other
Wound swab cultures are rarely useful unless there is clear clinical evidence of infection. Suspected deep intraabdominal abscess may require imaging and, if inconclusive, surgical exploration.
Treatment
Medications
Antibiotics are generally not indicated for early postoperative fever without evidence of infection. Critically ill patients or those with hemodynamic instability should receive empiric broad-spectrum antibiotics after thorough evaluation, but therapy should be discontinued after 48 hours if no infectious source is identified. Atelectasis management includes coughing exercises, incentive spirometry, chest physiotherapy, beta-2 agonists, intermittent positive-pressure breathing, and nebulization. Empiric antifungal therapy is not recommended initially.
Ongoing Care and Follow-Up
Drug fever is diagnosed by exclusion when other causes are ruled out. Surgical wounds and invasive device sites must be repeatedly examined for signs of infection.
Complications
Postoperative infections increase morbidity and mortality, may lead to sepsis, impair wound healing, and cause respiratory failure and other serious outcomes.
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KembaraXtra – Emergency & Acute Medicine – Peripheral Vascular Disease
Peripheral vascular disease (PVD), also known as peripheral artery disease (PAD), refers to obstruction of one or more peripheral arteries due to atherosclerosis, thrombosis, or embolism. Many patients also have coexisting coronary artery disease and cerebrovascular disease. Major risk factors include age, smoking, diabetes mellitus, hyperlipidemia, and hypertension. PVD is associated with significant morbidity and mortality related to systemic atherosclerosis. Complications include aneurysm formation, thrombosis, ulceration, limb loss, and progression to critical limb ischemia.
Chronic arterial insufficiency (CAI) results from progressive atherosclerotic narrowing that produces subacute ischemia and claudication. About 10% of patients progress to critical limb ischemia. Acute arterial insufficiency (AAI) is caused by arterial thrombosis (approximately 50%) or embolism and produces acute limb ischemia characterized by the “6 Ps.” Atheroembolism occurs when rupture or disruption of an atherosclerotic plaque in the aorta, iliac, or femoral arteries releases cholesterol emboli that obstruct small vessels. It is often precipitated by invasive arterial procedures such as cardiac catheterization.
Etiologies include atherosclerotic plaque obstruction, arterial thrombosis, cardiac emboli (commonly from atrial fibrillation, valvular disease, or cardiomyopathy), aneurysm, infection, tumor, vasculitis, foreign body, thrombosis superimposed on chronic disease, and atheroembolism.
Patients with CAI typically report claudication—aching calf pain in femoropopliteal disease or buttock and thigh pain in aortoiliac disease—brought on by exertion and relieved with rest or dependent positioning. Severe disease presents with rest pain, usually beginning in the foot, or rapidly progressive claudication and ulceration. Acute arterial insufficiency presents with sudden extremity pain that increases in severity, often beginning distally and progressing proximally. Pain may decrease once sensory loss occurs. Atheroembolism presents with cold, painful digits and may involve multiple organs including kidneys, mesentery, and skin, especially following recent vascular procedures.
On examination, sudden onset of pain and pallor in an extremity is limb- and life-threatening. In CAI, findings include diminished or absent peripheral pulses, delayed capillary refill, cool skin, prolonged venous filling time, bruits, pallor with elevation and dependent rubor, muscle and skin atrophy, thickened nails, hair loss, and toe or heel ulcerations. Acute arterial insufficiency presents with the 6 Ps: pain, pallor, pulselessness, poikilothermia, paresthesias, and paralysis. Identifying a potential embolic source such as atrial fibrillation is essential. Atheroembolism may show painful ischemic digits, “blue toe syndrome,” and livedo reticularis.
The ankle–brachial index (ABI) is an important bedside test in chronic disease. An ABI <0.9 is abnormal and <0.4-0.5 indicates severe disease. in patients with diabetes, calcified vessels may produce falsely elevated values (>1.3). Acute arterial insufficiency is primarily a clinical diagnosis based on the 6 Ps. Patients with acute-on-chronic disease may tolerate ischemia better due to collateral circulation. Atheroembolism is diagnosed clinically, with further evaluation to identify the embolic source.
Laboratory evaluation includes CBC, platelets, electrolytes, renal function, glucose, coagulation studies, and creatine phosphokinase to assess muscle ischemia. Additional studies may include inflammatory markers for vasculitis, blood cultures for suspected endocarditis, and hypercoagulable testing when indicated.
Doppler ultrasound is commonly used to identify the level of arterial occlusion and detect thrombosis or aneurysm. CT angiography is widely used as a first-line diagnostic tool and guides decisions for operative or endovascular intervention. Angiography allows simultaneous diagnosis and treatment with angioplasty, atherectomy, or thrombolysis. MRI is sensitive but less practical in emergency settings.
Differential diagnoses include acute thrombosis or embolism, arterial dissection, deep venous thrombosis, venous insufficiency, compartment syndrome, Buerger disease, spinal stenosis, neuropathy, bursitis, arthritis, and reflex sympathetic dystrophy.
Prehospital care includes maintaining hemodynamic stability, placing the limb at rest in a dependent position, providing oxygen when needed, and cardiac monitoring. In the emergency department, management includes IV fluids for hypotension, cardiac monitoring, supplemental oxygen, adequate analgesia, and avoidance of temperature extremes.
Management of chronic arterial insufficiency includes antiplatelet therapy with aspirin (75–325 mg daily) or clopidogrel (75 mg daily). Cilostazol, pentoxifylline, or dipyridamole may be used in selected patients. Risk-factor modification is essential and includes smoking cessation, lipid and blood pressure control, diabetes management, and structured exercise therapy. Revascularization options include balloon angioplasty, atherectomy, or bypass grafting depending on anatomy and severity.
Acute arterial insufficiency requires immediate IV heparin (80 U/kg bolus followed by infusion at 18 U/kg/hr), unless aortic dissection or aneurysm is suspected. Emergent consultation with vascular surgery or interventional radiology is mandatory. Revascularization must occur within 4–6 hours of symptom onset to prevent irreversible ischemia. Treatment options include thrombectomy, embolectomy, angioplasty, thrombolysis, or bypass grafting. Complications include compartment syndrome, irreversible limb ischemia requiring amputation, rhabdomyolysis, renal failure, and electrolyte disturbances.
Atheroembolism is managed conservatively when tissue involvement is limited and renal function preserved. Treatment is supportive with wound care and analgesia. Vascular surgery referral within 12–24 hours is recommended, and evaluation to prevent further embolic events is essential. Amputation may be required for irreversibly necrotic tissue.
All patients with acute arterial insufficiency require hospital admission for evaluation and revascularization. Patients with chronic disease should be admitted if they develop rapidly progressive claudication or ischemic rest pain. Atheroembolism warrants admission if there is significant tissue involvement, infection, pain, or renal compromise. Stable patients with mild chronic disease or limited atheroembolism may be discharged with close follow-up.
Early recognition of acute limb ischemia is critical, as time to reperfusion determines limb salvage and survival.
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Emergency And Acute Medicine – Pertussis
Pertussis is an acute respiratory tract infection transmitted by small respiratory droplets. The organism attaches to respiratory epithelial cells via fimbriae and produces toxins that cause ciliary dysfunction, accumulation of debris, increased mucus production, and inflammatory infiltration. Bronchiolar congestion, obstruction, and necrosis may develop. Airway obstruction from mucus plugging can lead to hypoxia, hypoventilation, and increased intrathoracic or intracranial pressure. Secondary bacterial pneumonia may worsen respiratory failure. Central nervous system injury may result from encephalitis, hypoxia, or elevated intracranial pressure. Uncomplicated illness typically lasts 6–10 weeks, although about half resolve in under 6 weeks. Mortality is highest in infants under 1 year, especially those younger than 1 month. Most deaths are due to secondary bacterial pneumonia. The incubation period is usually 7–10 days. Disease is most common in young children, but incidence is increasing among adolescents. Adults serve as the primary reservoir. Peak incidence occurs in late summer and fall. Vaccination with Tdap provides prevention. The causative organism is Bordetella pertussis, a fastidious gram-negative pleomorphic bacillus.
The illness classically progresses through three phases, although infants may not follow distinct stages. The catarrhal stage lasts 1–2 weeks and resembles a mild upper respiratory infection with rhinorrhea, low-grade fever, malaise, sore throat, lacrimation, and mild cough. The paroxysmal stage lasts 1–6 weeks and is characterized by severe coughing spells that end with a sudden inspiratory “whoop.” Paroxysms may be associated with cyanosis, apnea (especially in infants under 6 months), post-tussive emesis, and altered mental status due to hypoxia. The convalescent stage lasts 2–12 weeks with gradual improvement and decreasing frequency of cough. Adults and partially immunized children often have milder or atypical presentations, sometimes limited to persistent cough without a classic whoop.
Diagnosis in the emergency setting is primarily clinical, especially when a characteristic paroxysmal cough is observed or there is a known exposure. Laboratory confirmation may support the diagnosis. PCR testing from a posterior nasopharyngeal swab or aspirate has high sensitivity and specificity but may produce false positives and false negatives depending on timing and prior antibiotic use. Culture on Bordet–Gengou medium remains the gold standard due to high specificity but has low sensitivity and requires 7–12 days for results. Serology is useful later in the course. Leukocytosis with marked lymphocytosis is common and correlates with disease severity. Chest radiographs are often normal but may show perihilar infiltrates, atelectasis, or secondary pneumonia.
Differential diagnoses include other causes of prolonged or paroxysmal cough such as infections with Bordetella parapertussis, Chlamydia species, adenovirus, pneumonia, bronchiolitis, influenza, reactive airway disease, foreign body aspiration, and cystic fibrosis.
Initial management focuses on airway and respiratory support. Oxygen supplementation and suctioning of mucus plugs are important, particularly in infants. Droplet precautions are required for 5 days after initiation of effective antimicrobial therapy. Adequate hydration must be maintained. Continuous monitoring is recommended during severe paroxysms, especially in infants. Antibiotics are most effective during the catarrhal phase but are still indicated during the paroxysmal phase to reduce transmission. Azithromycin is the first-line agent. Alternatives include clarithromycin, erythromycin, or trimethoprim–sulfamethoxazole, although erythromycin carries a risk of pyloric stenosis in neonates. Bronchodilators and corticosteroids are generally not recommended. Tdap vaccination should be offered when appropriate, including during each pregnancy between 27 and 36 weeks gestation to protect newborns.
Admission is indicated for patients under 1 year of age, those with apnea, cyanosis, pneumonia, encephalitis, or significant respiratory distress. Children without respiratory compromise may be discharged with close follow-up, hydration guidance, and avoidance of cough triggers such as smoke and pollutants. Postexposure prophylaxis with antibiotics is recommended for all close contacts regardless of age or immunization status. Patients may return to school or work after 5 days of appropriate antibiotic therapy.
Complications include epistaxis, subconjunctival hemorrhage, pneumonia, pneumothorax, subcutaneous or mediastinal emphysema, bronchiectasis, hernias, rectal prolapse, seizures, encephalitis, intracranial hemorrhage, and spinal epidural hemorrhage. Infants require particular vigilance due to high risk of apnea and severe respiratory compromise. Cases must be reported to public health authorities, and strict droplet precautions are essential to prevent spread.
Pertussis is an acute respiratory tract infection transmitted by small respiratory droplets. The organism attaches to respiratory epithelial cells via fimbriae and produces toxins that cause ciliary dysfunction, accumulation of debris, increased mucus production, and inflammatory infiltration. Bronchiolar congestion, obstruction, and necrosis may develop. Airway obstruction from mucus plugging can lead to hypoxia, hypoventilation, and increased intrathoracic or intracranial pressure. Secondary bacterial pneumonia may worsen respiratory failure. Central nervous system injury may result from encephalitis, hypoxia, or elevated intracranial pressure. Uncomplicated illness typically lasts 6–10 weeks, although about half resolve in under 6 weeks. Mortality is highest in infants under 1 year, especially those younger than 1 month. Most deaths are due to secondary bacterial pneumonia. The incubation period is usually 7–10 days. Disease is most common in young children, but incidence is increasing among adolescents. Adults serve as the primary reservoir. Peak incidence occurs in late summer and fall. Vaccination with Tdap provides prevention. The causative organism is Bordetella pertussis, a fastidious gram-negative pleomorphic bacillus.
The illness classically progresses through three phases, although infants may not follow distinct stages. The catarrhal stage lasts 1–2 weeks and resembles a mild upper respiratory infection with rhinorrhea, low-grade fever, malaise, sore throat, lacrimation, and mild cough. The paroxysmal stage lasts 1–6 weeks and is characterized by severe coughing spells that end with a sudden inspiratory “whoop.” Paroxysms may be associated with cyanosis, apnea (especially in infants under 6 months), post-tussive emesis, and altered mental status due to hypoxia. The convalescent stage lasts 2–12 weeks with gradual improvement and decreasing frequency of cough. Adults and partially immunized children often have milder or atypical presentations, sometimes limited to persistent cough without a classic whoop.
Diagnosis in the emergency setting is primarily clinical, especially when a characteristic paroxysmal cough is observed or there is a known exposure. Laboratory confirmation may support the diagnosis. PCR testing from a posterior nasopharyngeal swab or aspirate has high sensitivity and specificity but may produce false positives and false negatives depending on timing and prior antibiotic use. Culture on Bordet–Gengou medium remains the gold standard due to high specificity but has low sensitivity and requires 7–12 days for results. Serology is useful later in the course. Leukocytosis with marked lymphocytosis is common and correlates with disease severity. Chest radiographs are often normal but may show perihilar infiltrates, atelectasis, or secondary pneumonia.
Differential diagnoses include other causes of prolonged or paroxysmal cough such as infections with Bordetella parapertussis, Chlamydia species, adenovirus, pneumonia, bronchiolitis, influenza, reactive airway disease, foreign body aspiration, and cystic fibrosis.
Initial management focuses on airway and respiratory support. Oxygen supplementation and suctioning of mucus plugs are important, particularly in infants. Droplet precautions are required for 5 days after initiation of effective antimicrobial therapy. Adequate hydration must be maintained. Continuous monitoring is recommended during severe paroxysms, especially in infants. Antibiotics are most effective during the catarrhal phase but are still indicated during the paroxysmal phase to reduce transmission. Azithromycin is the first-line agent. Alternatives include clarithromycin, erythromycin, or trimethoprim–sulfamethoxazole, although erythromycin carries a risk of pyloric stenosis in neonates. Bronchodilators and corticosteroids are generally not recommended. Tdap vaccination should be offered when appropriate, including during each pregnancy between 27 and 36 weeks gestation to protect newborns.
Admission is indicated for patients under 1 year of age, those with apnea, cyanosis, pneumonia, encephalitis, or significant respiratory distress. Children without respiratory compromise may be discharged with close follow-up, hydration guidance, and avoidance of cough triggers such as smoke and pollutants. Postexposure prophylaxis with antibiotics is recommended for all close contacts regardless of age or immunization status. Patients may return to school or work after 5 days of appropriate antibiotic therapy.
Complications include epistaxis, subconjunctival hemorrhage, pneumonia, pneumothorax, subcutaneous or mediastinal emphysema, bronchiectasis, hernias, rectal prolapse, seizures, encephalitis, intracranial hemorrhage, and spinal epidural hemorrhage. Infants require particular vigilance due to high risk of apnea and severe respiratory compromise. Cases must be reported to public health authorities, and strict droplet precautions are essential to prevent spread.
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KembaraXtra – Emergency & Acute Medicine – Perirectal Abscess
Perirectal abscess is a localized infection with accumulation of purulent material adjacent to the anus or rectum. It most commonly results from infection of the anal crypt glands with spread into adjacent potential spaces separated by muscle and fascia. Perianal abscesses are the most common and typically present with a visible, tender red bulge near the anus. Ischiorectal abscesses occur in a large potential space and may grow significantly before diagnosis; they can communicate posteriorly to form a horseshoe abscess. Intersphincteric abscesses remain confined between the internal and external sphincters. Supralevator abscesses are deep, located above the levator ani, often present with systemic symptoms, and usually require operative drainage under general anesthesia. Infections are typically polymicrobial with mixed enteric organisms. Associated conditions include diabetes, inflammatory bowel disease, malignancy, and immunocompromised states.
Patients commonly present with constant perianal, rectal, or pelvic pain. Pain is often worsened by defecation, sitting, or coughing. Deeper abscesses such as ischiorectal or supralevator may produce dull pelvic or rectal pain and may be less painful if located above the dentate line. Fever, chills, constipation, and drainage may occur. On examination, findings include perianal swelling, erythema, induration, fluctuance, and marked tenderness. An abscess in the inner buttock cleft is a red flag, as rectal abscesses can track outward. Digital rectal examination is essential and may reveal rectal wall swelling or focal tenderness. A fistulous tract may be palpable as a cord-like structure or identified with gentle probing.
Diagnosis is primarily clinical and based on careful history and thorough rectal examination. A high index of suspicion is required in patients with persistent perirectal pain. Routine laboratory testing and imaging are not required for simple perianal abscesses. Leukocytosis with left shift may be present. Blood cultures are reserved for patients with signs of sepsis. CT scan with IV contrast or MRI is helpful when a deeper abscess is suspected or when the diagnosis is unclear. MRI is particularly useful for identifying fistulous tracts. Endoanal ultrasound may also assist in selected cases.
The differential diagnosis includes anal fissure, thrombosed or inflamed hemorrhoids, sentinel pile, anal ulcer, proctitis, and anorectal carcinoma.
Prompt incision and drainage are the definitive treatments. Delay in drainage may worsen outcomes. Bedside drainage is appropriate only for localized perianal abscesses. A radial incision should be made close to the anal verge, the cavity explored to break loculations, and copious irrigation performed. Loose packing may be placed and removed after 48 hours. Operative drainage under general anesthesia is indicated for deeper abscesses or when adequate drainage cannot be achieved with local anesthesia.
Antibiotics are not routinely required after adequate drainage but are indicated in patients with extensive cellulitis, systemic infection, immunosuppression, valvular heart disease, prosthetic devices, or diabetes. Oral options include amoxicillin-clavulanate or a fluoroquinolone with consideration for MRSA coverage when indicated. Intravenous regimens may include cefoxitin, ampicillin-sulbactam, or combination therapy with ampicillin, gentamicin, and either clindamycin or metronidazole.
Postprocedural care includes sitz baths three times daily beginning 24 hours after drainage, high-fiber diet or bulking agents, and adequate analgesia.
Patients requiring operative drainage or those with systemic toxicity or sepsis should be admitted. Patients with adequate bedside drainage and no systemic illness may be discharged with close follow-up. All patients should be referred to a surgeon within 24–48 hours to evaluate for fistula formation, which occurs in approximately 25–50% of anorectal abscesses.
Careful assessment of the extent of infection is critical. Thorough rectal examination and probing are mandatory, and imaging should be obtained when deeper extension is suspected. Deep abscesses above the dentate line may present with minimal pain and isolated fever, increasing the risk of delayed diagnosis.
