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Emergency And Acute Medicine – Phalangeal Injuries, Foot
Phalangeal injuries of the foot are common, with the fifth (small) toe most frequently affected. These injuries usually result from direct trauma such as stubbing the toe, kicking a hard object, or dropping a heavy item onto the foot. Although many are minor, certain patterns—particularly those involving the great toe (hallux), intra-articular surfaces, or open wounds—require careful evaluation and possible orthopedic consultation.
Patients typically present with localized pain, swelling, bruising, and difficulty bearing weight. The history should include the time and mechanism of injury, prior trauma to the digit, and tetanus immunization status if a laceration is present. On examination, findings may include tenderness, swelling, crepitus, ecchymosis, and occasionally subungual hematoma. Lacerations or crush injuries may also be present. Neurovascular status of the affected digit must always be documented. Radiographs of the involved digit are essential for diagnosis, and the lateral view is often the most sensitive for detecting fractures or dislocations.
Fractures of the proximal phalanx or interphalangeal (IP) joint of the hallux require particular attention. Nondisplaced, non–intra-articular fractures can be treated with a short-leg walking cast with toe extension for comfort. Displaced fractures may require closed reduction under digital block anesthesia with longitudinal traction, followed by immobilization. Intra-articular fractures of the hallux warrant orthopedic consultation and are often managed with open reduction and internal fixation. Fractures involving the lesser toes rarely cause long-term disability. Nondisplaced fractures are typically treated with buddy taping and gauze padding between toes to prevent skin breakdown. Displaced fractures may be reduced under digital block anesthesia, followed by buddy taping or splinting and use of a hard-sole shoe with weight bearing as tolerated. Pain usually resolves within 2–3 weeks.
Interphalangeal joint dislocations are managed with closed reduction using digital block anesthesia and longitudinal traction with gentle pressure on the distal phalanx, followed by buddy taping. Unstable or irreducible dislocations require orthopedic consultation. Distal tuft fractures are commonly associated with subungual hematomas, which should be drained. Nail-bed lacerations may require repair. Buddy taping and weight bearing as tolerated are generally sufficient, with pain resolving in 2–3 weeks. Open fractures require urgent orthopedic consultation and prophylactic antibiotics.
Pain control is typically achieved with NSAIDs such as ibuprofen, though narcotic analgesics may be necessary for severe pain. Open fractures may require intravenous cefazolin in the emergency department and oral cephalexin for contaminated wounds. Admission is indicated for unstable or irreducible dislocations and open fractures requiring immediate orthopedic management. Most other fractures can be discharged with orthopedic follow-up in 2–3 weeks. Intra-articular fractures of the great toe require urgent specialist follow-up, while simple nondisplaced fractures of the lesser toes may be managed by primary care providers. Open, displaced, or intra-articular fractures—particularly those involving the hallux—should prompt early orthopedic consultation to reduce the risk of long-term functional impairment.
Phalangeal injuries of the foot are common, with the fifth (small) toe most frequently affected. These injuries usually result from direct trauma such as stubbing the toe, kicking a hard object, or dropping a heavy item onto the foot. Although many are minor, certain patterns—particularly those involving the great toe (hallux), intra-articular surfaces, or open wounds—require careful evaluation and possible orthopedic consultation.
Patients typically present with localized pain, swelling, bruising, and difficulty bearing weight. The history should include the time and mechanism of injury, prior trauma to the digit, and tetanus immunization status if a laceration is present. On examination, findings may include tenderness, swelling, crepitus, ecchymosis, and occasionally subungual hematoma. Lacerations or crush injuries may also be present. Neurovascular status of the affected digit must always be documented. Radiographs of the involved digit are essential for diagnosis, and the lateral view is often the most sensitive for detecting fractures or dislocations.
Fractures of the proximal phalanx or interphalangeal (IP) joint of the hallux require particular attention. Nondisplaced, non–intra-articular fractures can be treated with a short-leg walking cast with toe extension for comfort. Displaced fractures may require closed reduction under digital block anesthesia with longitudinal traction, followed by immobilization. Intra-articular fractures of the hallux warrant orthopedic consultation and are often managed with open reduction and internal fixation. Fractures involving the lesser toes rarely cause long-term disability. Nondisplaced fractures are typically treated with buddy taping and gauze padding between toes to prevent skin breakdown. Displaced fractures may be reduced under digital block anesthesia, followed by buddy taping or splinting and use of a hard-sole shoe with weight bearing as tolerated. Pain usually resolves within 2–3 weeks.
Interphalangeal joint dislocations are managed with closed reduction using digital block anesthesia and longitudinal traction with gentle pressure on the distal phalanx, followed by buddy taping. Unstable or irreducible dislocations require orthopedic consultation. Distal tuft fractures are commonly associated with subungual hematomas, which should be drained. Nail-bed lacerations may require repair. Buddy taping and weight bearing as tolerated are generally sufficient, with pain resolving in 2–3 weeks. Open fractures require urgent orthopedic consultation and prophylactic antibiotics.
Pain control is typically achieved with NSAIDs such as ibuprofen, though narcotic analgesics may be necessary for severe pain. Open fractures may require intravenous cefazolin in the emergency department and oral cephalexin for contaminated wounds. Admission is indicated for unstable or irreducible dislocations and open fractures requiring immediate orthopedic management. Most other fractures can be discharged with orthopedic follow-up in 2–3 weeks. Intra-articular fractures of the great toe require urgent specialist follow-up, while simple nondisplaced fractures of the lesser toes may be managed by primary care providers. Open, displaced, or intra-articular fractures—particularly those involving the hallux—should prompt early orthopedic consultation to reduce the risk of long-term functional impairment.
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Emergency And Acute Medicine – Phencyclidine Poisoning
Phencyclidine (PCP) is a dissociative anesthetic structurally related to ketamine that produces decreased perception of pain, agitation, and dissociation. It has a half-life of approximately 21–24 hours, which may be prolonged in overdose. Enterohepatic recirculation can contribute to prolonged or recurrent symptoms. PCP is a drug of abuse and is frequently encountered as an adulterant of marijuana. Street names include Angel Dust, Wicky Stick, Wicky Weed, Wacky Weed, Wet, Illy, Embalming Fluid, and Sherman. Pediatric exposure has been reported in toddlers through passive exposure.
Clinical presentation primarily involves the central nervous system. Patients may exhibit altered mental status ranging from agitation, bizarre or violent behavior, and belligerence to coma and seizures. Nystagmus—vertical, horizontal, or rotatory—is a characteristic finding. Cardiovascular manifestations include hypertension and tachycardia. Musculoskeletal complications are common due to decreased pain perception and intense muscle activity, leading to traumatic injuries and rhabdomyolysis. Hyperthermia may occur. History should focus on route of exposure, including smoking (often with marijuana) or ingestion.
Physical examination may reveal agitation or coma, hypertension, tachycardia, diaphoresis, nystagmus, hyperthermia, and vigorous muscle contractions. A careful assessment for occult trauma is essential because patients may not report pain appropriately.
Diagnosis is primarily clinical and supported by urine toxicology screening. However, false positives may occur with dextromethorphan, ketamine, and tramadol. Evaluation must exclude other causes of altered mental status. Laboratory studies include CBC, electrolytes, renal function, glucose, ethanol level, urinalysis for myoglobin, and creatine phosphokinase when rhabdomyolysis is suspected. Imaging such as chest radiography, extremity or spine radiographs, and head CT should be obtained when trauma or aspiration is suspected.
Differential diagnosis includes intoxication with cocaine, amphetamines, methamphetamine, MDMA, alcohols, ketamine, and other sympathomimetics. Drugs associated with nystagmus, such as lithium, carbamazepine, sedative–hypnotics, phenothiazines, alcohol, and dextromethorphan, should also be considered.
Management begins with attention to airway, breathing, and circulation. Combative patients may require restraints and additional personnel to ensure safety. Cardiac monitoring and IV access are indicated. In altered mental status, administer naloxone, thiamine, and glucose as appropriate. The patient should be placed in a quiet, low-stimulation environment. Benzodiazepines are first-line agents for agitation and seizures, with lorazepam or diazepam given in incremental doses. Haloperidol may be used cautiously but may lower the seizure threshold. Activated charcoal may be considered for recent oral coingestion. Aggressive IV hydration with normal saline is recommended, and sodium bicarbonate or mannitol may be used for rhabdomyolysis with a target urine pH of approximately 7.
Patients require admission if they have prolonged altered mental status, significant trauma, rhabdomyolysis, or hyperthermia. Those who become lucid after approximately six hours of observation without complications may be discharged. Psychiatry or social work referral is recommended for patients with suicidal ideation or chronic substance use.
PCP intoxication can result in severe traumatic injuries and life-threatening complications. Adequate chemical restraint with benzodiazepines is essential to prevent excessive muscle activity and subsequent rhabdomyolysis. False-positive urine toxicology screens may occur with dextromethorphan or tramadol. Ketamine abuse produces similar clinical features and should be considered in the differential diagnosis.
Phencyclidine (PCP) is a dissociative anesthetic structurally related to ketamine that produces decreased perception of pain, agitation, and dissociation. It has a half-life of approximately 21–24 hours, which may be prolonged in overdose. Enterohepatic recirculation can contribute to prolonged or recurrent symptoms. PCP is a drug of abuse and is frequently encountered as an adulterant of marijuana. Street names include Angel Dust, Wicky Stick, Wicky Weed, Wacky Weed, Wet, Illy, Embalming Fluid, and Sherman. Pediatric exposure has been reported in toddlers through passive exposure.
Clinical presentation primarily involves the central nervous system. Patients may exhibit altered mental status ranging from agitation, bizarre or violent behavior, and belligerence to coma and seizures. Nystagmus—vertical, horizontal, or rotatory—is a characteristic finding. Cardiovascular manifestations include hypertension and tachycardia. Musculoskeletal complications are common due to decreased pain perception and intense muscle activity, leading to traumatic injuries and rhabdomyolysis. Hyperthermia may occur. History should focus on route of exposure, including smoking (often with marijuana) or ingestion.
Physical examination may reveal agitation or coma, hypertension, tachycardia, diaphoresis, nystagmus, hyperthermia, and vigorous muscle contractions. A careful assessment for occult trauma is essential because patients may not report pain appropriately.
Diagnosis is primarily clinical and supported by urine toxicology screening. However, false positives may occur with dextromethorphan, ketamine, and tramadol. Evaluation must exclude other causes of altered mental status. Laboratory studies include CBC, electrolytes, renal function, glucose, ethanol level, urinalysis for myoglobin, and creatine phosphokinase when rhabdomyolysis is suspected. Imaging such as chest radiography, extremity or spine radiographs, and head CT should be obtained when trauma or aspiration is suspected.
Differential diagnosis includes intoxication with cocaine, amphetamines, methamphetamine, MDMA, alcohols, ketamine, and other sympathomimetics. Drugs associated with nystagmus, such as lithium, carbamazepine, sedative–hypnotics, phenothiazines, alcohol, and dextromethorphan, should also be considered.
Management begins with attention to airway, breathing, and circulation. Combative patients may require restraints and additional personnel to ensure safety. Cardiac monitoring and IV access are indicated. In altered mental status, administer naloxone, thiamine, and glucose as appropriate. The patient should be placed in a quiet, low-stimulation environment. Benzodiazepines are first-line agents for agitation and seizures, with lorazepam or diazepam given in incremental doses. Haloperidol may be used cautiously but may lower the seizure threshold. Activated charcoal may be considered for recent oral coingestion. Aggressive IV hydration with normal saline is recommended, and sodium bicarbonate or mannitol may be used for rhabdomyolysis with a target urine pH of approximately 7.
Patients require admission if they have prolonged altered mental status, significant trauma, rhabdomyolysis, or hyperthermia. Those who become lucid after approximately six hours of observation without complications may be discharged. Psychiatry or social work referral is recommended for patients with suicidal ideation or chronic substance use.
PCP intoxication can result in severe traumatic injuries and life-threatening complications. Adequate chemical restraint with benzodiazepines is essential to prevent excessive muscle activity and subsequent rhabdomyolysis. False-positive urine toxicology screens may occur with dextromethorphan or tramadol. Ketamine abuse produces similar clinical features and should be considered in the differential diagnosis.
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Emergency And Acute Medicine – Phenytoin Poisoning
Phenytoin poisoning occurs because phenytoin follows zero-order (capacity-limited) pharmacokinetics, meaning small increases in dose can produce disproportionately large increases in serum concentration. In overdose, the half-life may be significantly prolonged, up to 70 hours. Cardiovascular toxicity associated with IV phenytoin is often related to its diluent, propylene glycol. Fosphenytoin, a parenteral prodrug converted to active phenytoin, does not contain propylene glycol and is less likely to cause hypotension or dysrhythmias.
Toxicity may result from acute overdose, chronic accumulation, or acute-on-chronic ingestion. In patients receiving long-term therapy, unexplained toxicity should prompt consideration of a change in brand, dosage formulation, drug interaction, or altered serum albumin affecting free drug levels.
Clinical manifestations correlate with serum concentration. At 20–40 µg/mL, patients commonly develop nystagmus, dizziness, ataxia, drowsiness, nausea, vomiting, diplopia, and slurred speech. At 40–90 µg/mL, confusion and disorientation occur. Levels above 90 µg/mL may lead to coma, respiratory depression, and paradoxical seizures. Rapid IV administration can produce hypotension and bradycardia, particularly with standard IV phenytoin formulations. Chronic exposure may also cause hypersensitivity reactions including rash, fever, neutropenia, agranulocytosis, hepatitis, and cholangitis.
Evaluation begins with determining the time, route, and amount of ingestion. After oral overdose, peak levels may not be reached for 24 hours or longer, and absorption varies between preparations. Serum phenytoin concentrations should be repeated every four hours until they peak and begin to decline; once declining, levels may be monitored every 24 hours until below 30 µg/mL. In hypoalbuminemic patients or those with altered protein binding, measurement of a free phenytoin level is recommended. Fosphenytoin concentrations are measured as phenytoin and should be checked after full conversion (approximately 2 hours after IV infusion or 4 hours after IM injection).
Additional laboratory evaluation includes electrolytes, BUN, creatinine, and glucose. An anion gap metabolic acidosis may suggest coingestants, seizure activity, or propylene glycol toxicity. Blood glucose should be assessed in any patient with altered mental status.
Management is primarily supportive. Airway, breathing, and circulation should be stabilized with IV access and cardiac monitoring, especially in IV overdoses. In altered mental status, bedside glucose testing is essential, with administration of naloxone, dextrose, and thiamine as indicated. Hypotension should be treated with IV fluids and positioning, with dopamine considered for refractory cases. Paradoxical seizures are treated with benzodiazepines such as diazepam. A single dose of activated charcoal may be administered in appropriate oral ingestions; multiple-dose charcoal can increase phenytoin clearance but has not consistently shown clinical benefit.
Patients require admission if they have altered mental status, severe ataxia, rising phenytoin levels, levels greater than 25 µg/mL, or toxicity from IV administration, which warrants ICU monitoring. Fall precautions are important due to marked ataxia. Patients may be discharged when levels are 25 µg/mL or less, symptoms are resolving, and they are ambulatory without ataxia. Intentional ingestions require psychiatric evaluation, and close outpatient follow-up is necessary to reassess phenytoin levels and adjust therapy, particularly after any change in manufacturer or dosage formulation.
Key clinical reminders include recognition that even small dose increases can precipitate toxicity due to zero-order kinetics, and that serial phenytoin levels should be obtained every four hours until a clear downward trend is established.
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Emergency And Acute Medicine – Pheochromocytoma
Pheochromocytoma is a catecholamine-producing tumor arising from chromaffin tissue of the sympathetic nervous system. Most tumors originate in the adrenal medulla, with approximately 80% being solitary adrenal tumors (more commonly right-sided), 10% bilateral (often inherited), and 10% extra-adrenal (paragangliomas) located in the abdomen, thorax, neck, or bladder. About 10% are malignant. The condition is rare, occurring in approximately 2–8 per million people per year, and accounts for 0.2–0.4% of hypertensive patients, although it is more common in those with severe or refractory hypertension. It typically presents between the third and fifth decades of life, affects males and females equally, and is diagnosed postmortem in nearly half of cases. Approximately 10% are asymptomatic and discovered incidentally on imaging.
Up to 25% of cases are inherited in an autosomal dominant pattern and are associated with syndromes such as Multiple Endocrine Neoplasia type 2A, Multiple Endocrine Neoplasia type 2B, and von Hippel–Lindau disease. MEN 2A includes medullary thyroid carcinoma, pheochromocytoma, and hyperparathyroidism. MEN 2B includes medullary thyroid carcinoma, pheochromocytoma, mucosal neuromas, and skeletal abnormalities. Von Hippel–Lindau disease is associated with retinal and CNS hemangioblastomas, renal and pancreatic cysts, and pheochromocytoma. Other associations include neurofibromatosis, tuberous sclerosis, and paragangliomas.
The tumor synthesizes and stores catecholamines similarly to the normal adrenal medulla, predominantly secreting norepinephrine and, less commonly, epinephrine. Some epinephrine-predominant tumors may cause hypotensive episodes. Catecholamine release may occur spontaneously due to tumor necrosis or changes in blood flow, or may be triggered by trauma, exercise, surgery, anesthesia, glucagon, metoclopramide, steroids, tyramine-containing foods, iodinated contrast, tricyclic antidepressants, β-blockers, or sympathomimetics.
Hypertension is the most common manifestation and may be paroxysmal, sustained, or sustained with superimposed paroxysms. Classic paroxysms consist of abrupt episodes of severe hypertension, throbbing bilateral headache, tachycardia or palpitations, diaphoresis, pallor, anxiety, and tremulousness. Episodes typically last minutes to hours and increase in frequency and severity over time. Some patients are normotensive, particularly those with small tumors or familial disease. Chronic symptoms may include orthostatic hypotension due to reduced plasma volume, constipation or ileus from decreased peristalsis, weight loss, glucose intolerance, anxiety, and fatigue.
Acute crisis may present with prolonged severe hypertension or shock, hyperpyrexia, lactic acidosis, multiorgan failure, pulmonary edema from stress cardiomyopathy (including Takotsubo), stroke, myocardial infarction, aortic dissection, or acute abdomen due to tumor necrosis or mesenteric infarction. Physical findings often include severe hypertension with orthostatic changes, tachycardia, diaphoresis, pallor, tremor, mydriasis, and signs of hypertensive retinopathy. Café-au-lait spots or thyroid nodules may suggest associated syndromes. Tumors are usually not palpable.
Initial evaluation includes accurate blood pressure measurement with orthostatic readings and ECG to assess for ischemia or dysrhythmia. Laboratory findings may show elevated hemoglobin from hemoconcentration, leukocytosis from demargination, hyperglycemia, lactic acidosis, renal dysfunction, or hypercalcemia (in MEN 2A). The best screening test is plasma-free fractionated metanephrines, which are highly sensitive but may yield false positives. A normal result effectively excludes the diagnosis. Confirmation is typically performed with 24-hour urine collection for catecholamines and metanephrines, including creatinine to confirm adequate sampling. Numerous medications and substances can interfere with results.
Imaging with CT or MRI is used to localize tumors once biochemical confirmation is obtained. MRI is particularly useful for extra-adrenal lesions. Metaiodobenzylguanidine (MIBG) scanning has high specificity but limited sensitivity. Fine-needle aspiration is contraindicated due to risk of catecholamine surge.
Management of hypertensive crisis requires prompt α-adrenergic blockade. Phentolamine is traditionally used as an IV bolus followed by infusion, with aggressive fluid resuscitation to counteract vasodilation-induced hypotension. Alternatively, nicardipine or nitroprusside infusions may be used. β-blockers may be added only after adequate α-blockade to control reflex tachycardia. β-blockade must never be initiated before α-blockade, as unopposed α-stimulation can precipitate severe hypertension. Ventricular arrhythmias may require lidocaine or esmolol.
For preoperative or chronic management, phenoxybenzamine is initiated at least 7 days prior to surgery and titrated gradually. Selective α1-blockers such as doxazosin or terazosin are alternatives. β-blockers are added after adequate α-blockade if tachycardia persists. Calcium-channel blockers may also be used. Metyrosine can inhibit catecholamine synthesis in refractory cases.
Patients with suspected pheochromocytoma and labile blood pressure, hypertensive crisis, arrhythmias, or end-organ damage require admission. Stable patients with mild hypertension may be discharged with close follow-up and initiation of appropriate antihypertensive therapy. Plasma-free metanephrines should ideally be drawn during a hypertensive episode for maximal sensitivity.
Clinically, the combination of paroxysmal severe hypertension, headache, palpitations, and intense diaphoresis is highly suggestive of pheochromocytoma. Pallor rather than flushing is typical. Orthostatic hypotension is common and may worsen after α-blockade if volume repletion is inadequate. The diagnosis should be considered in unexplained shock, cardiomyopathy, recurrent hypertensive crises, or new-onset glucose intolerance with weight loss. Under no circumstances should β-blockers be administered before adequate α-blockade in suspected pheochromocytoma.
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Emergency And Acute Medicine – Phimosis
Phimosis is the inability to retract the foreskin (prepuce) over the glans penis. True (pathologic) phimosis results from scarring and fibrosis of the preputial opening, preventing retraction. It is important to distinguish this from physiologic phimosis, which is normal in young children due to natural adhesions between the glans and the inner prepuce. At birth, the foreskin is rarely retractable. Approximately 90% of foreskins are retractable by age 3 years and 99% by age 17, as smegma-producing epithelial cells shed and adhesions separate naturally. Parents should be instructed never to forcibly retract a child’s foreskin, as this may cause trauma and scarring.
True phimosis may develop from trauma due to forcible retraction, recurrent diaper dermatitis, repeated episodes of balanoposthitis (inflammation of the glans and foreskin), poor hygiene, poorly performed circumcision, or congenital anomalies. Chronic inflammation leads to fibrosis and narrowing of the preputial opening.
Patients may present with dysuria, hematuria, poor urinary stream, or ballooning of the foreskin during urination in severe cases. Examination may reveal a whitish, narrowed preputial orifice, along with edema, erythema, and tenderness of the foreskin. Associated balanoposthitis may be present. In extreme cases, obstructive uropathy or vascular compromise of the glans can occur, though these are uncommon.
In most cases, no laboratory or imaging workup is necessary. If severe stenosis causes suspected obstructive uropathy, evaluation of kidney function with BUN and creatinine and renal ultrasonography should be performed. When phimosis occurs secondary to recurrent balanoposthitis, screening for diabetes mellitus with urinalysis, serum glucose, or hemoglobin A1C is appropriate.
The main differential diagnosis is physiologic preputial adhesions in young children, which are normal and do not require intervention. Balanoposthitis without true phimosis should also be considered.
Pre-hospital personnel and caregivers should not attempt to retract the foreskin before medical evaluation, as this may worsen scarring or precipitate the more urgent condition of paraphimosis. Most patients require no immediate stabilization.
If obstructive uropathy is present, bladder decompression with urethral catheterization or suprapubic aspiration may be required. If vascular compromise of the glans occurs, an urgent dorsal slit procedure is necessary after adequate anesthesia, although this situation is rare in phimosis. Topical corticosteroids are often effective and represent first-line therapy. Betamethasone dipropionate 0.05–0.1% applied to the preputial orifice twice daily for 4–6 weeks has a high success rate in reducing phimosis. In pediatric patients requiring foreskin incision, procedural sedation is typically preferred over penile block.
Admission is indicated for obstructive uropathy or severe balanoposthitis with ischemia or necrosis. Patients who can void normally and have reliable urologic follow-up may be discharged. Referral to urology is recommended for evaluation of response to steroid therapy, possible dilation, operative repair, or elective circumcision if needed.
Physiologic phimosis should be managed with reassurance, age-appropriate expectations, and proper hygiene. Forced retraction should be avoided in children, especially between ages 3 and 17, when nonretractability may still be normal. Any signs of vascular compromise of the glans require urgent intervention to prevent necrosis.
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Emergency And Acute Medicine – Pityriasis Rosea
Pityriasis rosea is a self-limited inflammatory skin eruption of unknown origin that primarily affects children and young adults. The condition often begins with a single lesion known as a herald patch, which is an ovoid, erythematous, slightly raised plaque usually located on the trunk or proximal extremities. Within 7–14 days, a secondary eruption develops, consisting of multiple smaller, salmon-colored, elliptic papules with fine scaling. These lesions typically align along Langer lines on the trunk in a symmetric “Christmas tree” distribution. Nearly 80% of cases resolve spontaneously within 1–2 months.
The exact cause is unknown, although weak evidence suggests a viral association, particularly with human herpesvirus types 6 and 7. Several medications have been linked to pityriasis-like eruptions, including barbiturates, captopril, clonidine, gold, isotretinoin, metronidazole, bismuth, interferon, imatinib (Gleevec), and the hepatitis B vaccine. There are weak associations with eczema, asthma, and underlying malignancies.
Many patients report mild prodromal symptoms in the days preceding the rash, including malaise, gastrointestinal upset, or upper respiratory symptoms. On examination, the herald patch is typically 2–10 cm in diameter and seen in 50–90% of cases. The secondary eruption follows, appearing symmetrically along cleavage lines, predominantly on the trunk and proximal extremities. Pruritus is common and may vary in severity. Inverse pityriasis rosea, characterized by lesions on the face and distal extremities with minimal trunk involvement, is more frequently observed in children. Rare pediatric cases may include oral lesions such as punctate hemorrhages or ulcerations.
Diagnosis is clinical and based on characteristic history and physical findings. No routine laboratory testing is required. However, when the herald patch is absent or the presentation is atypical, alternative diagnoses must be considered. Secondary syphilis can mimic the rash and should prompt testing with a rapid plasma reagin (RPR) in patients with risk factors. A potassium hydroxide (KOH) preparation may help distinguish tinea corporis or tinea versicolor.
The differential diagnosis for the herald patch includes nummular eczema and tinea corporis. The secondary eruption may resemble secondary syphilis, drug eruption, guttate psoriasis, lichen planus, seborrheic dermatitis, scabies, dermatomyositis, cutaneous lymphoma, lupus, Kaposi sarcoma, or occult malignancy. Toxic appearance or mucous membrane involvement should prompt reconsideration of the diagnosis.
No stabilization is required in the emergency setting. Pityriasis rosea is self-limiting, and treatment is directed toward symptomatic relief, particularly for pruritus. Topical corticosteroids such as hydrocortisone 1% cream applied three times daily and oral antihistamines such as diphenhydramine may provide relief. In more severe cases, short courses of oral prednisone may be used. Erythromycin has also been reported to reduce symptom duration in some patients.
Hospital admission is not required. Patients with a clear diagnosis may be discharged with reassurance that the condition is benign and typically resolves within 1–2 months. Dermatology referral may be considered for severe, persistent, or atypical cases, especially if pruritus is refractory.
Pityriasis rosea most commonly affects the trunk and proximal extremities. Involvement of mucous membranes, distal extremities, or a toxic clinical appearance should prompt evaluation for alternative diagnoses.
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Emergency And Acute Medicine – Placental Abruption
Placental abruption is hemorrhage at the decidual–placental interface resulting in partial or complete separation of a normally implanted placenta before delivery of the fetus. It occurs in approximately 1% of all pregnancies and accounts for about 30% of bleeding episodes in the second half of pregnancy. It is responsible for 15% of fetal deaths, with neonatal mortality rates of 10–30%, and contributes to approximately 6% of maternal mortality. It is also referred to as abruptio placentae or accidental hemorrhage.
The primary cause is unknown, but the underlying process involves vascular injury with bleeding into the decidua basalis or mechanical shearing between the placenta and uterus, leading to clot formation and placental separation. Severe cases may result in disseminated intravascular coagulation (DIC) and significant maternal–fetal compromise. Many abruptions are thought to arise from chronic inflammatory or ischemic placental disease. Acute abruption may occur following trauma, rapid uterine decompression, or implantation over a uterine anomaly or fibroid.
Risk factors include prior abruption (10–20% recurrence risk), maternal hypertension and preeclampsia, advanced maternal age, increased parity, multiple gestation, uterine fibroids, tobacco use, cocaine abuse, trauma, premature rupture of membranes, oligohydramnios, polyhydramnios with rapid decompression, rapid delivery of the first twin, elevated second-trimester maternal serum alpha-fetoprotein, and thrombophilias. It is more common among African American and Caucasian women, with incidence increasing more rapidly among African American women.
Patients typically present after 20 weeks’ gestation with vaginal bleeding, which is painful in more than 80% of cases. However, bleeding may be absent in 20–25% due to concealed hemorrhage. Abdominal or back pain, uterine tenderness, frequent contractions, uterine tetany, nausea, vomiting, and unexplained preterm labor may occur. A history of trauma or cocaine use should be sought. On examination, uterine tenderness is common, and signs of hypotensive shock may appear late. Fetal distress may manifest as decreased fetal movement, bradycardia, or nonreassuring fetal heart rate tracings. Signs of DIC such as petechiae or bleeding from IV sites may be present. A sterile vaginal examination must be performed cautiously, particularly if placenta previa has not been excluded.
Diagnosis is primarily clinical. Immediate evaluation includes large-bore IV access, blood type and cross-match, rapid hemoglobin assessment, and continuous fetal and uterine monitoring. Laboratory studies include CBC, PT/PTT, fibrinogen level, and fibrin split products. Fibrinogen levels below 200 mg/dL and platelets below 100,000/μL strongly suggest abruption with coagulopathy. Kleihauer–Betke testing is indicated in Rh-negative patients. Ultrasound identifies abruption in only about 50% of cases, and a negative study does not exclude the diagnosis. MRI is sensitive but not practical in acute settings. CT performed for trauma evaluation may incidentally reveal abruption.
The differential diagnosis includes placenta previa, uterine rupture, preterm labor, vaginal or cervical lacerations, ovarian torsion, pyelonephritis, cholecystitis, appendicitis, and other intra-abdominal trauma.
Prehospital management includes transport in the left lateral recumbent position with full resuscitative measures if shock is suspected. Initial stabilization focuses on airway, breathing, and circulation with oxygen, cardiac monitoring, large-bore IV access, and aggressive crystalloid resuscitation. In the emergency department, continuous maternal cardiac and fetal monitoring is required. Blood products including packed red blood cells, fresh frozen plasma, cryoprecipitate, and platelets should be administered as indicated, often via a massive transfusion protocol. Immediate obstetric consultation is mandatory. Foley catheter placement allows close urine output monitoring. Tocolysis is generally contraindicated. In trauma-associated abruption, maternal stabilization takes priority.
Rh-immunoglobulin (300 μg IM at ≥12 weeks’ gestation) should be administered to Rh-negative patients, with dosing adjusted based on Kleihauer–Betke results. Corticosteroids for fetal lung maturity between 24 and 34 weeks and magnesium sulfate may be considered in consultation with obstetrics.
All confirmed or suspected cases require admission for maternal and fetal monitoring. ICU care is indicated for DIC, amniotic fluid embolism, or severe hemorrhage. Stable trauma patients without evidence of abruption after 4–6 hours of normal monitoring may be discharged in consultation with obstetrics, with instructions for pelvic rest and close follow-up.
Placental abruption remains a clinical diagnosis, as no single test reliably confirms or excludes it. Hypotension is often a late finding in pregnant patients with hypovolemia. Early anticipation of consumptive coagulopathy and prompt blood product administration are critical. Severe preeclampsia may mask hypovolemia, resulting in a normotensive but critically ill patient, and should be considered in any severe or unexplained abruption.
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Emergency And Acute Medicine – Placenta Previa
Placenta previa is defined as placental tissue overlying or positioned close to the internal cervical os. As the uterus enlarges and the cervix begins to dilate, placental vessels near the cervix may tear, resulting in vaginal bleeding. More than 90% of placenta previa diagnosed before 20 weeks’ gestation will resolve as the placenta “migrates” upward with uterine growth. However, if the placenta overlaps the internal os by more than 20 mm, previa is highly likely to persist at delivery. Greater degrees of overlap (15–23 mm or more) strongly predict persistence at term. Placenta previa accounts for approximately 20% of antepartum hemorrhage cases.
Placenta previa is classified into four types: complete (placenta completely covers the cervical os), partial (partially covers the os), marginal (placental edge reaches the margin of the os), and low-lying placenta (placental edge lies within 2 cm of the os). The overall incidence at term is approximately 0.4% of pregnancies. Maternal mortality is low (around 0.03%), but perinatal morbidity and mortality are increased—largely due to preterm delivery.
The exact etiology is unknown. Factors affecting implantation location include prior uterine curettage, abnormal endometrial vascularization, and delayed ovulation. Risk factors include multiparity (especially grand multiparity), multiple gestation, prior cesarean section (risk increases with number of previous C-sections), advanced maternal age, prior placenta previa, smoking, assisted reproduction, Asian maternal race, high-altitude residence, male fetus, and elevated maternal serum alpha-fetoprotein. Placenta previa is also associated with congenital anomalies, abnormal fetal presentation, preterm premature rupture of membranes, and amniotic fluid embolism. Placenta accreta spectrum disorders (accreta, increta, percreta) occur in 5–10% of patients with previa and may require cesarean hysterectomy due to severe bleeding.
The hallmark presentation is painless bright red vaginal bleeding after 20 weeks’ gestation. Seventy percent of patients present with painless bleeding, while about 20% may have associated uterine contractions. The first bleeding episode typically occurs between 27 and 32 weeks. Bleeding may range from minor spotting to massive hemorrhage, and recurrence is common. The severity or number of bleeding episodes does not necessarily correlate with the degree of placental coverage. Intercourse or heavy exercise may precipitate bleeding, though often there is no clear inciting event.
On examination, digital vaginal examination must never be performed in second- or third-trimester bleeding until placenta previa has been excluded by ultrasound, as this may precipitate severe hemorrhage. A sterile speculum exam is safe and may help identify whether bleeding originates from the cervical os, vagina, or another lesion. Signs of significant bleeding include blood pooling at the patient’s feet and vital sign instability such as tachycardia or hypotension. Continuous fetal heart rate monitoring is essential.
Diagnosis is made primarily by ultrasound. Transabdominal ultrasound is 93–98% accurate but may have false negatives (e.g., obesity, posterior placenta) and false positives (e.g., overdistended bladder). If placenta previa is suspected or findings are uncertain, transvaginal ultrasound should be performed, as it is essentially 100% accurate and does not increase bleeding risk. Color Doppler ultrasound may help identify placenta accreta. MRI can assist in evaluating invasive placental disorders.
Laboratory evaluation includes CBC, platelets, type and screen (or cross-match if transfusion anticipated), and Rh status. Kleihauer–Betke testing is performed in Rh-negative patients to detect fetomaternal hemorrhage. Coagulation studies are obtained if coagulopathy is suspected.
Prehospital management involves transport to a facility capable of managing high-risk or preterm deliveries. If hypotensive, the patient should be positioned in the left lateral recumbent position. Oxygen and IV access should be established. Initial stabilization includes airway, breathing, and circulation assessment, two large-bore IV lines, crystalloid resuscitation, and blood transfusion as needed. Blood transfusion is indicated for significant hypotension or hematocrit less than 30%. Fresh frozen plasma may be required for coagulopathy. Continuous fetal monitoring and immediate obstetric consultation are mandatory for symptomatic patients.
In the emergency department, patients with active bleeding require emergent obstetric consultation. Maintain NPO status and bed rest until obstetrics determines stability. Rh-negative patients should receive Rho(D) immune globulin (300 μg IM), with additional dosing guided by Kleihauer–Betke results. Magnesium sulfate may be used for preterm contractions when delivery is not indicated. Antenatal corticosteroids (e.g., betamethasone 12 mg IM every 24 hours for two doses) are recommended between 24 and 34 weeks to promote fetal lung maturity. Emergency cesarean delivery is indicated for ongoing hemorrhage or fetal compromise.
All patients with active bleeding from placenta previa should be admitted, as this condition constitutes a potential obstetric emergency. Selected stable patients whose bleeding has resolved may be managed outpatient in consultation with obstetrics. Asymptomatic patients with incidental findings may not require admission but should follow strict instructions, including pelvic rest and prompt reporting of any bleeding or contractions. If the placenta overlies the os by more than 20 mm, cesarean delivery is typically planned at 36–37 weeks.
Painless vaginal bleeding after 20 weeks’ gestation should be considered placenta previa until proven otherwise, whereas painful vaginal bleeding suggests placental abruption. Importantly, both conditions can coexist. Digital vaginal examination must be avoided until previa is excluded, while sterile speculum examination and transvaginal ultrasound are safe and appropriate diagnostic tools.
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Emergency And Acute Medicine – Pneumonia in Pediatric Patients
Pneumonia in children is an infection of the lung parenchyma most commonly resulting from oropharyngeal aspiration, although hematogenous spread may occur. The radiographic distribution often depends on the organism involved: interstitial patterns are typically seen with viral infections and Mycoplasma pneumoniae, lobar consolidation with Streptococcus pneumoniae, abscess formation with Staphylococcus aureus, and diffuse disease with Pneumocystis jirovecii. Clinical presentation and likely pathogens vary significantly with age.
In neonates younger than 2 weeks, common pathogens include group B Streptococcus, enteric gram-negative organisms, respiratory syncytial virus (RSV), herpes simplex virus, and S. aureus. Between 2 weeks and 3 months, pathogens include Chlamydia trachomatis, parainfluenza virus, RSV, S. pneumoniae, S. aureus, Haemophilus influenzae, and Bordetella pertussis. From 3 months to 8 years, viral etiologies predominate (RSV, parainfluenza, influenza, adenovirus), along with S. pneumoniae, H. influenzae in unimmunized children, group A streptococcus, S. aureus, and B. pertussis. In children older than 8 years, Mycoplasma pneumoniae is most common, followed by viral pathogens and S. pneumoniae. Recent immigrants may be at risk for Mycobacterium tuberculosis. Immunocompromised children are susceptible to organisms such as Pneumocystis jirovecii, Mycobacterium avium complex, M. tuberculosis, Klebsiella pneumoniae, and Pseudomonas aeruginosa. Less common causes include fungal infections and rickettsial organisms.
Common symptoms across all pediatric age groups include cough, fever, tachypnea, tachycardia, hypoxia, rales, and signs of respiratory distress such as retractions or grunting. A maculopapular rash may occur in up to 10% of cases. Infants younger than 6 months may present atypically with irritability, lethargy, apnea (especially RSV in premature infants), cyanosis, poor feeding, temperature instability, vomiting with coughing, nasal congestion, nasal flaring, or wheezing. A staccato cough in infants suggests Chlamydia trachomatis. Older children, particularly those over 5 years, are more likely to report pleuritic chest pain, productive cough, rigors, and chills. A thorough history should include immunization status, immune function, exposures, and progression of symptoms.
Pulse oximetry is essential in all suspected cases. Chest radiography remains the gold standard for diagnosis and should be obtained in children with signs of lower respiratory tract infection and in those younger than 36 months with marked leukocytosis (WBC >15,000 or absolute neutrophil count >9,000). Viral and Mycoplasma infections often produce interstitial, perihilar, or peribronchial infiltrates, whereas bacterial infections may demonstrate focal lobar consolidation, alveolar infiltrates, pleural effusion, or pneumatocele. Round pneumonia is considered pathognomonic for S. pneumoniae. Lateral decubitus films can help identify pleural effusions.
Laboratory studies may include a complete blood count, although sensitivity and specificity are limited. Marked leukocytosis (WBC ≥20,000 or ANC >9,000) increases the risk of pneumococcal bacteremia. Bordetella pertussis typically presents with leukocytosis and lymphocytosis. Blood cultures are recommended in children younger than 36 months and in toxic-appearing or hospitalized patients, though yield is low. Arterial blood gas analysis may be necessary in critically ill patients to assess respiratory insufficiency. Electrolytes should be checked in hypotensive children or when syndrome of inappropriate antidiuretic hormone secretion is suspected. Sputum cultures may be obtained in older children, and nasopharyngeal testing can identify RSV, C. trachomatis, and B. pertussis.
Initial management focuses on airway, breathing, and circulation. Children with moderate to severe illness may require aggressive airway management and intubation. High-flow oxygen should be administered for hypoxia. Intravenous fluid resuscitation with 0.9% normal saline (20 mL/kg bolus) is indicated for hypovolemia or shock. Bedside glucose should be checked in severely ill infants and toddlers, with prompt treatment of hypoglycemia. Ongoing monitoring with pulse oximetry is essential.
Empiric antibiotic therapy depends on age and clinical severity. Most well-appearing children aged 6 months and older can be treated as outpatients with oral antibiotics. For children aged 3 months to 5 years, amoxicillin is first-line therapy, with alternatives including amoxicillin–clavulanate or macrolides when atypical pathogens are suspected. For children aged 5 to 18 years, macrolides such as azithromycin or clarithromycin are commonly used for suspected Mycoplasma pneumoniae. Neonates requiring hospitalization should receive ampicillin plus cefotaxime or gentamicin, with azithromycin added if Chlamydia trachomatis or Bordetella pertussis is suspected. Infants 1–2 months old should receive ampicillin plus cefotaxime. Children older than 3 months requiring admission may receive cefotaxime, cefuroxime, or ceftriaxone, with vancomycin added for suspected penicillin-resistant S. pneumoniae, macrolides for atypical pathogens, and clindamycin for suspected group A streptococcal infection. Bronchodilators such as albuterol may be beneficial in children with concurrent reactive airway disease. Thoracentesis is indicated for significant pleural effusion.
Admission is warranted for toxic appearance, respiratory distress or failure, dehydration, apnea, infants younger than 2 months, infants younger than 6 months with lobar pneumonia, hypoxia (oxygen saturation <92% on room air at sea level), pleural effusion, poor outpatient response, immunocompromised status, or concerns about caregiver reliability. most mild cases can be discharged if there is no hypoxia, significant work of breathing, dehydration, vomiting, compliance concern, with follow-up ensured within 1–2 days.< />pan>
Early recognition and aggressive airway management are critical in children with severe sepsis or septic shock. Delays in antibiotic therapy should be avoided. Knowledge of local antimicrobial resistance patterns is essential to guide empiric therapy. Clear discharge instructions, reliable follow-up, and caregiver education are vital to ensure safe outpatient management.
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Emergency And Acute Medicine – Poisoning
Poisoning may be intentional or unintentional. Any patient presenting with an unexplained change in mental status should be evaluated for possible intoxication or overdose. Intentional poisoning may be related to depression, suicide attempts, homicide, or recreational drug abuse. Unintentional poisoning commonly occurs in children and may result from accidental ingestion, therapeutic errors such as double dosing, or recreational experimentation. In pediatric patients, most accidental ingestions occur in children aged 1–5 years. A history that is inconsistent or suspicious should raise concern for possible child abuse.
Clinical presentation varies depending on the substance involved. Neurologic findings may include lethargy, agitation, coma, hallucinations, or seizures. Respiratory effects may range from tachypnea to bradypnea or apnea, with possible inability to protect the airway. Cardiovascular manifestations include dysrhythmias and conduction abnormalities. Vital sign abnormalities may include hyperthermia or hypothermia, tachycardia or bradycardia, and hypertension or hypotension.
Recognition of toxidromes can guide management. Anticholinergic toxicity presents with altered mental status, dry skin and mucous membranes, fixed dilated pupils, tachycardia, hyperthermia, flushing, and urinary retention. Cholinergic toxicity presents with excessive secretions including salivation, lacrimation, urination, diaphoresis, miosis, bronchospasm, and wheezing. Opiate toxicity is characterized by central nervous system and respiratory depression with miosis. Sympathomimetic toxicity presents with CNS excitation, seizures, tachycardia, hypertension, and diaphoresis.
Initial evaluation requires complete vital signs including core temperature and a thorough physical examination, paying attention to pupils, skin findings, and unusual odors. Laboratory testing typically includes electrolytes, BUN, creatinine, and glucose. Calculation of the anion gap (normal 8–12) is essential when metabolic acidosis is suspected. Elevated anion gap metabolic acidosis can be remembered using the mnemonic “A CAT MUD PILES,” which includes causes such as alcoholic ketoacidosis, cyanide, carbon monoxide, salicylates, methanol, uremia, diabetic ketoacidosis, iron, lactic acidosis, and ethylene glycol. Serum osmol gap should be calculated when toxic alcohol ingestion is suspected. The calculated osmolality is 2(Na⁺) + glucose/18 + BUN/2.8 + ethanol/4.6 (if ethanol in mg/dL). An osmol gap greater than 10 suggests substances remembered by the mnemonic “ME DIE A”: methanol, ethanol, diuretics (mannitol, glycerin, sorbitol), isopropyl alcohol, ethylene glycol, and acetone. A normal osmol gap does not completely exclude toxic alcohol ingestion. Additional testing may include pregnancy testing, acetaminophen level in suicidal ingestions, toxicology screening, ECG for conduction abnormalities or QRS/QT prolongation, head CT for unexplained altered mental status, and chest radiograph if aspiration is suspected.
The differential diagnosis for altered mental status includes intracranial mass or hemorrhage, infection or sepsis, endocrine abnormalities, hypothermia, hypoxia, metabolic disturbances, and psychogenic causes. These must always be considered alongside toxicologic causes.
Pre-hospital management includes searching the scene for clues such as pill bottles or drug paraphernalia and transporting all medications for identification. Uncooperative patients may require restraint for safety. Comorbid trauma, medical illness, or environmental exposures should be considered. Activated charcoal may be administered pre-hospital in selected cases if transport time is prolonged.
Initial stabilization in the emergency department follows standard ABC principles. Endotracheal intubation is performed as needed for airway protection, oxygenation, and ventilation. Supplemental oxygen, pulse oximetry, cardiac monitoring, and IV access are established. Hypotension is treated with intravenous 0.9% normal saline boluses and vasopressors if persistent. Bradycardia may require atropine or pacing. In patients with altered mental status, administration of thiamine, dextrose (after checking glucose), and naloxone is appropriate.
Decontamination strategies depend on the timing and substance ingested. Orogastric lavage may be considered within one hour of potentially lethal ingestion without a known antidote, provided the airway is protected. Activated charcoal is most effective within a few hours of ingestion and is contraindicated in caustic ingestions, unprotected airways, or bowel obstruction. Charcoal does not effectively bind metals (iron, lithium), alcohols, or potassium. Whole-bowel irrigation with polyethylene glycol solution may be used for sustained-release preparations, iron or lithium ingestion, and body packers, but is contraindicated in bowel obstruction, perforation, or hypotension.
Enhanced elimination techniques include multiple-dose activated charcoal for drugs such as theophylline, carbamazepine, and phenobarbital. Urinary alkalinization is used for salicylates and phenobarbital. Hemodialysis is indicated for lithium, salicylates, theophylline, toxic alcohols, and valproate in selected cases. Seizures are treated initially with benzodiazepines such as diazepam or lorazepam. Persistent seizures may require phenobarbital. Phenytoin is generally not effective for toxicologic seizures unless related to epilepsy or status epilepticus of other etiology.
Specific antidotes are used when appropriate. Examples include N-acetylcysteine for acetaminophen toxicity, physostigmine for severe anticholinergic toxicity, flumazenil for selected benzodiazepine overdoses, glucagon for β-blocker toxicity, calcium and insulin for calcium-channel blocker overdose, oxygen or hyperbaric oxygen for carbon monoxide, vitamin K for warfarin toxicity, hydroxocobalamin or cyanide antidote kit for cyanide, digoxin-specific antibody fragments for digoxin toxicity, fomepizole or ethanol for methanol and ethylene glycol, deferoxamine for iron, pyridoxine for isoniazid, methylene blue for methemoglobinemia, naloxone for opioid toxicity, atropine and pralidoxime for organophosphates, and sodium bicarbonate for tricyclic antidepressant toxicity.
Admission is required for patients with altered mental status, cardiopulmonary instability, suicidal intent, significant laboratory abnormalities, or risk of delayed decompensation. Discharge may be considered for patients who are psychiatrically cleared, detoxified, hemodynamically stable, and medically safe. Accidental poisonings require prevention counseling, while intentional poisonings require psychiatric evaluation. Substance abuse referral should be considered when appropriate. In pregnancy, treatment of the mother is generally the best treatment for the fetus.
Clinicians must avoid overlooking non-toxicologic causes of altered mental status and should not rely solely on urine drug screens, as these test for a limited number of substances and may produce false-positive or false-negative results.
