​Emergency and Acute Medicine – Wolff–Parkinson–White (WPW) Syndrome


Wolff–Parkinson–White syndrome (WPW) is a cardiac conduction disorder caused by the presence of an accessory pathway (Kent bundle) that bypasses the atrioventricular (AV) node, allowing premature ventricular activation (pre-excitation). On ECG, the WPW pattern is characterized by a short PR interval (<0.12 sec), a delta (Δ) wave representing early ventricular depolarization, and a widened QRS complex (>0.10 sec). While the ECG pattern alone is termed WPW pattern, the diagnosis of WPW syndrome requires both these findings and associated tachydysrhythmias.


Accessory pathways occur in approximately 0.1–0.3% of the population and are most commonly located along the left lateral free wall, followed by the posteroseptal region. Conduction through these pathways may occur in antegrade, retrograde, or bidirectional fashion. The most common arrhythmia associated with WPW is orthodromic atrioventricular re-entrant tachycardia (AVRT) (≈70%), where impulses travel down the AV node and return via the accessory pathway, producing a narrow complex tachycardia. Less commonly, antidromic AVRT (≈30%) occurs, with conduction down the accessory pathway and back through the AV node, resulting in a wide complex tachycardia. WPW can also precipitate atrial fibrillation with rapid ventricular response, which carries a risk of degeneration into ventricular fibrillation and sudden death.


Patients may be asymptomatic or present with palpitations, chest pain, dyspnea, dizziness, diaphoresis, or syncope. Physical findings depend on the rhythm and hemodynamic status, ranging from stable tachycardia to signs of instability such as hypotension, altered mental status, cyanosis, or pulmonary edema. Sudden cardiac death is rare but can occur (approximately 1 per 1,000 patient-years).


Diagnosis is based primarily on ECG findings. During sinus rhythm, the classic triad includes short PR interval, delta wave, and widened QRS complex. During tachyarrhythmias, ECG patterns vary depending on the mechanism: orthodromic AVRT typically produces a narrow complex tachycardia (150–250 bpm), while antidromic AVRT produces a wide complex tachycardia. Atrial fibrillation in WPW appears as an irregular wide complex rhythm with variable QRS morphology, which is a dangerous presentation.


Management depends on patient stability and rhythm type. Unstable patients (hypotension, chest pain, altered mental status) require immediate synchronized cardioversion, starting at 100 J and escalating as needed. In stable patients, initial management includes vagal maneuvers such as the Valsalva maneuver or carotid sinus massage (if no contraindications).


For narrow complex tachycardia (orthodromic AVRT), pharmacologic therapy includes Adenosine (6 mg rapid IV bolus, followed by 12 mg if needed; pediatric: 0.1–0.2 mg/kg) or calcium channel blockers when the diagnosis is certain. For wide complex tachycardia or suspected WPW with atrial fibrillation, Amiodarone (150 mg IV over 10 minutes, followed by infusion) or Procainamide (6–13 mg/kg IV infusion) are preferred.


Critically important: AV nodal–blocking agents such as β-blockers, calcium channel blockers, digoxin, and lidocaine must be avoided in patients with WPW and wide complex tachycardia or atrial fibrillation, as they may enhance conduction through the accessory pathway and precipitate fatal ventricular arrhythmias.


Disposition depends on clinical presentation. Patients with instability, syncope, or refractory arrhythmias require admission and monitoring. Most stable patients who convert to sinus rhythm can be discharged with cardiology follow-up, including consideration of electrophysiologic studies and radiofrequency ablation, which offers definitive treatment.


Key clinical pearls include maintaining a high suspicion for WPW in any tachydysrhythmia, avoiding AV nodal blockers in uncertain wide complex rhythms, and addressing anticoagulation if arrhythmia duration exceeds 48 hours due to embolic risk.

Emergency and Acute Medicine – Drug Withdrawal




Drug Withdrawal refers to the constellation of symptoms that occur when a substance that has been used chronically is abruptly reduced or discontinued. The hallmark of many withdrawal syndromes—particularly those involving benzodiazepines, barbiturates, and opioids—is neuroexcitation, resulting from adaptive changes in the central nervous system. While withdrawal from sedative-hypnotics such as benzodiazepines and barbiturates can be life-threatening, opioid withdrawal is typically not fatal but can be extremely uncomfortable. Withdrawal from stimulants such as cocaine and amphetamines is also generally not life-threatening but can cause significant psychological distress.


The pathophysiology involves neuroadaptation to chronic drug exposure. With prolonged use, the body adjusts to the presence of the substance, leading to tolerance, where increasing doses are needed to achieve the same effect. When the drug is removed, these adaptations persist, resulting in withdrawal symptoms. It is important to distinguish tolerance from withdrawal, as they are related but separate phenomena.


Clinical features vary depending on the substance. Benzodiazepine and barbiturate withdrawal presents with anxiety, agitation, tremor, insomnia, tachycardia, hypertension, hyperthermia, and autonomic instability, with the potential for seizures and life-threatening complications. Opioid withdrawal is characterized by restlessness, irritability, drug craving, yawning, piloerection (“goosebumps”), mydriasis, nausea, vomiting, diarrhea, abdominal pain, tachycardia, and hypertension. Cocaine withdrawal typically manifests with depressed mood, fatigue, vivid dreams, sleep disturbances, and psychomotor changes, while amphetamine withdrawal presents with fatigue, irritability, anxiety, and sleep disturbances.


Diagnosis is primarily clinical and relies on a detailed substance use history, including the type of drug, time of last use, and any previous withdrawal episodes. Physical examination focuses on vital signs and signs of autonomic instability. Laboratory testing (electrolytes, renal function, glucose, CBC) may be helpful to identify complications or alternative diagnoses, although urine drug screening rarely changes acute management. Imaging is reserved for cases where the diagnosis is unclear or other pathology is suspected.


Management begins with initial stabilization, including airway, breathing, and circulation, IV access, fluid resuscitation, and monitoring. Treatment is then tailored to the specific withdrawal syndrome. For benzodiazepine or barbiturate withdrawal, aggressive supportive care and substitution with a long-acting agent of the same class are recommended, using medications such as Diazepam (5–10 mg IV repeated as needed; 5–20 mg PO for mild symptoms) or Lorazepam (1–2 mg PO or 2 mg IV repeated as needed). Severe cases or seizures may require Phenobarbital (15–20 mg/kg IV).


In opioid withdrawal, treatment is largely supportive. Symptom control includes antiemetics such as Ondansetron (4–8 mg PO/IV) and autonomic symptom relief with Clonidine (0.1–0.3 mg PO every 4–6 hours). Opioid replacement therapy may be considered in certain cases, especially when withdrawal complicates other medical conditions. For cocaine and amphetamine withdrawal, management is supportive, focusing on rest, hydration, and monitoring for psychiatric symptoms.


Disposition depends on severity and associated risks. Patients with moderate-to-severe symptoms, persistent withdrawal, psychosis, autonomic instability, or significant comorbid conditions require admission. Those with mild symptoms who respond to therapy and are psychiatrically stable may be discharged with appropriate follow-up. Referral to a detoxification or rehabilitation program is essential for long-term management.


A key clinical pearl is to avoid misdiagnosing other serious medical conditions as withdrawal, as infections, metabolic disturbances, or intracranial pathology may mimic withdrawal syndromes. Additionally, clinicians should ensure adequate dosing of benzodiazepines in sedative withdrawal, as under-treatment can lead to severe complications, including seizures.

​

Emergency and Acute Medicine – Alcohol Withdrawal




Alcohol Withdrawal is the most common withdrawal syndrome encountered in the emergency department and represents a spectrum of neuroexcitatory symptoms that occur after cessation or reduction of chronic alcohol use. The underlying mechanism involves neuroadaptation: chronic alcohol exposure enhances inhibitory GABA activity and suppresses excitatory NMDA receptors. When alcohol intake stops, this balance shifts toward excess excitation, leading to autonomic hyperactivity and neurologic symptoms. Repeated withdrawal episodes may worsen severity through a process known as kindling, increasing the risk of life-threatening complications.


Alcohol withdrawal progresses through a predictable timeline with four major clinical stages. Early withdrawal begins within 6–8 hours after the last drink and lasts 1–2 days, presenting with tremulousness, anxiety, palpitations, nausea, and anorexia. Withdrawal seizures typically occur between 6–48 hours and are usually brief, generalized seizures. Alcoholic hallucinosis develops within 12–48 hours and is characterized by visual (most common), tactile, or auditory hallucinations, often with a relatively clear sensorium. The most severe form, delirium tremens (DTs), occurs 48–96 hours after cessation and may last up to 5 days, presenting with tachycardia, hypertension, diaphoresis, agitation, and delirium. DTs occur in approximately 5% of patients but carry a high mortality rate of 5–15%.


Diagnosis is primarily clinical, based on history and physical examination. Key historical features include the time of last alcohol intake, history of prior withdrawal episodes, and severity of previous symptoms. Physical examination should focus on vital signs and signs of autonomic instability. Laboratory evaluation typically includes electrolytes, renal function, glucose, magnesium, CBC, and blood alcohol level, as well as screening for coexisting conditions such as infection. Imaging such as CT of the head is reserved for patients with altered mental status or unclear diagnosis.


Management begins with initial stabilization, including airway, breathing, and circulation, IV access, fluid resuscitation, and continuous monitoring. The cornerstone of treatment is benzodiazepines, which act by enhancing GABA activity and reducing CNS hyperexcitability. Commonly used agents include Diazepam (5–10 mg IV, repeat as needed; 5–20 mg PO for mild symptoms) and Lorazepam (2 mg IV or PO every 2–4 hours as needed). High or repeated dosing is often required to adequately control symptoms.


In severe or refractory cases, adjunctive therapies such as Phenobarbital (15–20 mg/kg IV for severe symptoms or status epilepticus) or Propofol (25–75 μg/kg/min infusion) may be used, particularly in ICU settings. Supportive care includes correction of electrolyte abnormalities and monitoring for complications such as arrhythmias or aspiration.


Disposition depends on severity. Patients with moderate-to-severe withdrawal, persistent symptoms, delirium tremens, or significant comorbidities require hospital admission, often to a monitored or intensive care setting. Patients with mild symptoms that respond well to therapy may be discharged with close follow-up and referral to a detoxification program.


A key clinical pearl is to avoid under-treatment with benzodiazepines, as inadequate dosing can lead to progression to severe withdrawal or DTs. Additionally, clinicians must remain vigilant for alternative diagnoses, as medical conditions such as infection, hypoglycemia, or intracranial pathology may mimic or coexist with alcohol withdrawal.

​

Emergency and Acute Medicine – Wheezing




Wheezing is a high-pitched, musical sound produced by turbulent airflow through narrowed airways, typically with a dominant frequency around 400 Hz. It occurs when airflow causes vibration of bronchial walls, similar to a reed instrument. Wheezing is most prominent when airway diameters are between 2–5 mm; larger airways produce lower-pitched sounds, while very small airways (<2 mm) may not transmit sound effectively due to energy loss. Airway narrowing may result from bronchoconstriction, inflammation, edema, or obstruction, and identifying the underlying mechanism is critical in acute care settings.


The causes of wheezing are broad and include both small-airway (pulmonary) and large-airway etiologies. Small-airway causes commonly include Asthma, Chronic Obstructive Pulmonary Disease, pulmonary edema, anaphylaxis, and aspiration. Certain drugs such as ACE inhibitors, β-blockers, aspirin, and NSAIDs may precipitate bronchospasm or allergic reactions. Less common causes include pulmonary embolism, carcinoid tumors, and occupational lung diseases like byssinosis. Large-airway causes include foreign body aspiration, vocal cord dysfunction, epiglottitis, tumors, and smoke inhalation. In pediatric populations, common causes include Bronchiolitis, asthma, croup, and congenital airway abnormalities such as tracheomalacia.


Clinically, wheezing presents as a whistling sound during breathing, often accompanied by dyspnea, cough, chest tightness, and respiratory distress. Diffuse wheezing suggests generalized airway disease such as asthma or pulmonary edema, while focal wheezing raises concern for localized obstruction such as pneumonia or foreign body. Associated findings may include tachypnea, tachycardia, cyanosis, and use of accessory muscles. A critical aspect of assessment is the patient’s mental status—fatigue, confusion, or lethargy may indicate impending respiratory failure and necessitate urgent airway management.


Evaluation begins with assessment of severity and oxygenation. Pulse oximetry is essential for monitoring oxygen saturation, while peak expiratory flow (PEF) helps quantify airway obstruction and response to treatment. Chest X-ray may be used to evaluate for pneumonia, pulmonary edema, or foreign body. Arterial blood gas (ABG) may be useful in severe cases to assess for rising CO₂ and acidosis, indicating respiratory fatigue. Additional investigations such as ECG or laryngoscopy may be indicated depending on suspected etiology.


Management focuses on rapid stabilization and reversal of airway obstruction. Initial treatment includes supplemental oxygen and airway support. Bronchodilators are first-line therapy, particularly Albuterol given as 2.5–5 mg nebulized every 20 minutes for 3 doses (pediatric: 0.15 mg/kg per dose, minimum 2.5 mg). Systemic corticosteroids such as Prednisone (40–80 mg PO; pediatric 1 mg/kg/day, max 60 mg) or Methylprednisolone (40–80 mg IV) are used to reduce airway inflammation and prevent relapse.


For moderate to severe cases, Ipratropium Bromide (0.5 mg nebulized every 20 minutes for 3 doses) can be added to β-agonist therapy. Additional therapies include magnesium sulfate (0.1 mL/kg of 50% solution IV over 20 minutes) in severe asthma, terbutaline (0.25 mg SC), and heliox in selected cases. In pediatric croup, racemic epinephrine (0.25–0.5 mL nebulized) may be used. Intubation is indicated for patients with impending respiratory failure, and Ketamine may be preferred due to its bronchodilatory properties.


Disposition depends on clinical response. Patients with persistent hypoxia, worsening symptoms, or underlying serious conditions require admission. Those who improve with treatment, achieve PEF >70% predicted, and maintain adequate oxygenation may be discharged with follow-up and clear return precautions. Patients with asthma should receive an action plan and appropriate outpatient referral.


A key clinical pearl is to always consider non-asthma causes of wheezing, especially in cases of focal findings or poor response to bronchodilators. Additionally, clinicians must be prepared for rapid airway deterioration, particularly when administering sedatives or managing severe respiratory distress.

​

Infectious Disease and Microbiology: Infectious Mononucleosis




Infectious mononucleosis (IM), also known as glandular fever, is a common self-limiting clinical syndrome caused primarily by Epstein–Barr virus. It is characterized by acute onset of fever, sore throat, lymphadenopathy, and atypical lymphocytosis. EBV is transmitted mainly through saliva, which is why the illness is often called the “kissing disease.” After infection, the virus persists lifelong in the host.


IM is common worldwide. In industrialized countries, EBV infection often occurs either in early childhood, when it is usually asymptomatic, or in late adolescence, when it is more likely to cause symptomatic mononucleosis. By adulthood, 90–95% of people have evidence of prior EBV infection. Risk factors include close contact with an infected person and immunosuppression, especially in transplant recipients. In rare cases, certain inherited immune defects can lead to severe, even life-threatening EBV infection.


The pathophysiology begins when EBV infects the oropharyngeal epithelium and then B lymphocytes. The immune response, especially proliferation of cytotoxic CD8+ T lymphocytes, is responsible for much of the clinical syndrome. These activated lymphocytes appear as atypical lymphocytes on the blood smear. Although the immune response controls the primary infection, EBV remains latent for life.


Clinically, young children are often asymptomatic or have only mild illness. In adolescents and young adults, the disease usually begins with fatigue, malaise, and myalgias, followed by fever and sore throat. Common symptoms include fever, sore throat, malaise, headache, anorexia, myalgias, and sometimes abdominal pain, nausea, or vomiting. On examination, patients commonly have cervical lymphadenopathy, pharyngitis or tonsillitis, splenomegaly, and sometimes hepatomegaly. Less common findings include palatal petechiae, periorbital edema, rash, and jaundice. A maculopapular rash may occur, especially after exposure to ampicillin or amoxicillin.


Diagnosis is usually supported by laboratory findings. Atypical lymphocytosis and relative or absolute lymphocytosis are common. Mild thrombocytopenia and elevated liver enzymes may also be present. Heterophile antibody tests such as the Monospot are widely used and are fairly sensitive and specific in symptomatic patients, although they may be negative early in illness or in young children. EBV-specific serology, including viral capsid antigen and EBV nuclear antigen antibodies, can help confirm the diagnosis when needed. Ultrasound may be used to assess splenomegaly, especially in athletes.


Treatment is mainly supportive. Most patients only need rest, fluids, and symptom relief with acetaminophen or nonsteroidal anti-inflammatory drugs. Corticosteroids are reserved for severe complications such as impending airway obstruction, severe thrombocytopenia, hemolytic anemia, myocarditis, pericarditis, or neurologic complications. Patients should avoid contact sports and strenuous physical activity for at least 3–4 weeks, or longer if splenomegaly persists, because of the risk of splenic rupture. Beta-lactam antibiotics such as ampicillin and amoxicillin should be avoided unless clearly indicated for another reason.


The prognosis is generally excellent, and most cases resolve within 1–2 weeks. However, fatigue may persist for weeks or even months in some patients. Complications are uncommon but may include autoimmune hemolytic anemia, thrombocytopenia, airway obstruction, hepatitis, myocarditis, pericarditis, neurologic syndromes, pneumonia, splenic rupture, and lymphoproliferative disorders in susceptible individuals.

​

​Emergency and Acute Medicine: Von Willebrand Disease


Von Willebrand Disease is the most common inherited bleeding disorder and results from either a deficiency or dysfunction of von Willebrand factor, a key protein involved in hemostasis. vWF plays two major roles: it mediates platelet adhesion to the vascular endothelium and serves as a carrier protein for Factor VIII. The disease affects approximately 1–2% of the general population and is usually inherited, though acquired forms can occur.


There are three major types of vWD. Type 1, the most common (about 70%), is a quantitative deficiency of vWF and is typically inherited in an autosomal dominant pattern, with symptoms ranging from mild to moderate bleeding. Type 2 involves qualitative defects in vWF function and includes several subtypes (2A, 2B, 2M, 2N), with type 2N characterized by reduced binding to factor VIII, leading to more significant coagulopathy. Type 3 is rare, inherited in an autosomal recessive pattern, and represents a severe deficiency or absence of vWF, resulting in serious bleeding manifestations. In addition to genetic causes, acquired vWD may occur due to conditions such as malignancies, autoimmune diseases, hypothyroidism, or certain medications.


Clinical presentation varies widely depending on the type and severity of the disorder. Many patients with type 1 or mild type 2 disease may be asymptomatic, while those with more severe forms present with mucocutaneous bleeding, including easy bruising, recurrent epistaxis, gum bleeding, and menorrhagia. Gastrointestinal bleeding, prolonged bleeding after procedures, and postoperative hemorrhage may also occur. In more severe cases, such as type 3 disease, patients may develop deep tissue bleeding and hemarthroses, resembling hemophilia. A detailed history often reveals a family history of bleeding and recurrent minor bleeding episodes, especially in pediatric and adolescent populations.


Physical examination is often normal, although findings may include ecchymoses, hematomas, or joint swelling in more severe cases. Special considerations include pregnancy, during which vWF levels may increase temporarily, often leading to fewer bleeding complications; however, levels drop postpartum, increasing the risk of delayed bleeding. In children, clinicians must always consider nonaccidental trauma when unexplained bruising or bleeding is present.


Diagnosis relies on laboratory evaluation. Platelet counts and morphology are typically normal, and prothrombin time (PT) is usually normal. Partial thromboplastin time (PTT) may be mildly prolonged due to reduced factor VIII levels. Specific tests include measurement of vWF antigen and activity, particularly the ristocetin cofactor assay, which evaluates vWF function through platelet agglutination. Bleeding time may be prolonged in more severe types but is less commonly used כיום due to poor reproducibility.


Management focuses on controlling bleeding and correcting the underlying defect. Initial stabilization includes standard resuscitation measures with fluids and blood products as needed, along with direct pressure to bleeding sites. The cornerstone of therapy for mild to moderate disease is Desmopressin, which promotes the release of endogenous vWF and increases factor VIII levels. It is administered at 0.3 μg/kg IV or subcutaneously (maximum 20 μg), or 300 μg intranasally (150 μg if <50 kg), with peak effect occurring within 30–60 minutes and lasting 6–8 hours. It is most effective in type 1 disease, variably effective in type 2, and not useful in type 3.


For severe bleeding or type 3 disease, vWF replacement therapy is required, typically using Humate-P at doses of 20–40 units/kg IV. Antifibrinolytic agents such as Tranexamic acid (20–25 mg/kg PO or IV every 8 hours) and Aminocaproic acid (50–60 mg/kg PO or IV every 4–6 hours) are useful adjuncts, particularly for mucosal bleeding. Although Cryoprecipitate and Fresh frozen plasma may contain vWF, they are generally reserved for life-threatening situations when safer products are unavailable due to infection risk. Patients should avoid antiplatelet medications such as NSAIDs, which can worsen bleeding.


Disposition depends on severity. Patients with significant or ongoing bleeding, especially those requiring IV therapy, should be admitted and managed in consultation with hematology. Those with controlled bleeding and reliable follow-up may be discharged with clear instructions. Long-term management includes hematology referral for definitive diagnosis, planning before surgical procedures, and education regarding bleeding risk.


A key clinical pearl is that patients may not know their specific subtype of bleeding disorder, and in emergency situations with significant bleeding, empiric treatment (e.g., FFP or vWF-containing products) may be necessary while awaiting definitive diagnosis.

Emergency and Acute Medicine: Vomiting (Pediatric)




Pediatric vomiting is a forceful, coordinated expulsion of gastric contents through the mouth, involving the phases of nausea, retching, and emesis. During vomiting, there is sustained contraction of the abdominal muscles and diaphragm, while the pylorus and antrum contract simultaneously. Unlike adults, vomiting in children—especially neonates and infants—requires a high index of suspicion for serious pathology, as it may be the first sign of life-threatening disease.


The etiology of pediatric vomiting is broad and age-dependent, encompassing gastrointestinal, metabolic, neurologic, infectious, and feeding-related causes. Gastrointestinal causes include conditions such as Hypertrophic pyloric stenosis, Intussusception, and Midgut volvulus, all of which may lead to obstruction and require urgent intervention. Metabolic causes include inborn errors of metabolism and diabetic ketoacidosis, while neurologic causes include intracranial hemorrhage, tumors, or hydrocephalus. Infectious etiologies such as gastroenteritis, urinary tract infections, pneumonia, and sepsis are also common. Feeding-related issues, including overfeeding or milk allergy, are particularly relevant in infants.


Clinical presentation varies depending on the underlying cause, but assessment of vomiting characteristics is critical. Nonbilious vomiting suggests obstruction proximal to the pylorus, whereas bilious (green) vomiting indicates obstruction distal to the ampulla of Vater and is a surgical emergency until proven otherwise. Bloody vomiting may indicate upper gastrointestinal bleeding, while “coffee-ground” emesis reflects digested blood. A feculent odor suggests distal bowel obstruction or peritonitis. Projectile vomiting in a 2–6 week old infant is classic for hypertrophic pyloric stenosis, while sudden onset vomiting with abdominal distention and systemic illness may suggest volvulus or intussusception.


On physical examination, clinicians should assess hydration status, vital signs, and overall appearance, as children can deteriorate rapidly. Signs such as tachycardia, poor perfusion, altered mental status, or shock indicate severe illness. Abdominal examination may reveal distention, tenderness, masses, or peritoneal signs suggesting obstruction or perforation. Additional examination should include evaluation of the genitourinary system (e.g., testicular torsion) and neurologic status.


The diagnostic workup is guided by clinical suspicion and aimed at excluding life-threatening causes. Laboratory studies may include glucose, electrolytes, and infection markers (CBC, cultures). Imaging plays a key role: abdominal radiographs can identify obstruction or perforation, while ultrasound is particularly useful for diagnosing pyloric stenosis and intussusception. CT scans may be required for complex cases such as appendicitis or masses. In some cases, nasogastric tube placement can aid in diagnosis and management by assessing gastric contents.


Management begins with initial stabilization, including airway, breathing, and circulation assessment. Fluid resuscitation with isotonic saline (0.9% NS) is essential, especially in dehydrated or hypovolemic children, while cautiously considering conditions such as increased intracranial pressure. Bedside glucose testing is important to detect hypoglycemia. Gastric decompression with a nasogastric or orogastric tube may be required in cases of obstruction or persistent vomiting. Treatment then focuses on identifying and addressing the underlying cause, with early surgical consultation when an acute abdomen is suspected. Antibiotics should be initiated if infection or peritonitis is present.


Antiemetic therapy may be used once serious causes have been excluded or addressed. First-line therapy includes Ondansetron, given at 0.1 mg/kg per dose (typically 4–8 mg) IV or PO every 6 hours. Second-line options include Metoclopramide at 0.1 mg/kg per dose PO every 6 hours, Prochlorperazine at 0.1 mg/kg per dose IV, IM, or PR every 6 hours, and Promethazine at 0.25 mg/kg per dose PO, PR, or IM every 6 hours. These medications should be used cautiously due to potential side effects, especially in younger children.


Disposition depends on the child’s clinical status and underlying cause. Admission is required for unstable vital signs, dehydration, inability to tolerate oral intake, or suspected serious pathology. Children may be discharged if they are stable, able to tolerate fluids, and serious causes have been excluded, with clear instructions given to caregivers regarding warning signs such as persistent vomiting, abdominal distention, decreased urine output, fever, lethargy, or behavioral changes.


A critical clinical pearl is that bilious vomiting in neonates is an emergency and should be assumed to represent intestinal obstruction (e.g., malrotation with volvulus) until proven otherwise. Additionally, clinicians must always consider non-gastrointestinal causes of vomiting, including neurologic, metabolic, and toxicologic etiologies, to avoid missing potentially life-threatening conditions.

​

​

Emergency and Acute Medicine: Warfarin Complications




Warfarin is a widely used oral anticoagulant that works by inhibiting vitamin K–dependent clotting factors (II, VII, IX, and X), thereby affecting both the extrinsic and common coagulation pathways. It is commonly prescribed for conditions such as venous thromboembolism, atrial fibrillation, and prosthetic heart valves. Its therapeutic effect is monitored using the International Normalized Ratio, with typical target ranges of 2–3 or 2.5–3.5 depending on indication. However, due to its narrow therapeutic window and numerous interactions, warfarin is associated with significant complications, most notably bleeding.


Bleeding is the most common complication, occurring in up to 15% of patients annually, with major bleeding events in about 5% and fatal bleeding (most often Intracranial hemorrhage) in less than 1%. The risk of bleeding increases significantly when the INR exceeds 4. Patients may present with a wide spectrum of symptoms, ranging from occult bleeding to life-threatening hemorrhage involving the gastrointestinal tract, central nervous system, or retroperitoneum. Conversely, subtherapeutic INR levels may result in breakthrough thrombosis, particularly in high-risk patients.


Several factors predispose patients to unstable INR levels and complications, including advanced age (>75 years), comorbidities such as hypertension, diabetes, renal or liver disease, malignancy, and hyperthyroidism. Drug and dietary interactions are especially important: antibiotics, Amiodarone, NSAIDs, and certain herbal supplements (e.g., ginkgo, garlic) can increase INR, while drugs like Rifampin, carbamazepine, and high vitamin K intake can decrease it. Warfarin is contraindicated in pregnancy due to its teratogenic effects.


A unique complication is warfarin-induced skin necrosis, which typically occurs within the first week of therapy and is associated with protein C deficiency. It presents as painful skin lesions that progress to necrosis with central eschar formation. Limb gangrene may also occur due to venous thrombosis. In cases of overdose or ingestion of long-acting anticoagulants (e.g., “superwarfarins” found in rodenticides), patients may initially be asymptomatic but develop prolonged coagulopathy requiring extended monitoring.


Evaluation requires a thorough history, including indication for anticoagulation, recent dose changes, medication interactions, and prior INR values. Physical examination should focus on signs of bleeding (e.g., ecchymosis, pallor, hypotension) and subtle neurologic changes suggestive of intracranial bleeding. Laboratory testing includes PT/INR, CBC, renal and liver function tests, and type and crossmatch if bleeding is suspected. Imaging, particularly CT scans, should be obtained liberally to detect occult bleeding, especially in trauma patients or those with neurologic symptoms.


Management depends on the INR level and presence of bleeding. For patients with INR <5 and no bleeding, the next dose may be held or reduced with close monitoring. For INR 5–9 without bleeding, holding warfarin and administering Vitamin K1 at 1–5 mg PO may be appropriate, especially in high-risk patients. For INR ≥9 without bleeding, vitamin K 2.5–5 mg PO is recommended. In cases of serious or life-threatening bleeding (any INR), immediate reversal is required with vitamin K 10 mg IV (slow infusion over 10–30 minutes) along with clotting factor replacement.


Rapid reversal is best achieved using Prothrombin complex concentrate, which contains clotting factors II, VII, IX, and X. Dosing is weight- and INR-dependent: 25 U/kg for INR 2–3.9, 35 U/kg for INR 4–5.9, and 50 U/kg for INR ≥6. PCC is preferred in cases of intracranial hemorrhage, massive bleeding, or when volume overload is a concern. Alternatively, Fresh frozen plasma may be used, typically 3–4 units (≈1 L), though it carries risks such as fluid overload and slower INR correction. In refractory or complex cases, adjuncts such as factor VIIa may be considered.


Disposition depends on severity. Patients with active bleeding, especially involving the CNS, GI tract, or retroperitoneum, require admission and often ICU-level care. Stable patients with asymptomatic supratherapeutic INR and reliable follow-up may be discharged with close monitoring. Follow-up within 24–48 hours for repeat INR testing is essential.


A key clinical pearl is to maintain a low threshold for imaging in anticoagulated patients, even after minor trauma, as serious bleeding may occur without obvious symptoms. Additionally, vitamin K should generally not be given for INR <5 without bleeding, and IV vitamin K should be reserved for severe cases due to the rare but serious risk of anaphylaxis.

​

Emergency and Acute Medicine: Warts




Warts are benign proliferative lesions of the skin and mucous membranes caused by infection with the Human papillomavirus. The virus infects the basal layer of epithelial tissue, leading to cellular proliferation and increased vascularity, which gives rise to the characteristic verrucous, hyperkeratotic appearance. Warts are extremely common, particularly in children and adolescents, and most resolve spontaneously due to a cell-mediated immune response—about one-third within 6 months, two-thirds within 2 years, and up to 90% within 5 years.


There are several clinical types of warts depending on location and HPV subtype. Verruca vulgaris (common warts) typically occur on the dorsum of the hands, fingers, and around nails and are usually asymptomatic. Verrucae plantaris (plantar warts) occur on weight-bearing areas of the feet such as the heels and metatarsal heads and are often painful due to pressure. Flat (juvenile) warts appear as small, smooth, flesh-colored lesions on sun-exposed areas such as the face, neck, and extremities and may spread with shaving. Anogenital warts, also known as condyloma acuminata, are sexually transmitted and commonly caused by HPV types 6 and 11, while types 16 and 18 are associated with cervical cancer. These lesions are often soft, multiple, and have a cauliflower-like appearance.


Transmission of HPV occurs through direct skin-to-skin contact, indirect contact via contaminated surfaces, or autoinoculation, especially in children who scratch or bite affected areas. The incubation period is variable, ranging from weeks to over a year. In pediatric cases, warts are common, but the presence of anogenital warts should raise concern for possible sexual abuse, particularly in younger children.


Diagnosis is primarily clinical, based on the characteristic appearance of lesions. Common and plantar warts disrupt normal skin lines and may show pinpoint bleeding when scraped. Flat warts are smooth and subtle, while anogenital warts are soft and pedunculated. Laboratory testing is generally unnecessary, although application of acetic acid can help highlight lesions by causing whitening. Biopsy is reserved for atypical, persistent, or suspicious lesions, especially in immunocompromised patients.


Management depends on the type, location, and patient preference. Many warts require no treatment, especially in children, due to high rates of spontaneous resolution. For cutaneous warts, first-line therapy includes topical salicylic acid, typically 17% over-the-counter or up to 70% prescription strength, applied after soaking the wart for 10–20 minutes, left on overnight, and followed by gentle debridement. Treatment is repeated regularly and may take weeks to months. Another simple method is duct tape occlusion therapy, which may be particularly useful in children.


For anogenital warts, treatment options include patient-applied therapies such as Imiquimod (5% cream applied three times per week for up to 16 weeks) and Podofilox (0.5% solution or gel applied twice daily for 3 days followed by 4 days off, repeated up to 4 cycles). Provider-administered treatments include podophyllin (10–25% weekly application), trichloroacetic acid (80–90% weekly for 6–10 weeks), and cryotherapy with liquid nitrogen every 1–2 weeks. These treatments require caution, especially in pregnancy or when applied to sensitive mucosal areas.


Preventive strategies include vaccination with Gardasil, which protects against HPV types 6, 11, 16, and 18 and is given as a 3-dose series over 6 months. This vaccine significantly reduces the risk of genital warts and HPV-related cancers. Another vaccine, Cervarix, targets oncogenic strains associated with cervical cancer.


Most patients can be managed as outpatients, but referral to dermatology or gynecology is appropriate for treatment-resistant cases, atypical lesions, or anogenital involvement. Follow-up is important to ensure treatment response and monitor for recurrence. Patients should be advised to return if lesions change, become painful, or fail to improve.


A key clinical pearl is that HPV vaccines do not protect against all HPV types, and patients may still develop warts despite vaccination. Additionally, clinicians should always consider the broader clinical context, including the possibility of immunosuppression or, in pediatric cases with anogenital lesions, safeguarding concerns.

​