MCCQE Part I surgery & emergency care questions

Tension pneumothorax is diagnosed clinically by the combination of hypotension, tracheal deviation away from the affected side, absent breath sounds, hyperresonance on percussion, and distended neck veins from impaired venous return. Air trapped in the pleural space under pressure collapses the ipsilateral lung and shifts the mediastinum, compressing the contralateral lung and great vessels. This is a clinical diagnosis that must be treated immediately without waiting for chest radiography. Hyperresonance distinguishes it from hemothorax, which presents with dullness to percussion.

• A. Diaphragmatic rupture typically shows bowel sounds in the chest and is diagnosed radiographically, not by tracheal deviation and hyperresonance.
• B. Flail chest presents with paradoxical chest wall movement, not tracheal deviation or unilateral absent breath sounds.
• C. Cardiac tamponade presents with muffled heart sounds and distended neck veins but normal, symmetric breath sounds without tracheal deviation.
• E. Massive hemothorax causes dullness to percussion and decreased breath sounds, not hyperresonance or tracheal deviation in this direction.

Patient B has decreased breath sounds and dullness to percussion over one hemithorax, consistent with blood accumulating in the pleural space, defining massive hemothorax. The combination of hypotension and jugular venous distension in trauma can reflect either obstructive shock from tamponade or massive hemothorax causing mediastinal shift and impaired venous return; auscultation findings distinguish them. Patient A's muffled heart sounds with clear, symmetric breath sounds instead point to cardiac tamponade (Beck's triad: hypotension, jugular venous distension, muffled heart sounds). Massive hemothorax is managed with immediate chest tube drainage and consideration of thoracotomy if output exceeds defined thresholds.

• B. Aortic transection presents with findings such as unequal upper extremity pulses or widened mediastinum, not isolated unilateral dullness and decreased breath sounds.
• C. Tension pneumothorax causes hyperresonance, not dullness, to percussion over the affected side.
• D. Cardiac tamponade presents with muffled heart sounds and symmetric, clear breath sounds, which is Patient A's presentation, not Patient B's.
• E. Pulmonary contusion does not typically cause unilateral dullness to percussion or significant hypotension from blood loss alone.

In a hemodynamically unstable patient with blunt abdominal trauma, FAST is the investigation of choice because it is rapid, portable, repeatable, and can be performed in the resuscitation bay without interrupting ongoing resuscitation. It identifies free intraperitoneal fluid (presumed hemoperitoneum) and pericardial fluid, which guides the decision for emergency laparotomy. CT provides more detailed information but requires transporting an unstable patient to the scanner, which is unsafe. Diagnostic peritoneal lavage is now largely obsolete, having been replaced by FAST in most trauma centres.

• A. MRI is too slow and impractical in the acute setting of an unstable trauma patient.
• B. Diagnostic peritoneal lavage is invasive and has been largely replaced by FAST as the rapid bedside test in unstable trauma patients.
• C. Plain abdominal radiography has poor sensitivity for detecting hemoperitoneum or solid organ injury.
• E. CT requires transport to the radiology suite and patient stability, making it inappropriate for a patient who remains hypotensive after fluid resuscitation.

In hemorrhagic shock from suspected ongoing intra-abdominal bleeding, massive transfusion protocols now favour balanced resuscitation with packed red blood cells, plasma, and platelets in a 1:1:1 ratio, which more closely mimics whole blood and reduces dilutional coagulopathy. Permissive hypotension, targeting a systolic blood pressure of approximately 90 mmHg until definitive hemorrhage control in the operating room, avoids disrupting early clot formation and limits further blood loss, except in patients with traumatic brain injury where higher pressures are needed for cerebral perfusion. Excessive crystalloid worsens coagulopathy, dilutes clotting factors, and is no longer recommended as the primary resuscitation fluid in hemorrhagic shock.

• B. Transfusing red cells alone without plasma and platelets leads to dilutional coagulopathy and does not address the platelet and clotting factor deficits of massive hemorrhage.
• C. Large-volume crystalloid resuscitation dilutes clotting factors, worsens coagulopathy, and can dislodge early clots, worsening outcomes in hemorrhagic shock.
• D. Vasopressors do not replace volume or address the underlying coagulopathy and blood loss, and raising pressure further can worsen hemorrhage before surgical control.
• E. Delaying transfusion for formal crossmatch is unsafe in an exsanguinating patient; uncrossmatched or type O blood should be used emergently.

In a hemodynamically unstable patient with an open-book pelvic fracture, immediate application of a pelvic binder at the level of the greater trochanters reduces pelvic volume, stabilizes the fracture, and tamponades venous and bony bleeding, which is the predominant source of pelvic hemorrhage. This simple, rapid intervention should be performed in the resuscitation bay before transfer for imaging or definitive fixation. CT angiography and angioembolization are valuable for identifying and treating arterial bleeding but should follow initial mechanical stabilization and are not the first step in an unstable patient.

• B. External fixation in the operating room is a subsequent step after temporary stabilization and resuscitation, not the immediate action in the trauma bay.
• C. Traction splints address long bone fractures, not pelvic ring instability, and are not indicated here.
• D. CT angiography requires patient transport and takes time; mechanical stabilization with a binder must occur first in an unstable patient.
• E. Angioembolization addresses arterial bleeding identified on imaging and follows, rather than precedes, initial pelvic binder application.

This hemodynamically stable patient who responds appropriately to initial fluid resuscitation, has no peritoneal signs, and has a CT scan without active contrast extravasation (blush) is an excellent candidate for nonoperative management of splenic injury, which is successful in the majority of blunt splenic trauma cases regardless of grade when hemodynamic stability is maintained. Management consists of admission, serial abdominal examinations, serial hemoglobin measurements, and bed rest with activity restriction. Operative intervention (splenectomy or splenorrhaphy) is reserved for hemodynamic instability, peritonitis, or failure of nonoperative management, and angioembolization is reserved for patients with contrast blush or ongoing bleeding, not routinely applied to a stable patient without a blush.

• A. Angioembolization is indicated for active contrast extravasation or ongoing instability, not for a stable patient without a blush on imaging.
• B. Exploratory laparotomy is unnecessary in a stable patient without peritonitis who is a candidate for nonoperative management.
• C. Emergency splenectomy is reserved for hemodynamic instability or failure of nonoperative management, neither of which is present here.
• D. Discharge is unsafe; this patient requires inpatient observation given the risk of delayed splenic bleeding.

Neurogenic shock results from disruption of descending sympathetic pathways after a high spinal cord injury (typically above T6), causing unopposed vagal tone, loss of vascular tone (vasodilation), and bradycardia rather than the tachycardia expected with hypovolemia. The warm, dry skin (not cool and clammy) and bradycardia in the setting of hypotension point to loss of sympathetic outflow rather than blood loss. Hemorrhagic shock classically produces tachycardia and cool, clammy skin due to compensatory sympathetic activation. Management of neurogenic shock emphasizes cautious fluids plus vasopressors, as aggressive fluid resuscitation alone will not correct the vasodilation.

• A. Hemorrhage would cause tachycardia and cool skin, not bradycardia with warm skin.
• B. Hemorrhage triggers sympathetic activation (tachycardia), not parasympathetic dominance.
• C. Myocardial contusion causes arrhythmia or pump failure, not this classic bradycardia-hypotension-warm skin triad.
• E. Catecholamine surges cause tachycardia, not bradycardia.

Burns involving the hands, feet, face, perineum, or major joints, as well as any circumferential burn, meet criteria for referral to a specialized burn centre regardless of the total body surface area involved, because of the high risk of functional impairment and need for specialized wound and rehabilitation care. This patient's burn involves the hand and wrist circumferentially, both independent referral criteria. Other criteria include burns greater than 10% TBSA, full-thickness burns of any size, electrical or chemical burns, and burns with inhalational injury or significant comorbidities. Local management without specialist input risks contracture and loss of hand function.

• B. Topical therapy and delayed follow-up are inappropriate given the referral criteria met by this burn's location and circumferential nature.
• C. Simple observation at a non-specialized centre does not address the need for burn-specific wound care and monitoring for compartment syndrome.
• D. Skin grafting decisions and surgery for complex burns should be made at a specialized burn centre, not locally.
• E. A circumferential hand burn requires specialist assessment for escharotomy risk and functional outcome, not routine home dressing care.

Standard pulse oximetry cannot distinguish carboxyhemoglobin from oxyhemoglobin and will display a falsely normal or near-normal saturation in carbon monoxide poisoning, so a normal reading does not exclude significant exposure. This patient's headache, nausea, confusion, and fire exposure are classic for carbon monoxide toxicity, and treatment with 100% oxygen via non-rebreather mask should begin immediately without waiting for confirmatory carboxyhemoglobin levels, as it accelerates dissociation of carbon monoxide from hemoglobin and reduces the half-life of carboxyhemoglobin from several hours to about 60-90 minutes. Co-oximetry (measuring carboxyhemoglobin directly) should be obtained to confirm the diagnosis and guide decisions about hyperbaric oxygen therapy, but treatment should not be delayed for this. Discharging the patient based on a reassuring pulse oximetry reading would be a dangerous error.

• A. There is no indication of opioid overdose; the history and symptoms point to carbon monoxide exposure.
• C. A normal pulse oximetry reading is falsely reassuring in carbon monoxide poisoning and does not exclude significant exposure.
• D. Oxygen therapy should begin immediately and should not be delayed for imaging.
• E. Co-oximetry (not relying on pulse oximetry trends) should be obtained regardless of the saturation reading given this clinical presentation.

This patient has clinical signs of compartment syndrome from a circumferential full-thickness burn: severe pain disproportionate to the injury, pain with passive stretch, and diminished distal pulses, caused by the inelastic eschar restricting swelling tissue beneath it. Escharotomy, a surgical incision through the eschar down to but not through the fascia along the mid-lateral or mid-medial lines, must be performed urgently to relieve pressure and restore perfusion. Waiting to reassess or relying on imaging risks irreversible ischemic damage and limb loss, since the diagnosis is clinical and time-sensitive. Mannitol and cooling do not address the mechanical constriction caused by the eschar.

• A. Delaying definitive treatment to reassess risks progression to irreversible muscle and nerve ischemia.
• B. Imaging would delay time-sensitive treatment; the diagnosis here is made clinically.
• C. Cooling and increased fluids do not address the underlying compartment syndrome caused by the eschar.
• D. Mannitol does not relieve the mechanical constriction caused by the inelastic eschar.

The treatment of frostbite is rapid rewarming by immersion in a water bath maintained at 37-39°C for 15-30 minutes until the tissue becomes soft and a red-purple colour returns. Water baths provide even, controlled heat transfer and avoid the burns or further tissue trauma caused by dry heat sources or friction. Rubbing or massaging frostbitten tissue causes mechanical damage to already fragile, ice-crystal-laden cells and should be avoided. Slow rewarming at room or ambient temperature prolongs tissue exposure to damaging intermediate temperatures and worsens outcomes compared with rapid controlled rewarming.

• A. Rubbing causes mechanical trauma to fragile frostbitten tissue and should never be used.
• B. Massage causes further mechanical damage to the tissue and does not aid rewarming.
• D. Slow rewarming at room temperature prolongs exposure to damaging temperatures and worsens tissue outcomes compared with rapid water-bath rewarming.
• E. Dry heat sources such as heating pads risk uneven heating and thermal burns to insensate tissue.

Severely hypothermic patients, particularly those with core temperatures below 28-30°C, are at high risk of ventricular fibrillation triggered by rough handling, movement, or mechanical stimulation of the irritable, cold myocardium. Gentle handling with minimal movement during extraction, transport, and rewarming is essential to avoid precipitating a lethal arrhythmia, and the patient should be kept horizontal rather than moved to sitting or standing positions. Core rewarming should proceed carefully, with cardiac monitoring continued throughout, while avoiding any unnecessary physical stimulation of the patient. Central venous catheterization and vigorous manipulation both carry a recognized risk of inducing ventricular fibrillation in this setting and should be avoided unless absolutely necessary.

• A. Vigorous compressions and limb manipulation in a hypothermic patient with a perfusing rhythm risk inducing ventricular fibrillation.
• B. Frequent repositioning introduces unnecessary mechanical stimulation that can precipitate arrhythmia in the hypothermic heart.
• C. Rapid repositioning to sitting can precipitate cardiac arrhythmia in a hypothermic, hemodynamically unstable patient.
• E. Central venous catheterization through the subclavian vein carries a particular risk of triggering ventricular fibrillation in severe hypothermia and should be avoided unless essential.

Right upper quadrant ultrasound is the first-line investigation for suspected acute cholecystitis because it is widely available, rapid, inexpensive, and has high sensitivity for gallstones, gallbladder wall thickening (>3 mm), pericholecystic fluid, and a sonographic Murphy's sign. This patient's positive Murphy's sign, fever, and leukocytosis fit the Tokyo Guidelines criteria for acute cholecystitis, and ultrasound confirms the diagnosis in the large majority of cases. CT and MRCP are reserved for equivocal ultrasound findings or suspected complications, while HIDA scan and ERCP have no role as the initial test here since there is no evidence of choledocholithiasis.

• A. CT is less sensitive than ultrasound for detecting gallstones and is not first-line for suspected cholecystitis.
• B. HIDA scan is more sensitive but less available and is used when ultrasound findings are equivocal, not as the initial test.
• C. MRCP is reserved for evaluating suspected common bile duct stones, not as the initial test for cholecystitis.
• D. ERCP is a therapeutic procedure for bile duct stones, not a diagnostic first step, and carries procedural risk.

This patient meets criteria for acute ascending cholangitis with Charcot's triad (fever, jaundice, RUQ pain) and features of severe (Grade III) disease per the Tokyo Guidelines, including hypotension and altered mental status despite initial resuscitation. Urgent biliary decompression, most commonly by ERCP with sphincterotomy and stone extraction or stent placement, is the definitive next step and should not be delayed since persistent biliary obstruction with infection can rapidly progress to septic shock and death. Cholecystectomy addresses the gallbladder but does not relieve the ductal obstruction causing sepsis, and it is deferred until after decompression and clinical stabilization.

• A. Observation is inappropriate given hemodynamic instability and altered mental status indicating severe cholangitis.
• B. Oral bile acid therapy is used for small cholesterol gallstones electively, not for acute obstructive cholangitis.
• D. Repeating ultrasound delays definitive decompression in a patient with ongoing septic shock.
• E. Cholecystectomy does not relieve the common bile duct obstruction and is not the urgent priority in septic cholangitis.

The diagnosis of acute pancreatitis requires two of three criteria: characteristic epigastric pain radiating to the back, serum lipase or amylase greater than three times the upper limit of normal, and characteristic findings on imaging. This patient has typical pain and a lipase level nearly four times the upper limit of normal, so the diagnosis is clinically established and imaging is not required to confirm it. CT is reserved for diagnostic uncertainty, failure to improve within 48 to 72 hours, or assessment of complications such as necrosis, not for routine confirmation. Early contrast CT can also worsen pancreatic injury and is avoided unless specifically indicated.

• A. CT is not required when clinical and biochemical criteria already establish the diagnosis; it is reserved for complications or uncertainty.
• C. MRCP is used to evaluate for choledocholithiasis as a cause, not to establish the diagnosis of pancreatitis itself.
• D. Only one of amylase or lipase needs to be elevated above threshold; both are not required.
• E. Diagnostic laparoscopy has no role in establishing the diagnosis of acute pancreatitis.

For mild gallstone pancreatitis, laparoscopic cholecystectomy should be performed during the index admission once the pancreatitis has clinically resolved, since delaying surgery significantly increases the risk of recurrent pancreatitis, cholecystitis, or other biliary complications while awaiting outpatient surgery. This patient has resolved pain, improving enzymes, and tolerance of oral intake, indicating she is a good candidate for same-admission cholecystectomy. ERCP is not indicated here because there is no evidence of persistent common bile duct obstruction. Delaying cholecystectomy to an outpatient date, whether weeks or months later, exposes the patient to unnecessary risk of recurrence.

• B. Delaying cholecystectomy by 6 weeks increases the risk of recurrent gallstone-related complications compared to same-admission surgery.
• C. ERCP is unnecessary without evidence of common bile duct stones or dilation on imaging.
• D. Omitting cholecystectomy leaves the underlying cause unaddressed and risks recurrent pancreatitis.
• E. A 6-month delay carries even greater risk of recurrent pancreatitis or cholecystitis before definitive surgery.

An upright chest X-ray demonstrating free air under the diaphragm (pneumoperitoneum) is a rapid, widely available test that strongly supports the diagnosis of a perforated hollow viscus such as a peptic ulcer, particularly in a patient with risk factors like chronic NSAID use and a sudden onset of severe pain progressing to peritonitis. While CT abdomen is more sensitive and often obtained if the diagnosis remains uncertain or for surgical planning, the upright chest X-ray is a quick initial test that can confirm the diagnosis and expedite the path to emergency surgery. Upper endoscopy and oral contrast studies are contraindicated or unhelpful in this setting due to the risk of worsening perforation or peritoneal contamination. The clinical priority once perforation is suspected is urgent surgical consultation for operative repair, usually by laparoscopic or open omental patch closure.

• A. Ultrasound is insensitive for detecting free intraperitoneal air compared to plain radiography or CT.
• B. Oral contrast risks further peritoneal contamination and is not used when perforation is suspected.
• C. Upper endoscopy risks insufflating air through the perforation and worsening peritoneal contamination.
• E. Diagnostic peritoneal lavage is an outdated technique not used in the modern evaluation of suspected perforation.

This patient has an adhesive small bowel obstruction, the most common cause of SBO in a patient with prior abdominal surgery, and shows no signs of strangulation such as fever, peritonitis, or leukocytosis. Initial management is conservative with nasogastric decompression, intravenous fluid resuscitation, bowel rest, and correction of electrolyte abnormalities, with serial examinations to monitor for signs of ischemia or clinical deterioration. Most adhesive SBOs resolve with this approach, and surgery is reserved for those with evidence of strangulation, peritonitis, or failure to improve after a trial of conservative management, typically 48 to 72 hours. Discharge without inpatient monitoring and decompression would be unsafe given ongoing obstruction.

• A. Percutaneous drainage has no role in the management of simple adhesive small bowel obstruction.
• B. An oral contrast challenge may be used to predict resolution but discharging a symptomatic obstructed patient home is unsafe.
• D. Colonoscopic decompression is used for large bowel obstruction or volvulus, not small bowel obstruction.
• E. Immediate surgery is not required in the absence of peritonitis, strangulation, or failure of conservative therapy.

The hallmark of acute mesenteric ischemia is pain out of proportion to physical findings, caused by embolic or thrombotic occlusion of the superior mesenteric artery leading to bowel wall ischemia before peritoneal signs develop. Atrial fibrillation is the classic risk factor, as a cardiac thrombus embolizes to the SMA. Elevated lactate reflects anaerobic metabolism from bowel ischemia. Early recognition is critical because peritonitis signifies transmural infarction and a much worse prognosis.

• A. Diverticulitis typically causes localized left lower quadrant tenderness proportional to the pain.
• B. Obstruction causes crampy pain with distension and high-pitched bowel sounds, not pain-exam mismatch.
• C. Pancreatitis causes epigastric pain with tenderness that correlates with severity and typically elevates lipase.
• D. A perforated ulcer causes peritonitis with marked guarding and rigidity matching the pain severity.

An incarcerated hernia that is non-reducible but without signs of strangulation (fever, tachycardia, erythema, or peritonitis) warrants urgent same-day surgical referral because of the risk of progression to strangulation, with gentle attempted reduction sometimes appropriate if performed promptly. A strangulated hernia, signaled by fever, tachycardia, overlying skin changes, and systemic toxicity, indicates compromised blood supply and bowel ischemia, requiring emergency surgery without delay to prevent bowel necrosis and perforation. Distinguishing these presentations guides the urgency of operative intervention and is a key safety point in surgical triage.

• A. Simple incarceration without strangulation signs does not require emergency surgery within the hour; urgent same-day referral is appropriate.
• B. The reasoning is reversed; the first has no systemic toxicity while the second shows clear signs of strangulation requiring emergency care.
• C. Both patients show concerning features (non-reducibility, systemic signs in the second) that preclude simple outpatient follow-up.
• D. Discharging a non-reducible incarcerated hernia for elective repair in 6 months risks progression to strangulation and bowel infarction.

The femoral canal is bounded by rigid structures, the inguinal ligament anteriorly, the lacunar ligament medially, and the pectineal ligament posteriorly, creating a narrow, unforgiving space. This anatomic rigidity means that even a small amount of herniated bowel or omentum can become trapped and have its blood supply compromised, giving femoral hernias a disproportionately high risk of incarceration and strangulation relative to their size. Because of this risk, femoral hernias are generally repaired promptly upon diagnosis even when asymptomatic, unlike many small reducible inguinal hernias which can sometimes be managed with watchful waiting. This anatomic principle is the basis for prioritizing earlier surgical referral for femoral hernias.

• A. Femoral hernias actually carry a higher lifetime risk of strangulation than inguinal hernias.
• B. Femoral hernias are typically small, and their small rigid defect is exactly what predisposes to strangulation.
• C. The femoral canal is narrow and rigid, not wide and compliant, which is precisely why strangulation risk is high.
• D. Femoral hernias can contain bowel, bladder, or omentum, and bowel involvement carries high strangulation risk.

Umbilical hernias are common in infants due to incomplete closure of the umbilical ring and the majority, especially those under 1.5 cm, close spontaneously by 4 to 5 years of age without intervention. Watchful waiting with reassurance is the appropriate management for an asymptomatic, easily reducible umbilical hernia in an otherwise healthy infant. Surgical referral is reserved for hernias that persist beyond age 4-5 years, are large (greater than 1.5-2 cm), or become incarcerated, strangulated, or symptomatic. Taping, binding, or coin application has no evidence of benefit and is not recommended.

• A. Ultrasound is unnecessary for a clinically straightforward, easily reducible umbilical hernia in an asymptomatic infant.
• C. Elective surgery is not indicated for an asymptomatic reducible umbilical hernia in infancy given the high rate of spontaneous closure.
• D. Taping or coin application does not accelerate closure and is not a recommended intervention.
• E. There is no indication of reflux-related pathology, and PPI therapy has no role in management of umbilical hernia.

This patient presents with the classic 6 P's of acute limb ischemia: pain, pallor, pulselessness, paresthesia, paralysis, and poikilothermia (coolness), likely from an embolus originating from atrial fibrillation. Motor and sensory deficits indicate advanced ischemia with a limited window, generally within 6 hours, before irreversible muscle and nerve damage occurs. Immediate anticoagulation with intravenous heparin should be started to prevent clot propagation while emergency vascular surgery is consulted for urgent revascularization, whether by embolectomy, thrombolysis, or bypass. Delay for outpatient measures or non-urgent testing risks limb loss.

• A. Cilostazol and compression stockings are treatments for chronic peripheral arterial disease, not acute limb-threatening ischemia.
• C. Oral anticoagulation and outpatient follow-up are far too delayed for a limb with sensory and motor deficits from acute ischemia.
• D. Ankle-brachial index and 24-hour reassessment are inappropriate delays when limb-threatening ischemia with neurologic deficit is present.
• E. Warmth increases tissue metabolic demand in an already ischemic limb and can worsen injury.

In patients with low pretest probability by the Wells score, a high-sensitivity D-dimer test is the appropriate initial investigation. If the D-dimer is negative, deep vein thrombosis is effectively excluded without further imaging. If positive, compression ultrasonography is then performed to confirm the diagnosis. This stepwise algorithm avoids unnecessary imaging in low-risk patients while maintaining high sensitivity for ruling out clot.

• A. Venography is invasive and obsolete as a first-line test; it is reserved for rare equivocal cases.
• B. CT venography is not a standard first-line test for suspected lower limb DVT.
• C. Ultrasonography is used after a positive D-dimer or in moderate-to-high pretest probability, not as the first step in low-risk patients.
• D. Empiric anticoagulation is not indicated before risk stratification and testing in a hemodynamically stable patient.

Direct oral anticoagulants such as rivaroxaban or apixaban are first-line therapy for most patients with acute deep vein thrombosis without cancer, renal failure, or antiphospholipid syndrome, per Thrombosis Canada and international guidelines. They do not require routine monitoring or bridging and have similar efficacy with less bleeding risk compared with warfarin. Warfarin requires several days of overlap with a parenteral anticoagulant to achieve therapeutic effect, which is no longer preferred when a DOAC can be used. Low-molecular-weight heparin monotherapy remains preferred in cancer-associated thrombosis.

• A. Warfarin with bridging is an older strategy, now reserved for situations where DOACs are contraindicated, such as severe renal impairment or valvular disease requiring vitamin K antagonist therapy.
• B. Unfractionated heparin alone is used for initial anticoagulation in specific situations like severe renal failure, not as first-line long-term therapy.
• C. Low-molecular-weight heparin monotherapy is preferred in cancer-associated thrombosis, not in this patient without malignancy.
• D. Aspirin is not adequate anticoagulation for treatment of acute proximal DVT.

For symptomatic carotid stenosis of 70 to 99% in a patient who has had a transient ischemic attack or non-disabling stroke, carotid endarterectomy performed within 2 weeks of the symptomatic event provides the greatest reduction in subsequent stroke risk. The benefit of surgery is time-sensitive, as the risk of recurrent stroke is highest in the days following the initial event. Medical therapy with antiplatelets and statins is continued perioperatively but does not replace surgical intervention at this degree of stenosis.

• A. Medical therapy alone is inadequate for symptomatic stenosis in this range; it is an adjunct to, not a substitute for, endarterectomy.
• B. Dual antiplatelet therapy alone is insufficient; surgical revascularization is indicated for this degree of symptomatic stenosis.
• C. Delaying for repeat imaging wastes the time-sensitive window during which endarterectomy provides maximal benefit.
• E. Endarterectomy is indicated now based on symptomatic 70-99% stenosis; waiting for progression to 90% delays a proven benefit.

Acute compartment syndrome is a clinical diagnosis in a patient with classic findings: pain out of proportion to injury, pain with passive stretch, and sensory changes, and it should prompt emergency fasciotomy without delay for confirmatory testing. Pulses and capillary refill are often preserved until late, so their presence does not exclude the diagnosis. Intracompartmental pressure measurement is reserved for equivocal cases or uncooperative or obtunded patients where clinical assessment is unreliable. Delaying treatment risks irreversible muscle and nerve necrosis within hours.

• A. Increasing opioids masks symptoms and delays diagnosis, risking irreversible tissue damage.
• B. MRI is not used to diagnose acute compartment syndrome and would cause dangerous delay.
• C. Pressure measurement is useful when the clinical picture is unclear, but this patient has classic findings and should proceed directly to fasciotomy without delay.
• D. Venous Doppler evaluates for DVT, not compartment syndrome, and would waste critical time.

Open fractures require prompt intravenous antibiotics, typically a first-generation cephalosporin such as cefazolin, administered as soon as possible after injury to reduce infection risk, along with surgical debridement and irrigation, ideally within 24 hours of injury. Antibiotic coverage is broadened to include gram-negative organisms in more severely contaminated or high-energy injuries. Delaying debridement beyond this window increases the risk of infection and osteomyelitis. Oral antibiotics and saline irrigation alone are inadequate for an open fracture with contamination.

• A. Oral antibiotics provide inadequate coverage, and delaying debridement to 72 hours increases infection risk.
• B. Vancomycin alone does not cover gram-negative organisms typically relevant in contaminated open fractures, and delaying debridement is inappropriate.
• D. Antibiotics should not be withheld; delaying treatment pending cultures significantly increases infection risk.
• E. A 5-day delay for debridement is unacceptable and substantially increases the risk of deep infection and osteomyelitis.

Surgical fixation of hip fractures within 48 hours of admission is associated with reduced 30-day mortality, fewer complications such as pressure ulcers and pneumonia, and improved functional outcomes in elderly patients. Unnecessary delay for extensive workup in a medically stable patient increases the risk of immobility-related complications without clear benefit. Non-operative management is reserved for patients who are not surgical candidates due to prohibitive risk or limited life expectancy, and carries significant morbidity from prolonged immobility.

• B. Elective delay of 2 weeks significantly increases mortality and complication risk compared with early fixation.
• C. Extensive delay for investigation in a stable patient increases complications without proven benefit and is not guideline-recommended.
• D. Non-operative management carries high morbidity and mortality from prolonged immobility and is reserved for patients unfit for any surgery.
• E. Waiting up to 7 days is associated with higher mortality compared with fixation within 48 hours in a medically stable patient.

Scaphoid fractures are notoriously difficult to detect on initial radiographs because the fracture line can be occult for up to two weeks. Given the high risk of avascular necrosis and nonunion from missed fractures (due to retrograde blood supply), the standard approach is to immobilize clinically suspected fractures in a thumb spica cast and repeat radiographs in 10-14 days, when bone resorption at the fracture site makes it visible. MRI or CT can detect occult fractures sooner but are not universally available as first-line in all Canadian settings, making cast immobilization with repeat imaging the practical and guideline-supported approach. Early immobilization also prevents further displacement while awaiting definitive imaging.

• B. Bone scan is not the standard initial approach and has largely been replaced by MRI/CT where occult fracture is strongly suspected.
• C. MRI is sensitive and can be used but is not required immediately in most centres; cast and repeat X-ray is the accepted first-line approach.
• D. Discharging without immobilization risks missing a fracture and progression to nonunion or avascular necrosis.
• E. Surgery is not indicated without a confirmed fracture.

Fat embolism syndrome classically occurs 24-72 hours after long bone or pelvic fractures and presents with the triad of hypoxemic respiratory distress, neurologic changes (confusion, agitation), and a petechial rash typically on the chest, axillae, and conjunctivae. Marrow fat released into the venous circulation at the fracture site embolizes to the pulmonary capillaries and causes a local inflammatory response and microvascular occlusion. Management is supportive, with early fracture fixation reducing the risk. The time course, petechiae, and neurologic involvement distinguish this from pulmonary embolism, which usually lacks petechiae and fever of this degree.

• A. ARDS from sepsis is possible but does not explain the characteristic petechiae and the classic 24-72 hour post-fracture timing.
• B. Pulmonary embolism typically presents with pleuritic chest pain and lacks the petechial rash and fever seen here.
• D. Aspiration pneumonia would not explain the petechial rash or the temporal relationship to the fracture.
• E. Cardiac tamponade presents with hypotension, jugular venous distension, and muffled heart sounds, not diffuse infiltrates and petechiae.

The Kocher criteria for differentiating septic arthritis from transient synovitis include fever greater than 38.5°C, inability to bear weight, ESR greater than 40 mm/h, and WBC count greater than 12 x 10^9/L (with CRP greater than 20 mg/L added by Caird as a strong independent predictor). This child meets four of these criteria, giving a very high predicted probability of septic arthritis, which requires urgent hip aspiration and surgical drainage to prevent cartilage destruction and femoral head damage. Transient synovitis is a diagnosis of exclusion typically presenting with normal or mildly elevated inflammatory markers and low-grade or no fever.

• A. Legg-Calve-Perthes disease is a chronic, insidious process without fever or markedly elevated inflammatory markers.
• B. Juvenile idiopathic arthritis usually presents with a more chronic course and often polyarticular involvement, not an acute single joint presentation with this degree of inflammatory marker elevation.
• C. Transient synovitis typically presents with normal or only mildly elevated inflammatory markers and lower fever, not this combination of findings.
• D. Osteoid osteoma causes night pain relieved by NSAIDs and does not cause fever or elevated inflammatory markers.

Slipped capital femoral epiphysis (SCFE) classically occurs in obese adolescents during the growth spurt, presenting with insidious groin, thigh, or knee pain and a limp. The hallmark finding is obligate external rotation of the hip during passive flexion, with loss of internal rotation, due to posterior and inferior displacement of the femoral epiphysis relative to the femoral neck. Diagnosis is confirmed with anteroposterior and frog-leg lateral radiographs of the pelvis, and treatment involves prompt surgical pinning to prevent further slippage and avascular necrosis. Weight-bearing should be stopped immediately once suspected to reduce the risk of progression to an unstable slip.

• A. Osteomyelitis would typically present with fever and systemic signs of infection, which are absent here.
• B. Transient synovitis is typically acute, often post-viral, and occurs in younger children, not adolescents with this chronic presentation.
• C. Legg-Calve-Perthes disease occurs in younger children (typically 4-10 years) and does not show the same obligate external rotation pattern.
• D. Developmental dysplasia of the hip is diagnosed in infancy and would not present as new-onset pain in a 13-year-old.

The anterior interosseous nerve is a purely motor branch of the median nerve that innervates the flexor pollicis longus and the flexor digitorum profundus to the index finger, both required to form the "OK" sign (pincer grip between thumb and index finger). It is the most commonly injured nerve in extension-type supracondylar fractures. Because it carries no sensory fibers, sensation remains intact, which is a key distinguishing feature from other nerve injuries in this fracture. Most anterior interosseous nerve palsies are neurapraxias that resolve spontaneously with observation over weeks to months.

• A. Ulnar nerve injury would cause weakness of finger abduction/adduction and sensory loss over the little finger, not the OK sign.
• B. Axillary nerve injury affects shoulder abduction and is not associated with supracondylar fractures.
• C. Radial nerve injury would cause wrist drop and inability to extend the fingers and thumb, not isolated pincer weakness.
• D. Musculocutaneous nerve injury affects elbow flexion and forearm sensation, not thumb-index pinch.

In a patient with good functional capacity, defined as being able to achieve at least 4 metabolic equivalents of task (such as climbing two flights of stairs or brisk walking) without cardiac symptoms, current Canadian Cardiovascular Society perioperative guidelines recommend proceeding to surgery without further cardiac testing, regardless of the type of noncardiac surgery. Functional capacity is a strong predictor of perioperative cardiac risk, and testing in asymptomatic patients with good functional capacity does not improve outcomes and only delays surgery. Further testing is reserved for patients with poor or unknown functional capacity combined with elevated clinical risk factors or significant surgery.

• B. Coronary angiography is invasive and unnecessary in an asymptomatic patient with good functional capacity.
• C. A resting ECG is not routinely required in asymptomatic patients with good functional capacity undergoing low-to-intermediate risk surgery.
• D. Stress testing is reserved for patients with poor functional capacity and elevated risk undergoing high-risk surgery, not this patient.
• E. Echocardiography is not indicated without symptoms or signs suggesting structural heart disease.

Total hip arthroplasty is a high-risk category for venous thromboembolism, and current guidelines recommend pharmacologic prophylaxis with low-molecular-weight heparin (or alternatively a direct oral anticoagulant or aspirin after an initial LMWH course in some protocols) for a minimum of 10-14 days, with extension up to 35 days post-operatively given the prolonged risk period after major hip surgery. Mechanical prophylaxis alone is insufficient for this high-risk category and is typically used as an adjunct or when pharmacologic prophylaxis is contraindicated. Extended-duration prophylaxis reduces the incidence of symptomatic VTE, which can occur even after hospital discharge in hip arthroplasty patients.

• A. Unfractionated heparin twice daily and only 5 days duration is inadequate for this high-risk major orthopedic surgery.
• B. Omitting prophylaxis in high-risk major orthopedic surgery significantly increases VTE risk and is not guideline-supported.
• C. Mechanical prophylaxis alone is insufficient in this high VTE risk category without a contraindication to pharmacologic agents.
• D. Aspirin alone for only 7 days provides inadequate duration and is generally used as a step-down option after initial LMWH, not as sole initial prophylaxis.

Fever on postoperative day 1-2 is most commonly due to atelectasis from shallow breathing, splinting, and retained secretions after general anesthesia and abdominal surgery. Basal crackles that clear with coughing, without purulent sputum or focal consolidation, support this diagnosis rather than pneumonia or another infectious source. The classic timeline mnemonic places atelectasis in the first 1-2 days, urinary tract infection around days 3-5, wound infection days 5-7, and venous thromboembolism from day 5 onward. Management is incentive spirometry, early mobilization, and adequate analgesia rather than antibiotics.

• A. Surgical site infection usually appears after day 5 and the wound looks clean.
• B. DVT-related fever typically occurs from day 5 onward and the calves are non-tender.
• D. There is no diarrhea or recent antibiotic exposure to suggest C. difficile colitis.
• E. Urinary tract infection typically presents later (days 3-5) and urinalysis here is normal.

Postoperative ileus is a self-limited, functional impairment of coordinated gastrointestinal motility caused by surgical handling, inflammatory mediators, opioid analgesia, and autonomic disruption, typically resolving within 2-4 days. It is distinguished from mechanical obstruction by diffuse gas distribution throughout the small and large bowel with gas present in the rectum, and the absence of a discrete transition point on imaging. Mechanical obstruction, in contrast, shows a transition zone between dilated proximal and collapsed distal bowel, often with absent rectal gas and crampy colicky pain. Management of ileus is supportive, including fluid and electrolyte correction, early mobilization, and minimizing opioids.

• A. Intussusception is rare in adults and would show a focal transition point, not diffuse gas with rectal gas present.
• B. Adhesive obstruction would show a focal transition point and typically presents later, not with uniform gas distribution.
• C. Internal hernia causes a focal mechanical transition point, not diffuse gas throughout the bowel.
• D. Mesenteric ischemia presents with severe pain out of proportion to exam and signs of peritonism, not diffuse painless distension.

Evidence-based surgical site infection bundles call for prophylactic antibiotics administered within 60 minutes before incision so that adequate tissue levels are present at the time of the first cut, maintenance of intraoperative normothermia (core temperature at least 36°C), and perioperative glucose control targeting below 10 mmol/L, avoiding both hyperglycemia and hypoglycemia. Tight glucose targets below 6 mmol/L increase the risk of hypoglycemia without added benefit and are not recommended. Antibiotics given after incision or too far in advance fail to achieve adequate tissue concentration at the time of contamination.

• A. Withholding insulin until glucose exceeds 14 mmol/L allows prolonged hyperglycemia, which impairs neutrophil function and wound healing.
• C. Hypothermia impairs immune function and vasoconstricts tissue, increasing surgical site infection risk.
• D. Administering antibiotics 3 hours preoperatively results in subtherapeutic tissue levels by the time of incision.
• E. Antibiotics given after skin closure do not provide tissue coverage during the period of contamination risk and the glucose target is too tight, risking hypoglycemia.

Canadian law recognizes the doctrine of implied (or presumed) consent in emergencies, allowing physicians to proceed with necessary treatment when a patient lacks capacity, no substitute decision-maker is immediately available, and delay would result in death or serious harm. This principle is codified in provincial health care consent legislation and reflects the ethical duty of beneficence outweighing the procedural requirement for explicit consent in true emergencies. The physician should document the clinical urgency, the patient's incapacity, and the absence of an available substitute decision-maker. Once the patient's condition allows, ongoing care decisions should involve the patient or an appropriate substitute decision-maker as soon as feasible.

• A. Delaying a life-saving intervention to locate a substitute decision-maker in a true emergency would cause preventable harm or death.
• C. Court orders are reserved for non-emergent disputed treatment decisions, not immediately life-threatening emergencies.
• D. The patient is unconscious and hemodynamically unstable; waiting for him to regain consciousness would be fatal.
• E. A second surgeon's signature does not substitute for legally valid consent and is not required under the emergency doctrine.

The Canadian Task Force on Preventive Health Care recommends screening average-risk adults aged 50 to 74 years with fecal occult blood testing or fecal immunochemical testing every 2 years, or flexible sigmoidoscopy every 10 years, as first-line strategies. Fecal testing is preferred for population-based screening because it is non-invasive, inexpensive, and has demonstrated mortality benefit in randomized trials. Colonoscopy is reserved as a follow-up investigation for positive screening tests or for higher-risk individuals, not as a first-line population screening tool in Canada. Screening should begin at age 50 in average-risk individuals, not earlier or later.

• A. Average-risk screening should begin at age 50, not be deferred to age 60.
• C. CT colonography is not a recommended first-line screening modality by the Canadian Task Force.
• D. Flexible sigmoidoscopy is recommended every 10 years, not every 5 years, and screening begins at age 50, not 45.
• E. Colonoscopy is not recommended as a first-line population screening test in Canada and age 40 is too early for an average-risk patient.

The Canadian Task Force on Preventive Health Care recommends that average-risk women aged 40 to 49 engage in shared decision-making with their physician, discussing the modest mortality benefit against the higher risk of false positives, overdiagnosis, and unnecessary biopsies before deciding whether to start screening earlier than age 50. For women aged 50 to 74, the Task Force recommends biennial mammography. Annual mammography is not recommended by the Task Force at any age for average-risk women, and MRI is reserved for women at high hereditary risk, such as BRCA mutation carriers.

• A. Breast MRI is reserved for women at high hereditary risk, not for average-risk screening.
• B. Starting screening without informed shared decision-making does not respect the patient's autonomy given the trade-offs involved at this age.
• C. Annual mammography is not the interval recommended by the Canadian Task Force at any age for average-risk women.
• E. Shared decision-making regarding earlier screening should occur now rather than deferring the conversation entirely to age 50.

In a patient with a normal thyroid-stimulating hormone level, thyroid ultrasound is the recommended first investigation for a palpable thyroid nodule because it characterizes size, composition, and sonographic features such as microcalcifications, irregular margins, and increased central vascularity that predict malignancy risk and determine whether fine-needle aspiration is indicated based on size and risk stratification. A radioactive iodine uptake scan is reserved for patients with a suppressed thyroid-stimulating hormone to evaluate for a hyperfunctioning nodule, which is not the case here. Proceeding directly to biopsy without ultrasound risks missing nodules that need sampling from a specific suspicious area or performing unnecessary biopsy on a benign-appearing nodule.

• A. Radioactive iodine uptake scanning is indicated when the thyroid-stimulating hormone is suppressed, suggesting a hyperfunctioning nodule, not in this euthyroid patient.
• B. Core needle biopsy is not the standard first biopsy technique for thyroid nodules; ultrasound-guided fine-needle aspiration is preferred.
• C. Empiric levothyroxine suppression therapy has no proven benefit in shrinking thyroid nodules and delays appropriate risk stratification.
• E. Fine-needle aspiration should be guided by ultrasound risk stratification and nodule characteristics rather than performed blindly.

A seatbelt sign (linear abdominal wall ecchymosis) is associated with underlying bowel and mesenteric injury, which can be missed on initial CT because free fluid or subtle wall thickening may be minimal early and perforation can be delayed. Mesenteric vessel injury or a contusion can progress to full-thickness necrosis and perforation over 24-48 hours, presenting with fever, tachycardia, and peritonitis as seen here. This is a classic pitfall of seatbelt sign patients, who require a period of observation or repeat imaging even when the initial CT is unremarkable. The clinical picture of delayed peritonitis after blunt trauma with a seatbelt sign should prompt urgent surgical evaluation for laparotomy.

• A. The spleen is a solid organ and injury would typically be visible on the initial CT; delayed rupture usually presents with hemorrhage, not fever and peritonitis.
• B. An infected abdominal wall hematoma would cause localized, not diffuse, tenderness and would not typically cause this degree of peritonitis.
• C. Retroperitoneal hematoma usually causes flank or back pain and hypotension from blood loss, not fever and peritonitis.
• D. Traumatic pancreatitis typically presents with epigastric pain and elevated amylase/lipase, not diffuse peritonitis from a lower abdominal seatbelt mechanism.

This patient's history of a brief lucid interval after head trauma followed by rapid neurologic deterioration, with a dilated pupil and contralateral hemiparesis, is classic for an epidural hematoma, most often caused by laceration of the middle meningeal artery associated with a temporal bone fracture. Blood accumulates between the dura and the skull, and because the dura is tightly adherent to the sutures, the hematoma is confined and forms a biconvex (lens-shaped) hyperdensity on CT that does not cross suture lines. The dilated, sluggish pupil reflects uncinate herniation compressing the ipsilateral oculomotor nerve, a neurosurgical emergency requiring urgent evacuation. Rapid recognition and surgical decompression are critical to prevent fatal brainstem compression.

• B. Blood in the basal cisterns suggests subarachnoid hemorrhage, which does not typically present with this lucid interval pattern.
• C. Punctate grey-white junction hyperdensities suggest diffuse axonal injury, which presents with immediate loss of consciousness rather than a lucid interval.
• D. Diffuse grey-white loss of differentiation describes diffuse cerebral edema or hypoxic-ischemic injury, not a focal mass lesion.
• E. A crescent-shaped collection crossing suture lines describes a subdural hematoma, which is less classically associated with a lucid interval.

This patient has a symptomatic acute subdural hematoma with significant midline shift in the setting of supratherapeutic warfarin anticoagulation, a situation with high risk of hematoma expansion and herniation. Current guidelines recommend immediate reversal of warfarin with 4-factor prothrombin complex concentrate, which rapidly restores clotting factors, combined with intravenous vitamin K for sustained reversal, and urgent neurosurgical consultation for possible evacuation. Fresh frozen plasma is slower to prepare and administer and less effective than PCC for rapid reversal in life-threatening bleeding. Time to anticoagulation reversal is directly linked to outcome in anticoagulant-associated intracranial hemorrhage, so delay must be avoided.

• A. Withholding reversal risks hematoma expansion and herniation; urgent reversal and neurosurgical input are required.
• B. Protamine reverses heparin, not warfarin, and is not appropriate here; outpatient follow-up is unsafe with midline shift.
• C. Platelets do not reverse warfarin's effect on vitamin K-dependent clotting factors, and a general ward is inappropriate for this acuity.
• E. FFP alone is slower acting and less effective than PCC for rapid warfarin reversal in this emergency.

Periorbital ecchymosis not explained by direct orbital trauma (raccoon eyes), postauricular ecchymosis (Battle sign), and clear rhinorrhea that separates into a central clot and a halo of clear fluid on gauze (the halo sign, suggesting cerebrospinal fluid mixed with blood) together indicate a basilar skull fracture, typically through the anterior or middle cranial fossa. These signs result from blood and CSF tracking along fascial planes from the fracture site. Basilar skull fracture requires CT imaging, often with non-contrast CT of the head and temporal bone, and these patients should avoid nasogastric tubes and nasal instrumentation until the fracture is excluded. Clinical recognition is important because the fracture itself may not always be visible on standard axial CT cuts.

• A. An isolated nasal bone fracture does not cause periorbital ecchymosis bilaterally, mastoid bruising, or CSF rhinorrhea.
• C. An orbital blowout fracture causes periorbital signs localized to the affected side and does not explain Battle sign or CSF leak.
• D. Le Fort II fracture involves the maxilla and nasal bones with malocclusion and facial mobility, not the triad described here.
• E. Anterior epistaxis produces frank blood, not the halo sign of CSF mixed with blood, and would not explain bruising at the mastoid.

The Canadian CT Head Rule identifies high-risk and medium-risk criteria for clinically important brain injury in patients with minor head injury and GCS 13-15. High-risk criteria, which predict need for neurosurgical intervention, include GCS less than 15 at 2 hours, suspected open or depressed skull fracture, signs of basilar skull fracture, two or more episodes of vomiting, and age 65 years or older. Two or more vomiting episodes is one of the high-risk criteria and mandates CT imaging. Mild headache, brief light-headedness, and age under 65 are not criteria in this rule, and retrograde amnesia duration beyond 30 minutes falls under a lower-risk (medium-risk) criterion, not the 20 minutes described.

• A. Retrograde amnesia must be 30 minutes or more before impact to meet the medium-risk criterion; 20 minutes does not qualify.
• B. Age 65 years or older is the threshold criterion; 45 years does not meet it.
• C. A single episode of light-headedness without loss of consciousness is not one of the rule's criteria.
• D. Mild headache severity alone is not a criterion in the Canadian CT Head Rule.

The combination of widening pulse pressure (rising systolic with stable or falling diastolic pressure), bradycardia, and an irregular respiratory pattern constitutes Cushing's triad, a late and ominous sign of markedly elevated intracranial pressure causing brainstem compression. As intracranial pressure rises toward mean arterial pressure, cerebral perfusion pressure falls, triggering a reflex increase in systemic blood pressure (the Cushing reflex) to maintain cerebral perfusion; this hypertension in turn stimulates baroreceptors, producing reflex bradycardia, while brainstem compression disrupts the medullary respiratory centers. This is a medical emergency requiring immediate measures to reduce intracranial pressure and neurosurgical evaluation, as herniation may be imminent. Hypovolemic shock would cause tachycardia and hypotension, the opposite of this pattern.

• A. Hypovolemic shock classically produces tachycardia and hypotension, not bradycardia and hypertension.
• B. An acute MI would not typically produce this specific triad of hypertension, bradycardia, and irregular respirations in this trauma context.
• D. Autonomic dysreflexia occurs with spinal cord lesions above T6 and classically causes hypertension with bradycardia but would not explain an irregular brainstem-type respiratory pattern in a patient with a head injury, not a cord lesion.
• E. Opioid-induced respiratory depression causes slow, shallow breathing but does not explain the hypertension and bradycardia seen here.

Central cord syndrome typically occurs in older adults with pre-existing cervical spondylosis after a hyperextension injury, which causes buckling of the ligamentum flavum and cord compression centrally. The cervical spinal tracts are organized somatotopically with cervical (arm) fibers located more centrally and lumbosacral (leg) fibers more peripherally in the corticospinal and spinothalamic tracts, so central injury produces motor weakness and pain/temperature loss that is disproportionately greater in the upper limbs than the lower limbs. Position and vibration sense, carried in the dorsal columns, are often relatively preserved. Most patients have a favorable prognosis for partial recovery with conservative management, though significant deficits can persist.

• A. Brown-Séquard syndrome results from hemisection of the cord, causing ipsilateral motor and dorsal column loss with contralateral pain/temperature loss, not the bilateral arm-predominant pattern described.
• B. Anterior cord syndrome causes bilateral motor loss and loss of pain/temperature sensation with preserved dorsal column function, but affects the legs and arms more equally and is typically caused by anterior spinal artery infarction, not hyperextension in spondylosis.
• C. Posterior cord syndrome is rare and causes loss of proprioception and vibration sense with preserved motor and pain/temperature function, the opposite of this presentation.
• D. Complete cord transection causes total loss of motor and sensory function below the lesion, not this selective arm-predominant pattern.