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Emergency And Acute Medicine – Amyotrophic Lateral Sclerosis
Core Overview
Amyotrophic lateral sclerosis (ALS) is a progressive, incurable neurodegenerative disease affecting the motor system at all levels. It involves degeneration of both upper and lower motor neurons, leading to muscle weakness, wasting, fasciculations, hyperreflexia, and Babinski signs. Some patients develop associated frontotemporal dementia. The disease eventually results in respiratory failure due to weakness of the diaphragm and other respiratory muscles. ALS most commonly begins between 40 and 70 years of age, affects men more than women, and typically leads to death within 3–5 years of diagnosis, most often from respiratory paralysis.
Causes And Risk Factors
The exact cause of ALS remains unknown. Approximately 10% of cases are familial. Cigarette smoking and heavy metal exposure have been identified as possible risk factors. Pathologically, there is selective loss of upper and lower motor neurons with relative sparing of sensory and other nonmotor neurons.
Clinical Presentation
The most common presentation is asymmetric limb weakness, seen in about 80% of patients. Symptoms may begin in the arms (cervical onset) or legs (lumbar onset) and eventually involve all limbs. Bulbar-onset ALS is the second most common presentation and manifests with dysarthria and dysphagia. Both upper motor neuron signs (hyperreflexia, Babinski sign) and lower motor neuron signs (atrophy, weakness, fasciculations) are present. Extraocular muscles, sphincter control, sensation, and cognition are typically spared early.
History Considerations
Most patients presenting to the emergency department already have a known diagnosis. History should focus on acute complications and functional decline, especially respiratory symptoms. When ALS is suspected in a patient presenting with “weakness,” it is essential to distinguish true neuromuscular weakness from fatigue, dyspnea, pain, or poor exercise tolerance caused by other conditions. True weakness often presents as difficulty performing specific tasks, such as washing hair, gripping objects, climbing stairs, or speaking and swallowing.
Physical Examination
A focused neurologic examination is essential, although ALS is rarely diagnosed definitively in the ED. Upper motor neuron involvement produces stiffness and slow, poorly coordinated movements, while lower motor neuron disease causes muscle wasting, weakness, cramps, and fasciculations. Brisk reflexes and visible muscle atrophy are common findings. The examination should primarily aim to exclude other potentially reversible conditions.
Essential Emergency Evaluation
ALS is a clinical diagnosis and is rarely made for the first time in the emergency department. Recognition of possible ALS warrants referral for outpatient neurologic evaluation. In patients with known ALS and worsening symptoms, evaluation should focus on treatable complications. Forced vital capacity (FVC) is a key assessment; values below 50% of predicted indicate advanced disease and often require ventilatory support. Comparison with prior baseline measurements is crucial.
Diagnostic Studies
Laboratory testing may be useful in cases of undifferentiated weakness to identify alternative diagnoses, such as electrolyte abnormalities or myopathy (elevated CPK). Imaging such as cervical spine radiographs or head CT may be needed after falls or to exclude other neurologic pathology. Electromyography can help confirm the diagnosis but is not typically performed in the ED.
Conditions To Differentiate
Important mimics include cervical spinal cord compression, thyrotoxicosis, heavy metal poisoning, neurosyphilis, Lyme disease, lymphoma-related neuropathy, myasthenia gravis, and esophageal malignancy in bulbar presentations. Acute onset, sensory deficits, or significant pain should prompt evaluation for alternative diagnoses.
Emergency Management Principles
There is no curative therapy for ALS. Riluzole modestly prolongs survival but is not an emergency treatment. ED care focuses on symptom control and management of complications. Respiratory failure is the most critical emergency issue and requires careful assessment of advanced directives before initiating invasive ventilation. Noninvasive ventilation should be attempted first when appropriate, as weaning from mechanical ventilation is often difficult.
Supportive And Symptom-Based Treatment
Pain from immobility or joint stress may respond to NSAIDs. Insomnia can be treated with antihistamines, antidepressants, or benzodiazepines. Excessive salivation and aspiration risk may be reduced with anticholinergic agents. Muscle cramps often improve with baclofen or tizanidine. Constipation related to immobility should be managed with laxatives, stool softeners, and dietary modification.
Disposition And Follow-Up
Admission is indicated for respiratory insufficiency, dehydration, inability to be cared for at home, infection, or other serious complications. Patients with suspected ALS and stable condition may be discharged with urgent neurology referral. Those with known ALS and mild, manageable complications may be discharged if respiratory status is stable and outpatient care is feasible.
Clinical Lessons And Common Errors
ALS is a relentlessly progressive motor neuron disease with no cure. Many patients have advance directives that must be clarified before aggressive interventions. A forced vital capacity below 50% of predicted is a key marker of advanced disease and usually signals the need for ventilatory support.
Core Overview
Amyotrophic lateral sclerosis (ALS) is a progressive, incurable neurodegenerative disease affecting the motor system at all levels. It involves degeneration of both upper and lower motor neurons, leading to muscle weakness, wasting, fasciculations, hyperreflexia, and Babinski signs. Some patients develop associated frontotemporal dementia. The disease eventually results in respiratory failure due to weakness of the diaphragm and other respiratory muscles. ALS most commonly begins between 40 and 70 years of age, affects men more than women, and typically leads to death within 3–5 years of diagnosis, most often from respiratory paralysis.
Causes And Risk Factors
The exact cause of ALS remains unknown. Approximately 10% of cases are familial. Cigarette smoking and heavy metal exposure have been identified as possible risk factors. Pathologically, there is selective loss of upper and lower motor neurons with relative sparing of sensory and other nonmotor neurons.
Clinical Presentation
The most common presentation is asymmetric limb weakness, seen in about 80% of patients. Symptoms may begin in the arms (cervical onset) or legs (lumbar onset) and eventually involve all limbs. Bulbar-onset ALS is the second most common presentation and manifests with dysarthria and dysphagia. Both upper motor neuron signs (hyperreflexia, Babinski sign) and lower motor neuron signs (atrophy, weakness, fasciculations) are present. Extraocular muscles, sphincter control, sensation, and cognition are typically spared early.
History Considerations
Most patients presenting to the emergency department already have a known diagnosis. History should focus on acute complications and functional decline, especially respiratory symptoms. When ALS is suspected in a patient presenting with “weakness,” it is essential to distinguish true neuromuscular weakness from fatigue, dyspnea, pain, or poor exercise tolerance caused by other conditions. True weakness often presents as difficulty performing specific tasks, such as washing hair, gripping objects, climbing stairs, or speaking and swallowing.
Physical Examination
A focused neurologic examination is essential, although ALS is rarely diagnosed definitively in the ED. Upper motor neuron involvement produces stiffness and slow, poorly coordinated movements, while lower motor neuron disease causes muscle wasting, weakness, cramps, and fasciculations. Brisk reflexes and visible muscle atrophy are common findings. The examination should primarily aim to exclude other potentially reversible conditions.
Essential Emergency Evaluation
ALS is a clinical diagnosis and is rarely made for the first time in the emergency department. Recognition of possible ALS warrants referral for outpatient neurologic evaluation. In patients with known ALS and worsening symptoms, evaluation should focus on treatable complications. Forced vital capacity (FVC) is a key assessment; values below 50% of predicted indicate advanced disease and often require ventilatory support. Comparison with prior baseline measurements is crucial.
Diagnostic Studies
Laboratory testing may be useful in cases of undifferentiated weakness to identify alternative diagnoses, such as electrolyte abnormalities or myopathy (elevated CPK). Imaging such as cervical spine radiographs or head CT may be needed after falls or to exclude other neurologic pathology. Electromyography can help confirm the diagnosis but is not typically performed in the ED.
Conditions To Differentiate
Important mimics include cervical spinal cord compression, thyrotoxicosis, heavy metal poisoning, neurosyphilis, Lyme disease, lymphoma-related neuropathy, myasthenia gravis, and esophageal malignancy in bulbar presentations. Acute onset, sensory deficits, or significant pain should prompt evaluation for alternative diagnoses.
Emergency Management Principles
There is no curative therapy for ALS. Riluzole modestly prolongs survival but is not an emergency treatment. ED care focuses on symptom control and management of complications. Respiratory failure is the most critical emergency issue and requires careful assessment of advanced directives before initiating invasive ventilation. Noninvasive ventilation should be attempted first when appropriate, as weaning from mechanical ventilation is often difficult.
Supportive And Symptom-Based Treatment
Pain from immobility or joint stress may respond to NSAIDs. Insomnia can be treated with antihistamines, antidepressants, or benzodiazepines. Excessive salivation and aspiration risk may be reduced with anticholinergic agents. Muscle cramps often improve with baclofen or tizanidine. Constipation related to immobility should be managed with laxatives, stool softeners, and dietary modification.
Disposition And Follow-Up
Admission is indicated for respiratory insufficiency, dehydration, inability to be cared for at home, infection, or other serious complications. Patients with suspected ALS and stable condition may be discharged with urgent neurology referral. Those with known ALS and mild, manageable complications may be discharged if respiratory status is stable and outpatient care is feasible.
Clinical Lessons And Common Errors
ALS is a relentlessly progressive motor neuron disease with no cure. Many patients have advance directives that must be clarified before aggressive interventions. A forced vital capacity below 50% of predicted is a key marker of advanced disease and usually signals the need for ventilatory support.
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Emergency And Acute Medicine – Traumatic Amputation And Replantation
Core Overview
Traumatic amputations are classified as partial or complete. Partial amputations retain some tissue connection between the distal and proximal segments and are managed with revascularization, while complete amputations have no connecting tissue and may be managed with replantation. From an emergency standpoint, both are approached the same way: stabilize the patient, protect the amputated part, control hemorrhage, and arrange urgent specialist involvement.
Causes
Traumatic amputations commonly occur from machinery and powered tools, household appliances, lawnmowers, entrapment between objects, motor vehicle collisions, crush and blast injuries, gunshot or knife wounds, degloving injuries (including ring avulsions), and animal bites.
Key History Points
The exact time of injury is crucial because ischemia time strongly predicts replantation success. Irreversible muscle necrosis begins around 6 hours of ischemia, and tolerable ischemia depends on temperature and muscle content. Digits tolerate longer ischemia because they contain less muscle, with warm ischemia of roughly 8–12 hours and cool ischemia up to 24 hours. Larger limbs tolerate less, with warm ischemia around 4–6 hours and cold ischemia around 10–12 hours. Mechanism matters: clean “guillotine” injuries have better outcomes than crush or avulsion injuries. Document handedness, occupation and hobbies, and comorbidities that reduce success such as diabetes, peripheral vascular disease, rheumatologic disease, and smoking.
Focused Examination
Assessment and documentation of the injured extremity should be detailed. Neurologic compromise includes loss of sensation, reduced two-point discrimination, and loss of active range of motion. In partial amputations, vascular compromise is suggested by a dusky or cyanotic distal segment, delayed capillary refill over 2 seconds, diminished or absent pulses by palpation or Doppler, and the “ribbon sign” from arterial twisting. Use the Allen test for hand injuries when relevant, and consider pulse oximetry on the distal segment. Soft tissue assessment should include skin, muscle, tendon, and nail bed integrity, and identification of exposed bone and fractures.
Essential Emergency Approach
Emergency department priorities include obtaining a rapid, accurate history and exam, stabilizing the patient, preserving the amputated part, and arranging urgent consultation or transfer if replantation is possible. Imaging and labs should never delay time-sensitive transfer when ischemia limits are approaching.
Investigations
Preoperative labs and wound cultures may be obtained if requested for operative planning. Radiographs of both the stump and the amputated part are helpful, but should not delay transport. Further procedures are guided by the surgical team.
Prehospital Priorities
All amputated tissue should be collected, including small fragments of bone, skin, and soft tissue. Patients and parts should be transported to a microvascular replantation center when feasible, unless other life-threatening injuries require immediate transport to a trauma center. Air transport should be considered if ischemia time is a concern.
Initial Stabilization And Hemorrhage Control
Early surgical consultation is critical. Establish IV access and control bleeding by elevating the limb and applying direct pressure with a bulky dressing; use pressure points if needed. Tourniquet use is appropriate if these fail, such as a blood pressure cuff inflated to about 30 mm Hg above systolic pressure. Partial amputations can bleed significantly because vessels may not retract or spasm effectively. Avoid actions that worsen tissue viability, including vascular clamps, cautery, vessel ligation, debridement, and repeated manipulation or examinations.
Care Of The Amputated Part And Stump
Gently remove gross contamination and irrigate with saline only, avoiding antiseptics. Wrap the amputated part in saline-moistened gauze, place it in a clean dry plastic bag or specimen container, then place that sealed container in an ice-water slurry (half ice, half water) or refrigerate at about 4°C. Do not place the part directly on ice or directly into ice water, and avoid dry ice to prevent freezing injury. Irrigate the stump with saline and cover with saline-dampened gauze, splint as needed, and keep partial amputations near anatomic alignment. Preserve all tissue fragments as they may be useful for grafting. Proximal arterial cannulation and perfusion solutions may be considered for major limb amputations only under surgical direction.
Emergency Department Management
Provide tetanus prophylaxis and adequate IV analgesia, keep the patient NPO, and administer prophylactic antibiotics when tissue is devitalized, bone is exposed, or there is contamination. Antibiotic coverage should include Streptococcus, Staphylococcus aureus, and Clostridium perfringens. Treat patients as candidates for surgical salvage until a specialist determines otherwise, and prioritize minimizing ischemia time through early transfer when indicated.
Replantation Considerations
Decision-making incorporates age, occupation, handedness, motivation, general health, and comorbidities such as diabetes and peripheral vascular disease. Common indications include thumb amputations at any level, multiple digit loss, hand amputations through the palm or distal wrist, select digit levels (often distal to the flexor digitorum superficialis insertion and proximal to the DIP joint), some ring avulsion injuries, certain forearm-level injuries when sharp or moderately avulsed, and most pediatric amputations due to favorable functional recovery.
Situations Where Replantation Is Usually Avoided
Replantation is less favorable with severely crushed or mangled parts, multi-level injuries, severe tendon avulsions at the musculotendinous junction, single-digit amputations proximal to the flexor digitorum superficialis insertion, unstable patients with major concurrent injuries, patients unsuitable for anesthesia, and excessively prolonged ischemia times. Lower-extremity replantation is rarely attempted except in selected pediatric cases.
Fingertip Amputation Approach
Fingertip injuries distal to the DIP joint are common. Priorities are preserving length, achieving durable sensate coverage, minimizing pain, and preserving the nail unit when possible. If there is no exposed phalanx, saline irrigation and petrolatum-soaked gauze with healing by secondary intention is often appropriate, especially for wounds under about 1 cm². If there is a small amount of exposed phalanx, trimming bone below the soft-tissue level and closing primarily or allowing secondary healing may be used. Any persistent exposed bone typically requires operative management and specialist consultation. Treat exposed phalanx as an open fracture, so antibiotics are indicated. Splinting helps prevent repeat trauma, and nail bed preservation improves function and cosmesis.
Nonlimb Amputations
Penis, ear, and nose amputations should be handled with the same preservation technique and urgent referral to the appropriate specialist. Successful penile replantation becomes unlikely beyond about 24 hours of cold ischemia or 6 hours of warm ischemia. Ear and nasal replantation may be attempted with variable outcomes depending on injury characteristics and available expertise.
Pediatric And Geriatric Notes
Children should generally be considered for replantation, and fingertip amputations in children can often regenerate with secondary intention, even with volar involvement. Pediatric fingertip injuries distal to the nail lunula may be replanted more successfully than in adults. Advanced age alone is not an absolute contraindication, but medical comorbidities often limit candidacy.
Medications
First-line antibiotic coverage commonly includes cefazolin, with vancomycin as an alternative when indicated. If clostridial contamination is a concern, broader coverage such as piperacillin/tazobactam may be considered based on local protocols and specialist input.
Disposition And Follow-Up
Patients undergoing replantation or revascularization require admission. Selected minor fingertip amputations or mild degloving injuries with stable vasculature may be discharged with close surgical or orthopedic follow-up. Patients with significant skin loss may require later grafting and should be monitored closely.
Clinical Tips And Common Errors
Every effort should be made to minimize ischemia time through rapid consultation or transfer. Avoid any direct contact of the amputated part with ice to prevent freezing injury. Always complete a thorough trauma survey to avoid missing other serious injuries that may be less obvious but life-threatening.
Core Overview
Traumatic amputations are classified as partial or complete. Partial amputations retain some tissue connection between the distal and proximal segments and are managed with revascularization, while complete amputations have no connecting tissue and may be managed with replantation. From an emergency standpoint, both are approached the same way: stabilize the patient, protect the amputated part, control hemorrhage, and arrange urgent specialist involvement.
Causes
Traumatic amputations commonly occur from machinery and powered tools, household appliances, lawnmowers, entrapment between objects, motor vehicle collisions, crush and blast injuries, gunshot or knife wounds, degloving injuries (including ring avulsions), and animal bites.
Key History Points
The exact time of injury is crucial because ischemia time strongly predicts replantation success. Irreversible muscle necrosis begins around 6 hours of ischemia, and tolerable ischemia depends on temperature and muscle content. Digits tolerate longer ischemia because they contain less muscle, with warm ischemia of roughly 8–12 hours and cool ischemia up to 24 hours. Larger limbs tolerate less, with warm ischemia around 4–6 hours and cold ischemia around 10–12 hours. Mechanism matters: clean “guillotine” injuries have better outcomes than crush or avulsion injuries. Document handedness, occupation and hobbies, and comorbidities that reduce success such as diabetes, peripheral vascular disease, rheumatologic disease, and smoking.
Focused Examination
Assessment and documentation of the injured extremity should be detailed. Neurologic compromise includes loss of sensation, reduced two-point discrimination, and loss of active range of motion. In partial amputations, vascular compromise is suggested by a dusky or cyanotic distal segment, delayed capillary refill over 2 seconds, diminished or absent pulses by palpation or Doppler, and the “ribbon sign” from arterial twisting. Use the Allen test for hand injuries when relevant, and consider pulse oximetry on the distal segment. Soft tissue assessment should include skin, muscle, tendon, and nail bed integrity, and identification of exposed bone and fractures.
Essential Emergency Approach
Emergency department priorities include obtaining a rapid, accurate history and exam, stabilizing the patient, preserving the amputated part, and arranging urgent consultation or transfer if replantation is possible. Imaging and labs should never delay time-sensitive transfer when ischemia limits are approaching.
Investigations
Preoperative labs and wound cultures may be obtained if requested for operative planning. Radiographs of both the stump and the amputated part are helpful, but should not delay transport. Further procedures are guided by the surgical team.
Prehospital Priorities
All amputated tissue should be collected, including small fragments of bone, skin, and soft tissue. Patients and parts should be transported to a microvascular replantation center when feasible, unless other life-threatening injuries require immediate transport to a trauma center. Air transport should be considered if ischemia time is a concern.
Initial Stabilization And Hemorrhage Control
Early surgical consultation is critical. Establish IV access and control bleeding by elevating the limb and applying direct pressure with a bulky dressing; use pressure points if needed. Tourniquet use is appropriate if these fail, such as a blood pressure cuff inflated to about 30 mm Hg above systolic pressure. Partial amputations can bleed significantly because vessels may not retract or spasm effectively. Avoid actions that worsen tissue viability, including vascular clamps, cautery, vessel ligation, debridement, and repeated manipulation or examinations.
Care Of The Amputated Part And Stump
Gently remove gross contamination and irrigate with saline only, avoiding antiseptics. Wrap the amputated part in saline-moistened gauze, place it in a clean dry plastic bag or specimen container, then place that sealed container in an ice-water slurry (half ice, half water) or refrigerate at about 4°C. Do not place the part directly on ice or directly into ice water, and avoid dry ice to prevent freezing injury. Irrigate the stump with saline and cover with saline-dampened gauze, splint as needed, and keep partial amputations near anatomic alignment. Preserve all tissue fragments as they may be useful for grafting. Proximal arterial cannulation and perfusion solutions may be considered for major limb amputations only under surgical direction.
Emergency Department Management
Provide tetanus prophylaxis and adequate IV analgesia, keep the patient NPO, and administer prophylactic antibiotics when tissue is devitalized, bone is exposed, or there is contamination. Antibiotic coverage should include Streptococcus, Staphylococcus aureus, and Clostridium perfringens. Treat patients as candidates for surgical salvage until a specialist determines otherwise, and prioritize minimizing ischemia time through early transfer when indicated.
Replantation Considerations
Decision-making incorporates age, occupation, handedness, motivation, general health, and comorbidities such as diabetes and peripheral vascular disease. Common indications include thumb amputations at any level, multiple digit loss, hand amputations through the palm or distal wrist, select digit levels (often distal to the flexor digitorum superficialis insertion and proximal to the DIP joint), some ring avulsion injuries, certain forearm-level injuries when sharp or moderately avulsed, and most pediatric amputations due to favorable functional recovery.
Situations Where Replantation Is Usually Avoided
Replantation is less favorable with severely crushed or mangled parts, multi-level injuries, severe tendon avulsions at the musculotendinous junction, single-digit amputations proximal to the flexor digitorum superficialis insertion, unstable patients with major concurrent injuries, patients unsuitable for anesthesia, and excessively prolonged ischemia times. Lower-extremity replantation is rarely attempted except in selected pediatric cases.
Fingertip Amputation Approach
Fingertip injuries distal to the DIP joint are common. Priorities are preserving length, achieving durable sensate coverage, minimizing pain, and preserving the nail unit when possible. If there is no exposed phalanx, saline irrigation and petrolatum-soaked gauze with healing by secondary intention is often appropriate, especially for wounds under about 1 cm². If there is a small amount of exposed phalanx, trimming bone below the soft-tissue level and closing primarily or allowing secondary healing may be used. Any persistent exposed bone typically requires operative management and specialist consultation. Treat exposed phalanx as an open fracture, so antibiotics are indicated. Splinting helps prevent repeat trauma, and nail bed preservation improves function and cosmesis.
Nonlimb Amputations
Penis, ear, and nose amputations should be handled with the same preservation technique and urgent referral to the appropriate specialist. Successful penile replantation becomes unlikely beyond about 24 hours of cold ischemia or 6 hours of warm ischemia. Ear and nasal replantation may be attempted with variable outcomes depending on injury characteristics and available expertise.
Pediatric And Geriatric Notes
Children should generally be considered for replantation, and fingertip amputations in children can often regenerate with secondary intention, even with volar involvement. Pediatric fingertip injuries distal to the nail lunula may be replanted more successfully than in adults. Advanced age alone is not an absolute contraindication, but medical comorbidities often limit candidacy.
Medications
First-line antibiotic coverage commonly includes cefazolin, with vancomycin as an alternative when indicated. If clostridial contamination is a concern, broader coverage such as piperacillin/tazobactam may be considered based on local protocols and specialist input.
Disposition And Follow-Up
Patients undergoing replantation or revascularization require admission. Selected minor fingertip amputations or mild degloving injuries with stable vasculature may be discharged with close surgical or orthopedic follow-up. Patients with significant skin loss may require later grafting and should be monitored closely.
Clinical Tips And Common Errors
Every effort should be made to minimize ischemia time through rapid consultation or transfer. Avoid any direct contact of the amputated part with ice to prevent freezing injury. Always complete a thorough trauma survey to avoid missing other serious injuries that may be less obvious but life-threatening.
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Emergency And Acute Medicine – Amphetamine Poisoning
Core Overview
Amphetamine toxicity results from increased release of norepinephrine, dopamine, and serotonin, reduced catecholamine reuptake, and direct stimulation of α- and β-adrenergic receptors. These effects lead to a classic sympathomimetic toxidrome that can range from mild agitation to life-threatening hyperthermia, cardiovascular collapse, and multiorgan failure.
Underlying Causes
Amphetamine poisoning may occur from prescription stimulants such as amphetamine, dextroamphetamine, methamphetamine, methylphenidate, phentermine, and related agents. Illicit or “designer” drugs include methamphetamine (“crystal,” “ice,” “crank”), MDMA (“ecstasy”), MDA, methcathinone, and mephedrone, sometimes sold as “bath salts.” These substances are often synthesized in clandestine laboratories and may be smoked, injected, or insufflated, leading to rapid onset and prolonged toxicity.
Clinical Features
Central nervous system findings include agitation, delirium, hyperactivity, tremors, mydriasis, headache, hyperreflexia, seizures, status epilepticus, and coma. Psychiatric manifestations include euphoria, anxiety, aggression, hallucinations, and compulsive behaviors. Cardiovascular effects include tachycardia, hypertensive crisis, dysrhythmias, and potential cardiovascular collapse. Systemic complications include hyperthermia, diaphoresis, rhabdomyolysis, myoglobinuria, acute renal failure, disseminated intravascular coagulation, and anorexia.
History And Physical Examination
History should establish the substance used, dose, timing, route of exposure, and possible coingestions. Symptoms suggesting end-organ injury such as chest pain, dyspnea, headache, confusion, or vomiting should be sought. Physical examination commonly reveals agitation, tachycardia, diaphoresis, and mydriasis. Severe intoxication may present with hyperthermia, hypertensive crisis, seizures, hypotension, or respiratory distress. Careful evaluation for trauma, infection, focal neurologic deficits, cardiac murmurs, pneumothorax, and soft-tissue infections is essential.
Essential Emergency Evaluation
Vital signs must be closely monitored, with core temperature measurement required if hyperthermia is suspected. A temperature greater than 40°C is an ominous sign and mandates immediate intervention. Continuous cardiac monitoring and ECG assessment are essential to detect ischemia or dysrhythmias.
Diagnostic Testing
Laboratory evaluation includes electrolytes, glucose, BUN, creatinine, creatine phosphokinase, urinalysis for blood and myoglobin, and coagulation studies if DIC is suspected. Hyperkalemia and acidosis may accompany rhabdomyolysis and renal failure. Urine toxicology screening may identify coingestants, although some synthetic stimulants may not be detected. Aspirin and acetaminophen levels should be obtained if intentional overdose is possible. Imaging includes chest radiography for pulmonary edema or ARDS and head CT for altered mental status, focal deficits, or severe headache.
Conditions To Differentiate
Important alternative diagnoses include sepsis, thyroid storm, serotonin syndrome, neuroleptic malignant syndrome, pheochromocytoma, subarachnoid hemorrhage, cocaine toxicity, ethanol or sedative withdrawal, anticholinergic toxicity, and other causes of seizures or hypertensive emergencies.
Emergency Department Management
Prehospital care focuses on safety, IV access, and prevention of self-injury. Initial stabilization prioritizes airway, breathing, and circulation, IV fluid resuscitation, cardiac monitoring, and administration of naloxone, glucose, and thiamine if mental status is altered. Activated charcoal may be used early, and whole-bowel irrigation is indicated for body packers. Benzodiazepines are first-line therapy for agitation, seizures, and hypertension related to catecholamine excess. Severe hypertension may require α-blockade with phentolamine or vasodilators such as nitroprusside; β-blockers should be avoided. Hyperthermia requires aggressive sedation, active cooling, and paralysis with nondepolarizing agents if necessary. Rhabdomyolysis is treated with IV fluids to maintain adequate urine output, and dialysis is considered for renal failure or refractory hyperkalemia.
Disposition And Follow-Up
Admission is required for patients with hyperthermia, persistent altered mental status, hypertensive crisis, seizures, rhabdomyolysis, or ongoing tachycardia. Asymptomatic patients who remain stable after observation may be discharged. Referral for substance use treatment, detoxification, and rehabilitation should be arranged when appropriate.
Key Clinical Lessons And Common Errors
Severe amphetamine toxicity carries high morbidity and mortality if hyperthermia and agitation are not rapidly controlled. Core temperature monitoring is critical, and aggressive sedation with benzodiazepines plus active cooling is lifesaving. Rhabdomyolysis and hyperkalemia must be anticipated and treated early. Physical restraints should be minimized when possible, as they may worsen hyperthermia and acidosis. Benzodiazepines remain the cornerstone of treatment for symptomatic methamphetamine and amphetamine intoxication.
Core Overview
Amphetamine toxicity results from increased release of norepinephrine, dopamine, and serotonin, reduced catecholamine reuptake, and direct stimulation of α- and β-adrenergic receptors. These effects lead to a classic sympathomimetic toxidrome that can range from mild agitation to life-threatening hyperthermia, cardiovascular collapse, and multiorgan failure.
Underlying Causes
Amphetamine poisoning may occur from prescription stimulants such as amphetamine, dextroamphetamine, methamphetamine, methylphenidate, phentermine, and related agents. Illicit or “designer” drugs include methamphetamine (“crystal,” “ice,” “crank”), MDMA (“ecstasy”), MDA, methcathinone, and mephedrone, sometimes sold as “bath salts.” These substances are often synthesized in clandestine laboratories and may be smoked, injected, or insufflated, leading to rapid onset and prolonged toxicity.
Clinical Features
Central nervous system findings include agitation, delirium, hyperactivity, tremors, mydriasis, headache, hyperreflexia, seizures, status epilepticus, and coma. Psychiatric manifestations include euphoria, anxiety, aggression, hallucinations, and compulsive behaviors. Cardiovascular effects include tachycardia, hypertensive crisis, dysrhythmias, and potential cardiovascular collapse. Systemic complications include hyperthermia, diaphoresis, rhabdomyolysis, myoglobinuria, acute renal failure, disseminated intravascular coagulation, and anorexia.
History And Physical Examination
History should establish the substance used, dose, timing, route of exposure, and possible coingestions. Symptoms suggesting end-organ injury such as chest pain, dyspnea, headache, confusion, or vomiting should be sought. Physical examination commonly reveals agitation, tachycardia, diaphoresis, and mydriasis. Severe intoxication may present with hyperthermia, hypertensive crisis, seizures, hypotension, or respiratory distress. Careful evaluation for trauma, infection, focal neurologic deficits, cardiac murmurs, pneumothorax, and soft-tissue infections is essential.
Essential Emergency Evaluation
Vital signs must be closely monitored, with core temperature measurement required if hyperthermia is suspected. A temperature greater than 40°C is an ominous sign and mandates immediate intervention. Continuous cardiac monitoring and ECG assessment are essential to detect ischemia or dysrhythmias.
Diagnostic Testing
Laboratory evaluation includes electrolytes, glucose, BUN, creatinine, creatine phosphokinase, urinalysis for blood and myoglobin, and coagulation studies if DIC is suspected. Hyperkalemia and acidosis may accompany rhabdomyolysis and renal failure. Urine toxicology screening may identify coingestants, although some synthetic stimulants may not be detected. Aspirin and acetaminophen levels should be obtained if intentional overdose is possible. Imaging includes chest radiography for pulmonary edema or ARDS and head CT for altered mental status, focal deficits, or severe headache.
Conditions To Differentiate
Important alternative diagnoses include sepsis, thyroid storm, serotonin syndrome, neuroleptic malignant syndrome, pheochromocytoma, subarachnoid hemorrhage, cocaine toxicity, ethanol or sedative withdrawal, anticholinergic toxicity, and other causes of seizures or hypertensive emergencies.
Emergency Department Management
Prehospital care focuses on safety, IV access, and prevention of self-injury. Initial stabilization prioritizes airway, breathing, and circulation, IV fluid resuscitation, cardiac monitoring, and administration of naloxone, glucose, and thiamine if mental status is altered. Activated charcoal may be used early, and whole-bowel irrigation is indicated for body packers. Benzodiazepines are first-line therapy for agitation, seizures, and hypertension related to catecholamine excess. Severe hypertension may require α-blockade with phentolamine or vasodilators such as nitroprusside; β-blockers should be avoided. Hyperthermia requires aggressive sedation, active cooling, and paralysis with nondepolarizing agents if necessary. Rhabdomyolysis is treated with IV fluids to maintain adequate urine output, and dialysis is considered for renal failure or refractory hyperkalemia.
Disposition And Follow-Up
Admission is required for patients with hyperthermia, persistent altered mental status, hypertensive crisis, seizures, rhabdomyolysis, or ongoing tachycardia. Asymptomatic patients who remain stable after observation may be discharged. Referral for substance use treatment, detoxification, and rehabilitation should be arranged when appropriate.
Key Clinical Lessons And Common Errors
Severe amphetamine toxicity carries high morbidity and mortality if hyperthermia and agitation are not rapidly controlled. Core temperature monitoring is critical, and aggressive sedation with benzodiazepines plus active cooling is lifesaving. Rhabdomyolysis and hyperkalemia must be anticipated and treated early. Physical restraints should be minimized when possible, as they may worsen hyperthermia and acidosis. Benzodiazepines remain the cornerstone of treatment for symptomatic methamphetamine and amphetamine intoxication.
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Emergency And Acute Medicine – Amenorrhea
Core Overview
Amenorrhea refers to the absence of menstruation. Primary amenorrhea is defined as the absence of spontaneous uterine bleeding by age 16 years or within 5 years of breast development, which normally begins by age 13. Secondary amenorrhea is the absence of uterine bleeding for 3 months in a woman with previously regular menses or for 9 months in a woman with prior oligomenorrhea. Secondary amenorrhea is more common, and pregnancy is the most frequent cause encountered in emergency care.
Underlying Causes
Primary amenorrhea is most commonly due to gonadal failure, hypothalamic–pituitary disorders, chromosomal abnormalities, structural abnormalities such as imperforate hymen, or conditions such as Turner syndrome. Secondary amenorrhea is frequently related to pregnancy, lactation, or the postpartum state. Other causes include Asherman syndrome, dysfunction of the hypothalamic–pituitary–ovarian axis, polycystic ovarian syndrome, endocrinopathies, extremes of body weight, intense physical exercise, medications, autoimmune disease, ovarian failure, and menopause.
Clinical Features
History should focus on age at menarche, menstrual pattern, sexual activity, exercise habits, weight change, chronic illness, medication use, prior chemotherapy or CNS radiation, family history, and infertility. Physical examination may reveal signs of low estrogen such as atrophic vaginal mucosa and mood changes, or signs of hyperandrogenism including truncal obesity, hirsutism, acne, and male-pattern baldness. Thyroid examination, pelvic or genital examination, and Tanner staging are essential components of assessment.
Essential Emergency Evaluation
A pregnancy test is mandatory in all patients presenting with amenorrhea. If pregnancy testing is negative and the patient is otherwise stable, no additional emergent testing is typically required in the emergency department.
Diagnostic Testing
If pregnancy is excluded, further laboratory evaluation such as TSH, prolactin, LH, and FSH can be deferred to outpatient follow-up with gynecology or primary care. Imaging is not required emergently unless there is concern for ectopic pregnancy or another acute process based on the patient’s presentation. No diagnostic procedures are typically required in the emergency setting.
Conditions To Differentiate
Pregnancy must always be excluded first, including ectopic pregnancy when clinically suspected.
Emergency Department Management
Prehospital care is supportive. If amenorrhea is related to pregnancy, management should follow pregnancy-specific protocols. In the emergency department, treatment consists primarily of reassurance, patient education, and appropriate referral for outpatient evaluation.
Disposition And Follow-Up
Admission is not required unless there is concern for ectopic pregnancy or another emergent condition. Most patients can be safely discharged with referral to gynecology. Follow-up with a gynecologist is recommended for definitive evaluation and management.
Key Clinical Lessons And Common Errors
Pregnancy is the most important and common cause of amenorrhea in the emergency department and must always be ruled out. Urine pregnancy testing may yield false-negative results in dilute urine or early pregnancy, and serum testing should be considered when clinical suspicion is high, particularly for ectopic pregnancy. Eating disorders such as anorexia nervosa should be considered, especially in adolescents presenting with amenorrhea.
Core Overview
Amenorrhea refers to the absence of menstruation. Primary amenorrhea is defined as the absence of spontaneous uterine bleeding by age 16 years or within 5 years of breast development, which normally begins by age 13. Secondary amenorrhea is the absence of uterine bleeding for 3 months in a woman with previously regular menses or for 9 months in a woman with prior oligomenorrhea. Secondary amenorrhea is more common, and pregnancy is the most frequent cause encountered in emergency care.
Underlying Causes
Primary amenorrhea is most commonly due to gonadal failure, hypothalamic–pituitary disorders, chromosomal abnormalities, structural abnormalities such as imperforate hymen, or conditions such as Turner syndrome. Secondary amenorrhea is frequently related to pregnancy, lactation, or the postpartum state. Other causes include Asherman syndrome, dysfunction of the hypothalamic–pituitary–ovarian axis, polycystic ovarian syndrome, endocrinopathies, extremes of body weight, intense physical exercise, medications, autoimmune disease, ovarian failure, and menopause.
Clinical Features
History should focus on age at menarche, menstrual pattern, sexual activity, exercise habits, weight change, chronic illness, medication use, prior chemotherapy or CNS radiation, family history, and infertility. Physical examination may reveal signs of low estrogen such as atrophic vaginal mucosa and mood changes, or signs of hyperandrogenism including truncal obesity, hirsutism, acne, and male-pattern baldness. Thyroid examination, pelvic or genital examination, and Tanner staging are essential components of assessment.
Essential Emergency Evaluation
A pregnancy test is mandatory in all patients presenting with amenorrhea. If pregnancy testing is negative and the patient is otherwise stable, no additional emergent testing is typically required in the emergency department.
Diagnostic Testing
If pregnancy is excluded, further laboratory evaluation such as TSH, prolactin, LH, and FSH can be deferred to outpatient follow-up with gynecology or primary care. Imaging is not required emergently unless there is concern for ectopic pregnancy or another acute process based on the patient’s presentation. No diagnostic procedures are typically required in the emergency setting.
Conditions To Differentiate
Pregnancy must always be excluded first, including ectopic pregnancy when clinically suspected.
Emergency Department Management
Prehospital care is supportive. If amenorrhea is related to pregnancy, management should follow pregnancy-specific protocols. In the emergency department, treatment consists primarily of reassurance, patient education, and appropriate referral for outpatient evaluation.
Disposition And Follow-Up
Admission is not required unless there is concern for ectopic pregnancy or another emergent condition. Most patients can be safely discharged with referral to gynecology. Follow-up with a gynecologist is recommended for definitive evaluation and management.
Key Clinical Lessons And Common Errors
Pregnancy is the most important and common cause of amenorrhea in the emergency department and must always be ruled out. Urine pregnancy testing may yield false-negative results in dilute urine or early pregnancy, and serum testing should be considered when clinical suspicion is high, particularly for ectopic pregnancy. Eating disorders such as anorexia nervosa should be considered, especially in adolescents presenting with amenorrhea.
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Emergency And Acute Medicine – Amebiasis
Core Overview
Amebiasis is an invasive parasitic infection with both intestinal and extraintestinal manifestations. It is endemic worldwide, particularly in regions with poor sanitation. High-risk populations include travelers to or immigrants from endemic areas, institutionalized individuals, men who have sex with men, individuals engaging in oral–anal sexual practices, and those with HIV infection. Severe disease and complications are more likely in immunocompromised patients, pregnant or postpartum individuals, those at extremes of age, and patients with malnutrition or malignancy.
Causative Organism And Transmission
The disease is caused by Entamoeba histolytica, an anaerobic, nonflagellated protozoan. Humans are the sole reservoir. Transmission occurs via the fecal–oral route, leading to invasive colitis after ingestion. Extraintestinal spread occurs hematogenously.
Clinical Manifestations
Intestinal disease typically presents 1 week to 1 month after exposure. Most cases involve acute nondysenteric colitis with afebrile diarrhea and minimal abdominal findings. Classic dysentery presents with bloody, mucoid diarrhea, abdominal pain, tenesmus, and weight loss, with fever being uncommon. Fulminant colitis manifests with severe toxicity, rigid abdomen, high risk of perforation, and mortality exceeding 40%. Toxic megacolon presents with profuse diarrhea, fever, abdominal distension, and peritonitis, often associated with corticosteroid use. Chronic complications include ameboma, amebic strictures, and chronic colitis.
Extraintestinal disease most commonly involves amebic liver abscess, typically a solitary lesion in the right lobe. Patients present with fever, right upper quadrant pain, hepatomegaly, and minimal diarrhea. Complications include rupture into pleural, peritoneal, or pericardial spaces. Rare manifestations include brain, lung, splenic, perinephric, genital, and cutaneous amebiasis.
History And Physical Examination
A careful exposure history and assessment of risk factors are essential. Physical examination should focus on identifying signs of dehydration, peritonitis, sepsis, shock, abdominal masses, or hepatomegaly. Digital rectal examination frequently reveals gross or occult blood.
Diagnostic Evaluation
Stool PCR is the diagnostic gold standard with near-perfect sensitivity and specificity. Stool antigen testing and serology are valuable adjuncts, particularly in suspected liver abscess where stool studies may be negative. Stool microscopy is no longer recommended due to poor sensitivity. Laboratory findings may include leukocytosis, elevated alkaline phosphatase and ALT in liver abscess, and electrolyte abnormalities from dehydration.
Imaging with abdominal ultrasound or CT is used to identify liver abscesses and assess rupture risk. Colonoscopy with biopsy provides definitive diagnosis for colitis, dysentery, ameboma, and strictures. Fine-needle aspiration of liver abscess is reserved for diagnostic uncertainty or treatment failure.
Conditions To Differentiate
Intestinal amebiasis must be distinguished from enteroinvasive bacterial infections, inflammatory bowel disease, ischemic colitis, malignancy, pancreatitis, and bowel obstruction. Liver abscess should be differentiated from bacterial abscess, echinococcal cyst, tuberculosis, malignancy, and cholecystitis. Cutaneous disease may mimic carcinoma or sexually transmitted infections.
Initial Stabilization And Supportive Care
Management begins with airway, breathing, and circulation assessment. Intravenous isotonic fluids are indicated for dehydration or shock. Antidiarrheal agents should be avoided. Electrolyte abnormalities must be corrected promptly.
Definitive Emergency Department Management
Systemic therapy with metronidazole or tinidazole is first-line for invasive disease. All patients must receive subsequent luminal therapy to eradicate intestinal colonization. Luminal agents should never be used alone. If stool and serology are negative but suspicion remains high, gastroenterology consultation and repeat testing are warranted. Surgical intervention is required for toxic megacolon, perforation, or refractory disease. Liver abscesses may require drainage if large, left-sided, ruptured, or unresponsive to medical therapy.
Special Population Considerations
In pregnancy, metronidazole should be used cautiously in the first trimester but not withheld in life-threatening disease. Certain agents, including tinidazole and tetracycline, are contraindicated. Pediatric patients are at higher risk for fulminant colitis and require careful monitoring.
Disposition And Follow-Up
Hospital admission is indicated for patients with shock, sepsis, peritonitis, severe dehydration, electrolyte imbalance, fulminant colitis, bowel obstruction, extraintestinal abscesses, or failure of outpatient therapy. Discharge may be appropriate for stable patients with mild disease who can tolerate oral therapy. Follow-up with gastroenterology or infectious disease is recommended within one week.
Key Clinical Lessons And Common Errors
Avoid antidiarrheal medications in suspected amebiasis. Always treat with both a systemic amebicide and a luminal agent unless contraindicated. Maintain vigilance for high-mortality complications such as fulminant colitis and extraintestinal disease, as delayed recognition significantly worsens outcomes.
Core Overview
Amebiasis is an invasive parasitic infection with both intestinal and extraintestinal manifestations. It is endemic worldwide, particularly in regions with poor sanitation. High-risk populations include travelers to or immigrants from endemic areas, institutionalized individuals, men who have sex with men, individuals engaging in oral–anal sexual practices, and those with HIV infection. Severe disease and complications are more likely in immunocompromised patients, pregnant or postpartum individuals, those at extremes of age, and patients with malnutrition or malignancy.
Causative Organism And Transmission
The disease is caused by Entamoeba histolytica, an anaerobic, nonflagellated protozoan. Humans are the sole reservoir. Transmission occurs via the fecal–oral route, leading to invasive colitis after ingestion. Extraintestinal spread occurs hematogenously.
Clinical Manifestations
Intestinal disease typically presents 1 week to 1 month after exposure. Most cases involve acute nondysenteric colitis with afebrile diarrhea and minimal abdominal findings. Classic dysentery presents with bloody, mucoid diarrhea, abdominal pain, tenesmus, and weight loss, with fever being uncommon. Fulminant colitis manifests with severe toxicity, rigid abdomen, high risk of perforation, and mortality exceeding 40%. Toxic megacolon presents with profuse diarrhea, fever, abdominal distension, and peritonitis, often associated with corticosteroid use. Chronic complications include ameboma, amebic strictures, and chronic colitis.
Extraintestinal disease most commonly involves amebic liver abscess, typically a solitary lesion in the right lobe. Patients present with fever, right upper quadrant pain, hepatomegaly, and minimal diarrhea. Complications include rupture into pleural, peritoneal, or pericardial spaces. Rare manifestations include brain, lung, splenic, perinephric, genital, and cutaneous amebiasis.
History And Physical Examination
A careful exposure history and assessment of risk factors are essential. Physical examination should focus on identifying signs of dehydration, peritonitis, sepsis, shock, abdominal masses, or hepatomegaly. Digital rectal examination frequently reveals gross or occult blood.
Diagnostic Evaluation
Stool PCR is the diagnostic gold standard with near-perfect sensitivity and specificity. Stool antigen testing and serology are valuable adjuncts, particularly in suspected liver abscess where stool studies may be negative. Stool microscopy is no longer recommended due to poor sensitivity. Laboratory findings may include leukocytosis, elevated alkaline phosphatase and ALT in liver abscess, and electrolyte abnormalities from dehydration.
Imaging with abdominal ultrasound or CT is used to identify liver abscesses and assess rupture risk. Colonoscopy with biopsy provides definitive diagnosis for colitis, dysentery, ameboma, and strictures. Fine-needle aspiration of liver abscess is reserved for diagnostic uncertainty or treatment failure.
Conditions To Differentiate
Intestinal amebiasis must be distinguished from enteroinvasive bacterial infections, inflammatory bowel disease, ischemic colitis, malignancy, pancreatitis, and bowel obstruction. Liver abscess should be differentiated from bacterial abscess, echinococcal cyst, tuberculosis, malignancy, and cholecystitis. Cutaneous disease may mimic carcinoma or sexually transmitted infections.
Initial Stabilization And Supportive Care
Management begins with airway, breathing, and circulation assessment. Intravenous isotonic fluids are indicated for dehydration or shock. Antidiarrheal agents should be avoided. Electrolyte abnormalities must be corrected promptly.
Definitive Emergency Department Management
Systemic therapy with metronidazole or tinidazole is first-line for invasive disease. All patients must receive subsequent luminal therapy to eradicate intestinal colonization. Luminal agents should never be used alone. If stool and serology are negative but suspicion remains high, gastroenterology consultation and repeat testing are warranted. Surgical intervention is required for toxic megacolon, perforation, or refractory disease. Liver abscesses may require drainage if large, left-sided, ruptured, or unresponsive to medical therapy.
Special Population Considerations
In pregnancy, metronidazole should be used cautiously in the first trimester but not withheld in life-threatening disease. Certain agents, including tinidazole and tetracycline, are contraindicated. Pediatric patients are at higher risk for fulminant colitis and require careful monitoring.
Disposition And Follow-Up
Hospital admission is indicated for patients with shock, sepsis, peritonitis, severe dehydration, electrolyte imbalance, fulminant colitis, bowel obstruction, extraintestinal abscesses, or failure of outpatient therapy. Discharge may be appropriate for stable patients with mild disease who can tolerate oral therapy. Follow-up with gastroenterology or infectious disease is recommended within one week.
Key Clinical Lessons And Common Errors
Avoid antidiarrheal medications in suspected amebiasis. Always treat with both a systemic amebicide and a luminal agent unless contraindicated. Maintain vigilance for high-mortality complications such as fulminant colitis and extraintestinal disease, as delayed recognition significantly worsens outcomes.
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Emergency And Acute Medicine – Alkalosis
Core Overview
Alkalosis refers to disorders in which blood pH is elevated above normal. This may occur due to excessive loss of carbon dioxide from hyperventilation (respiratory alkalosis) or from an increase in serum bicarbonate concentration (metabolic alkalosis). Respiratory alkalosis results from increased alveolar ventilation leading to reduced PaCO₂, commonly triggered by hypoxemia, metabolic acidosis, or direct stimulation of central or peripheral chemoreceptors. It is rarely life-threatening and typically occurs with pH values below 7.50.
Metabolic alkalosis develops when hydrogen ions are lost or bicarbonate is gained. Persistence requires impaired renal excretion of bicarbonate, often due to volume depletion, electrolyte abnormalities, or hormonal influences. Severe alkalemia carries high mortality, particularly when pH exceeds 7.55–7.65.
Underlying Causes
Respiratory alkalosis may arise from central nervous system conditions such as anxiety, pain, fever, stroke, infection, or intracranial lesions. Hypoxemia from altitude exposure, anemia, or pulmonary shunting is a frequent trigger. Drugs and hormones including salicylates, catecholamines, nicotine, progesterone, pregnancy, and hyperthyroidism may also contribute. Thoracic conditions such as pulmonary embolism, pneumonia, pneumothorax, sepsis, hepatic failure, and heat exhaustion are additional causes.
Metabolic alkalosis is commonly due to gastrointestinal hydrogen loss from vomiting, nasogastric suction, bulimia, or chloride-losing diarrhea. Renal losses occur with diuretics, mineralocorticoid excess, post-hypercapnia states, and inherited tubulopathies such as Bartter or Gitelman syndromes. Other mechanisms include intracellular hydrogen shifts, extracellular volume contraction, bicarbonate administration, and massive transfusions.
Clinical Manifestations
Symptoms result from reduced cerebral blood flow, electrolyte disturbances, and the underlying disease process. Neuromuscular irritability due to hypocalcemia is common and may present with weakness, myalgias, tetany, paresthesias, carpal–pedal spasm, seizures, or altered mental status. Cardiac arrhythmias may occur in association with hypokalemia. Signs of dehydration, hypoxemia, and neuromuscular excitability such as Chvostek or Trousseau signs may be present.
Initial Evaluation
Assessment begins with serum electrolytes demonstrating elevated bicarbonate in metabolic alkalosis and evaluation for hypokalemia or hypocalcemia. Renal function testing helps identify dehydration or renal failure. Blood gas analysis confirms alkalemia and distinguishes respiratory from metabolic causes. Expected compensatory responses should be calculated to detect mixed acid–base disorders. Measurement of urine chloride is essential in metabolic alkalosis to differentiate saline-responsive from saline-resistant causes.
Diagnostic Studies
Additional laboratory testing may include glucose, ionized calcium, magnesium, pregnancy testing, and targeted studies based on clinical suspicion such as CBC, cultures, liver function tests, aspirin levels, toxicology screening, renin, aldosterone, cortisol, and thyroid studies. Imaging with chest radiography may reveal pulmonary or cardiac pathology. Electrocardiography is useful for identifying conduction abnormalities related to electrolyte disturbances.
Conditions To Consider
Respiratory alkalosis requires exclusion of organic pathology before diagnosing anxiety-related hyperventilation. Metabolic alkalosis may be categorized as saline responsive (e.g., gastric losses, diuretics, post-hypercapnia states) or saline resistant (e.g., hyperaldosteronism, Cushing syndrome, inherited renal disorders, exogenous alkali exposure).
Emergency Management Principles
Initial stabilization focuses on airway, breathing, and circulation with oxygen, IV access, and cardiac monitoring. Altered mental status warrants administration of glucose, thiamine, and naloxone as indicated.
Respiratory alkalosis is managed by treating the underlying cause, with cautious use of anxiolytics when appropriate.
Management of metabolic alkalosis depends on urine chloride. Volume-depleted patients benefit from isotonic saline and potassium repletion. Saline-resistant cases require treatment of the underlying endocrine or renal disorder, potassium supplementation, aldosterone antagonists, or acetazolamide. Severe refractory alkalosis may rarely require dilute hydrochloric acid infusion or hemodialysis.
Pharmacologic Therapy
Therapeutic agents may include dextrose for hypoglycemia, potassium supplementation, naloxone, thiamine, acetazolamide, spironolactone, antiemetics, and proton pump inhibitors. Dilute hydrochloric acid infusion is reserved for life-threatening alkalemia and must be administered via a central line with close monitoring.
Disposition And Follow-Up
Hospital admission is required for severe alkalemia, altered mental status, dysrhythmias, significant electrolyte abnormalities, hemodynamic instability, or serious underlying disease. ICU care is indicated for pH values greater than 7.55. Patients may be discharged once alkalosis resolves and contributing factors are corrected.
Key Clinical Insights And Common Errors
Respiratory alkalosis is driven by increased minute ventilation resulting in low PaCO₂ and elevated pH. Metabolic alkalosis typically reflects increased bicarbonate retention due to volume, potassium, or chloride depletion. Contraction alkalosis occurs with extracellular fluid loss concentrating serum bicarbonate. Mixed acid–base disorders should be suspected when pH appears normal despite abnormal PaCO₂ or bicarbonate, or when compensatory responses are inappropriate.
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Emergency and Acute Medicine – Adrenal Insufficiency
Overview and Clinical Significance
Adrenal insufficiency occurs when cortisol production is inadequate to meet the body’s physiologic or stress-related demands. In emergency and acute care, the most critical presentation is acute adrenal insufficiency (Addisonian crisis), a life-threatening condition characterized by hypotension, electrolyte disturbances, and shock. Because laboratory confirmation is often delayed or unavailable in the emergency department, early recognition and empiric treatment are essential to prevent morbidity and mortality.
Etiology and Pathophysiology
Adrenal insufficiency is classified as primary, secondary, or tertiary. Primary adrenal insufficiency results from destruction or dysfunction of the adrenal glands and leads to deficiencies in cortisol and often aldosterone. Causes include autoimmune disease, congenital adrenal hyperplasia, infections (such as tuberculosis or fungal disease), metastatic cancer, infiltrative disorders, bilateral adrenal hemorrhage, and medication-related suppression (e.g., etomidate, ketoconazole). Secondary adrenal insufficiency arises from pituitary dysfunction or chronic suppression of ACTH, most commonly due to prolonged glucocorticoid therapy. Tertiary adrenal insufficiency results from hypothalamic dysfunction. An Addisonian crisis is often triggered by infection, trauma, surgery, dehydration, pregnancy, abrupt steroid withdrawal, or initiation of thyroid hormone in an undiagnosed patient.
Clinical Presentation
Symptoms are frequently nonspecific and may include fatigue, weakness, anorexia, nausea, vomiting, abdominal pain, salt craving, dizziness, and muscle or joint pain. Physical findings often include hypotension, tachycardia, fever or hypothermia, weight loss, and altered mental status. Findings more specific to primary adrenal insufficiency include hyperpigmentation, vitiligo, dehydration, hyperkalemia, and hyponatremia. In Addisonian crisis, patients may present in circulatory shock with severe hypotension, hypoglycemia, electrolyte abnormalities, and acute kidney injury.
Diagnostic Evaluation
Diagnosis in the emergency department is primarily clinical. Laboratory findings typically demonstrate hyponatremia, hyperkalemia, elevated BUN and creatinine from volume depletion, and low or inappropriately normal glucose levels. A random serum cortisol level below 20 μg/dL in a critically ill or hypotensive patient strongly suggests adrenal insufficiency, but treatment should not be delayed while awaiting results. Definitive confirmation with a cosyntropin (ACTH) stimulation test is usually performed after stabilization. If steroids must be administered before testing, dexamethasone is preferred because it does not interfere with cortisol assays.
Emergency Management
Initial management follows airway, breathing, and circulation principles. Aggressive volume resuscitation with isotonic saline is critical to correct hypovolemia and hypotension. Immediate glucocorticoid replacement is required, with intravenous hydrocortisone as first-line therapy; dexamethasone is an acceptable alternative. Hypoglycemia should be treated with intravenous dextrose, and life-threatening hyperkalemia managed using standard emergency protocols. Identification and treatment of precipitating factors, particularly infection or medication nonadherence, are essential components of care.
Disposition and Key Pitfalls
All patients with acute adrenal insufficiency require hospital admission, and those with hemodynamic instability should be managed in an intensive care setting. With timely therapy, blood pressure and clinical status typically improve within several hours. A major pitfall in emergency care is failure to recognize adrenal insufficiency in patients with unexplained hypotension or shock refractory to fluids and vasopressors. When suspected, steroid therapy should be administered immediately, as early treatment is lifesaving and should never be delayed for diagnostic confirmation.
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Emergency and Acute Medicine – Acute Coronary Syndrome: Myocardial Infarction
Overview and Definitions
Myocardial infarction (MI) results from an acute imbalance between myocardial oxygen supply and demand, leading to ischemia and irreversible myocardial injury. It is a core component of acute coronary syndrome (ACS), which includes unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). Differentiation among these entities is essential, as management strategies and urgency of reperfusion differ substantially.
Etiology and Pathophysiology
The most common cause of MI is atherosclerotic coronary artery disease with plaque rupture and superallowing thrombus formation, resulting in partial or complete coronary occlusion. Other mechanisms include coronary vasospasm (variant/Prinzmetal angina), microvascular dysfunction, coronary embolism, arteritis (e.g., lupus, Takayasu arteritis, Kawasaki disease), prolonged hypotension, severe anemia, carbon monoxide poisoning, thyroid storm, or structural abnormalities such as aneurysm or ectasia. Cocaine and amphetamine use may precipitate MI through intense vasospasm and thrombosis.
Major risk factors include hypercholesterolemia, diabetes mellitus, hypertension, smoking, male sex, postmenopausal status in women, and a family history of premature coronary artery disease.
Clinical Presentation
Chest pain is the most common presenting symptom. Patients typically describe substernal pressure, heaviness, squeezing, burning, or tightness. Pain may radiate to the arms, shoulders, back, neck, or jaw. Anginal equivalents, particularly common in older adults, women, and patients with diabetes, include dyspnea, diaphoresis, nausea or vomiting, abdominal pain, syncope, or unexplained weakness.
Symptoms often last longer than 30 minutes and may occur at rest or with exertion. Many patients report preceding crescendo angina. Pain is usually not positional or pleuritic and is often only partially relieved by rest or nitroglycerin. A clenched fist over the chest (Levine sign) is suggestive of ischemic pain.
Physical Examination
The physical exam may be normal, especially early. Possible findings include tachycardia, hypertension during pain, S3 or S4 gallop, a new murmur from papillary muscle dysfunction with mitral regurgitation, diminished peripheral pulses, or signs of acute decompensated heart failure.
Essential Emergency Evaluation
History remains the most critical element in differentiating MI from noncardiac causes of chest pain. Rapid assessment and early testing are required to avoid delays in reperfusion therapy.
Electrocardiography
A 12-lead ECG is the cornerstone of diagnosis and must be obtained immediately. ECG findings help distinguish STEMI from NSTEMI and nonischemic causes of ST elevation such as pericarditis, early repolarization, left ventricular hypertrophy with strain, prior infarction with aneurysm, or hyperkalemia.
Diagnostic criteria for STEMI include new ST-segment elevation at the J point in two contiguous leads (with sex- and lead-specific thresholds). ST depression in leads V1–V2 may indicate posterior infarction.
New or presumed new left bundle branch block alone is no longer considered diagnostic of STEMI; however, Sgarbossa criteria can identify MI in patients with LBBB. Echocardiography may reveal regional wall motion abnormalities or mechanical complications.
Laboratory and Imaging Studies
Cardiac biomarkers (troponin I or T, CK-MB) confirm myocardial necrosis and guide risk stratification. Additional testing includes electrolytes, calcium, magnesium, renal function, and digoxin level when relevant. Chest radiography may reveal pulmonary edema, cardiomegaly, or alternative diagnoses such as aortic dissection.
Differential Diagnosis
The differential for MI-like chest pain includes aortic dissection, pulmonary embolism, pericarditis, pneumonia, pneumothorax, esophageal disorders, biliary disease, peptic ulcer disease, anxiety or panic disorder, and musculoskeletal chest pain.
Prehospital and Initial ED Management
Early management includes IV access, cardiac monitoring, oxygen if hypoxic, aspirin administration, and sublingual nitroglycerin for symptom relief. When feasible, a prehospital ECG with advance notification to the receiving facility improves outcomes.
Definitive Emergency Treatment
STEMI is a time-critical emergency requiring immediate reperfusion. Primary percutaneous coronary intervention (PCI) is preferred and should occur within 90 minutes of first medical contact. If PCI is not available within 120 minutes, fibrinolytic therapy should be administered promptly.
All patients without contraindications should receive aspirin. Dual antiplatelet therapy with clopidogrel, prasugrel, or ticagrelor is used based on reperfusion strategy and patient factors. Nitrates are administered if systolic blood pressure is adequate and there is no evidence of right ventricular infarction.
β-blockers are recommended within the first 24 hours unless contraindicated. Anticoagulation with unfractionated heparin, bivalirudin, or low-molecular-weight heparin is used depending on whether PCI or thrombolysis is planned. Morphine may be used judiciously for pain control.
Life-threatening dysrhythmias and conduction disturbances must be managed promptly, with pacing or defibrillation as indicated. Patients in cardiogenic shock require urgent transfer to a catheterization laboratory for revascularization and mechanical circulatory support when necessary.
Disposition and Follow-Up
All patients with confirmed myocardial infarction require hospital admission, typically to a coronary care or intensive care unit. Patients with uncertain diagnoses often benefit from observation with serial ECGs, biomarkers, and advanced testing. No patient with MI should be discharged from the emergency department.
Clinical Pearls and Pitfalls
Rapid recognition and reperfusion save myocardium and lives—time is muscle. Door-to-needle time for thrombolysis should be within 30 minutes when PCI is unavailable. A single normal ECG or negative biomarker does not exclude MI early in the course. New LBBB alone should not be considered diagnostic without supportive findings. Maintain a high index of suspicion in patients with atypical presentations.
Overview and Definitions
Myocardial infarction (MI) results from an acute imbalance between myocardial oxygen supply and demand, leading to ischemia and irreversible myocardial injury. It is a core component of acute coronary syndrome (ACS), which includes unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). Differentiation among these entities is essential, as management strategies and urgency of reperfusion differ substantially.
Etiology and Pathophysiology
The most common cause of MI is atherosclerotic coronary artery disease with plaque rupture and superallowing thrombus formation, resulting in partial or complete coronary occlusion. Other mechanisms include coronary vasospasm (variant/Prinzmetal angina), microvascular dysfunction, coronary embolism, arteritis (e.g., lupus, Takayasu arteritis, Kawasaki disease), prolonged hypotension, severe anemia, carbon monoxide poisoning, thyroid storm, or structural abnormalities such as aneurysm or ectasia. Cocaine and amphetamine use may precipitate MI through intense vasospasm and thrombosis.
Major risk factors include hypercholesterolemia, diabetes mellitus, hypertension, smoking, male sex, postmenopausal status in women, and a family history of premature coronary artery disease.
Clinical Presentation
Chest pain is the most common presenting symptom. Patients typically describe substernal pressure, heaviness, squeezing, burning, or tightness. Pain may radiate to the arms, shoulders, back, neck, or jaw. Anginal equivalents, particularly common in older adults, women, and patients with diabetes, include dyspnea, diaphoresis, nausea or vomiting, abdominal pain, syncope, or unexplained weakness.
Symptoms often last longer than 30 minutes and may occur at rest or with exertion. Many patients report preceding crescendo angina. Pain is usually not positional or pleuritic and is often only partially relieved by rest or nitroglycerin. A clenched fist over the chest (Levine sign) is suggestive of ischemic pain.
Physical Examination
The physical exam may be normal, especially early. Possible findings include tachycardia, hypertension during pain, S3 or S4 gallop, a new murmur from papillary muscle dysfunction with mitral regurgitation, diminished peripheral pulses, or signs of acute decompensated heart failure.
Essential Emergency Evaluation
History remains the most critical element in differentiating MI from noncardiac causes of chest pain. Rapid assessment and early testing are required to avoid delays in reperfusion therapy.
Electrocardiography
A 12-lead ECG is the cornerstone of diagnosis and must be obtained immediately. ECG findings help distinguish STEMI from NSTEMI and nonischemic causes of ST elevation such as pericarditis, early repolarization, left ventricular hypertrophy with strain, prior infarction with aneurysm, or hyperkalemia.
Diagnostic criteria for STEMI include new ST-segment elevation at the J point in two contiguous leads (with sex- and lead-specific thresholds). ST depression in leads V1–V2 may indicate posterior infarction.
New or presumed new left bundle branch block alone is no longer considered diagnostic of STEMI; however, Sgarbossa criteria can identify MI in patients with LBBB. Echocardiography may reveal regional wall motion abnormalities or mechanical complications.
Laboratory and Imaging Studies
Cardiac biomarkers (troponin I or T, CK-MB) confirm myocardial necrosis and guide risk stratification. Additional testing includes electrolytes, calcium, magnesium, renal function, and digoxin level when relevant. Chest radiography may reveal pulmonary edema, cardiomegaly, or alternative diagnoses such as aortic dissection.
Differential Diagnosis
The differential for MI-like chest pain includes aortic dissection, pulmonary embolism, pericarditis, pneumonia, pneumothorax, esophageal disorders, biliary disease, peptic ulcer disease, anxiety or panic disorder, and musculoskeletal chest pain.
Prehospital and Initial ED Management
Early management includes IV access, cardiac monitoring, oxygen if hypoxic, aspirin administration, and sublingual nitroglycerin for symptom relief. When feasible, a prehospital ECG with advance notification to the receiving facility improves outcomes.
Definitive Emergency Treatment
STEMI is a time-critical emergency requiring immediate reperfusion. Primary percutaneous coronary intervention (PCI) is preferred and should occur within 90 minutes of first medical contact. If PCI is not available within 120 minutes, fibrinolytic therapy should be administered promptly.
All patients without contraindications should receive aspirin. Dual antiplatelet therapy with clopidogrel, prasugrel, or ticagrelor is used based on reperfusion strategy and patient factors. Nitrates are administered if systolic blood pressure is adequate and there is no evidence of right ventricular infarction.
β-blockers are recommended within the first 24 hours unless contraindicated. Anticoagulation with unfractionated heparin, bivalirudin, or low-molecular-weight heparin is used depending on whether PCI or thrombolysis is planned. Morphine may be used judiciously for pain control.
Life-threatening dysrhythmias and conduction disturbances must be managed promptly, with pacing or defibrillation as indicated. Patients in cardiogenic shock require urgent transfer to a catheterization laboratory for revascularization and mechanical circulatory support when necessary.
Disposition and Follow-Up
All patients with confirmed myocardial infarction require hospital admission, typically to a coronary care or intensive care unit. Patients with uncertain diagnoses often benefit from observation with serial ECGs, biomarkers, and advanced testing. No patient with MI should be discharged from the emergency department.
Clinical Pearls and Pitfalls
Rapid recognition and reperfusion save myocardium and lives—time is muscle. Door-to-needle time for thrombolysis should be within 30 minutes when PCI is unavailable. A single normal ECG or negative biomarker does not exclude MI early in the course. New LBBB alone should not be considered diagnostic without supportive findings. Maintain a high index of suspicion in patients with atypical presentations.
- Published on
Emergency and Acute Medicine – Acute Coronary Syndrome: Myocardial Infarction
Overview and Definitions
Myocardial infarction (MI) results from an acute imbalance between myocardial oxygen supply and demand, leading to ischemia and irreversible myocardial injury. It is a core component of acute coronary syndrome (ACS), which includes unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). Differentiation among these entities is essential, as management strategies and urgency of reperfusion differ substantially.
Etiology and Pathophysiology
The most common cause of MI is atherosclerotic coronary artery disease with plaque rupture and superallowing thrombus formation, resulting in partial or complete coronary occlusion. Other mechanisms include coronary vasospasm (variant/Prinzmetal angina), microvascular dysfunction, coronary embolism, arteritis (e.g., lupus, Takayasu arteritis, Kawasaki disease), prolonged hypotension, severe anemia, carbon monoxide poisoning, thyroid storm, or structural abnormalities such as aneurysm or ectasia. Cocaine and amphetamine use may precipitate MI through intense vasospasm and thrombosis.
Major risk factors include hypercholesterolemia, diabetes mellitus, hypertension, smoking, male sex, postmenopausal status in women, and a family history of premature coronary artery disease.
Clinical Presentation
Chest pain is the most common presenting symptom. Patients typically describe substernal pressure, heaviness, squeezing, burning, or tightness. Pain may radiate to the arms, shoulders, back, neck, or jaw. Anginal equivalents, particularly common in older adults, women, and patients with diabetes, include dyspnea, diaphoresis, nausea or vomiting, abdominal pain, syncope, or unexplained weakness.
Symptoms often last longer than 30 minutes and may occur at rest or with exertion. Many patients report preceding crescendo angina. Pain is usually not positional or pleuritic and is often only partially relieved by rest or nitroglycerin. A clenched fist over the chest (Levine sign) is suggestive of ischemic pain.
Physical Examination
The physical exam may be normal, especially early. Possible findings include tachycardia, hypertension during pain, S3 or S4 gallop, a new murmur from papillary muscle dysfunction with mitral regurgitation, diminished peripheral pulses, or signs of acute decompensated heart failure.
Essential Emergency Evaluation
History remains the most critical element in differentiating MI from noncardiac causes of chest pain. Rapid assessment and early testing are required to avoid delays in reperfusion therapy.
Electrocardiography
A 12-lead ECG is the cornerstone of diagnosis and must be obtained immediately. ECG findings help distinguish STEMI from NSTEMI and nonischemic causes of ST elevation such as pericarditis, early repolarization, left ventricular hypertrophy with strain, prior infarction with aneurysm, or hyperkalemia.
Diagnostic criteria for STEMI include new ST-segment elevation at the J point in two contiguous leads (with sex- and lead-specific thresholds). ST depression in leads V1–V2 may indicate posterior infarction.
New or presumed new left bundle branch block alone is no longer considered diagnostic of STEMI; however, Sgarbossa criteria can identify MI in patients with LBBB. Echocardiography may reveal regional wall motion abnormalities or mechanical complications.
Laboratory and Imaging Studies
Cardiac biomarkers (troponin I or T, CK-MB) confirm myocardial necrosis and guide risk stratification. Additional testing includes electrolytes, calcium, magnesium, renal function, and digoxin level when relevant. Chest radiography may reveal pulmonary edema, cardiomegaly, or alternative diagnoses such as aortic dissection.
Differential Diagnosis
The differential for MI-like chest pain includes aortic dissection, pulmonary embolism, pericarditis, pneumonia, pneumothorax, esophageal disorders, biliary disease, peptic ulcer disease, anxiety or panic disorder, and musculoskeletal chest pain.
Prehospital and Initial ED Management
Early management includes IV access, cardiac monitoring, oxygen if hypoxic, aspirin administration, and sublingual nitroglycerin for symptom relief. When feasible, a prehospital ECG with advance notification to the receiving facility improves outcomes.
Definitive Emergency Treatment
STEMI is a time-critical emergency requiring immediate reperfusion. Primary percutaneous coronary intervention (PCI) is preferred and should occur within 90 minutes of first medical contact. If PCI is not available within 120 minutes, fibrinolytic therapy should be administered promptly.
All patients without contraindications should receive aspirin. Dual antiplatelet therapy with clopidogrel, prasugrel, or ticagrelor is used based on reperfusion strategy and patient factors. Nitrates are administered if systolic blood pressure is adequate and there is no evidence of right ventricular infarction.
β-blockers are recommended within the first 24 hours unless contraindicated. Anticoagulation with unfractionated heparin, bivalirudin, or low-molecular-weight heparin is used depending on whether PCI or thrombolysis is planned. Morphine may be used judiciously for pain control.
Life-threatening dysrhythmias and conduction disturbances must be managed promptly, with pacing or defibrillation as indicated. Patients in cardiogenic shock require urgent transfer to a catheterization laboratory for revascularization and mechanical circulatory support when necessary.
Disposition and Follow-Up
All patients with confirmed myocardial infarction require hospital admission, typically to a coronary care or intensive care unit. Patients with uncertain diagnoses often benefit from observation with serial ECGs, biomarkers, and advanced testing. No patient with MI should be discharged from the emergency department.
Clinical Pearls and Pitfalls
Rapid recognition and reperfusion save myocardium and lives—time is muscle. Door-to-needle time for thrombolysis should be within 30 minutes when PCI is unavailable. A single normal ECG or negative biomarker does not exclude MI early in the course. New LBBB alone should not be considered diagnostic without supportive findings. Maintain a high index of suspicion in patients with atypical presentations.
Overview and Definitions
Myocardial infarction (MI) results from an acute imbalance between myocardial oxygen supply and demand, leading to ischemia and irreversible myocardial injury. It is a core component of acute coronary syndrome (ACS), which includes unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). Differentiation among these entities is essential, as management strategies and urgency of reperfusion differ substantially.
Etiology and Pathophysiology
The most common cause of MI is atherosclerotic coronary artery disease with plaque rupture and superallowing thrombus formation, resulting in partial or complete coronary occlusion. Other mechanisms include coronary vasospasm (variant/Prinzmetal angina), microvascular dysfunction, coronary embolism, arteritis (e.g., lupus, Takayasu arteritis, Kawasaki disease), prolonged hypotension, severe anemia, carbon monoxide poisoning, thyroid storm, or structural abnormalities such as aneurysm or ectasia. Cocaine and amphetamine use may precipitate MI through intense vasospasm and thrombosis.
Major risk factors include hypercholesterolemia, diabetes mellitus, hypertension, smoking, male sex, postmenopausal status in women, and a family history of premature coronary artery disease.
Clinical Presentation
Chest pain is the most common presenting symptom. Patients typically describe substernal pressure, heaviness, squeezing, burning, or tightness. Pain may radiate to the arms, shoulders, back, neck, or jaw. Anginal equivalents, particularly common in older adults, women, and patients with diabetes, include dyspnea, diaphoresis, nausea or vomiting, abdominal pain, syncope, or unexplained weakness.
Symptoms often last longer than 30 minutes and may occur at rest or with exertion. Many patients report preceding crescendo angina. Pain is usually not positional or pleuritic and is often only partially relieved by rest or nitroglycerin. A clenched fist over the chest (Levine sign) is suggestive of ischemic pain.
Physical Examination
The physical exam may be normal, especially early. Possible findings include tachycardia, hypertension during pain, S3 or S4 gallop, a new murmur from papillary muscle dysfunction with mitral regurgitation, diminished peripheral pulses, or signs of acute decompensated heart failure.
Essential Emergency Evaluation
History remains the most critical element in differentiating MI from noncardiac causes of chest pain. Rapid assessment and early testing are required to avoid delays in reperfusion therapy.
Electrocardiography
A 12-lead ECG is the cornerstone of diagnosis and must be obtained immediately. ECG findings help distinguish STEMI from NSTEMI and nonischemic causes of ST elevation such as pericarditis, early repolarization, left ventricular hypertrophy with strain, prior infarction with aneurysm, or hyperkalemia.
Diagnostic criteria for STEMI include new ST-segment elevation at the J point in two contiguous leads (with sex- and lead-specific thresholds). ST depression in leads V1–V2 may indicate posterior infarction.
New or presumed new left bundle branch block alone is no longer considered diagnostic of STEMI; however, Sgarbossa criteria can identify MI in patients with LBBB. Echocardiography may reveal regional wall motion abnormalities or mechanical complications.
Laboratory and Imaging Studies
Cardiac biomarkers (troponin I or T, CK-MB) confirm myocardial necrosis and guide risk stratification. Additional testing includes electrolytes, calcium, magnesium, renal function, and digoxin level when relevant. Chest radiography may reveal pulmonary edema, cardiomegaly, or alternative diagnoses such as aortic dissection.
Differential Diagnosis
The differential for MI-like chest pain includes aortic dissection, pulmonary embolism, pericarditis, pneumonia, pneumothorax, esophageal disorders, biliary disease, peptic ulcer disease, anxiety or panic disorder, and musculoskeletal chest pain.
Prehospital and Initial ED Management
Early management includes IV access, cardiac monitoring, oxygen if hypoxic, aspirin administration, and sublingual nitroglycerin for symptom relief. When feasible, a prehospital ECG with advance notification to the receiving facility improves outcomes.
Definitive Emergency Treatment
STEMI is a time-critical emergency requiring immediate reperfusion. Primary percutaneous coronary intervention (PCI) is preferred and should occur within 90 minutes of first medical contact. If PCI is not available within 120 minutes, fibrinolytic therapy should be administered promptly.
All patients without contraindications should receive aspirin. Dual antiplatelet therapy with clopidogrel, prasugrel, or ticagrelor is used based on reperfusion strategy and patient factors. Nitrates are administered if systolic blood pressure is adequate and there is no evidence of right ventricular infarction.
β-blockers are recommended within the first 24 hours unless contraindicated. Anticoagulation with unfractionated heparin, bivalirudin, or low-molecular-weight heparin is used depending on whether PCI or thrombolysis is planned. Morphine may be used judiciously for pain control.
Life-threatening dysrhythmias and conduction disturbances must be managed promptly, with pacing or defibrillation as indicated. Patients in cardiogenic shock require urgent transfer to a catheterization laboratory for revascularization and mechanical circulatory support when necessary.
Disposition and Follow-Up
All patients with confirmed myocardial infarction require hospital admission, typically to a coronary care or intensive care unit. Patients with uncertain diagnoses often benefit from observation with serial ECGs, biomarkers, and advanced testing. No patient with MI should be discharged from the emergency department.
Clinical Pearls and Pitfalls
Rapid recognition and reperfusion save myocardium and lives—time is muscle. Door-to-needle time for thrombolysis should be within 30 minutes when PCI is unavailable. A single normal ECG or negative biomarker does not exclude MI early in the course. New LBBB alone should not be considered diagnostic without supportive findings. Maintain a high index of suspicion in patients with atypical presentations.
- Published on
Emergency and Acute Medicine – Acromioclavicular (AC) Joint Injury
Anatomy and Injury Overview
The acromioclavicular (AC) joint is formed by the distal clavicle articulating with the acromion of the scapula. Stability is provided by the acromioclavicular (AC) ligament, the coracoclavicular (CC) ligament, and dynamic support from the deltoid and trapezius muscles. The AC ligament primarily maintains horizontal stability, while the CC ligament provides vertical stability. Injury occurs along a predictable spectrum, classically described by the Rockwood classification, which reflects progressive disruption of these stabilizing structures.
Rockwood Classification
Type I injuries involve a sprain of the AC ligament without rupture. The CC ligament, deltoid, and trapezius remain intact, and radiographs are normal; diagnosis is clinical, with localized AC joint tenderness.
Type II injuries feature rupture of the AC ligament with horizontal instability of the distal clavicle and a sprained but intact CC ligament. Mild deltoid and trapezius injury may be present. Imaging shows slight widening of the AC joint (normally <5 mm) with a normal cc distance (11–13 mm).< />pan>
Type III injuries include rupture of both the AC and CC ligaments, producing horizontal and vertical instability. The deltoid and trapezius are detached, and radiographs demonstrate widening of the AC joint with superior displacement of the distal clavicle, typically about 100%.
Types IV, V, and VI represent severe injuries and are best appreciated on axillary or lateral views. All require operative management and carry a higher risk of prolonged disability. Type IV involves posterior displacement of the clavicle into the trapezius; Type V shows marked superior displacement with a 100–300% increase in CC distance and dramatic shoulder droop; Type VI, usually associated with high-energy trauma, features inferior displacement of the clavicle into a subacromial or subcoracoid position and is often accompanied by neurovascular injury.
Mechanism and Epidemiology
AC joint injuries are most common in young, active males, particularly during contact sports. The typical mechanism is a direct blow to the superior or lateral shoulder with the arm adducted, such as during a fall. Less commonly, injury occurs indirectly through a fall on an outstretched hand or elbow, transmitting force to the AC joint.
Clinical Presentation
Patients usually report pain over the superior or anterior shoulder following trauma, worsened by cross-body movement, reaching behind the back, or overhead activity. The severity of symptoms correlates with the degree of ligament disruption. Associated neurovascular complaints or cervical spine symptoms should heighten concern for severe injury.
Physical Examination
Examination is best performed with the patient seated or standing, as gravity accentuates instability. Inspection may reveal swelling, ecchymosis, deformity, asymmetry, or skin tenting. A prominent distal clavicle with a sagging acromion suggests at least a Type II injury.
Palpation should proceed systematically from the sternoclavicular joint along the clavicle to the AC joint, CC ligament, coracoid process, scapula, and proximal humerus. AC joint tenderness suggests AC ligament injury, while horizontal instability indicates rupture. Tenderness or vertical instability implicates CC ligament disruption.
Provocative maneuvers include the cross-body adduction test, which compresses the AC joint and reproduces pain, and the O’Brien test, which may elicit superior shoulder pain in AC pathology. A complete distal neurovascular examination, including assessment of the brachial plexus, and a careful cervical spine evaluation are essential.
Diagnostic Evaluation
Diagnosis relies on history, examination, and targeted imaging. Dedicated AC joint radiographs with bilateral comparison are recommended when injury is suspected, as standard shoulder views may obscure subtle findings. The Zanca view (10–15° cephalic tilt) improves visualization of the AC joint, while axillary views are critical for identifying posterior or inferior clavicular displacement. Stress views are no longer routinely recommended. Advanced imaging with CT or MRI is reserved for surgical planning or complex injuries, and angiography may be indicated if vascular compromise is suspected.
Differential Diagnosis
Conditions that may mimic AC joint injury include shoulder dislocation, clavicle or acromion fractures, rotator cuff pathology, tendinitis, adhesive capsulitis, cervical radiculopathy, osteoarthritis, osteomyelitis, and—in children—distal clavicle physeal fractures.
Management in the Emergency Setting
Initial care includes ice application, sling immobilization, analgesia, and cervical spine precautions when indicated.
Type I and II injuries are managed conservatively with rest, ice, NSAIDs, brief sling use (typically 3–7 days), and early range-of-motion exercises. Most patients return to normal activity within 2–4 weeks once painless strength and motion are restored.
Type III injuries require sling immobilization, analgesia, and early orthopedic referral (within 72 hours). Management is controversial, with treatment individualized based on patient age, activity level, occupation, hand dominance, and reinjury risk.
Types IV, V, and VI injuries necessitate immediate orthopedic consultation and operative repair.
A recognized long-term complication of AC joint injury is post-traumatic arthritis.
Pediatric Considerations
In children, the clavicle is encased in a periosteal sleeve, with the CC ligament contained within and the AC ligament external and more vulnerable. True AC joint dislocations are uncommon in pediatrics and are usually Type I or II. Distal clavicle physeal fractures are more frequent. Younger children with Type III injuries are typically managed conservatively, while adolescents may require more aggressive treatment. Types IV–VI generally require surgery.
Disposition and Follow-Up
Patients with Type I or II injuries may be discharged with orthopedic follow-up in 2–4 weeks. Type III injuries require urgent orthopedic evaluation, and Types IV–VI typically warrant admission for operative management. Open injuries and pediatric cases should receive prompt specialist assessment.
Clinical Pearls and Pitfalls
Normal CC spacing distinguishes Type I and II injuries and supports conservative management. Type III injuries demonstrate complete superior displacement and require early orthopedic input. Types IV–VI share ligamentous disruption with Type III injuries but differ by clavicular position and uniformly require surgical repair.
Anatomy and Injury Overview
The acromioclavicular (AC) joint is formed by the distal clavicle articulating with the acromion of the scapula. Stability is provided by the acromioclavicular (AC) ligament, the coracoclavicular (CC) ligament, and dynamic support from the deltoid and trapezius muscles. The AC ligament primarily maintains horizontal stability, while the CC ligament provides vertical stability. Injury occurs along a predictable spectrum, classically described by the Rockwood classification, which reflects progressive disruption of these stabilizing structures.
Rockwood Classification
Type I injuries involve a sprain of the AC ligament without rupture. The CC ligament, deltoid, and trapezius remain intact, and radiographs are normal; diagnosis is clinical, with localized AC joint tenderness.
Type II injuries feature rupture of the AC ligament with horizontal instability of the distal clavicle and a sprained but intact CC ligament. Mild deltoid and trapezius injury may be present. Imaging shows slight widening of the AC joint (normally <5 mm) with a normal cc distance (11–13 mm).< />pan>
Type III injuries include rupture of both the AC and CC ligaments, producing horizontal and vertical instability. The deltoid and trapezius are detached, and radiographs demonstrate widening of the AC joint with superior displacement of the distal clavicle, typically about 100%.
Types IV, V, and VI represent severe injuries and are best appreciated on axillary or lateral views. All require operative management and carry a higher risk of prolonged disability. Type IV involves posterior displacement of the clavicle into the trapezius; Type V shows marked superior displacement with a 100–300% increase in CC distance and dramatic shoulder droop; Type VI, usually associated with high-energy trauma, features inferior displacement of the clavicle into a subacromial or subcoracoid position and is often accompanied by neurovascular injury.
Mechanism and Epidemiology
AC joint injuries are most common in young, active males, particularly during contact sports. The typical mechanism is a direct blow to the superior or lateral shoulder with the arm adducted, such as during a fall. Less commonly, injury occurs indirectly through a fall on an outstretched hand or elbow, transmitting force to the AC joint.
Clinical Presentation
Patients usually report pain over the superior or anterior shoulder following trauma, worsened by cross-body movement, reaching behind the back, or overhead activity. The severity of symptoms correlates with the degree of ligament disruption. Associated neurovascular complaints or cervical spine symptoms should heighten concern for severe injury.
Physical Examination
Examination is best performed with the patient seated or standing, as gravity accentuates instability. Inspection may reveal swelling, ecchymosis, deformity, asymmetry, or skin tenting. A prominent distal clavicle with a sagging acromion suggests at least a Type II injury.
Palpation should proceed systematically from the sternoclavicular joint along the clavicle to the AC joint, CC ligament, coracoid process, scapula, and proximal humerus. AC joint tenderness suggests AC ligament injury, while horizontal instability indicates rupture. Tenderness or vertical instability implicates CC ligament disruption.
Provocative maneuvers include the cross-body adduction test, which compresses the AC joint and reproduces pain, and the O’Brien test, which may elicit superior shoulder pain in AC pathology. A complete distal neurovascular examination, including assessment of the brachial plexus, and a careful cervical spine evaluation are essential.
Diagnostic Evaluation
Diagnosis relies on history, examination, and targeted imaging. Dedicated AC joint radiographs with bilateral comparison are recommended when injury is suspected, as standard shoulder views may obscure subtle findings. The Zanca view (10–15° cephalic tilt) improves visualization of the AC joint, while axillary views are critical for identifying posterior or inferior clavicular displacement. Stress views are no longer routinely recommended. Advanced imaging with CT or MRI is reserved for surgical planning or complex injuries, and angiography may be indicated if vascular compromise is suspected.
Differential Diagnosis
Conditions that may mimic AC joint injury include shoulder dislocation, clavicle or acromion fractures, rotator cuff pathology, tendinitis, adhesive capsulitis, cervical radiculopathy, osteoarthritis, osteomyelitis, and—in children—distal clavicle physeal fractures.
Management in the Emergency Setting
Initial care includes ice application, sling immobilization, analgesia, and cervical spine precautions when indicated.
Type I and II injuries are managed conservatively with rest, ice, NSAIDs, brief sling use (typically 3–7 days), and early range-of-motion exercises. Most patients return to normal activity within 2–4 weeks once painless strength and motion are restored.
Type III injuries require sling immobilization, analgesia, and early orthopedic referral (within 72 hours). Management is controversial, with treatment individualized based on patient age, activity level, occupation, hand dominance, and reinjury risk.
Types IV, V, and VI injuries necessitate immediate orthopedic consultation and operative repair.
A recognized long-term complication of AC joint injury is post-traumatic arthritis.
Pediatric Considerations
In children, the clavicle is encased in a periosteal sleeve, with the CC ligament contained within and the AC ligament external and more vulnerable. True AC joint dislocations are uncommon in pediatrics and are usually Type I or II. Distal clavicle physeal fractures are more frequent. Younger children with Type III injuries are typically managed conservatively, while adolescents may require more aggressive treatment. Types IV–VI generally require surgery.
Disposition and Follow-Up
Patients with Type I or II injuries may be discharged with orthopedic follow-up in 2–4 weeks. Type III injuries require urgent orthopedic evaluation, and Types IV–VI typically warrant admission for operative management. Open injuries and pediatric cases should receive prompt specialist assessment.
Clinical Pearls and Pitfalls
Normal CC spacing distinguishes Type I and II injuries and supports conservative management. Type III injuries demonstrate complete superior displacement and require early orthopedic input. Types IV–VI share ligamentous disruption with Type III injuries but differ by clavicular position and uniformly require surgical repair.
