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Emergency and acute medicine – penetrating chest trauma
Cause and mechanism
Penetrating chest trauma most commonly results from gunshot wounds or stab wounds. Less frequently, injury occurs from impalement on a sharp object following a fall or high-energy impact. These mechanisms place intrathoracic organs and major vessels at high risk for rapid deterioration.
Clinical features
Patients may present with an object impaled in the chest wall or an obvious penetrating wound with variable external bleeding. Common symptoms include chest pain, dyspnea, and respiratory distress. Altered mental status may occur secondary to hypoxemia or shock. Physical findings can include absent or asymmetric breath sounds, hypotension, and jugular venous distention, suggesting pneumothorax, hemothorax, or cardiac tamponade.
Initial evaluation
A rapid assessment of airway, breathing, and circulation is mandatory. The focused exam should evaluate respiratory effort, chest wall excursion, crepitus, subcutaneous emphysema, breath sounds, and heart sounds. An upright chest radiograph is preferred to identify pneumothorax, although a supine film should be obtained first if spinal precautions are required. Baseline hemoglobin, pulse oximetry, arterial blood gas, serum lactate, and type and screen should be obtained early.
Diagnostic studies
Echocardiography is indicated when tamponade is suspected or when a wound is near the heart. In penetrating precordial injuries, hemopericardium may decompress into the pleural space, so repeat pericardial ultrasound after chest tube placement is recommended. Electrocardiography assists in identifying myocardial injury. With gunshot wounds, imaging must account for all entry and exit sites, and additional studies of the abdomen or pelvis may be required. Arteriography is indicated if great vessel injury is suspected. Esophageal evaluation with contrast swallow or endoscopy and bronchoscopy should be considered when aerodigestive injury is possible.
Differential considerations
Life-threatening diagnoses include pneumothorax, tension or open pneumothorax, hemothorax, pulmonary contusion, myocardial contusion or rupture, pericardial tamponade, traumatic aortic injury, tracheobronchial or esophageal injury, diaphragmatic rupture, intra-abdominal injury, and spinal cord injury.
Prehospital priorities
All patients with signs of life should be transported rapidly to a trauma center. Full spinal immobilization is indicated when spinal injury is suspected. Impaled objects must never be removed in the field because they may be tamponading major bleeding. Suspected tension pneumothorax requires immediate needle decompression. Large open pneumothoraces should be covered with a three-sided occlusive dressing to prevent tension physiology. Transport should not be delayed for intravenous access.
Early resuscitation
Airway, breathing, and circulation management is the priority. Endotracheal intubation is indicated for respiratory distress, hypoxia, or hypotension. Supplemental oxygen should be provided to stable patients. Two large-bore peripheral IV lines should be established, with cautious fluid resuscitation. In penetrating aortic injury, permissive hypotension with a systolic pressure around 90 mm Hg is recommended until surgical control is achieved. Suspected tension pneumothorax requires immediate needle thoracostomy followed by chest tube placement without waiting for imaging. Pericardial tamponade with instability warrants emergency pericardiocentesis followed by rapid operative intervention.
Emergency department management
The trauma surgeon should be notified immediately. Tube thoracostomy is required for pneumothorax or hemothorax, using appropriately sized tubes. Aggressive crystalloid resuscitation should be avoided when pulmonary contusion is present. Wounds below the nipple line or posterior scapular tip raise concern for intra-abdominal injury and require further evaluation with ultrasound, CT, diagnostic peritoneal lavage, or operative exploration. Chest wounds should not be probed, and impaled objects should only be removed in the operating room. All foreign material should be preserved as forensic evidence. Tetanus prophylaxis should be updated as indicated.
Medications and supportive care
Analgesia and sedation should be provided using small, titrated doses of short-acting agents to avoid respiratory compromise. High-dose steroids for spinal cord injury remain controversial and should follow institutional protocols. Broad-spectrum intravenous antibiotics are indicated if wounds are grossly contaminated.
Disposition and outcomes
All patients with penetrating chest trauma require hospital admission. Hemodynamically unstable patients should proceed directly to the operating room. Emergency department thoracotomy may be lifesaving in selected patients with penetrating torso trauma who had signs of life in the field and short prehospital CPR duration. Large initial chest tube output or persistent bleeding mandates surgical intervention. Patients with isolated minor chest wall wounds and normal imaging may be observed briefly and discharged if repeat evaluation excludes intrathoracic injury and the patient remains stable.
Cause and mechanism
Penetrating chest trauma most commonly results from gunshot wounds or stab wounds. Less frequently, injury occurs from impalement on a sharp object following a fall or high-energy impact. These mechanisms place intrathoracic organs and major vessels at high risk for rapid deterioration.
Clinical features
Patients may present with an object impaled in the chest wall or an obvious penetrating wound with variable external bleeding. Common symptoms include chest pain, dyspnea, and respiratory distress. Altered mental status may occur secondary to hypoxemia or shock. Physical findings can include absent or asymmetric breath sounds, hypotension, and jugular venous distention, suggesting pneumothorax, hemothorax, or cardiac tamponade.
Initial evaluation
A rapid assessment of airway, breathing, and circulation is mandatory. The focused exam should evaluate respiratory effort, chest wall excursion, crepitus, subcutaneous emphysema, breath sounds, and heart sounds. An upright chest radiograph is preferred to identify pneumothorax, although a supine film should be obtained first if spinal precautions are required. Baseline hemoglobin, pulse oximetry, arterial blood gas, serum lactate, and type and screen should be obtained early.
Diagnostic studies
Echocardiography is indicated when tamponade is suspected or when a wound is near the heart. In penetrating precordial injuries, hemopericardium may decompress into the pleural space, so repeat pericardial ultrasound after chest tube placement is recommended. Electrocardiography assists in identifying myocardial injury. With gunshot wounds, imaging must account for all entry and exit sites, and additional studies of the abdomen or pelvis may be required. Arteriography is indicated if great vessel injury is suspected. Esophageal evaluation with contrast swallow or endoscopy and bronchoscopy should be considered when aerodigestive injury is possible.
Differential considerations
Life-threatening diagnoses include pneumothorax, tension or open pneumothorax, hemothorax, pulmonary contusion, myocardial contusion or rupture, pericardial tamponade, traumatic aortic injury, tracheobronchial or esophageal injury, diaphragmatic rupture, intra-abdominal injury, and spinal cord injury.
Prehospital priorities
All patients with signs of life should be transported rapidly to a trauma center. Full spinal immobilization is indicated when spinal injury is suspected. Impaled objects must never be removed in the field because they may be tamponading major bleeding. Suspected tension pneumothorax requires immediate needle decompression. Large open pneumothoraces should be covered with a three-sided occlusive dressing to prevent tension physiology. Transport should not be delayed for intravenous access.
Early resuscitation
Airway, breathing, and circulation management is the priority. Endotracheal intubation is indicated for respiratory distress, hypoxia, or hypotension. Supplemental oxygen should be provided to stable patients. Two large-bore peripheral IV lines should be established, with cautious fluid resuscitation. In penetrating aortic injury, permissive hypotension with a systolic pressure around 90 mm Hg is recommended until surgical control is achieved. Suspected tension pneumothorax requires immediate needle thoracostomy followed by chest tube placement without waiting for imaging. Pericardial tamponade with instability warrants emergency pericardiocentesis followed by rapid operative intervention.
Emergency department management
The trauma surgeon should be notified immediately. Tube thoracostomy is required for pneumothorax or hemothorax, using appropriately sized tubes. Aggressive crystalloid resuscitation should be avoided when pulmonary contusion is present. Wounds below the nipple line or posterior scapular tip raise concern for intra-abdominal injury and require further evaluation with ultrasound, CT, diagnostic peritoneal lavage, or operative exploration. Chest wounds should not be probed, and impaled objects should only be removed in the operating room. All foreign material should be preserved as forensic evidence. Tetanus prophylaxis should be updated as indicated.
Medications and supportive care
Analgesia and sedation should be provided using small, titrated doses of short-acting agents to avoid respiratory compromise. High-dose steroids for spinal cord injury remain controversial and should follow institutional protocols. Broad-spectrum intravenous antibiotics are indicated if wounds are grossly contaminated.
Disposition and outcomes
All patients with penetrating chest trauma require hospital admission. Hemodynamically unstable patients should proceed directly to the operating room. Emergency department thoracotomy may be lifesaving in selected patients with penetrating torso trauma who had signs of life in the field and short prehospital CPR duration. Large initial chest tube output or persistent bleeding mandates surgical intervention. Patients with isolated minor chest wall wounds and normal imaging may be observed briefly and discharged if repeat evaluation excludes intrathoracic injury and the patient remains stable.
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Emergency and acute medicine – Chemical Weapons Poisoning
General overview
Chemical weapons poisoning refers to exposure to toxic agents designed to cause injury or death by affecting the central nervous system, lungs, cardiovascular system, skin, eyes, or gastrointestinal tract. These agents may be encountered in warfare, terrorism, industrial accidents, or mass casualty incidents and often involve multiple victims presenting simultaneously.
Types of agents and mechanisms
Blood agents such as cyanide disrupt cellular respiration by binding to cytochrome oxidase and uncoupling oxidative phosphorylation, leading to rapid tissue hypoxia.
Blister agents, including sulfur mustard, nitrogen mustard, lewisite, and phosgene oxime, cause alkylation and cross-linking of DNA and proteins, resulting in cellular membrane damage and delayed tissue necrosis.
Lacrimators and riot control agents, such as CN (Mace), CS, oleoresin capsaicin, chloropicrin, and adamsite, primarily irritate mucous membranes.
Pulmonary irritants, also known as choking agents, vary by water solubility. Highly soluble agents like ammonia mainly affect the upper airway, intermediate agents such as chlorine damage both upper and lower airways through free radical formation, and low-solubility agents like phosgene cause delayed pulmonary edema after hydrolysis in the lungs.
Nerve agents, including sarin, tabun, soman, and VX, inhibit acetylcholinesterase, resulting in widespread cholinergic overstimulation at muscarinic, nicotinic, and central nervous system receptors.
Incapacitating agents such as 3-quinuclidinyl benzilate (BZ) produce an anticholinergic toxidrome through antimuscarinic effects.
Clinical features
History often suggests exposure through reports of multiple affected individuals, fires, industrial incidents, or known chemical release.
Blood agents cause early tachypnea, hypertension, and tachycardia followed by respiratory depression, hypotension, bradycardia, seizures, coma, and rapid death. Cyanosis is uncommon, and metabolic acidosis is prominent.
Blister agents lead to delayed skin erythema, edema, pruritus, vesiculation, and necrosis, along with severe ocular injury, airway sloughing, bronchospasm, and bone marrow suppression.
Lacrimators cause intense eye pain, lacrimation, blepharospasm, temporary blindness, skin irritation, cough, and chest tightness.
Pulmonary irritants produce dyspnea, cough, bronchospasm, chest pain, and delayed pulmonary edema that may appear up to 24 hours after exposure.
Nerve agents produce the classic SLUDGEBAM syndrome with salivation, lacrimation, urination, defecation, gastrointestinal cramps, emesis, bronchorrhea, bronchoconstriction, bradycardia, miosis, seizures, muscle fasciculations, weakness, and paralysis.
Incapacitating agents result in anticholinergic findings including hyperthermia, dry skin, flushed appearance, delirium, tachycardia, urinary retention, and decreased bowel sounds.
Evaluation and recognition
Diagnosis is primarily clinical and based on exposure history and toxidrome recognition. Physical examination may reveal clues such as bitter almond odor and severe acidosis in cyanide poisoning, blistering and skin sloughing with mustard agents, or marked secretions and miosis with nerve agents.
Laboratory and imaging findings
Arterial blood gases may show severe metabolic acidosis and elevated lactate in cyanide exposure. Complete blood counts can reveal leukopenia, thrombocytopenia, or anemia after mustard exposure. Electrolytes, renal function, creatine phosphokinase, and urinalysis assist in monitoring systemic injury. Erythrocyte cholinesterase activity supports nerve agent exposure. Chest radiography is useful to assess pulmonary edema.
Differential considerations
Conditions that may mimic chemical weapons exposure include asthma or COPD exacerbations, Stevens–Johnson syndrome, toxic epidermal necrolysis, organophosphate pesticide poisoning, botulism, radiation injury, congestive heart failure, and anaphylactoid reactions.
Prehospital priorities
Prevent secondary contamination by using appropriate personal protective equipment. Immediate decontamination is critical, with removal of clothing and either dry or wet decontamination depending on the agent. Atropine should be administered early in suspected nerve agent exposure even if tachycardia is present.
Initial stabilization
Airway, breathing, and circulation take priority. Patients require rapid decontamination, copious irrigation of skin and eyes, supplemental oxygen, cardiac monitoring, pulse oximetry, and intravenous access with isotonic fluids. Health care workers must remain protected throughout care.
Emergency department management
Treatment focuses on decontamination, supportive care, and agent-specific antidotes. Cyanide exposure requires high-flow oxygen, seizure control, and hydroxocobalamin as first-line therapy, with traditional cyanide antidote kits as alternatives.
Blister agents are managed with supportive and burn care, fluid and electrolyte monitoring, and management of hematologic complications.
Pulmonary irritants and lacrimators are treated with supportive respiratory care, bronchodilators, eye irrigation, and observation for delayed pulmonary edema.
Nerve agent poisoning requires aggressive airway management, repeated high-dose atropine titrated to respiratory improvement, pralidoxime to reverse neuromuscular effects, and benzodiazepines for seizures.
Incapacitating agents are managed with supportive care, hydration, benzodiazepines for agitation, and consideration of physostigmine in consultation with a poison center.
Pharmacologic therapy
Key medications include atropine, pralidoxime, hydroxocobalamin, benzodiazepines, bronchodilators, and components of the cyanide antidote kit, dosed according to severity and patient age.
Disposition and monitoring
Patients with significant exposure or symptoms require hospital or intensive care admission for monitoring and supportive care. Those exposed to riot control agents alone may be observed in the emergency department and discharged if symptoms resolve.
Clinical pearls
Effective decontamination is essential to protect both patients and clinicians. Recognition of toxidromes allows early, life-saving antidote administration. Delayed complications, particularly pulmonary edema after choking agents, require vigilant observation even when initial symptoms are mild.
General overview
Chemical weapons poisoning refers to exposure to toxic agents designed to cause injury or death by affecting the central nervous system, lungs, cardiovascular system, skin, eyes, or gastrointestinal tract. These agents may be encountered in warfare, terrorism, industrial accidents, or mass casualty incidents and often involve multiple victims presenting simultaneously.
Types of agents and mechanisms
Blood agents such as cyanide disrupt cellular respiration by binding to cytochrome oxidase and uncoupling oxidative phosphorylation, leading to rapid tissue hypoxia.
Blister agents, including sulfur mustard, nitrogen mustard, lewisite, and phosgene oxime, cause alkylation and cross-linking of DNA and proteins, resulting in cellular membrane damage and delayed tissue necrosis.
Lacrimators and riot control agents, such as CN (Mace), CS, oleoresin capsaicin, chloropicrin, and adamsite, primarily irritate mucous membranes.
Pulmonary irritants, also known as choking agents, vary by water solubility. Highly soluble agents like ammonia mainly affect the upper airway, intermediate agents such as chlorine damage both upper and lower airways through free radical formation, and low-solubility agents like phosgene cause delayed pulmonary edema after hydrolysis in the lungs.
Nerve agents, including sarin, tabun, soman, and VX, inhibit acetylcholinesterase, resulting in widespread cholinergic overstimulation at muscarinic, nicotinic, and central nervous system receptors.
Incapacitating agents such as 3-quinuclidinyl benzilate (BZ) produce an anticholinergic toxidrome through antimuscarinic effects.
Clinical features
History often suggests exposure through reports of multiple affected individuals, fires, industrial incidents, or known chemical release.
Blood agents cause early tachypnea, hypertension, and tachycardia followed by respiratory depression, hypotension, bradycardia, seizures, coma, and rapid death. Cyanosis is uncommon, and metabolic acidosis is prominent.
Blister agents lead to delayed skin erythema, edema, pruritus, vesiculation, and necrosis, along with severe ocular injury, airway sloughing, bronchospasm, and bone marrow suppression.
Lacrimators cause intense eye pain, lacrimation, blepharospasm, temporary blindness, skin irritation, cough, and chest tightness.
Pulmonary irritants produce dyspnea, cough, bronchospasm, chest pain, and delayed pulmonary edema that may appear up to 24 hours after exposure.
Nerve agents produce the classic SLUDGEBAM syndrome with salivation, lacrimation, urination, defecation, gastrointestinal cramps, emesis, bronchorrhea, bronchoconstriction, bradycardia, miosis, seizures, muscle fasciculations, weakness, and paralysis.
Incapacitating agents result in anticholinergic findings including hyperthermia, dry skin, flushed appearance, delirium, tachycardia, urinary retention, and decreased bowel sounds.
Evaluation and recognition
Diagnosis is primarily clinical and based on exposure history and toxidrome recognition. Physical examination may reveal clues such as bitter almond odor and severe acidosis in cyanide poisoning, blistering and skin sloughing with mustard agents, or marked secretions and miosis with nerve agents.
Laboratory and imaging findings
Arterial blood gases may show severe metabolic acidosis and elevated lactate in cyanide exposure. Complete blood counts can reveal leukopenia, thrombocytopenia, or anemia after mustard exposure. Electrolytes, renal function, creatine phosphokinase, and urinalysis assist in monitoring systemic injury. Erythrocyte cholinesterase activity supports nerve agent exposure. Chest radiography is useful to assess pulmonary edema.
Differential considerations
Conditions that may mimic chemical weapons exposure include asthma or COPD exacerbations, Stevens–Johnson syndrome, toxic epidermal necrolysis, organophosphate pesticide poisoning, botulism, radiation injury, congestive heart failure, and anaphylactoid reactions.
Prehospital priorities
Prevent secondary contamination by using appropriate personal protective equipment. Immediate decontamination is critical, with removal of clothing and either dry or wet decontamination depending on the agent. Atropine should be administered early in suspected nerve agent exposure even if tachycardia is present.
Initial stabilization
Airway, breathing, and circulation take priority. Patients require rapid decontamination, copious irrigation of skin and eyes, supplemental oxygen, cardiac monitoring, pulse oximetry, and intravenous access with isotonic fluids. Health care workers must remain protected throughout care.
Emergency department management
Treatment focuses on decontamination, supportive care, and agent-specific antidotes. Cyanide exposure requires high-flow oxygen, seizure control, and hydroxocobalamin as first-line therapy, with traditional cyanide antidote kits as alternatives.
Blister agents are managed with supportive and burn care, fluid and electrolyte monitoring, and management of hematologic complications.
Pulmonary irritants and lacrimators are treated with supportive respiratory care, bronchodilators, eye irrigation, and observation for delayed pulmonary edema.
Nerve agent poisoning requires aggressive airway management, repeated high-dose atropine titrated to respiratory improvement, pralidoxime to reverse neuromuscular effects, and benzodiazepines for seizures.
Incapacitating agents are managed with supportive care, hydration, benzodiazepines for agitation, and consideration of physostigmine in consultation with a poison center.
Pharmacologic therapy
Key medications include atropine, pralidoxime, hydroxocobalamin, benzodiazepines, bronchodilators, and components of the cyanide antidote kit, dosed according to severity and patient age.
Disposition and monitoring
Patients with significant exposure or symptoms require hospital or intensive care admission for monitoring and supportive care. Those exposed to riot control agents alone may be observed in the emergency department and discharged if symptoms resolve.
Clinical pearls
Effective decontamination is essential to protect both patients and clinicians. Recognition of toxidromes allows early, life-saving antidote administration. Delayed complications, particularly pulmonary edema after choking agents, require vigilant observation even when initial symptoms are mild.
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Emergency and Acute Medicine – Emergency Cesarean Section
Alert
The sole indication for an emergency department physician to perform an emergency perimortem cesarean section is a gravid female (>24 weeks gestation) in cardiopulmonary arrest who has not responded to initial resuscitative measures, regardless of cause. The most important predictor of fetal survival is the time interval between maternal cardiac arrest and cesarean delivery. The procedure should begin within 4 minutes of maternal arrest with a goal of fetal delivery within 1 minute. Immediate consultation with obstetrics, pediatrics, and surgery (if trauma related) should be obtained, but the procedure must not be delayed while awaiting consultant arrival. Emergent cesarean section should not be performed if gestational age is <24 weeks.< />pan>
Overview and Definition
Emergency (perimortem) cesarean section is a resuscitative intervention performed during maternal cardiopulmonary arrest to improve maternal hemodynamics by relieving aortocaval compression and to allow potential fetal survival. Uterine decompression improves venous return, cardiac output, and the effectiveness of cardiopulmonary resuscitation.
Etiology
Trauma, both penetrating and blunt, is the most common cause of maternal mortality. Nontraumatic causes include pulmonary embolism, cerebral vascular accident, amniotic fluid embolism, disseminated intravascular coagulation, placenta previa, eclampsia, and medical conditions such as asthma, congestive heart failure, myocardial infarction, and drug overdose.
Diagnosis
Diagnosis is clinical and based on the presence of cardiopulmonary arrest in a gravid female estimated to be beyond 24 weeks gestation.
Signs and Symptoms
The patient is unresponsive, apneic, and pulseless. Gestational age is estimated clinically.
Physical Examination
A uterus palpated at least four fingerbreadths above the umbilicus corresponds to an estimated gestational age of ≥24 weeks.
Essential Assessment
Rapid confirmation of apnea and pulselessness should occur simultaneously with evaluation for reversible causes of arrest including hypoxia, hypovolemia, acidosis, electrolyte abnormalities, hypoglycemia, hypothermia, trauma, thromboembolism, toxins, tension pneumothorax, cardiac tamponade, and supine hypotension syndrome. Fundal height in centimeters approximates gestational age in weeks. Ultrasound may be used only if immediately available and without delay.
Diagnostic Tests and Interpretation
No imaging or laboratory studies are required to establish the diagnosis. Fetal heart tones should not be assessed if this delays intervention.
Prehospital Care
Scene time should be minimized. The patient should be positioned in the left lateral decubitus position to relieve inferior vena cava compression. In trauma patients requiring spinal immobilization, manual uterine displacement or elevation of the right hip should be performed.
Initial Stabilization
Standard ACLS measures should be initiated, including airway management with a smaller endotracheal tube, high-flow oxygen, cardiac monitoring, and large-bore IV access with aggressive fluid resuscitation. If gestational age is ≥24 weeks and no return of spontaneous circulation occurs after 4 minutes of resuscitation, immediate cesarean section is indicated.
Emergency Department Procedure
Do not delay for consultants. Perform a vertical midline abdominal incision from the pubic hairline to approximately 5 cm above the umbilicus. Incise through fascia and peritoneum, retract the bladder inferiorly, make a vertical uterine incision, deliver the fetus, clamp and cut the umbilical cord, deliver the placenta, reassess maternal circulation, and continue resuscitative efforts.
Disposition
The neonate requires admission to the neonatal intensive care unit. If maternal circulation returns, the mother requires intensive care unit admission. Neither patient should be discharged from the emergency department.
Pearls and Pitfalls
Only gravid patients ≥24 weeks gestation qualify for perimortem cesarean section. The decision must be made within 4 minutes of maternal arrest, and delivery should be completed within 1 minute. Speed and decisiveness are critical.
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Emergency and Acute Medicine – Bladder Injury
Overview and Definitions
Bladder injury most commonly results from blunt trauma. Approximately 10% of patients with pelvic fractures sustain significant bladder injury, and 80–90% of bladder ruptures are associated with pelvic fractures. Overall mortality ranges from 17–22%, increasing to nearly 60% in combined intraperitoneal and extraperitoneal ruptures.
Etiology and Classification
Trauma accounts for about 82% of bladder injuries. Blunt mechanisms include motor vehicle accidents (87%), falls (7%), and assault (6%). Penetrating injuries are most often due to gunshot wounds (85%) and stabbings (15%). Iatrogenic causes account for 14% and include TURP, urologic, gynecologic, obstetric, abdominal, and orthopedic hip procedures, biopsies, indwelling Foley catheters, and IUD placement. Intoxication accounts for 2.9%, and spontaneous rupture occurs in less than 1%.
Extraperitoneal rupture (62%) is usually associated with pelvic fractures and results from blunt force or bone fragments. Intraperitoneal rupture (25%) occurs from direct compression of a distended bladder, typically involving the bladder dome. Combined intraperitoneal and extraperitoneal rupture (12%) carries the highest mortality due to associated injuries. Bladder contusion involves injury to the endothelial lining or muscularis with an intact bladder wall and may cause gross hematuria with normal imaging; it usually resolves without intervention.
In children, the bladder is intra-abdominal until late adolescence, making intraperitoneal rupture more common and overall bladder injury more frequent due to a less rigid pelvis.
Clinical Presentation
The classic triad includes gross hematuria, suprapubic pain, and difficulty voiding. History should focus on traumatic mechanism or recent procedures. On examination, the urethral meatus must be inspected; if blood is present, Foley catheter placement should be deferred until a retrograde urethrogram is performed, as concomitant urethral injury occurs in 10–29% of cases.
Evaluation and Diagnostic Testing
Initial evaluation includes urinalysis, which shows gross hematuria in 95–100% of significant injuries and microscopic hematuria in about 5%. BUN may be elevated due to intraperitoneal urine resorption, and electrolyte abnormalities such as hyperkalemia or hypernatremia may be present.
Retrograde cystography or CT cystography is the diagnostic modality of choice, with sensitivity around 95% and specificity near 100%. If urethral injury is suspected, a retrograde urethrogram is performed first. Proper cystography requires adequate bladder distension with diluted contrast and postdrainage imaging, as up to 10% of ruptures are detected only after bladder emptying. Extraperitoneal ruptures show teardrop- or star-shaped extravasation, whereas intraperitoneal ruptures demonstrate contrast outlining bowel loops or filling paracolic gutters. FAST examination showing free pelvic fluid should heighten suspicion for bladder injury.
Differential Diagnosis
Consider peritoneal trauma, urethral injury, and renal or ureteral trauma.
Management
Prehospital bladder catheterization should be avoided. Initial management follows standard ABCs with early urologic consultation. Extraperitoneal nonpenetrating ruptures may be managed with Foley catheter drainage (20F or larger) for approximately 14 days, with most lacerations sealing within 3 weeks; surgical repair is recommended if the patient is undergoing pelvic or abdominal surgery for other injuries. Intraperitoneal ruptures require surgical exploration and repair. Bladder contusions require no specific intervention. Broad-spectrum antibiotics are indicated for intraperitoneal rupture.
Disposition and Follow-Up
Admission is required for patients with associated major trauma or those needing surgical intervention. Bladder contusions without rupture and without other injuries may be discharged. Most bladder ruptures require admission, and discharge should occur only after urologic clearance. Urology follow-up is required for all outpatient-managed injuries, with Foley catheter removal typically at 14 days for conservatively managed extraperitoneal ruptures.
Clinical Insights and Common Errors
Free pelvic fluid on CT or ultrasound should prompt concern for bladder injury. Unresponsive, intoxicated, or altered patients require careful evaluation. Any penetrating injury to the lower abdomen with hematuria warrants cystography.
Overview and Definitions
Bladder injury most commonly results from blunt trauma. Approximately 10% of patients with pelvic fractures sustain significant bladder injury, and 80–90% of bladder ruptures are associated with pelvic fractures. Overall mortality ranges from 17–22%, increasing to nearly 60% in combined intraperitoneal and extraperitoneal ruptures.
Etiology and Classification
Trauma accounts for about 82% of bladder injuries. Blunt mechanisms include motor vehicle accidents (87%), falls (7%), and assault (6%). Penetrating injuries are most often due to gunshot wounds (85%) and stabbings (15%). Iatrogenic causes account for 14% and include TURP, urologic, gynecologic, obstetric, abdominal, and orthopedic hip procedures, biopsies, indwelling Foley catheters, and IUD placement. Intoxication accounts for 2.9%, and spontaneous rupture occurs in less than 1%.
Extraperitoneal rupture (62%) is usually associated with pelvic fractures and results from blunt force or bone fragments. Intraperitoneal rupture (25%) occurs from direct compression of a distended bladder, typically involving the bladder dome. Combined intraperitoneal and extraperitoneal rupture (12%) carries the highest mortality due to associated injuries. Bladder contusion involves injury to the endothelial lining or muscularis with an intact bladder wall and may cause gross hematuria with normal imaging; it usually resolves without intervention.
In children, the bladder is intra-abdominal until late adolescence, making intraperitoneal rupture more common and overall bladder injury more frequent due to a less rigid pelvis.
Clinical Presentation
The classic triad includes gross hematuria, suprapubic pain, and difficulty voiding. History should focus on traumatic mechanism or recent procedures. On examination, the urethral meatus must be inspected; if blood is present, Foley catheter placement should be deferred until a retrograde urethrogram is performed, as concomitant urethral injury occurs in 10–29% of cases.
Evaluation and Diagnostic Testing
Initial evaluation includes urinalysis, which shows gross hematuria in 95–100% of significant injuries and microscopic hematuria in about 5%. BUN may be elevated due to intraperitoneal urine resorption, and electrolyte abnormalities such as hyperkalemia or hypernatremia may be present.
Retrograde cystography or CT cystography is the diagnostic modality of choice, with sensitivity around 95% and specificity near 100%. If urethral injury is suspected, a retrograde urethrogram is performed first. Proper cystography requires adequate bladder distension with diluted contrast and postdrainage imaging, as up to 10% of ruptures are detected only after bladder emptying. Extraperitoneal ruptures show teardrop- or star-shaped extravasation, whereas intraperitoneal ruptures demonstrate contrast outlining bowel loops or filling paracolic gutters. FAST examination showing free pelvic fluid should heighten suspicion for bladder injury.
Differential Diagnosis
Consider peritoneal trauma, urethral injury, and renal or ureteral trauma.
Management
Prehospital bladder catheterization should be avoided. Initial management follows standard ABCs with early urologic consultation. Extraperitoneal nonpenetrating ruptures may be managed with Foley catheter drainage (20F or larger) for approximately 14 days, with most lacerations sealing within 3 weeks; surgical repair is recommended if the patient is undergoing pelvic or abdominal surgery for other injuries. Intraperitoneal ruptures require surgical exploration and repair. Bladder contusions require no specific intervention. Broad-spectrum antibiotics are indicated for intraperitoneal rupture.
Disposition and Follow-Up
Admission is required for patients with associated major trauma or those needing surgical intervention. Bladder contusions without rupture and without other injuries may be discharged. Most bladder ruptures require admission, and discharge should occur only after urologic clearance. Urology follow-up is required for all outpatient-managed injuries, with Foley catheter removal typically at 14 days for conservatively managed extraperitoneal ruptures.
Clinical Insights and Common Errors
Free pelvic fluid on CT or ultrasound should prompt concern for bladder injury. Unresponsive, intoxicated, or altered patients require careful evaluation. Any penetrating injury to the lower abdomen with hematuria warrants cystography.
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Emergency and Acute Medicine – Human Bite
Overview
Human bites are the third most common type of bite injury, following dog and cat bites. Up to 75% occur during aggressive encounters, while 15–20% are related to sexual activity (“love nips”). Human bites carry a higher risk of infection than animal bites because of the dense oral bacterial flora.
Types of Human Bites
Occlusional bites occur when human teeth directly bite the skin, producing lacerations or crush injuries; these are more prone to infection than animal bites. Clenched-fist injuries (CFIs), also known as fight bites, are the most serious form. They typically present as small wounds over the metacarpophalangeal joints of the dominant hand and occur when a clenched fist strikes another person’s teeth. When the hand relaxes, the puncture site may seal, trapping oral bacteria within the joint. Tendons can carry bacteria into deeper potential spaces of the hand, markedly increasing the risk of deep and extensive infection.
Microbiology and Etiology
Human bite infections are polymicrobial, involving aerobic and anaerobic organisms. The most common pathogens are Streptococcus and Staphylococcus species. Other organisms include Eikenella corrodens, Haemophilus influenzae, Peptostreptococcus, and Corynebacterium. E. corrodens exhibits synergism with Streptococcus, Staphylococcus aureus, Bacteroides, and gram-negative organisms. Although rare, viral transmission through human bites has been reported, including hepatitis viruses, HIV, and herpes simplex virus.
Clinical Presentation
Most human bites involve the upper extremities (60–75%), followed by the head and neck (15–20%), trunk (10–20%), and lower extremities (approximately 5%). Common complications include cellulitis, deep-space infections such as septic arthritis and osteomyelitis, fractures, and tendon injuries. Hand bites have the highest infection rates.
History and Examination
History should include the time of injury, patient allergies, immune status, tetanus immunization status, and HIV or hepatitis B status of the person inflicting the bite, if known. On examination, carefully document wound location and extent, swelling, crush injury, devitalized tissue, range of motion, tendon and nerve function, signs of infection including regional adenopathy, and any joint or bone involvement.
Essential Evaluation
A meticulous examination is critical, especially for clenched-fist injuries. The deepest part of the wound must be examined while the fingers are taken through a full range of motion to identify extensor tendon lacerations or joint capsule violation.
Diagnostic Testing
Aerobic and anaerobic cultures should be obtained from clinically infected wounds; cultures are not indicated for noninfected bites. CBC is appropriate when there are signs of significant infection. Electrolytes, glucose, BUN, and creatinine should be checked in diabetic patients or those with severe infections. Imaging is usually unnecessary, but plain radiographs are indicated for suspected fractures, foreign bodies such as teeth, baseline evaluation when bone or joint space is violated, or infection near bone or joint spaces. Ultrasound may help differentiate abscess from cellulitis.
Differential Diagnosis and Special Considerations
Animal bites typically cause more punctures and lacerations, whereas human bites more often produce crush injuries. In suspected sexual abuse, look for central bruising or “hickeys,” linear abrasions or bruises on both dorsal and palmar or plantar surfaces, and multiple lesions on different extremities. An intercanine distance greater than 3 cm suggests permanent dentition and an attacker older than 8 years. If abuse is suspected, collect saliva using a saline-moistened swab placed in a paper envelope, obtain photographs, and notify authorities.
Prehospital and Initial Management
Control bleeding with direct pressure. Ensure airway patency and adequate tissue perfusion.
Emergency Department Management
Irrigate wounds copiously with normal saline using an 18-gauge needle or plastic catheter directed along the wound tract, avoiding forceful injection into tissues. Débride foreign material, necrotic tissue, and devitalized skin, but do not débride puncture wounds. Remove eschar to allow drainage and irrigation of underlying pus.
Clenched-fist injuries require immobilization and splinting in a functional position with bulky hand dressing, elevation, and early consultation with a hand surgeon for possible operative irrigation and exploration. Use a sling for outpatients and tubular stockinette suspension for inpatients. Do not perform primary repair of avulsion wounds.
Wound Closure
Primary closure increases infection risk and should be avoided in infected wounds or those older than 24 hours. Closure of wounds older than 8 hours is controversial. Facial wounds may be closed up to 24 hours after injury with counseling regarding infection risk. Infected wounds and those presenting after 24 hours should be left open, with possible delayed primary closure or approximation using Steri-Strips. Clenched-fist injuries should never be sutured.
Antibiotic Therapy and Prophylaxis
Prophylactic antibiotics are controversial for low-risk bites but are recommended for moderate to severe injuries, crush injuries with edema, bone or joint involvement, hand bites, wounds near prosthetic joints, and patients with diabetes, prior splenectomy, or immunosuppression. Tetanus prophylaxis should be updated as indicated. Refer patients for possible HIV testing and surveillance when appropriate.
Medications
First-line therapy includes amoxicillin–clavulanate orally, ampicillin–sulbactam IV, piperacillin–tazobactam IV, ticarcillin–clavulanate IV, or ceftriaxone plus metronidazole. Second-line regimens involve combination therapy with trimethoprim–sulfamethoxazole, penicillin VK, ciprofloxacin, or doxycycline, each combined with anaerobic coverage using clindamycin or metronidazole.
Disposition
Admission is indicated for infected wounds at presentation, severe or progressive cellulitis or lymphangitis, systemic infection, or failure of outpatient antibiotics. Healthy patients with localized infection may be discharged on antibiotics with 24-hour follow-up, while noninfected wounds require reassessment within 48 hours.
Special Populations
In geriatric patients, human bite marks rarely occur accidentally and should raise concern for elder abuse. In pediatric patients, human bite marks are also uncommon and suggest possible abuse; an intercanine distance greater than 3 cm indicates an adult attacker.
Follow-Up and Referral
All infected hand wounds require hand specialist follow-up. Suspected child abuse mandates referral to appropriate authorities.
Key Clinical Cautions
Always examine clenched-fist wounds through full finger motion to detect tendon or joint involvement. Early hand surgery consultation is essential for all clenched-fist injuries because of their high infection rate.
Overview
Human bites are the third most common type of bite injury, following dog and cat bites. Up to 75% occur during aggressive encounters, while 15–20% are related to sexual activity (“love nips”). Human bites carry a higher risk of infection than animal bites because of the dense oral bacterial flora.
Types of Human Bites
Occlusional bites occur when human teeth directly bite the skin, producing lacerations or crush injuries; these are more prone to infection than animal bites. Clenched-fist injuries (CFIs), also known as fight bites, are the most serious form. They typically present as small wounds over the metacarpophalangeal joints of the dominant hand and occur when a clenched fist strikes another person’s teeth. When the hand relaxes, the puncture site may seal, trapping oral bacteria within the joint. Tendons can carry bacteria into deeper potential spaces of the hand, markedly increasing the risk of deep and extensive infection.
Microbiology and Etiology
Human bite infections are polymicrobial, involving aerobic and anaerobic organisms. The most common pathogens are Streptococcus and Staphylococcus species. Other organisms include Eikenella corrodens, Haemophilus influenzae, Peptostreptococcus, and Corynebacterium. E. corrodens exhibits synergism with Streptococcus, Staphylococcus aureus, Bacteroides, and gram-negative organisms. Although rare, viral transmission through human bites has been reported, including hepatitis viruses, HIV, and herpes simplex virus.
Clinical Presentation
Most human bites involve the upper extremities (60–75%), followed by the head and neck (15–20%), trunk (10–20%), and lower extremities (approximately 5%). Common complications include cellulitis, deep-space infections such as septic arthritis and osteomyelitis, fractures, and tendon injuries. Hand bites have the highest infection rates.
History and Examination
History should include the time of injury, patient allergies, immune status, tetanus immunization status, and HIV or hepatitis B status of the person inflicting the bite, if known. On examination, carefully document wound location and extent, swelling, crush injury, devitalized tissue, range of motion, tendon and nerve function, signs of infection including regional adenopathy, and any joint or bone involvement.
Essential Evaluation
A meticulous examination is critical, especially for clenched-fist injuries. The deepest part of the wound must be examined while the fingers are taken through a full range of motion to identify extensor tendon lacerations or joint capsule violation.
Diagnostic Testing
Aerobic and anaerobic cultures should be obtained from clinically infected wounds; cultures are not indicated for noninfected bites. CBC is appropriate when there are signs of significant infection. Electrolytes, glucose, BUN, and creatinine should be checked in diabetic patients or those with severe infections. Imaging is usually unnecessary, but plain radiographs are indicated for suspected fractures, foreign bodies such as teeth, baseline evaluation when bone or joint space is violated, or infection near bone or joint spaces. Ultrasound may help differentiate abscess from cellulitis.
Differential Diagnosis and Special Considerations
Animal bites typically cause more punctures and lacerations, whereas human bites more often produce crush injuries. In suspected sexual abuse, look for central bruising or “hickeys,” linear abrasions or bruises on both dorsal and palmar or plantar surfaces, and multiple lesions on different extremities. An intercanine distance greater than 3 cm suggests permanent dentition and an attacker older than 8 years. If abuse is suspected, collect saliva using a saline-moistened swab placed in a paper envelope, obtain photographs, and notify authorities.
Prehospital and Initial Management
Control bleeding with direct pressure. Ensure airway patency and adequate tissue perfusion.
Emergency Department Management
Irrigate wounds copiously with normal saline using an 18-gauge needle or plastic catheter directed along the wound tract, avoiding forceful injection into tissues. Débride foreign material, necrotic tissue, and devitalized skin, but do not débride puncture wounds. Remove eschar to allow drainage and irrigation of underlying pus.
Clenched-fist injuries require immobilization and splinting in a functional position with bulky hand dressing, elevation, and early consultation with a hand surgeon for possible operative irrigation and exploration. Use a sling for outpatients and tubular stockinette suspension for inpatients. Do not perform primary repair of avulsion wounds.
Wound Closure
Primary closure increases infection risk and should be avoided in infected wounds or those older than 24 hours. Closure of wounds older than 8 hours is controversial. Facial wounds may be closed up to 24 hours after injury with counseling regarding infection risk. Infected wounds and those presenting after 24 hours should be left open, with possible delayed primary closure or approximation using Steri-Strips. Clenched-fist injuries should never be sutured.
Antibiotic Therapy and Prophylaxis
Prophylactic antibiotics are controversial for low-risk bites but are recommended for moderate to severe injuries, crush injuries with edema, bone or joint involvement, hand bites, wounds near prosthetic joints, and patients with diabetes, prior splenectomy, or immunosuppression. Tetanus prophylaxis should be updated as indicated. Refer patients for possible HIV testing and surveillance when appropriate.
Medications
First-line therapy includes amoxicillin–clavulanate orally, ampicillin–sulbactam IV, piperacillin–tazobactam IV, ticarcillin–clavulanate IV, or ceftriaxone plus metronidazole. Second-line regimens involve combination therapy with trimethoprim–sulfamethoxazole, penicillin VK, ciprofloxacin, or doxycycline, each combined with anaerobic coverage using clindamycin or metronidazole.
Disposition
Admission is indicated for infected wounds at presentation, severe or progressive cellulitis or lymphangitis, systemic infection, or failure of outpatient antibiotics. Healthy patients with localized infection may be discharged on antibiotics with 24-hour follow-up, while noninfected wounds require reassessment within 48 hours.
Special Populations
In geriatric patients, human bite marks rarely occur accidentally and should raise concern for elder abuse. In pediatric patients, human bite marks are also uncommon and suggest possible abuse; an intercanine distance greater than 3 cm indicates an adult attacker.
Follow-Up and Referral
All infected hand wounds require hand specialist follow-up. Suspected child abuse mandates referral to appropriate authorities.
Key Clinical Cautions
Always examine clenched-fist wounds through full finger motion to detect tendon or joint involvement. Early hand surgery consultation is essential for all clenched-fist injuries because of their high infection rate.
- Published on
Emergency and Acute Medicine – Bipolar Disorder
Core Concepts And Definitions
Mania has a broad and often subtle presentation that may be difficult to recognize in the emergency setting. Manifestations range from irritability or cheerfulness to agitation, delirium, or frank psychosis, with the full extent of illness often revealed only through collateral history. Onset may be gradual or abrupt, with episodes typically lasting weeks to months and only rarely becoming chronic. Hypomania represents a milder form without marked functional impairment. Mixed mood states involve concurrent manic and depressive features and should be managed as mania in the emergency department. Bipolar disorder, formerly termed manic-depressive illness, is defined by one or more episodes of hypomania, mania, or mixed mood, often accompanied by depressive episodes. Bipolar II disorder refers to patients who experience hypomania but never full mania. The illness commonly begins in adolescence or early adulthood, with episodes varying widely in severity, duration, and frequency. Treatment responsiveness ranges from excellent to highly refractory. Schizoaffective disorder is characterized by mood episodes accompanied by psychotic symptoms that persist even during euthymic periods.
Etiologic Considerations
Bipolar disorder is most often a primary psychiatric illness with a strong genetic association. Secondary causes must be considered, particularly in patients over 40 years of age presenting with a first episode, atypical or mixed features, or altered sensorium. Medical, neurologic, endocrine, or toxicologic conditions may precipitate manic syndromes.
Clinical Features And Assessment
History should focus on recent manic symptoms, often requiring information from family or other informants. Key features include elevated, expansive, or irritable mood; increased energy and activity; reduced need for sleep; pressured speech; distractibility; racing thoughts; impulsivity; grandiosity; poor judgment; and engagement in high-risk behaviors. Past episodes of mania or depression, medication nonadherence, recent antidepressant initiation or discontinuation, substance use, and family history of bipolar disorder are critical elements. Medical history should assess for endocrine, metabolic, or neurologic disease and current or recent medications.
On examination, patients often appear hyperactive or agitated, with loud, rapid, or pressured speech. Affect is commonly irritable and labile, with intermittent tearfulness or dysphoria that may obscure diagnosis. Thought processes may be rapid, tangential, incoherent, or delirious. Thought content may include mood-congruent psychosis such as grandiose delusions or mood-incongruent psychotic features indistinguishable from other psychotic disorders. Judgment is typically impaired, with inflated self-esteem and uncharacteristic financial, sexual, or social indiscretions. Sensorium is usually intact, though confusion or delirium can occur.
Essential Evaluation
A focused physical and neurologic examination with vital signs is mandatory. Because mania can mimic delirium, a full medical evaluation may be required to exclude secondary causes.
Diagnostic Testing
Laboratory studies include toxicology screening, blood alcohol level, electrolytes, glucose, complete blood count, thyroid-stimulating hormone, and serum levels of lithium, carbamazepine, or valproate when relevant. Additional testing is guided by clinical context. Neuroimaging is reserved for suspected neurologic pathology.
Differential Diagnosis
Consider primary mania, schizoaffective disorder, psychotic disorders, agitated depression, personality disorders, attention-deficit disorder, conduct or impulse-control disorders, intoxication or withdrawal from alcohol or sedative-hypnotics, stimulant intoxication, medication-induced states including antidepressants, corticosteroids, thyroid hormone, anticholinergics, and antiparkinsonian agents, as well as metabolic, endocrine, infectious, inflammatory, vascular, neoplastic, and postictal neurologic conditions.
Initial Management And Safety Measures
Patients with mania carry a high risk of violence and impulsivity. Management begins with a calm, nonconfrontational approach in a low-stimulation environment, with adequate security support. Physical restraints and sedation may be required. Cooperative but agitated patients may be treated with oral antipsychotics or benzodiazepines. Uncooperative or severely agitated patients are commonly managed with combined haloperidol and lorazepam administered orally, intramuscularly, or intravenously, though monotherapy with either class may be appropriate. Alternative parenteral agents include lorazepam, olanzapine, ziprasidone, or chlorpromazine, with dose reductions in elderly or frail patients.
Emergency Department Treatment Strategies
Outpatient management may include short-term antipsychotics for symptom control, sleep-promoting agents, discontinuation of antidepressants if implicated, and initiation or resumption of mood stabilizers, recognizing that therapeutic effects may take days to weeks. Inpatient care is indicated for severe agitation, psychosis, unsafe behavior, or medical instability, with sedation and mood stabilizer initiation coordinated with psychiatry.
Pharmacologic Options
Acute agitation may be treated with lorazepam 2 mg orally or intramuscularly, repeatable as needed, or haloperidol 5 mg orally with similar repetition limits. Combination therapy using haloperidol 5 mg with lorazepam 1–2 mg is commonly effective. Parenteral alternatives include olanzapine, ziprasidone, aripiprazole, or chlorpromazine, with attention to hypotension and QT prolongation risks. Maintenance and outpatient medications include lithium, valproate, carbamazepine, lamotrigine, and atypical antipsychotics such as quetiapine, risperidone, olanzapine, and aripiprazole, often combined with benzodiazepines. Lamotrigine requires strict gradual titration to minimize risk of severe dermatologic reactions, particularly after interruptions. Pregnancy significantly complicates management, as lithium, valproate, and carbamazepine carry substantial teratogenic risk, especially early in gestation.
Disposition And Follow-Up
Involuntary hospitalization is required when patients pose a danger to themselves or others, exhibit severe impairment in self-care, display unsafe behaviors due to impaired judgment, or require diagnostic clarification. Patients with mild symptoms may be discharged if safety supports are in place, treatment adherence is likely, and prompt outpatient psychiatric follow-up within one to three days is arranged. Some patients may decline treatment despite not meeting criteria for involuntary commitment; education regarding future care options should be provided to patients and families.
Key Clinical Insights And Common Errors
Mania often presents with irritability or dysphoria rather than euphoria. Patients presenting with depression should always be screened for past or current manic or hypomanic symptoms, as misdiagnosis is common. Comorbid substance use is frequent and complicates management. Early identification of prodromal manic symptoms may prevent full episodes. In children, bipolar disorder frequently manifests as behavioral disinhibition or persistent irritability rather than classic mood elevation.
Core Concepts And Definitions
Mania has a broad and often subtle presentation that may be difficult to recognize in the emergency setting. Manifestations range from irritability or cheerfulness to agitation, delirium, or frank psychosis, with the full extent of illness often revealed only through collateral history. Onset may be gradual or abrupt, with episodes typically lasting weeks to months and only rarely becoming chronic. Hypomania represents a milder form without marked functional impairment. Mixed mood states involve concurrent manic and depressive features and should be managed as mania in the emergency department. Bipolar disorder, formerly termed manic-depressive illness, is defined by one or more episodes of hypomania, mania, or mixed mood, often accompanied by depressive episodes. Bipolar II disorder refers to patients who experience hypomania but never full mania. The illness commonly begins in adolescence or early adulthood, with episodes varying widely in severity, duration, and frequency. Treatment responsiveness ranges from excellent to highly refractory. Schizoaffective disorder is characterized by mood episodes accompanied by psychotic symptoms that persist even during euthymic periods.
Etiologic Considerations
Bipolar disorder is most often a primary psychiatric illness with a strong genetic association. Secondary causes must be considered, particularly in patients over 40 years of age presenting with a first episode, atypical or mixed features, or altered sensorium. Medical, neurologic, endocrine, or toxicologic conditions may precipitate manic syndromes.
Clinical Features And Assessment
History should focus on recent manic symptoms, often requiring information from family or other informants. Key features include elevated, expansive, or irritable mood; increased energy and activity; reduced need for sleep; pressured speech; distractibility; racing thoughts; impulsivity; grandiosity; poor judgment; and engagement in high-risk behaviors. Past episodes of mania or depression, medication nonadherence, recent antidepressant initiation or discontinuation, substance use, and family history of bipolar disorder are critical elements. Medical history should assess for endocrine, metabolic, or neurologic disease and current or recent medications.
On examination, patients often appear hyperactive or agitated, with loud, rapid, or pressured speech. Affect is commonly irritable and labile, with intermittent tearfulness or dysphoria that may obscure diagnosis. Thought processes may be rapid, tangential, incoherent, or delirious. Thought content may include mood-congruent psychosis such as grandiose delusions or mood-incongruent psychotic features indistinguishable from other psychotic disorders. Judgment is typically impaired, with inflated self-esteem and uncharacteristic financial, sexual, or social indiscretions. Sensorium is usually intact, though confusion or delirium can occur.
Essential Evaluation
A focused physical and neurologic examination with vital signs is mandatory. Because mania can mimic delirium, a full medical evaluation may be required to exclude secondary causes.
Diagnostic Testing
Laboratory studies include toxicology screening, blood alcohol level, electrolytes, glucose, complete blood count, thyroid-stimulating hormone, and serum levels of lithium, carbamazepine, or valproate when relevant. Additional testing is guided by clinical context. Neuroimaging is reserved for suspected neurologic pathology.
Differential Diagnosis
Consider primary mania, schizoaffective disorder, psychotic disorders, agitated depression, personality disorders, attention-deficit disorder, conduct or impulse-control disorders, intoxication or withdrawal from alcohol or sedative-hypnotics, stimulant intoxication, medication-induced states including antidepressants, corticosteroids, thyroid hormone, anticholinergics, and antiparkinsonian agents, as well as metabolic, endocrine, infectious, inflammatory, vascular, neoplastic, and postictal neurologic conditions.
Initial Management And Safety Measures
Patients with mania carry a high risk of violence and impulsivity. Management begins with a calm, nonconfrontational approach in a low-stimulation environment, with adequate security support. Physical restraints and sedation may be required. Cooperative but agitated patients may be treated with oral antipsychotics or benzodiazepines. Uncooperative or severely agitated patients are commonly managed with combined haloperidol and lorazepam administered orally, intramuscularly, or intravenously, though monotherapy with either class may be appropriate. Alternative parenteral agents include lorazepam, olanzapine, ziprasidone, or chlorpromazine, with dose reductions in elderly or frail patients.
Emergency Department Treatment Strategies
Outpatient management may include short-term antipsychotics for symptom control, sleep-promoting agents, discontinuation of antidepressants if implicated, and initiation or resumption of mood stabilizers, recognizing that therapeutic effects may take days to weeks. Inpatient care is indicated for severe agitation, psychosis, unsafe behavior, or medical instability, with sedation and mood stabilizer initiation coordinated with psychiatry.
Pharmacologic Options
Acute agitation may be treated with lorazepam 2 mg orally or intramuscularly, repeatable as needed, or haloperidol 5 mg orally with similar repetition limits. Combination therapy using haloperidol 5 mg with lorazepam 1–2 mg is commonly effective. Parenteral alternatives include olanzapine, ziprasidone, aripiprazole, or chlorpromazine, with attention to hypotension and QT prolongation risks. Maintenance and outpatient medications include lithium, valproate, carbamazepine, lamotrigine, and atypical antipsychotics such as quetiapine, risperidone, olanzapine, and aripiprazole, often combined with benzodiazepines. Lamotrigine requires strict gradual titration to minimize risk of severe dermatologic reactions, particularly after interruptions. Pregnancy significantly complicates management, as lithium, valproate, and carbamazepine carry substantial teratogenic risk, especially early in gestation.
Disposition And Follow-Up
Involuntary hospitalization is required when patients pose a danger to themselves or others, exhibit severe impairment in self-care, display unsafe behaviors due to impaired judgment, or require diagnostic clarification. Patients with mild symptoms may be discharged if safety supports are in place, treatment adherence is likely, and prompt outpatient psychiatric follow-up within one to three days is arranged. Some patients may decline treatment despite not meeting criteria for involuntary commitment; education regarding future care options should be provided to patients and families.
Key Clinical Insights And Common Errors
Mania often presents with irritability or dysphoria rather than euphoria. Patients presenting with depression should always be screened for past or current manic or hypomanic symptoms, as misdiagnosis is common. Comorbid substance use is frequent and complicates management. Early identification of prodromal manic symptoms may prevent full episodes. In children, bipolar disorder frequently manifests as behavioral disinhibition or persistent irritability rather than classic mood elevation.
- Published on
Emergency and Acute Medicine – Biologic Weapons
Overview And Scope
Biologic weapons are naturally occurring organisms or toxins that are deliberately purified and disseminated to cause mass morbidity, mortality, and societal disruption. These agents include bacteria, viruses, fungi, and toxins, with more than 400 potential or actualized pathogens capable of weaponization. They are relatively inexpensive compared with other weapons of mass destruction, highly potent, and can be deployed covertly. Their stealth derives from natural incubation periods, as agents are typically invisible, odorless, and tasteless. Patients often present to multiple health care facilities with nonspecific complaints, delaying recognition of a covert release. Exposure occurs through direct skin contact, inhalation of aerosolized particles, or ingestion via contaminated food or water.
Causative Agents
Bacterial agents include Bacillus anthracis (anthrax), Yersinia pestis (plague), Vibrio cholerae (cholera), Francisella tularensis (tularemia), Brucella species (brucellosis), and Coxiella burnetii (Q fever). Viral agents include variola virus (smallpox), alphaviruses causing viral encephalitides such as Venezuelan, Eastern, and Western equine encephalitis, and viral hemorrhagic fevers including Ebola, Marburg, Lassa, and dengue. Toxin-based weapons include ricin, staphylococcal enterotoxin B, botulinum toxin, and mycotoxins.
Clinical Recognition And Patterns
Clinicians must remain alert for unusual illness patterns suggestive of intentional release. Warning signs include geographic clustering of illness among individuals who live or work near one another, atypical age distributions for common diseases, multiple patients presenting with unexplained similar syndromes, a single case of disease caused by a rare or eradicated pathogen, and surges of patients with similar symptoms accompanied by increasing morbidity and mortality.
Key Syndromic Presentations
Inhalational anthrax presents with fever, chills, malaise, cough, dyspnea, chest pain, nausea, diaphoresis, myalgias, tachycardia, and possible meningeal signs. Cutaneous anthrax begins as a painless pruritic papule that evolves into a vesicle and then a necrotic ulcer with a black eschar and surrounding nonpitting edema. Plague manifests with abrupt fever, chills, cough, hemoptysis, dyspnea, headache, vomiting, painful lymphadenopathy (buboes), confusion, abdominal pain, oliguria, ecchymosis, and acral gangrene. Weaponized tularemia most commonly presents in a typhoidal form with fever, headache, malaise, and nonproductive cough, carrying high mortality if untreated. Q fever causes a flu-like illness with pleuritic chest pain and patchy infiltrates on chest imaging, with low mortality even without treatment. Brucellosis presents after a prolonged incubation with flu-like and neuropsychiatric symptoms and focal joint or genitourinary pain. Smallpox begins with a prodrome of fever and myalgias followed by a characteristic centrifugal rash progressing synchronously from macules to pustules and crusts, with high untreated mortality. Viral hemorrhagic fevers evolve from a flu-like illness to gastrointestinal symptoms, organ dysfunction, hemorrhage, shock, and high fatality rates.
Initial Assessment And Workup
Bioterrorism should be suspected when relatively young, healthy patients present with influenza-like illness and deteriorate rapidly or when characteristic cutaneous findings appear. Laboratory evaluation includes complete blood count, electrolytes, renal function, arterial blood gas analysis, blood and wound cultures, coagulation studies, and cerebrospinal fluid analysis when indicated. Imaging is guided by suspected agent, with chest radiography revealing mediastinal widening and pleural effusions in anthrax or bronchopneumonia in plague. Laboratories must be alerted when high-risk pathogens are suspected.
Differential Diagnosis
Consider common infectious mimics such as influenza, bacterial pneumonia, meningitis, varicella, tularemia, and staphylococcal or streptococcal skin infections, as well as noninfectious causes depending on presentation. Distinguishing features include rash distribution, lesion staging, involvement of palms and soles, and systemic toxicity.
Prehospital And Early Management
Universal precautions with appropriate respiratory protection, including N95 masks, are essential. Initial stabilization follows standard airway, breathing, and circulation principles, with intravenous fluids for hypotension, supplemental oxygen for hypoxemia, and vasopressors for refractory shock. Respiratory and contact isolation should be instituted immediately for suspected cases.
Emergency Department Management
Supportive care includes antipyretics and early initiation of disease-specific therapy. Anthrax requires prompt antibiotics, with ciprofloxacin or doxycycline as first-line agents, often in combination with other antibiotics depending on severity and susceptibility. Plague mandates antibiotics within 24 hours, typically streptomycin or gentamicin, with chloramphenicol added for meningitis or severe illness. Brucellosis is treated with prolonged doxycycline-based regimens combined with streptomycin or rifampin. Q fever is often self-limited, though doxycycline shortens illness duration. Smallpox management is supportive, with vaccination within four days of exposure reducing disease severity; secondary bacterial infections should be treated, and exposed staff vaccinated. Management of tularemia and viral hemorrhagic fevers follows established disease-specific protocols.
Disposition And Public Health Coordination
Admission decisions depend on clinical severity and the broader disaster context. Toxic, hypoxic, or unstable patients require inpatient care with isolation. Mild, noncontagious cases may be managed as outpatients when appropriate. Suspected or confirmed cases must be reported immediately to local and state health authorities, with infectious disease and toxicology consultation obtained. Postexposure prophylaxis, vaccination, and occupational health follow-up are critical for exposed personnel.
Critical Insights And Common Errors
Early recognition is challenging, requiring a consistently high index of suspicion. Failure to use appropriate personal protective equipment places health care workers at risk. Geographic clustering of illness, unusual presentations, and rapid clinical deterioration should prompt consideration of a biologic weapon and early initiation of therapy or prophylaxis to reduce morbidity and mortality.
Overview And Scope
Biologic weapons are naturally occurring organisms or toxins that are deliberately purified and disseminated to cause mass morbidity, mortality, and societal disruption. These agents include bacteria, viruses, fungi, and toxins, with more than 400 potential or actualized pathogens capable of weaponization. They are relatively inexpensive compared with other weapons of mass destruction, highly potent, and can be deployed covertly. Their stealth derives from natural incubation periods, as agents are typically invisible, odorless, and tasteless. Patients often present to multiple health care facilities with nonspecific complaints, delaying recognition of a covert release. Exposure occurs through direct skin contact, inhalation of aerosolized particles, or ingestion via contaminated food or water.
Causative Agents
Bacterial agents include Bacillus anthracis (anthrax), Yersinia pestis (plague), Vibrio cholerae (cholera), Francisella tularensis (tularemia), Brucella species (brucellosis), and Coxiella burnetii (Q fever). Viral agents include variola virus (smallpox), alphaviruses causing viral encephalitides such as Venezuelan, Eastern, and Western equine encephalitis, and viral hemorrhagic fevers including Ebola, Marburg, Lassa, and dengue. Toxin-based weapons include ricin, staphylococcal enterotoxin B, botulinum toxin, and mycotoxins.
Clinical Recognition And Patterns
Clinicians must remain alert for unusual illness patterns suggestive of intentional release. Warning signs include geographic clustering of illness among individuals who live or work near one another, atypical age distributions for common diseases, multiple patients presenting with unexplained similar syndromes, a single case of disease caused by a rare or eradicated pathogen, and surges of patients with similar symptoms accompanied by increasing morbidity and mortality.
Key Syndromic Presentations
Inhalational anthrax presents with fever, chills, malaise, cough, dyspnea, chest pain, nausea, diaphoresis, myalgias, tachycardia, and possible meningeal signs. Cutaneous anthrax begins as a painless pruritic papule that evolves into a vesicle and then a necrotic ulcer with a black eschar and surrounding nonpitting edema. Plague manifests with abrupt fever, chills, cough, hemoptysis, dyspnea, headache, vomiting, painful lymphadenopathy (buboes), confusion, abdominal pain, oliguria, ecchymosis, and acral gangrene. Weaponized tularemia most commonly presents in a typhoidal form with fever, headache, malaise, and nonproductive cough, carrying high mortality if untreated. Q fever causes a flu-like illness with pleuritic chest pain and patchy infiltrates on chest imaging, with low mortality even without treatment. Brucellosis presents after a prolonged incubation with flu-like and neuropsychiatric symptoms and focal joint or genitourinary pain. Smallpox begins with a prodrome of fever and myalgias followed by a characteristic centrifugal rash progressing synchronously from macules to pustules and crusts, with high untreated mortality. Viral hemorrhagic fevers evolve from a flu-like illness to gastrointestinal symptoms, organ dysfunction, hemorrhage, shock, and high fatality rates.
Initial Assessment And Workup
Bioterrorism should be suspected when relatively young, healthy patients present with influenza-like illness and deteriorate rapidly or when characteristic cutaneous findings appear. Laboratory evaluation includes complete blood count, electrolytes, renal function, arterial blood gas analysis, blood and wound cultures, coagulation studies, and cerebrospinal fluid analysis when indicated. Imaging is guided by suspected agent, with chest radiography revealing mediastinal widening and pleural effusions in anthrax or bronchopneumonia in plague. Laboratories must be alerted when high-risk pathogens are suspected.
Differential Diagnosis
Consider common infectious mimics such as influenza, bacterial pneumonia, meningitis, varicella, tularemia, and staphylococcal or streptococcal skin infections, as well as noninfectious causes depending on presentation. Distinguishing features include rash distribution, lesion staging, involvement of palms and soles, and systemic toxicity.
Prehospital And Early Management
Universal precautions with appropriate respiratory protection, including N95 masks, are essential. Initial stabilization follows standard airway, breathing, and circulation principles, with intravenous fluids for hypotension, supplemental oxygen for hypoxemia, and vasopressors for refractory shock. Respiratory and contact isolation should be instituted immediately for suspected cases.
Emergency Department Management
Supportive care includes antipyretics and early initiation of disease-specific therapy. Anthrax requires prompt antibiotics, with ciprofloxacin or doxycycline as first-line agents, often in combination with other antibiotics depending on severity and susceptibility. Plague mandates antibiotics within 24 hours, typically streptomycin or gentamicin, with chloramphenicol added for meningitis or severe illness. Brucellosis is treated with prolonged doxycycline-based regimens combined with streptomycin or rifampin. Q fever is often self-limited, though doxycycline shortens illness duration. Smallpox management is supportive, with vaccination within four days of exposure reducing disease severity; secondary bacterial infections should be treated, and exposed staff vaccinated. Management of tularemia and viral hemorrhagic fevers follows established disease-specific protocols.
Disposition And Public Health Coordination
Admission decisions depend on clinical severity and the broader disaster context. Toxic, hypoxic, or unstable patients require inpatient care with isolation. Mild, noncontagious cases may be managed as outpatients when appropriate. Suspected or confirmed cases must be reported immediately to local and state health authorities, with infectious disease and toxicology consultation obtained. Postexposure prophylaxis, vaccination, and occupational health follow-up are critical for exposed personnel.
Critical Insights And Common Errors
Early recognition is challenging, requiring a consistently high index of suspicion. Failure to use appropriate personal protective equipment places health care workers at risk. Geographic clustering of illness, unusual presentations, and rapid clinical deterioration should prompt consideration of a biologic weapon and early initiation of therapy or prophylaxis to reduce morbidity and mortality.
- Published on
Emergency and Acute Medicine – Bell’s Palsy
Overview And Clinical Definition
Bell’s palsy is an acute, idiopathic peripheral seventh cranial nerve (facial nerve) palsy. It is the most common cause of facial nerve paralysis in both adults and children. Spontaneous recovery occurs in approximately 85% of patients without treatment. Prognosis correlates with severity, with partial lesions recovering more reliably than complete paralysis. Clinical improvement usually begins within two weeks, often with return of taste sensation first, and recovery is typically complete within two to three months. Advanced age and delayed recovery are associated with worse outcomes. Men and women are affected equally, most commonly between the third and fifth decades, though all ages may be affected. Diabetes and pregnancy increase risk, and annual incidence ranges from 15 to 40 per 100,000.
Etiology And Pathophysiology
By definition, Bell’s palsy is idiopathic, though viral reactivation—most notably herpes simplex virus—is strongly suspected. Other infectious causes of peripheral facial nerve palsy include Lyme disease, Epstein–Barr virus, and varicella-zoster virus. The underlying mechanism is thought to be edema and degeneration of the facial nerve within the stylomastoid foramen. Because the forehead receives bilateral cortical innervation, only peripheral or brainstem lesions produce unilateral forehead weakness; isolated cortical lesions spare forehead movement.
Clinical Presentation
Patients typically report sudden onset unilateral facial droop with incomplete eyelid closure and loss of forehead muscle tone. Maximal weakness is reached within five days in nearly all cases, and within two days in about half. Associated features include excessive tearing or eye dryness, reduced blinking, subjective facial numbness, drooling, altered taste, hyperacusis, mastoid fullness or pain, and a frequent viral prodrome. On examination, there is isolated unilateral facial weakness involving both upper and lower face. Loss of forehead movement confirms a peripheral lesion. The remainder of the neurologic examination, including other cranial nerves and limb motor function, should be normal. The Bell phenomenon, upward rolling of the eye during attempted eyelid closure, may be observed.
Diagnostic Evaluation
Diagnosis is clinical and based on history and physical examination. Routine laboratory testing and imaging are not required. Lyme serology should be obtained in endemic regions or when clinical suspicion exists. Testing for infectious mononucleosis may be appropriate when EBV is suspected. Imaging is reserved for atypical cases or when alternative diagnoses such as tumor, mastoiditis, or central nervous system pathology are suspected.
Differential Diagnosis
Important alternatives include brainstem lesions, which typically involve additional cranial nerves or extraocular movement abnormalities; Lyme disease; Ramsay Hunt syndrome, suggested by vesicular rash, tinnitus, or vertigo; infectious mononucleosis; parotid or acoustic tumors; trauma; postoperative or infectious middle ear pathology; meningitis; Guillain–Barré syndrome; basilar artery aneurysm; early HIV infection; and bilateral facial palsy due to systemic disease such as sarcoidosis or leukemia. Rare recurrence of idiopathic palsy can occur without change in management.
Emergency Management
Patients with isolated peripheral facial nerve palsy are hemodynamically stable. Primary ED management focuses on eye protection to prevent corneal injury due to impaired eyelid closure. Lubricating ophthalmic preparations are essential, with eye patching at night as needed. Oral corticosteroids started within one week of symptom onset, ideally within 72 hours, improve recovery rates with minimal risk. Antiviral therapy combined with steroids may offer additional benefit in severe cases, though evidence is mixed. When Lyme disease is suspected, appropriate antibiotic therapy should be initiated. Surgical decompression is rarely considered and remains controversial, reserved for severe cases without improvement.
Medications
First-line therapy includes artificial tears or lubricating ophthalmic ointment as needed and prednisone 30–40 mg orally twice daily for seven days, with pediatric dosing adjusted by weight. In more severe presentations, valacyclovir 1 g orally three times daily for seven days may be added.
Disposition And Follow-Up
Hospital admission is not required for isolated Bell’s palsy. Patients may be safely discharged with outpatient management. Follow-up within one week is recommended to assess recovery and ensure adequate eye protection.
Key Clinical Lessons And Common Errors
Isolated seventh nerve weakness must involve both upper and lower face to support Bell’s palsy. Preservation of forehead movement indicates a central lesion and mandates further evaluation. A normal neurologic examination elsewhere is essential for diagnosis. Eye protection is critical to prevent corneal injury. Corticosteroids improve outcomes when given early, while antivirals remain optional and situation dependent.
Overview And Clinical Definition
Bell’s palsy is an acute, idiopathic peripheral seventh cranial nerve (facial nerve) palsy. It is the most common cause of facial nerve paralysis in both adults and children. Spontaneous recovery occurs in approximately 85% of patients without treatment. Prognosis correlates with severity, with partial lesions recovering more reliably than complete paralysis. Clinical improvement usually begins within two weeks, often with return of taste sensation first, and recovery is typically complete within two to three months. Advanced age and delayed recovery are associated with worse outcomes. Men and women are affected equally, most commonly between the third and fifth decades, though all ages may be affected. Diabetes and pregnancy increase risk, and annual incidence ranges from 15 to 40 per 100,000.
Etiology And Pathophysiology
By definition, Bell’s palsy is idiopathic, though viral reactivation—most notably herpes simplex virus—is strongly suspected. Other infectious causes of peripheral facial nerve palsy include Lyme disease, Epstein–Barr virus, and varicella-zoster virus. The underlying mechanism is thought to be edema and degeneration of the facial nerve within the stylomastoid foramen. Because the forehead receives bilateral cortical innervation, only peripheral or brainstem lesions produce unilateral forehead weakness; isolated cortical lesions spare forehead movement.
Clinical Presentation
Patients typically report sudden onset unilateral facial droop with incomplete eyelid closure and loss of forehead muscle tone. Maximal weakness is reached within five days in nearly all cases, and within two days in about half. Associated features include excessive tearing or eye dryness, reduced blinking, subjective facial numbness, drooling, altered taste, hyperacusis, mastoid fullness or pain, and a frequent viral prodrome. On examination, there is isolated unilateral facial weakness involving both upper and lower face. Loss of forehead movement confirms a peripheral lesion. The remainder of the neurologic examination, including other cranial nerves and limb motor function, should be normal. The Bell phenomenon, upward rolling of the eye during attempted eyelid closure, may be observed.
Diagnostic Evaluation
Diagnosis is clinical and based on history and physical examination. Routine laboratory testing and imaging are not required. Lyme serology should be obtained in endemic regions or when clinical suspicion exists. Testing for infectious mononucleosis may be appropriate when EBV is suspected. Imaging is reserved for atypical cases or when alternative diagnoses such as tumor, mastoiditis, or central nervous system pathology are suspected.
Differential Diagnosis
Important alternatives include brainstem lesions, which typically involve additional cranial nerves or extraocular movement abnormalities; Lyme disease; Ramsay Hunt syndrome, suggested by vesicular rash, tinnitus, or vertigo; infectious mononucleosis; parotid or acoustic tumors; trauma; postoperative or infectious middle ear pathology; meningitis; Guillain–Barré syndrome; basilar artery aneurysm; early HIV infection; and bilateral facial palsy due to systemic disease such as sarcoidosis or leukemia. Rare recurrence of idiopathic palsy can occur without change in management.
Emergency Management
Patients with isolated peripheral facial nerve palsy are hemodynamically stable. Primary ED management focuses on eye protection to prevent corneal injury due to impaired eyelid closure. Lubricating ophthalmic preparations are essential, with eye patching at night as needed. Oral corticosteroids started within one week of symptom onset, ideally within 72 hours, improve recovery rates with minimal risk. Antiviral therapy combined with steroids may offer additional benefit in severe cases, though evidence is mixed. When Lyme disease is suspected, appropriate antibiotic therapy should be initiated. Surgical decompression is rarely considered and remains controversial, reserved for severe cases without improvement.
Medications
First-line therapy includes artificial tears or lubricating ophthalmic ointment as needed and prednisone 30–40 mg orally twice daily for seven days, with pediatric dosing adjusted by weight. In more severe presentations, valacyclovir 1 g orally three times daily for seven days may be added.
Disposition And Follow-Up
Hospital admission is not required for isolated Bell’s palsy. Patients may be safely discharged with outpatient management. Follow-up within one week is recommended to assess recovery and ensure adequate eye protection.
Key Clinical Lessons And Common Errors
Isolated seventh nerve weakness must involve both upper and lower face to support Bell’s palsy. Preservation of forehead movement indicates a central lesion and mandates further evaluation. A normal neurologic examination elsewhere is essential for diagnosis. Eye protection is critical to prevent corneal injury. Corticosteroids improve outcomes when given early, while antivirals remain optional and situation dependent.
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Emergency and Acute Medicine – Animal Bite
Overview
Most animal bites are provoked. Dogs cause the majority of bites, with large dogs responsible for the most severe injuries; pit bulls account for the highest number of fatalities. Children represent about 70% of fatalities, most often from bites to the face or neck. The majority of dog bites involve animals owned by family or friends. Cat bites usually involve household pets and have a high infection rate, approximately 50% among those seeking care, because of deep puncture wounds. Rat bites occur mainly in laboratory workers or children of low socioeconomic status. Rabies transmission from rats is rare, and prophylaxis is not routinely indicated.
Special Syndromes
Catscratch disease (CSD) is diagnosed when three of four criteria are present: contact with a cat and a scratch or inoculation lesion, positive catscratch skin test, characteristic lymph node histopathology, and exclusion of other causes of lymphadenopathy. Rat-bite fever (RBF) is uncommon in the United States but carries a high mortality rate and does not require an actual bite, as transmission may occur through handling rats.
Microbiology and Etiology
Dog and cat bites commonly involve Pasteurella multocida, found twice as often in cat bites as dog bites and present in up to 80% of cat bite infections, typically within 24 hours. Staphylococcus and Streptococcus infections usually appear after 24 hours. Other pathogens include anaerobes and Capnocytophaga canimorsus (dog bites). Catscratch disease is caused by Bartonella henselae. Rat-bite fever is caused by Spirillum minus and Streptobacillus moniliformis.
Epidemiology of Bites
Dog bites account for 80–90% of all mammalian bites, cat bites 5–15%, human bites 2–5%, and rat bites 2–3%.
Clinical Presentation
Dog bites most commonly cause crush injuries but may also produce tears, avulsions, punctures, and scratches. Infection rates are lower than with cat or human bites and typically present with cellulitis, malodorous gray discharge, fever, and lymphadenopathy. Cat bites usually cause puncture wounds and have infection rates of 30–50%. Catscratch disease begins with a small macule or vesicle that becomes a papule within 3–10 days, followed weeks later by tender, nonsuppurative regional lymphadenopathy that resolves over 2–4 months, often with low-grade fever and malaise. Rat-bite fever due to S. moniliformis presents 2–10 days after exposure with fever, rigors, migratory polyarthralgias, headache, nausea, and vomiting; S. minus has a 1–3 week incubation and is more common in Asia.
History and Examination
History should include animal behavior, provocation, ownership, location, time since injury, tetanus status, allergies, and immunocompromising conditions. Examination must document wound location and extent, swelling, crush injury, devitalized tissue, range of motion, tendon and nerve function, joint or bone involvement, and signs of infection including regional adenopathy.
Diagnostic Evaluation
Aerobic and anaerobic cultures are indicated for infected wounds but not for clinically uninfected bites. Catscratch disease may be confirmed by elevated Bartonella henselae titers or a positive catscratch antigen skin test, defined as induration ≥5 mm at 48–72 hours. Plain radiographs are indicated for suspected fractures, foreign bodies such as teeth, baseline evaluation of bone or joint space violation, and infection near bone or joints to assess for osteomyelitis.
Differential Diagnosis
Consider human bites, other animal bites, reactive lymphadenopathy, chronic lymphadenitis, infection, drug reactions, malignancy, and congenital causes of lymphadenopathy.
Prehospital and Initial Care
Apply direct pressure to control bleeding. In the emergency department, prioritize hemostasis and airway stabilization for bites to the face or neck.
Emergency Department Management
Irrigate wounds copiously with normal saline using an 18-gauge plastic catheter directed along the wound tract; avoid forceful injection into tissue planes. Débride foreign material, necrotic tissue, and eschar, but do not débride puncture wounds. Wound closure increases infection risk and must be individualized. Do not close infected wounds or wounds older than 24 hours. Facial wounds may be closed with patient counseling regarding infection risk. Infected wounds, delayed presentations, and deep hand wounds should be left open, with delayed primary closure if appropriate.
Antibiotic Therapy
Antibiotics are indicated for infected wounds, cat bites, hand injuries, crush injuries, puncture wounds, full-thickness wounds of hand, face, or lower extremity, wounds involving joints, tendons, ligaments, or fractures, immunocompromised patients, wounds requiring surgical débridement, and presentations more than 8 hours after injury. Elevate the affected extremity.
Tetanus and Rabies Prophylaxis
Update tetanus prophylaxis as indicated. Rabies prophylaxis is unnecessary unless rabies is suspected. Rodents and rabbits rarely transmit rabies; skunks, raccoons, bats, and foxes are major reservoirs.
Condition-Specific Treatment
Catscratch disease is usually self-limited; provide analgesia, local heat, and avoid lymph node trauma. Antibiotics are controversial but may be considered in severe disease or immunocompromised patients. Rat-bite fever requires IV penicillin or doxycycline due to significant mortality risk.
Medications
First-line options include amoxicillin–clavulanate orally, ampicillin–sulbactam IV, penicillin IV, piperacillin–tazobactam IV, ticarcillin–clavulanate IV, or ceftriaxone plus metronidazole. Second-line regimens involve combination therapy with trimethoprim–sulfamethoxazole, penicillin VK, ciprofloxacin, or doxycycline plus anaerobic coverage with clindamycin or metronidazole.
Disposition
Admit patients with infected wounds at presentation, severe or progressive cellulitis or lymphangitis, systemic infection, failure of outpatient therapy, or severe catscratch disease with prolonged fever or marked lymphadenopathy. Healthy patients with localized infection may be discharged on antibiotics with 24-hour follow-up. Noninfected wounds require follow-up within 48 hours.
Follow-Up and Referral
Refer infected hand wounds to a hand specialist. Ensure close follow-up as outlined above.
Key Clinical Cautions
Animal bites are reportable to authorities in many jurisdictions.
Overview
Most animal bites are provoked. Dogs cause the majority of bites, with large dogs responsible for the most severe injuries; pit bulls account for the highest number of fatalities. Children represent about 70% of fatalities, most often from bites to the face or neck. The majority of dog bites involve animals owned by family or friends. Cat bites usually involve household pets and have a high infection rate, approximately 50% among those seeking care, because of deep puncture wounds. Rat bites occur mainly in laboratory workers or children of low socioeconomic status. Rabies transmission from rats is rare, and prophylaxis is not routinely indicated.
Special Syndromes
Catscratch disease (CSD) is diagnosed when three of four criteria are present: contact with a cat and a scratch or inoculation lesion, positive catscratch skin test, characteristic lymph node histopathology, and exclusion of other causes of lymphadenopathy. Rat-bite fever (RBF) is uncommon in the United States but carries a high mortality rate and does not require an actual bite, as transmission may occur through handling rats.
Microbiology and Etiology
Dog and cat bites commonly involve Pasteurella multocida, found twice as often in cat bites as dog bites and present in up to 80% of cat bite infections, typically within 24 hours. Staphylococcus and Streptococcus infections usually appear after 24 hours. Other pathogens include anaerobes and Capnocytophaga canimorsus (dog bites). Catscratch disease is caused by Bartonella henselae. Rat-bite fever is caused by Spirillum minus and Streptobacillus moniliformis.
Epidemiology of Bites
Dog bites account for 80–90% of all mammalian bites, cat bites 5–15%, human bites 2–5%, and rat bites 2–3%.
Clinical Presentation
Dog bites most commonly cause crush injuries but may also produce tears, avulsions, punctures, and scratches. Infection rates are lower than with cat or human bites and typically present with cellulitis, malodorous gray discharge, fever, and lymphadenopathy. Cat bites usually cause puncture wounds and have infection rates of 30–50%. Catscratch disease begins with a small macule or vesicle that becomes a papule within 3–10 days, followed weeks later by tender, nonsuppurative regional lymphadenopathy that resolves over 2–4 months, often with low-grade fever and malaise. Rat-bite fever due to S. moniliformis presents 2–10 days after exposure with fever, rigors, migratory polyarthralgias, headache, nausea, and vomiting; S. minus has a 1–3 week incubation and is more common in Asia.
History and Examination
History should include animal behavior, provocation, ownership, location, time since injury, tetanus status, allergies, and immunocompromising conditions. Examination must document wound location and extent, swelling, crush injury, devitalized tissue, range of motion, tendon and nerve function, joint or bone involvement, and signs of infection including regional adenopathy.
Diagnostic Evaluation
Aerobic and anaerobic cultures are indicated for infected wounds but not for clinically uninfected bites. Catscratch disease may be confirmed by elevated Bartonella henselae titers or a positive catscratch antigen skin test, defined as induration ≥5 mm at 48–72 hours. Plain radiographs are indicated for suspected fractures, foreign bodies such as teeth, baseline evaluation of bone or joint space violation, and infection near bone or joints to assess for osteomyelitis.
Differential Diagnosis
Consider human bites, other animal bites, reactive lymphadenopathy, chronic lymphadenitis, infection, drug reactions, malignancy, and congenital causes of lymphadenopathy.
Prehospital and Initial Care
Apply direct pressure to control bleeding. In the emergency department, prioritize hemostasis and airway stabilization for bites to the face or neck.
Emergency Department Management
Irrigate wounds copiously with normal saline using an 18-gauge plastic catheter directed along the wound tract; avoid forceful injection into tissue planes. Débride foreign material, necrotic tissue, and eschar, but do not débride puncture wounds. Wound closure increases infection risk and must be individualized. Do not close infected wounds or wounds older than 24 hours. Facial wounds may be closed with patient counseling regarding infection risk. Infected wounds, delayed presentations, and deep hand wounds should be left open, with delayed primary closure if appropriate.
Antibiotic Therapy
Antibiotics are indicated for infected wounds, cat bites, hand injuries, crush injuries, puncture wounds, full-thickness wounds of hand, face, or lower extremity, wounds involving joints, tendons, ligaments, or fractures, immunocompromised patients, wounds requiring surgical débridement, and presentations more than 8 hours after injury. Elevate the affected extremity.
Tetanus and Rabies Prophylaxis
Update tetanus prophylaxis as indicated. Rabies prophylaxis is unnecessary unless rabies is suspected. Rodents and rabbits rarely transmit rabies; skunks, raccoons, bats, and foxes are major reservoirs.
Condition-Specific Treatment
Catscratch disease is usually self-limited; provide analgesia, local heat, and avoid lymph node trauma. Antibiotics are controversial but may be considered in severe disease or immunocompromised patients. Rat-bite fever requires IV penicillin or doxycycline due to significant mortality risk.
Medications
First-line options include amoxicillin–clavulanate orally, ampicillin–sulbactam IV, penicillin IV, piperacillin–tazobactam IV, ticarcillin–clavulanate IV, or ceftriaxone plus metronidazole. Second-line regimens involve combination therapy with trimethoprim–sulfamethoxazole, penicillin VK, ciprofloxacin, or doxycycline plus anaerobic coverage with clindamycin or metronidazole.
Disposition
Admit patients with infected wounds at presentation, severe or progressive cellulitis or lymphangitis, systemic infection, failure of outpatient therapy, or severe catscratch disease with prolonged fever or marked lymphadenopathy. Healthy patients with localized infection may be discharged on antibiotics with 24-hour follow-up. Noninfected wounds require follow-up within 48 hours.
Follow-Up and Referral
Refer infected hand wounds to a hand specialist. Ensure close follow-up as outlined above.
Key Clinical Cautions
Animal bites are reportable to authorities in many jurisdictions.
- Published on
Emergency and Acute Medicine – Bath Salts (Synthetic Cathinones) Poisoning
Overview And Definitions
“Bath salts” is a nonspecific term used for designer drugs containing synthetic cathinones, most commonly 3,4-methylenedioxypyrovalerone (MDPV) in the United States, along with mephedrone, methylone, and numerous related compounds. These substances are highly addictive central nervous system stimulants with frequent hallucinogenic effects, producing clinical manifestations similar to cocaine, methamphetamine, or MDMA. Products are marketed under names such as Aura, Cloud 9, Ivory Wave, Vanilla Sky, and White Rush, often labeled “not for human consumption” and falsely sold as bath salts, plant food, or insect repellents to evade regulation. They appear as powders, tablets, or crystals of varying colors and may be ingested, snorted, smoked, or injected. Reported complications include severe delirium, psychosis, violent behavior, hyperthermia, rhabdomyolysis, multiorgan failure, DIC, myocardial infarction, stroke, and death.
Epidemiology
Use in the United States was first reported in 2010, with earlier reports in Europe dating to 2004. By 2011, synthetic cathinones were described as a major emerging drug problem, prompting temporary DEA Schedule I classification. Despite regulation, availability persists through retail outlets and online sources, with thousands of poison center reports nationwide.
Etiology And Pathophysiology
MDPV and related agents are structurally similar to cathinone, a stimulant alkaloid derived from the khat plant. Toxicity results primarily from potent effects on dopamine, norepinephrine, and serotonin reuptake and release. Frequent chemical modification of these agents complicates detection and regulation, and the toxic contribution of adulterants remains poorly defined.
Clinical Presentation
History is often limited or unobtainable, with collateral information from bystanders frequently required. Suspicion should be high when severe agitation or delirium occurs without an alternative explanation. Physical findings are nonspecific but typically reflect a sympathomimetic toxidrome, including hyperthermia, tachycardia, hypertension, dysrhythmias, diaphoresis, mydriasis, hyperreflexia, seizures, respiratory distress, and rhabdomyolysis. Prominent neuropsychiatric manifestations include agitation, hallucinations, paranoia, psychosis, excited delirium, aggression, panic attacks, insomnia, and suicidal ideation.
Evaluation
Assessment focuses on determining severity of intoxication and excluding competing medical or toxicologic causes of altered mental status. No routine ED assay reliably detects MDPV; confirmatory testing is limited to reference laboratories and is not available acutely. Laboratory evaluation should include CBC, basic metabolic panel, liver profile, coagulation studies, creatine kinase, lactate, and acid–base status, with toxicology screens used to identify coingestants. Imaging such as head CT is reserved for trauma or focal neurologic concern. ECG monitoring is essential to assess QRS and QT intervals and detect dysrhythmias.
Differential Diagnosis
Consider cocaine or amphetamine intoxication, anticholinergic toxicity, MDMA exposure, ethanol intoxication or withdrawal, serotonin syndrome, primary psychiatric illness, and infectious or metabolic causes of delirium.
Emergency Management
Prehospital care prioritizes airway protection, oxygenation, IV access, glucose assessment, and rapid transport. In the ED, management is supportive with continuous cardiac and temperature monitoring. Benzodiazepines are first-line therapy for agitation, seizures, and sympathomimetic effects. Active cooling measures, including ice packs, misting, fans, cooling blankets, and cooled IV fluids, are indicated for hyperthermia. Physical restraints should be used sparingly and only to prevent immediate harm. Severe or refractory cases may require endotracheal intubation, with propofol preferred for sedation when necessary. Antipsychotics should be used cautiously due to risks of seizure threshold reduction, extrapyramidal effects, and dysrhythmias. Consultation with a poison control center or medical toxicologist is strongly recommended.
Medications
Lorazepam is administered in 2–4 mg IV or IM increments, and diazepam in 10–30 mg IV or IM increments, titrated to effect.
Disposition And Follow-Up
All symptomatic patients require hospital admission for observation and monitoring. Severe intoxication with hyperthermia, cardiovascular instability, uncontrolled hypertension, or persistent altered mental status warrants ICU care. Only patients who remain completely asymptomatic after an adequate observation period may be discharged, with timing guided by poison control consultation. Outpatient follow-up with primary care is advised after discharge.
Key Clinical Considerations And Diagnostic Traps
A sympathomimetic toxidrome accompanied by delirium or psychosis should prompt consideration of synthetic cathinone exposure. Hyperthermia is a major driver of morbidity and must be treated aggressively. Management is largely supportive, with benzodiazepines forming the cornerstone of therapy, as no antidote exists.
Overview And Definitions
“Bath salts” is a nonspecific term used for designer drugs containing synthetic cathinones, most commonly 3,4-methylenedioxypyrovalerone (MDPV) in the United States, along with mephedrone, methylone, and numerous related compounds. These substances are highly addictive central nervous system stimulants with frequent hallucinogenic effects, producing clinical manifestations similar to cocaine, methamphetamine, or MDMA. Products are marketed under names such as Aura, Cloud 9, Ivory Wave, Vanilla Sky, and White Rush, often labeled “not for human consumption” and falsely sold as bath salts, plant food, or insect repellents to evade regulation. They appear as powders, tablets, or crystals of varying colors and may be ingested, snorted, smoked, or injected. Reported complications include severe delirium, psychosis, violent behavior, hyperthermia, rhabdomyolysis, multiorgan failure, DIC, myocardial infarction, stroke, and death.
Epidemiology
Use in the United States was first reported in 2010, with earlier reports in Europe dating to 2004. By 2011, synthetic cathinones were described as a major emerging drug problem, prompting temporary DEA Schedule I classification. Despite regulation, availability persists through retail outlets and online sources, with thousands of poison center reports nationwide.
Etiology And Pathophysiology
MDPV and related agents are structurally similar to cathinone, a stimulant alkaloid derived from the khat plant. Toxicity results primarily from potent effects on dopamine, norepinephrine, and serotonin reuptake and release. Frequent chemical modification of these agents complicates detection and regulation, and the toxic contribution of adulterants remains poorly defined.
Clinical Presentation
History is often limited or unobtainable, with collateral information from bystanders frequently required. Suspicion should be high when severe agitation or delirium occurs without an alternative explanation. Physical findings are nonspecific but typically reflect a sympathomimetic toxidrome, including hyperthermia, tachycardia, hypertension, dysrhythmias, diaphoresis, mydriasis, hyperreflexia, seizures, respiratory distress, and rhabdomyolysis. Prominent neuropsychiatric manifestations include agitation, hallucinations, paranoia, psychosis, excited delirium, aggression, panic attacks, insomnia, and suicidal ideation.
Evaluation
Assessment focuses on determining severity of intoxication and excluding competing medical or toxicologic causes of altered mental status. No routine ED assay reliably detects MDPV; confirmatory testing is limited to reference laboratories and is not available acutely. Laboratory evaluation should include CBC, basic metabolic panel, liver profile, coagulation studies, creatine kinase, lactate, and acid–base status, with toxicology screens used to identify coingestants. Imaging such as head CT is reserved for trauma or focal neurologic concern. ECG monitoring is essential to assess QRS and QT intervals and detect dysrhythmias.
Differential Diagnosis
Consider cocaine or amphetamine intoxication, anticholinergic toxicity, MDMA exposure, ethanol intoxication or withdrawal, serotonin syndrome, primary psychiatric illness, and infectious or metabolic causes of delirium.
Emergency Management
Prehospital care prioritizes airway protection, oxygenation, IV access, glucose assessment, and rapid transport. In the ED, management is supportive with continuous cardiac and temperature monitoring. Benzodiazepines are first-line therapy for agitation, seizures, and sympathomimetic effects. Active cooling measures, including ice packs, misting, fans, cooling blankets, and cooled IV fluids, are indicated for hyperthermia. Physical restraints should be used sparingly and only to prevent immediate harm. Severe or refractory cases may require endotracheal intubation, with propofol preferred for sedation when necessary. Antipsychotics should be used cautiously due to risks of seizure threshold reduction, extrapyramidal effects, and dysrhythmias. Consultation with a poison control center or medical toxicologist is strongly recommended.
Medications
Lorazepam is administered in 2–4 mg IV or IM increments, and diazepam in 10–30 mg IV or IM increments, titrated to effect.
Disposition And Follow-Up
All symptomatic patients require hospital admission for observation and monitoring. Severe intoxication with hyperthermia, cardiovascular instability, uncontrolled hypertension, or persistent altered mental status warrants ICU care. Only patients who remain completely asymptomatic after an adequate observation period may be discharged, with timing guided by poison control consultation. Outpatient follow-up with primary care is advised after discharge.
Key Clinical Considerations And Diagnostic Traps
A sympathomimetic toxidrome accompanied by delirium or psychosis should prompt consideration of synthetic cathinone exposure. Hyperthermia is a major driver of morbidity and must be treated aggressively. Management is largely supportive, with benzodiazepines forming the cornerstone of therapy, as no antidote exists.
