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Emergency and acute medicine – acute cholangitis
Overview and pathophysiology
Acute cholangitis is a purulent infection of the biliary tree that develops when there is partial or complete obstruction of the common bile duct. Obstruction may be caused by gallstones, tumors, cysts, or strictures, leading to increased intraluminal pressure and bacterial overgrowth. This process commonly results in bacteremia and sepsis and may extend to involve the liver and gallbladder. Mirizzi syndrome refers to bile duct obstruction caused by extrinsic compression from gallbladder or cystic duct stones or edema.
Causative factors
Infection typically arises from ascending bacteria originating in the duodenum, gallbladder infection, portal venous seeding, hematogenous spread with hepatic secretion, or lymphatic spread. Common organisms include intestinal coliforms such as Escherichia coli, Enterococcus species, and anaerobes including Bacteroides and Clostridium. In patients with AIDS, sclerosing cholangitis may occur, characterized by papillary stenosis, sclerosing cholangitis, and extrahepatic biliary obstruction; organisms such as cytomegalovirus, Cryptosporidium, and microsporidia are frequently isolated, although their exact causal role remains uncertain.
Clinical presentation
The classic presentation is Charcot triad, consisting of fever with chills, right upper quadrant abdominal pain, and jaundice, although all three features are present in only about half of patients. Progression to hypotension and altered mental status indicates severe biliary sepsis, known as Reynolds pentad. Abdominal pain is present in most patients and usually localizes to the right upper quadrant. Fever is common, while clinically apparent jaundice may be absent in a significant proportion of cases. In AIDS-related cholangitis, symptoms tend to be more indolent, with relatively normal bilirubin levels.
Initial evaluation
Early evaluation should include assessment for sepsis and organ dysfunction. Recommended studies include complete blood count, liver function tests, amylase and lipase, urinalysis, blood cultures, and electrocardiography in patients at risk for cardiac disease. Right upper quadrant ultrasound is the initial imaging study of choice to assess for biliary dilation and gallstones, with hepatobiliary scintigraphy considered when ultrasound findings are inconclusive.
Laboratory and imaging findings
Laboratory testing typically demonstrates leukocytosis with a left shift, unless the patient is immunocompromised or in advanced sepsis. Liver function tests show a cholestatic pattern with elevated direct bilirubin and alkaline phosphatase, while transaminase elevations are usually mild. Amylase and lipase are normal or only slightly elevated. Ultrasound helps identify the level of obstruction and gallstone etiology. Hepatobiliary scintigraphy is sensitive early in the disease before ductal dilation develops. CT imaging may assist in excluding alternative diagnoses. MR cholangiopancreatography is highly accurate but generally unnecessary if therapeutic ERCP is planned.
Differential considerations
Conditions that may mimic cholangitis include acute cholecystitis, hepatitis, hepatic abscess, acute pancreatitis, right-sided pyelonephritis, right lower lobe pneumonia or pulmonary embolism, perforated peptic ulcer, appendicitis, and sepsis with nonspecific liver enzyme elevation.
Early management
Initial management focuses on aggressive treatment of sepsis. Prompt intravenous fluid resuscitation is essential to correct dehydration and hemodynamic compromise. Most patients show clinical improvement within the first 24 hours of appropriate antibiotic therapy. Vasopressors may be required for hypotension refractory to fluids.
Emergency department treatment
Broad-spectrum intravenous antibiotics should be initiated early to cover gram-negative coliforms, anaerobes, and Enterococcus. Acceptable regimens include beta-lactam/beta-lactamase inhibitor combinations, carbapenems, or combination therapy with an aminoglycoside. Alternative regimens should be used in patients with penicillin allergy or renal insufficiency. Patients should be kept nil per os, with nasogastric decompression if vomiting or ileus is present. Analgesia and antiemetics may be provided once hemodynamic stability is ensured. Early gastroenterology and surgical consultation is mandatory. If there is no clinical response within 12–24 hours, urgent biliary decompression via ERCP, percutaneous drainage, or surgery is required.
Disposition and follow-up
All patients with acute cholangitis require hospital admission, with intensive care unit placement for those with septic shock or organ failure. There are no criteria for emergency department discharge. Definitive management involves continued intravenous antibiotics and timely biliary drainage when indicated.
Key clinical points
Acute cholangitis is a medical emergency with high risk of sepsis. Early recognition, aggressive fluid resuscitation, prompt administration of broad-spectrum antibiotics, and rapid consultation for biliary drainage are critical to improving outcomes.
Overview and pathophysiology
Acute cholangitis is a purulent infection of the biliary tree that develops when there is partial or complete obstruction of the common bile duct. Obstruction may be caused by gallstones, tumors, cysts, or strictures, leading to increased intraluminal pressure and bacterial overgrowth. This process commonly results in bacteremia and sepsis and may extend to involve the liver and gallbladder. Mirizzi syndrome refers to bile duct obstruction caused by extrinsic compression from gallbladder or cystic duct stones or edema.
Causative factors
Infection typically arises from ascending bacteria originating in the duodenum, gallbladder infection, portal venous seeding, hematogenous spread with hepatic secretion, or lymphatic spread. Common organisms include intestinal coliforms such as Escherichia coli, Enterococcus species, and anaerobes including Bacteroides and Clostridium. In patients with AIDS, sclerosing cholangitis may occur, characterized by papillary stenosis, sclerosing cholangitis, and extrahepatic biliary obstruction; organisms such as cytomegalovirus, Cryptosporidium, and microsporidia are frequently isolated, although their exact causal role remains uncertain.
Clinical presentation
The classic presentation is Charcot triad, consisting of fever with chills, right upper quadrant abdominal pain, and jaundice, although all three features are present in only about half of patients. Progression to hypotension and altered mental status indicates severe biliary sepsis, known as Reynolds pentad. Abdominal pain is present in most patients and usually localizes to the right upper quadrant. Fever is common, while clinically apparent jaundice may be absent in a significant proportion of cases. In AIDS-related cholangitis, symptoms tend to be more indolent, with relatively normal bilirubin levels.
Initial evaluation
Early evaluation should include assessment for sepsis and organ dysfunction. Recommended studies include complete blood count, liver function tests, amylase and lipase, urinalysis, blood cultures, and electrocardiography in patients at risk for cardiac disease. Right upper quadrant ultrasound is the initial imaging study of choice to assess for biliary dilation and gallstones, with hepatobiliary scintigraphy considered when ultrasound findings are inconclusive.
Laboratory and imaging findings
Laboratory testing typically demonstrates leukocytosis with a left shift, unless the patient is immunocompromised or in advanced sepsis. Liver function tests show a cholestatic pattern with elevated direct bilirubin and alkaline phosphatase, while transaminase elevations are usually mild. Amylase and lipase are normal or only slightly elevated. Ultrasound helps identify the level of obstruction and gallstone etiology. Hepatobiliary scintigraphy is sensitive early in the disease before ductal dilation develops. CT imaging may assist in excluding alternative diagnoses. MR cholangiopancreatography is highly accurate but generally unnecessary if therapeutic ERCP is planned.
Differential considerations
Conditions that may mimic cholangitis include acute cholecystitis, hepatitis, hepatic abscess, acute pancreatitis, right-sided pyelonephritis, right lower lobe pneumonia or pulmonary embolism, perforated peptic ulcer, appendicitis, and sepsis with nonspecific liver enzyme elevation.
Early management
Initial management focuses on aggressive treatment of sepsis. Prompt intravenous fluid resuscitation is essential to correct dehydration and hemodynamic compromise. Most patients show clinical improvement within the first 24 hours of appropriate antibiotic therapy. Vasopressors may be required for hypotension refractory to fluids.
Emergency department treatment
Broad-spectrum intravenous antibiotics should be initiated early to cover gram-negative coliforms, anaerobes, and Enterococcus. Acceptable regimens include beta-lactam/beta-lactamase inhibitor combinations, carbapenems, or combination therapy with an aminoglycoside. Alternative regimens should be used in patients with penicillin allergy or renal insufficiency. Patients should be kept nil per os, with nasogastric decompression if vomiting or ileus is present. Analgesia and antiemetics may be provided once hemodynamic stability is ensured. Early gastroenterology and surgical consultation is mandatory. If there is no clinical response within 12–24 hours, urgent biliary decompression via ERCP, percutaneous drainage, or surgery is required.
Disposition and follow-up
All patients with acute cholangitis require hospital admission, with intensive care unit placement for those with septic shock or organ failure. There are no criteria for emergency department discharge. Definitive management involves continued intravenous antibiotics and timely biliary drainage when indicated.
Key clinical points
Acute cholangitis is a medical emergency with high risk of sepsis. Early recognition, aggressive fluid resuscitation, prompt administration of broad-spectrum antibiotics, and rapid consultation for biliary drainage are critical to improving outcomes.
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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 – chancroid
Basic description
Chancroid is a sexually transmitted genital ulcer disease associated with an increased risk of HIV acquisition. It is common in parts of Africa, Southeast Asia, and Latin America but uncommon in the United States, where herpes simplex virus and syphilis are far more frequent causes of genital ulcers. Despite this, chancroid is likely underreported due to diagnostic challenges.
Cause and microbiology
The disease is caused by Haemophilus ducreyi, a highly infectious gram-negative bacterium transmitted through sexual contact.
Clinical presentation
Chancroid typically begins as a small erythematous papule or pustule that rapidly ulcerates into a painful lesion measuring 1–20 mm. The ulcers are soft, friable, and have ragged, irregular borders with an excavated appearance. The base contains moist granulation tissue and may produce purulent or hemorrhagic exudate.
In men, lesions most often involve the penile shaft, glans, foreskin, or anus, whereas in women they may occur on the cervix, vagina, vulva, perineum, or anus. Symptoms usually appear 4–7 days after exposure, with an incubation period ranging from 1–35 days.
Painful inguinal lymphadenopathy develops in approximately half of affected men and less frequently in women. These nodes are typically unilateral, may become suppurative, and can rupture to form chronic draining sinuses. Dysuria and dyspareunia may occur due to lesion contact. Several variants exist, including phagedenic chancroid with rapid tissue destruction, giant chancroid with a single large ulcer, serpiginous ulcers that spread superficially, and follicular chancroid with multiple small perifollicular lesions.
Diagnostic approach
Diagnosis is primarily clinical but often inaccurate because laboratory confirmation is difficult. The Centers for Disease Control and Prevention defines a probable diagnosis as the presence of typical painful genital ulcers with negative testing for syphilis and herpes simplex virus. A definite diagnosis requires isolation of H. ducreyi on culture, which is rarely feasible in routine practice.
Laboratory evaluation
Gram stain is unreliable and shows characteristic gram-negative coccobacilli in a linear “school-of-fish” pattern in only 50–80% of cases. Culture requires specialized media and has variable sensitivity. Polymerase chain reaction testing is sensitive and specific but not widely available. Serologic testing for syphilis, herpes simplex virus, and HIV is recommended because coinfection is common.
Differential diagnosis
Infectious considerations include syphilis, genital herpes, granuloma inguinale, and lymphogranuloma venereum. Noninfectious causes such as drug reactions, pyoderma gangrenosum, and Behçet disease should also be considered when presentation is atypical.
Management principles
Standard infection control precautions should be used during evaluation. Treatment should not be delayed when clinical criteria for probable chancroid are met.
Emergency department treatment
First-line therapy includes single-dose azithromycin or intramuscular ceftriaxone, with ceftriaxone preferred during pregnancy. Alternative regimens include ciprofloxacin for three days (avoided in pregnancy and lactation) or erythromycin for seven days. Suppurative lymph nodes larger than 5 cm should be aspirated with a large-bore needle through intact skin to prevent chronic sinus formation. Patients should undergo concurrent testing for HIV, syphilis, and herpes simplex virus, with repeat testing at three months if initially negative.
Medications
Recommended regimens include azithromycin 1 g orally once or ceftriaxone 250 mg intramuscularly once. Alternatives are ciprofloxacin 500 mg orally twice daily for three days or erythromycin base 500 mg orally four times daily for seven days.
Disposition and follow-up
Patients should abstain from sexual activity or use condoms until complete lesion healing. Clinical improvement is usually seen within two days, with ulcer resolution in 3–7 days, though healing may be delayed in HIV-positive or uncircumcised patients.
Ongoing care recommendations
All sexual partners with exposure within 10 days of symptom onset should be examined and treated regardless of symptoms. HIV-positive patients require close follow-up, particularly when treated with single-dose regimens due to higher failure rates.
Key clinical pearls
Treatment should be initiated based on clinical probability rather than awaiting culture confirmation. Treatment failure should prompt evaluation for nonadherence, antimicrobial resistance, or coinfection, particularly syphilis.
Basic description
Chancroid is a sexually transmitted genital ulcer disease associated with an increased risk of HIV acquisition. It is common in parts of Africa, Southeast Asia, and Latin America but uncommon in the United States, where herpes simplex virus and syphilis are far more frequent causes of genital ulcers. Despite this, chancroid is likely underreported due to diagnostic challenges.
Cause and microbiology
The disease is caused by Haemophilus ducreyi, a highly infectious gram-negative bacterium transmitted through sexual contact.
Clinical presentation
Chancroid typically begins as a small erythematous papule or pustule that rapidly ulcerates into a painful lesion measuring 1–20 mm. The ulcers are soft, friable, and have ragged, irregular borders with an excavated appearance. The base contains moist granulation tissue and may produce purulent or hemorrhagic exudate.
In men, lesions most often involve the penile shaft, glans, foreskin, or anus, whereas in women they may occur on the cervix, vagina, vulva, perineum, or anus. Symptoms usually appear 4–7 days after exposure, with an incubation period ranging from 1–35 days.
Painful inguinal lymphadenopathy develops in approximately half of affected men and less frequently in women. These nodes are typically unilateral, may become suppurative, and can rupture to form chronic draining sinuses. Dysuria and dyspareunia may occur due to lesion contact. Several variants exist, including phagedenic chancroid with rapid tissue destruction, giant chancroid with a single large ulcer, serpiginous ulcers that spread superficially, and follicular chancroid with multiple small perifollicular lesions.
Diagnostic approach
Diagnosis is primarily clinical but often inaccurate because laboratory confirmation is difficult. The Centers for Disease Control and Prevention defines a probable diagnosis as the presence of typical painful genital ulcers with negative testing for syphilis and herpes simplex virus. A definite diagnosis requires isolation of H. ducreyi on culture, which is rarely feasible in routine practice.
Laboratory evaluation
Gram stain is unreliable and shows characteristic gram-negative coccobacilli in a linear “school-of-fish” pattern in only 50–80% of cases. Culture requires specialized media and has variable sensitivity. Polymerase chain reaction testing is sensitive and specific but not widely available. Serologic testing for syphilis, herpes simplex virus, and HIV is recommended because coinfection is common.
Differential diagnosis
Infectious considerations include syphilis, genital herpes, granuloma inguinale, and lymphogranuloma venereum. Noninfectious causes such as drug reactions, pyoderma gangrenosum, and Behçet disease should also be considered when presentation is atypical.
Management principles
Standard infection control precautions should be used during evaluation. Treatment should not be delayed when clinical criteria for probable chancroid are met.
Emergency department treatment
First-line therapy includes single-dose azithromycin or intramuscular ceftriaxone, with ceftriaxone preferred during pregnancy. Alternative regimens include ciprofloxacin for three days (avoided in pregnancy and lactation) or erythromycin for seven days. Suppurative lymph nodes larger than 5 cm should be aspirated with a large-bore needle through intact skin to prevent chronic sinus formation. Patients should undergo concurrent testing for HIV, syphilis, and herpes simplex virus, with repeat testing at three months if initially negative.
Medications
Recommended regimens include azithromycin 1 g orally once or ceftriaxone 250 mg intramuscularly once. Alternatives are ciprofloxacin 500 mg orally twice daily for three days or erythromycin base 500 mg orally four times daily for seven days.
Disposition and follow-up
Patients should abstain from sexual activity or use condoms until complete lesion healing. Clinical improvement is usually seen within two days, with ulcer resolution in 3–7 days, though healing may be delayed in HIV-positive or uncircumcised patients.
Ongoing care recommendations
All sexual partners with exposure within 10 days of symptom onset should be examined and treated regardless of symptoms. HIV-positive patients require close follow-up, particularly when treated with single-dose regimens due to higher failure rates.
Key clinical pearls
Treatment should be initiated based on clinical probability rather than awaiting culture confirmation. Treatment failure should prompt evaluation for nonadherence, antimicrobial resistance, or coinfection, particularly syphilis.
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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 – acute cholecystitis
Definition and pathogenesis
Acute cholecystitis refers to inflammation of the gallbladder, most often resulting from obstruction of bile flow. The condition is usually precipitated by prolonged blockage of the gallbladder neck or cystic duct, leading to bile stasis, rising intraluminal pressure, mucosal injury, and subsequent inflammatory changes such as edema and increased vascularity.
Underlying causes
The most common form is acute calculous cholecystitis, caused by gallstone obstruction in the gallbladder neck, cystic duct, or occasionally the common bile duct. Secondary bacterial infection with coliforms and anaerobes may occur, although their primary role remains debated. Acalculous cholecystitis accounts for roughly 10% of cases and typically develops in critically ill patients due to biliary stasis and gallbladder ischemia, followed by inflammation and infection. In children, calculous cholecystitis is rare, whereas the acalculous form is more common and often associated with systemic infections such as sepsis, scarlet fever, Kawasaki disease, or parasitic illness.
Clinical features
Patients with calculous cholecystitis usually present with dull, aching epigastric or right upper quadrant pain that may radiate to the right scapula, shoulder, or thoracic spine. Pain persisting longer than six hours favors cholecystitis over uncomplicated biliary colic. As inflammation progresses, pain becomes sharper and more localized due to parietal peritoneal irritation. Nausea, vomiting, fever, and chills are common but not universal, and jaundice occurs in a minority of patients. A history of prior biliary colic or known gallstones supports the diagnosis. In contrast, acalculous cholecystitis often presents atypically in critically ill patients, with minimal localized abdominal pain and features of sepsis without an obvious source.
Physical examination findings
Localized right upper quadrant tenderness with percussion sensitivity or rebound may develop as inflammation advances. A positive Murphy sign—sudden inspiratory arrest during gentle palpation of the right upper quadrant—is present in most cases. In severe disease, signs of peritonitis or systemic toxicity may be evident.
Initial evaluation
Essential investigations include a complete blood count, liver function tests, amylase and lipase, urinalysis, and pregnancy testing when appropriate. Electrocardiography is recommended in patients at risk for coronary artery disease to exclude cardiac causes of pain. Imaging with right upper quadrant ultrasound is the preferred initial diagnostic test, with hepatobiliary scintigraphy reserved for equivocal cases or suspected acalculous cholecystitis.
Laboratory and imaging characteristics
Leukocytosis supports the diagnosis but may be absent in many patients. Liver enzymes and pancreatic markers are usually normal or only mildly elevated; disproportionate elevations in bilirubin or alkaline phosphatase raise concern for common bile duct obstruction or cholangitis. Ultrasound typically demonstrates gallbladder wall thickening, pericholecystic fluid, or gallstones and has high sensitivity and specificity. Hepatobiliary scintigraphy is highly sensitive and specific when ultrasound findings are inconclusive. CT imaging is useful to exclude complications such as perforation, emphysematous cholecystitis, or alternative intra-abdominal pathology.
Diagnostic considerations
Conditions that may mimic acute cholecystitis include biliary colic, cholangitis, hepatitis, hepatic abscess, pancreatitis, peptic ulcer disease, intestinal perforation, right lower lobe pneumonia, myocardial infarction, abdominal aortic aneurysm, appendicitis, and pyelonephritis.
Early management
Initial treatment focuses on supportive care, including intravenous access, fluid resuscitation for dehydration or sepsis, supplemental oxygen, and cardiac monitoring until myocardial ischemia is excluded. Patients should be kept nil per os, with nasogastric decompression if vomiting or ileus is present.
Emergency department therapy
Broad-spectrum intravenous antibiotics covering gram-negative coliforms, anaerobes, and Enterococcus species should be started promptly. Suitable regimens include beta-lactam/beta-lactamase inhibitor combinations, with aminoglycosides added if sepsis or cholangitis is suspected. Alternative regimens are required for patients with penicillin allergy. Antiemetics and opioid analgesics may be administered once the diagnosis is reasonably secure, with caution regarding sphincter of Oddi spasm. Early surgical consultation is mandatory.
Disposition and follow-up
All patients with acute cholecystitis require hospital admission for intravenous antibiotics, analgesia, fluid management, and definitive surgical treatment, typically cholecystectomy within 24–72 hours. Unstable patients or those with complications such as perforation or sepsis require urgent operative intervention. Discharge from the emergency department is not appropriate.
Clinical pearls
Ultrasound is the first-line imaging modality in suspected cholecystitis. Hepatobiliary scintigraphy should be obtained when ultrasound is inconclusive or acalculous cholecystitis is suspected. Early recognition, prompt antibiotics, and timely surgical involvement are essential to prevent complications.
Definition and pathogenesis
Acute cholecystitis refers to inflammation of the gallbladder, most often resulting from obstruction of bile flow. The condition is usually precipitated by prolonged blockage of the gallbladder neck or cystic duct, leading to bile stasis, rising intraluminal pressure, mucosal injury, and subsequent inflammatory changes such as edema and increased vascularity.
Underlying causes
The most common form is acute calculous cholecystitis, caused by gallstone obstruction in the gallbladder neck, cystic duct, or occasionally the common bile duct. Secondary bacterial infection with coliforms and anaerobes may occur, although their primary role remains debated. Acalculous cholecystitis accounts for roughly 10% of cases and typically develops in critically ill patients due to biliary stasis and gallbladder ischemia, followed by inflammation and infection. In children, calculous cholecystitis is rare, whereas the acalculous form is more common and often associated with systemic infections such as sepsis, scarlet fever, Kawasaki disease, or parasitic illness.
Clinical features
Patients with calculous cholecystitis usually present with dull, aching epigastric or right upper quadrant pain that may radiate to the right scapula, shoulder, or thoracic spine. Pain persisting longer than six hours favors cholecystitis over uncomplicated biliary colic. As inflammation progresses, pain becomes sharper and more localized due to parietal peritoneal irritation. Nausea, vomiting, fever, and chills are common but not universal, and jaundice occurs in a minority of patients. A history of prior biliary colic or known gallstones supports the diagnosis. In contrast, acalculous cholecystitis often presents atypically in critically ill patients, with minimal localized abdominal pain and features of sepsis without an obvious source.
Physical examination findings
Localized right upper quadrant tenderness with percussion sensitivity or rebound may develop as inflammation advances. A positive Murphy sign—sudden inspiratory arrest during gentle palpation of the right upper quadrant—is present in most cases. In severe disease, signs of peritonitis or systemic toxicity may be evident.
Initial evaluation
Essential investigations include a complete blood count, liver function tests, amylase and lipase, urinalysis, and pregnancy testing when appropriate. Electrocardiography is recommended in patients at risk for coronary artery disease to exclude cardiac causes of pain. Imaging with right upper quadrant ultrasound is the preferred initial diagnostic test, with hepatobiliary scintigraphy reserved for equivocal cases or suspected acalculous cholecystitis.
Laboratory and imaging characteristics
Leukocytosis supports the diagnosis but may be absent in many patients. Liver enzymes and pancreatic markers are usually normal or only mildly elevated; disproportionate elevations in bilirubin or alkaline phosphatase raise concern for common bile duct obstruction or cholangitis. Ultrasound typically demonstrates gallbladder wall thickening, pericholecystic fluid, or gallstones and has high sensitivity and specificity. Hepatobiliary scintigraphy is highly sensitive and specific when ultrasound findings are inconclusive. CT imaging is useful to exclude complications such as perforation, emphysematous cholecystitis, or alternative intra-abdominal pathology.
Diagnostic considerations
Conditions that may mimic acute cholecystitis include biliary colic, cholangitis, hepatitis, hepatic abscess, pancreatitis, peptic ulcer disease, intestinal perforation, right lower lobe pneumonia, myocardial infarction, abdominal aortic aneurysm, appendicitis, and pyelonephritis.
Early management
Initial treatment focuses on supportive care, including intravenous access, fluid resuscitation for dehydration or sepsis, supplemental oxygen, and cardiac monitoring until myocardial ischemia is excluded. Patients should be kept nil per os, with nasogastric decompression if vomiting or ileus is present.
Emergency department therapy
Broad-spectrum intravenous antibiotics covering gram-negative coliforms, anaerobes, and Enterococcus species should be started promptly. Suitable regimens include beta-lactam/beta-lactamase inhibitor combinations, with aminoglycosides added if sepsis or cholangitis is suspected. Alternative regimens are required for patients with penicillin allergy. Antiemetics and opioid analgesics may be administered once the diagnosis is reasonably secure, with caution regarding sphincter of Oddi spasm. Early surgical consultation is mandatory.
Disposition and follow-up
All patients with acute cholecystitis require hospital admission for intravenous antibiotics, analgesia, fluid management, and definitive surgical treatment, typically cholecystectomy within 24–72 hours. Unstable patients or those with complications such as perforation or sepsis require urgent operative intervention. Discharge from the emergency department is not appropriate.
Clinical pearls
Ultrasound is the first-line imaging modality in suspected cholecystitis. Hepatobiliary scintigraphy should be obtained when ultrasound is inconclusive or acalculous cholecystitis is suspected. Early recognition, prompt antibiotics, and timely surgical involvement are essential to prevent complications.
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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 – Benzodiazepine Poisoning
Clinical Overview
Benzodiazepines enhance the activity of γ-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the central nervous system, by binding to a specific allosteric site and increasing the frequency of chloride channel opening. This results in neuronal membrane hyperpolarization and suppression of cellular excitation. Additional effects include depression of spinal reflexes and the reticular activating system. Benzodiazepines are rapidly absorbed from the gastrointestinal tract, are highly protein bound, have a large volume of distribution, and undergo hepatic metabolism. Duration of action is inversely related to lipophilicity, with more lipophilic agents entering the CNS faster; clinically, the duration of effect follows lorazepam greater than diazepam greater than midazolam. Toxicity is potentiated when combined with other sedative–hypnotics such as ethanol, barbiturates, or propofol.
Clinical Manifestations
Central nervous system effects include sedation, drowsiness, slurred speech, delirium, coma, and typically midrange or small pupils. Neuromuscular findings include incoordination, slowed voluntary movements, ataxia, hypotension, and hyporeflexia or areflexia. Cardiovascular depression is usually mild, and isolated benzodiazepine ingestion is rarely lethal. Respiratory depression is generally mild compared with barbiturates but is more pronounced with short-acting agents and intravenous formulations. Gastrointestinal symptoms may include nausea, vomiting, and diarrhea. Other findings include hypothermia. Complications can include cerebral hypoxia, rhabdomyolysis, and pressure-related neuropathies, though there is no long-term organ toxicity. In pediatric patients, paradoxical agitation or restlessness may occur.
Diagnostic Approach
Diagnosis is primarily clinical, based on a history of ingestion or injection and findings of CNS depression, with lack of response to naloxone. Continuous pulse oximetry is essential. Laboratory evaluation includes electrolytes, blood urea nitrogen, creatinine, serum glucose, thyroid studies, arterial blood gas when indicated, and urinalysis for myoglobin in comatose patients or those immobilized for prolonged periods. Qualitative urine benzodiazepine screens may confirm exposure but do not correlate with severity and can yield false negatives, as many agents such as clonazepam, lorazepam, midazolam, and alprazolam are not detected. Serum benzodiazepine levels are not useful acutely. Additional studies include alcohol level, barbiturate level if suspected, acetaminophen and salicylate levels in possible self-harm, pregnancy testing, ECG, chest radiography for aspiration, and head CT when clinically indicated.
Differential Considerations
Alternative causes of depressed mental status include hypoglycemia, other sedative–hypnotics, antidepressants or antipsychotics, opioids, anticonvulsants, carbon monoxide or cyanide exposure, alcohol intoxication, hypoxemia, hypothermia, head trauma, CNS infection, and metabolic or electrolyte derangements.
Initial And Emergency Management
Prehospital care focuses on airway protection, oxygenation, cardiac monitoring, intravenous access, rapid glucose assessment, and retrieval of pill containers when overdose is suspected. Initial stabilization prioritizes airway, breathing, and circulation with supplemental oxygen, intravenous isotonic fluids, and continuous monitoring. Naloxone, thiamine, and dextrose should be administered in comatose or altered patients to address reversible causes.
In the emergency department, gastric lavage may be considered only within one hour of a life-threatening ingestion with a protected airway. Activated charcoal may be administered orally or via nasogastric tube if the airway is secure. There is no role for forced diuresis, dialysis, or charcoal hemoperfusion.
Role Of Flumazenil
Flumazenil is a competitive benzodiazepine receptor antagonist that rapidly reverses benzodiazepine-induced coma, with onset in one to two minutes and a short duration of action. Its use is limited to carefully selected patients, such as non-habituated individuals with isolated benzodiazepine overdose, normal vital signs, normal ECG, and no coingestions. It is most useful in iatrogenic sedation. Flumazenil should not be used empirically or in patients with seizure risk, tricyclic antidepressant coingestion, benzodiazepine dependence, abnormal vital signs, hypoxia, dysrhythmias, hypotension, or increased intracranial pressure, as it may precipitate withdrawal seizures or arrhythmias.
Pharmacologic Therapy
Activated charcoal may be given at 1 g/kg if appropriate. Hypoglycemia should be treated with intravenous dextrose, and thiamine administered when indicated. Flumazenil dosing begins with 0.2 mg IV over 30 seconds, titrated cautiously to effect, with close monitoring for resedation. Continuous infusion may be required in select cases. Naloxone and thiamine remain part of supportive care when the diagnosis is uncertain.
Disposition And Follow-Up
Admission is required for patients with persistent or profound CNS depression, respiratory or cardiovascular compromise, or significant coingestions. Patients may be discharged after at least four hours of observation if asymptomatic; those receiving flumazenil require extended observation for recurrent sedation. Intentional overdoses warrant psychiatric evaluation. Patients with chronic benzodiazepine use should be counseled regarding withdrawal risks, including autonomic instability, tremor, paresthesias, and seizures.
Key Clinical Insights And Common Errors
Benzodiazepine toxicity is primarily supportive in management, and isolated overdoses are seldom fatal. Clinical presentation is more informative than drug levels or toxicology screens. Flumazenil should be reserved for select cases, as inappropriate use can precipitate seizures or dysrhythmias. Intravenous formulations containing propylene glycol may cause elevated osmolar gap and anion gap metabolic acidosis, a consideration often overlooked in critically ill patients.
Clinical Overview
Benzodiazepines enhance the activity of γ-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the central nervous system, by binding to a specific allosteric site and increasing the frequency of chloride channel opening. This results in neuronal membrane hyperpolarization and suppression of cellular excitation. Additional effects include depression of spinal reflexes and the reticular activating system. Benzodiazepines are rapidly absorbed from the gastrointestinal tract, are highly protein bound, have a large volume of distribution, and undergo hepatic metabolism. Duration of action is inversely related to lipophilicity, with more lipophilic agents entering the CNS faster; clinically, the duration of effect follows lorazepam greater than diazepam greater than midazolam. Toxicity is potentiated when combined with other sedative–hypnotics such as ethanol, barbiturates, or propofol.
Clinical Manifestations
Central nervous system effects include sedation, drowsiness, slurred speech, delirium, coma, and typically midrange or small pupils. Neuromuscular findings include incoordination, slowed voluntary movements, ataxia, hypotension, and hyporeflexia or areflexia. Cardiovascular depression is usually mild, and isolated benzodiazepine ingestion is rarely lethal. Respiratory depression is generally mild compared with barbiturates but is more pronounced with short-acting agents and intravenous formulations. Gastrointestinal symptoms may include nausea, vomiting, and diarrhea. Other findings include hypothermia. Complications can include cerebral hypoxia, rhabdomyolysis, and pressure-related neuropathies, though there is no long-term organ toxicity. In pediatric patients, paradoxical agitation or restlessness may occur.
Diagnostic Approach
Diagnosis is primarily clinical, based on a history of ingestion or injection and findings of CNS depression, with lack of response to naloxone. Continuous pulse oximetry is essential. Laboratory evaluation includes electrolytes, blood urea nitrogen, creatinine, serum glucose, thyroid studies, arterial blood gas when indicated, and urinalysis for myoglobin in comatose patients or those immobilized for prolonged periods. Qualitative urine benzodiazepine screens may confirm exposure but do not correlate with severity and can yield false negatives, as many agents such as clonazepam, lorazepam, midazolam, and alprazolam are not detected. Serum benzodiazepine levels are not useful acutely. Additional studies include alcohol level, barbiturate level if suspected, acetaminophen and salicylate levels in possible self-harm, pregnancy testing, ECG, chest radiography for aspiration, and head CT when clinically indicated.
Differential Considerations
Alternative causes of depressed mental status include hypoglycemia, other sedative–hypnotics, antidepressants or antipsychotics, opioids, anticonvulsants, carbon monoxide or cyanide exposure, alcohol intoxication, hypoxemia, hypothermia, head trauma, CNS infection, and metabolic or electrolyte derangements.
Initial And Emergency Management
Prehospital care focuses on airway protection, oxygenation, cardiac monitoring, intravenous access, rapid glucose assessment, and retrieval of pill containers when overdose is suspected. Initial stabilization prioritizes airway, breathing, and circulation with supplemental oxygen, intravenous isotonic fluids, and continuous monitoring. Naloxone, thiamine, and dextrose should be administered in comatose or altered patients to address reversible causes.
In the emergency department, gastric lavage may be considered only within one hour of a life-threatening ingestion with a protected airway. Activated charcoal may be administered orally or via nasogastric tube if the airway is secure. There is no role for forced diuresis, dialysis, or charcoal hemoperfusion.
Role Of Flumazenil
Flumazenil is a competitive benzodiazepine receptor antagonist that rapidly reverses benzodiazepine-induced coma, with onset in one to two minutes and a short duration of action. Its use is limited to carefully selected patients, such as non-habituated individuals with isolated benzodiazepine overdose, normal vital signs, normal ECG, and no coingestions. It is most useful in iatrogenic sedation. Flumazenil should not be used empirically or in patients with seizure risk, tricyclic antidepressant coingestion, benzodiazepine dependence, abnormal vital signs, hypoxia, dysrhythmias, hypotension, or increased intracranial pressure, as it may precipitate withdrawal seizures or arrhythmias.
Pharmacologic Therapy
Activated charcoal may be given at 1 g/kg if appropriate. Hypoglycemia should be treated with intravenous dextrose, and thiamine administered when indicated. Flumazenil dosing begins with 0.2 mg IV over 30 seconds, titrated cautiously to effect, with close monitoring for resedation. Continuous infusion may be required in select cases. Naloxone and thiamine remain part of supportive care when the diagnosis is uncertain.
Disposition And Follow-Up
Admission is required for patients with persistent or profound CNS depression, respiratory or cardiovascular compromise, or significant coingestions. Patients may be discharged after at least four hours of observation if asymptomatic; those receiving flumazenil require extended observation for recurrent sedation. Intentional overdoses warrant psychiatric evaluation. Patients with chronic benzodiazepine use should be counseled regarding withdrawal risks, including autonomic instability, tremor, paresthesias, and seizures.
Key Clinical Insights And Common Errors
Benzodiazepine toxicity is primarily supportive in management, and isolated overdoses are seldom fatal. Clinical presentation is more informative than drug levels or toxicology screens. Flumazenil should be reserved for select cases, as inappropriate use can precipitate seizures or dysrhythmias. Intravenous formulations containing propylene glycol may cause elevated osmolar gap and anion gap metabolic acidosis, a consideration often overlooked in critically ill patients.
- Published on
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 – 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 – 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.
