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Emergency And Acute Medicine – Postpartum Hemorrhage
Postpartum hemorrhage (PPH) is defined as excessive bleeding after 20 weeks of gestation and is categorized as primary (occurring within 24 hours of delivery) or secondary (occurring more than 24 hours but within 12 weeks postpartum). It is defined quantitatively as blood loss greater than 500 mL after vaginal delivery or greater than 1,000 mL after cesarean section. PPH occurs in approximately 4% of vaginal deliveries and 6% of cesarean sections. It is the leading cause of maternal death worldwide, accounting for about 25% of pregnancy-related deaths, with nearly half of postpartum deaths attributed to hemorrhage. The majority of cases are caused by uterine atony (50–60%), retained placenta (20–30%), or cervical and vaginal lacerations (10%). Serious complications include hypovolemic shock, need for blood transfusion, acute respiratory distress syndrome, renal or hepatic failure, Sheehan syndrome, disseminated intravascular coagulation (DIC), infertility, and death.
The causes of PPH are commonly remembered as the “4 Ts”: Tone (uterine atony), Tissue (retained placental tissue), Trauma (lacerations or uterine rupture), and Thrombin (coagulopathies). Immediate causes include uterine atony, genital tract lacerations, retained placental tissue, placenta accreta, uterine rupture or inversion, puerperal hematoma, and coagulation disorders. Delayed PPH is often due to retained products of conception, postpartum endometritis, withdrawal of exogenous estrogen, hematoma, or underlying coagulopathies such as idiopathic thrombocytopenic purpura, thrombotic thrombocytopenic purpura, von Willebrand disease, or DIC. Risk factors include prior PPH, advanced maternal age, multiple gestations, prolonged labor, polyhydramnios, instrumental delivery, fetal demise, anticoagulation therapy, placental abruption, fibroids, prolonged oxytocin use, cesarean section, placenta previa or accreta, chorioamnionitis, and general anesthesia.
Clinically, patients present with ongoing vaginal bleeding that is often painless. Signs of hypovolemia include tachycardia, tachypnea, narrow pulse pressure, decreased urine output, cool clammy skin, poor capillary refill, and altered mental status. Notably, hypotension may not occur until blood loss exceeds 1,500 mL. Delayed PPH typically presents with copious vaginal bleeding days to weeks after delivery. History should focus on delivery complications, episiotomy, prior clotting disorders, and symptoms of hypovolemia such as dizziness, syncope, pallor, and decreased urine output. Physical examination requires thorough inspection of the perineum, vagina, cervix, and uterus, including external inspection, speculum examination, and bimanual examination.
Evaluation includes rapid assessment of uterine tone, retained products, and genital tract trauma. Laboratory studies should include complete blood count, platelet count, prothrombin time, partial thromboplastin time, fibrinogen level, and type and cross-match for blood products. Hemoglobin should be rapidly determined. Ultrasound may help identify retained products in delayed PPH or intrauterine or intra-abdominal fluid collections, though manual examination is often more sensitive and may be both diagnostic and therapeutic. Puerperal hematomas should be considered when pain accompanies tachycardia and hypotension.
Management requires simultaneous hemorrhage control and aggressive resuscitation. Immediate priorities include airway support, supplemental oxygen, cardiac monitoring, establishment of large-bore IV access, rapid crystalloid infusion, blood product resuscitation as needed, and Foley catheter placement to monitor urine output. Uterine atony is treated first with bimanual uterine massage and administration of uterotonics. Oxytocin is first-line therapy, followed by methylergonovine (avoided in hypertensive patients) and 15-methyl prostaglandin F2α (used cautiously in asthma). Genital tract lacerations must be identified and repaired promptly with absorbable sutures. Uterine inversion requires immediate manual repositioning using the Johnson maneuver; if unsuccessful, tocolytic agents such as terbutaline or magnesium sulfate may be administered to facilitate reduction. Surgical intervention is required if medical therapy fails, and hysterectomy is necessary in approximately 1 in 1,000 deliveries. Radiologic embolization may also be considered.
Uterine tamponade with balloon devices such as a Foley catheter, Rusch catheter, Sengstaken–Blakemore tube, or Bakri balloon may serve as temporizing measures for continued bleeding. Coagulopathies require targeted treatment with fresh-frozen plasma, platelets, or cryoprecipitate. Active management of the third stage of labor—including prompt uterotonic administration, cord traction with uterine countertraction, and uterine massage—reduces PPH risk.
All patients with immediate PPH require admission to a monitored setting, with early obstetric consultation and ICU care if hemodynamic instability or DIC is present. Patients with endometritis require admission for intravenous antibiotics. Selected cases of delayed PPH that are easily controlled and hemodynamically stable may be managed outpatient with close obstetric follow-up and oral methylergonovine when appropriate. Close follow-up is essential, and patients should seek immediate care if bleeding recurs.
Early recognition, rapid resuscitation, aggressive use of uterotonics, and timely obstetric intervention are critical. Most maternal deaths from PPH result from delayed diagnosis or inadequate resuscitation. Prompt action and multidisciplinary coordination are essential to prevent morbidity and mortality.
Postpartum hemorrhage (PPH) is defined as excessive bleeding after 20 weeks of gestation and is categorized as primary (occurring within 24 hours of delivery) or secondary (occurring more than 24 hours but within 12 weeks postpartum). It is defined quantitatively as blood loss greater than 500 mL after vaginal delivery or greater than 1,000 mL after cesarean section. PPH occurs in approximately 4% of vaginal deliveries and 6% of cesarean sections. It is the leading cause of maternal death worldwide, accounting for about 25% of pregnancy-related deaths, with nearly half of postpartum deaths attributed to hemorrhage. The majority of cases are caused by uterine atony (50–60%), retained placenta (20–30%), or cervical and vaginal lacerations (10%). Serious complications include hypovolemic shock, need for blood transfusion, acute respiratory distress syndrome, renal or hepatic failure, Sheehan syndrome, disseminated intravascular coagulation (DIC), infertility, and death.
The causes of PPH are commonly remembered as the “4 Ts”: Tone (uterine atony), Tissue (retained placental tissue), Trauma (lacerations or uterine rupture), and Thrombin (coagulopathies). Immediate causes include uterine atony, genital tract lacerations, retained placental tissue, placenta accreta, uterine rupture or inversion, puerperal hematoma, and coagulation disorders. Delayed PPH is often due to retained products of conception, postpartum endometritis, withdrawal of exogenous estrogen, hematoma, or underlying coagulopathies such as idiopathic thrombocytopenic purpura, thrombotic thrombocytopenic purpura, von Willebrand disease, or DIC. Risk factors include prior PPH, advanced maternal age, multiple gestations, prolonged labor, polyhydramnios, instrumental delivery, fetal demise, anticoagulation therapy, placental abruption, fibroids, prolonged oxytocin use, cesarean section, placenta previa or accreta, chorioamnionitis, and general anesthesia.
Clinically, patients present with ongoing vaginal bleeding that is often painless. Signs of hypovolemia include tachycardia, tachypnea, narrow pulse pressure, decreased urine output, cool clammy skin, poor capillary refill, and altered mental status. Notably, hypotension may not occur until blood loss exceeds 1,500 mL. Delayed PPH typically presents with copious vaginal bleeding days to weeks after delivery. History should focus on delivery complications, episiotomy, prior clotting disorders, and symptoms of hypovolemia such as dizziness, syncope, pallor, and decreased urine output. Physical examination requires thorough inspection of the perineum, vagina, cervix, and uterus, including external inspection, speculum examination, and bimanual examination.
Evaluation includes rapid assessment of uterine tone, retained products, and genital tract trauma. Laboratory studies should include complete blood count, platelet count, prothrombin time, partial thromboplastin time, fibrinogen level, and type and cross-match for blood products. Hemoglobin should be rapidly determined. Ultrasound may help identify retained products in delayed PPH or intrauterine or intra-abdominal fluid collections, though manual examination is often more sensitive and may be both diagnostic and therapeutic. Puerperal hematomas should be considered when pain accompanies tachycardia and hypotension.
Management requires simultaneous hemorrhage control and aggressive resuscitation. Immediate priorities include airway support, supplemental oxygen, cardiac monitoring, establishment of large-bore IV access, rapid crystalloid infusion, blood product resuscitation as needed, and Foley catheter placement to monitor urine output. Uterine atony is treated first with bimanual uterine massage and administration of uterotonics. Oxytocin is first-line therapy, followed by methylergonovine (avoided in hypertensive patients) and 15-methyl prostaglandin F2α (used cautiously in asthma). Genital tract lacerations must be identified and repaired promptly with absorbable sutures. Uterine inversion requires immediate manual repositioning using the Johnson maneuver; if unsuccessful, tocolytic agents such as terbutaline or magnesium sulfate may be administered to facilitate reduction. Surgical intervention is required if medical therapy fails, and hysterectomy is necessary in approximately 1 in 1,000 deliveries. Radiologic embolization may also be considered.
Uterine tamponade with balloon devices such as a Foley catheter, Rusch catheter, Sengstaken–Blakemore tube, or Bakri balloon may serve as temporizing measures for continued bleeding. Coagulopathies require targeted treatment with fresh-frozen plasma, platelets, or cryoprecipitate. Active management of the third stage of labor—including prompt uterotonic administration, cord traction with uterine countertraction, and uterine massage—reduces PPH risk.
All patients with immediate PPH require admission to a monitored setting, with early obstetric consultation and ICU care if hemodynamic instability or DIC is present. Patients with endometritis require admission for intravenous antibiotics. Selected cases of delayed PPH that are easily controlled and hemodynamically stable may be managed outpatient with close obstetric follow-up and oral methylergonovine when appropriate. Close follow-up is essential, and patients should seek immediate care if bleeding recurs.
Early recognition, rapid resuscitation, aggressive use of uterotonics, and timely obstetric intervention are critical. Most maternal deaths from PPH result from delayed diagnosis or inadequate resuscitation. Prompt action and multidisciplinary coordination are essential to prevent morbidity and mortality.
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Emergency And Acute Medicine – Postpartum Infection
Postpartum infection most commonly presents as postpartum endometritis (PPE), which may occur early (within 48 hours) or late (3 days to 6 weeks after delivery). Early PPE is more frequently associated with cesarean section and occurs in 1–3% of uncomplicated vaginal deliveries. The classic triad consists of fever, lower abdominal pain with uterine tenderness, and foul-smelling lochia. Late PPE usually follows vaginal delivery. The risk of PPE may be as high as 85–95% in high-risk nonelective cesarean sections. Complications, which are more common after cesarean delivery, include pelvic thrombophlebitis, pelvic abscess, and bacteremia.
Septic pelvic thrombophlebitis is a diagnosis of exclusion and may present as acute thrombosis, most commonly involving the right ovarian vein within the first 48 hours, characterized by progressive lower abdominal pain and persistent spiking (“picket fence”) fevers with tachycardia. Septic abortion is an ascending polymicrobial infection through an open cervical os, often associated with retained products of conception or nonsterile techniques. Mastitis ranges from mild localized breast inflammation to systemic illness and abscess formation, occurring in 1–30% of postpartum patients, most commonly within the first 3 months and peaking at 2–3 weeks. Urinary tract infection and pyelonephritis, along with mastitis, account for the majority of postpartum infections.
Postpartum endometritis is typically polymicrobial due to ascending infection from the lower genital tract, involving both anaerobic and aerobic organisms. Common pathogens include group A and B streptococci, enterococci, Gardnerella vaginalis, Escherichia coli, Enterobacter, Bacteroides, and Peptostreptococcus. Late infections may involve Ureaplasma urealyticum, Mycoplasma hominis, and Chlamydia trachomatis. Septic abortion is usually polymicrobial and may include E. coli, Bacteroides, anaerobic gram-negative rods, group B streptococci, Staphylococcus species, and sexually transmitted organisms such as gonorrhea and Chlamydia. Mastitis is most commonly caused by Staphylococcus aureus, followed by streptococci and gram-negative organisms.
Patients typically present with fever and chills, abdominal or uterine tenderness, and foul-smelling lochia in cases of endometritis. Septic abortion may resemble endometritis but can progress to shock, acute respiratory distress syndrome, or disseminated intravascular coagulation. Mastitis presents with fever, unilateral breast pain, engorgement, erythema, and tenderness. Other infection sources include wound infections with redness and swelling, and urinary tract infections with dysuria, frequency, flank pain, and costovertebral angle tenderness. A careful birth history should assess mode of delivery, duration of labor, rupture of membranes, instrumentation, exposure to sexually transmitted infections, and immunocompromised status.
Evaluation includes abdominal and pelvic examination, cervical cultures for Chlamydia, and endometrial cultures when indicated. Laboratory testing should include complete blood count, urinalysis and urine culture, and blood cultures. Imaging with CT or MRI is useful for suspected ovarian vein thrombosis, while ultrasound can identify abscess or retained products of conception. Plain radiographs may reveal retained foreign bodies or free air in septic abortion.
Management begins with airway, breathing, and circulation stabilization, particularly in patients with signs of sepsis or shock. Intravenous access, crystalloid resuscitation, supplemental oxygen, and cardiac monitoring are essential. Broad-spectrum intravenous antibiotics should be initiated promptly. Endometritis is commonly treated with regimens such as cefoxitin, cefotetan, piperacillin–tazobactam, ampicillin–sulbactam, or clindamycin plus gentamicin. Septic abortion requires broad triple antibiotic coverage targeting gram-positive, gram-negative, and anaerobic organisms, along with prompt dilation and curettage to remove retained tissue. Mastitis is treated with oral antibiotics such as dicloxacillin, cephalexin, clindamycin, or erythromycin, with vancomycin reserved for suspected or confirmed MRSA. Inpatient urinary tract infections or pyelonephritis may be treated with intravenous ciprofloxacin, ceftriaxone, or piperacillin–tazobactam.
Septic pelvic thrombophlebitis may require anticoagulation with heparin in addition to antibiotics. Infected wounds or abscesses require drainage, and necrotizing fasciitis mandates urgent surgical debridement with broad-spectrum antibiotics and possible adjunctive hyperbaric oxygen therapy. Continuous monitoring for hemodynamic instability, respiratory compromise, and progression to sepsis is critical.
Patients with endometritis, septic abortion, or suspected septic pelvic thrombophlebitis require hospital admission. Mild, nontoxic patients may be considered for outpatient management only with close obstetric consultation and follow-up. All patients should receive close follow-up with obstetrics or primary care to ensure clinical resolution and to monitor for complications. Early recognition, prompt antimicrobial therapy, and aggressive supportive care are essential to prevent morbidity and mortality in postpartum infections.
Postpartum infection most commonly presents as postpartum endometritis (PPE), which may occur early (within 48 hours) or late (3 days to 6 weeks after delivery). Early PPE is more frequently associated with cesarean section and occurs in 1–3% of uncomplicated vaginal deliveries. The classic triad consists of fever, lower abdominal pain with uterine tenderness, and foul-smelling lochia. Late PPE usually follows vaginal delivery. The risk of PPE may be as high as 85–95% in high-risk nonelective cesarean sections. Complications, which are more common after cesarean delivery, include pelvic thrombophlebitis, pelvic abscess, and bacteremia.
Septic pelvic thrombophlebitis is a diagnosis of exclusion and may present as acute thrombosis, most commonly involving the right ovarian vein within the first 48 hours, characterized by progressive lower abdominal pain and persistent spiking (“picket fence”) fevers with tachycardia. Septic abortion is an ascending polymicrobial infection through an open cervical os, often associated with retained products of conception or nonsterile techniques. Mastitis ranges from mild localized breast inflammation to systemic illness and abscess formation, occurring in 1–30% of postpartum patients, most commonly within the first 3 months and peaking at 2–3 weeks. Urinary tract infection and pyelonephritis, along with mastitis, account for the majority of postpartum infections.
Postpartum endometritis is typically polymicrobial due to ascending infection from the lower genital tract, involving both anaerobic and aerobic organisms. Common pathogens include group A and B streptococci, enterococci, Gardnerella vaginalis, Escherichia coli, Enterobacter, Bacteroides, and Peptostreptococcus. Late infections may involve Ureaplasma urealyticum, Mycoplasma hominis, and Chlamydia trachomatis. Septic abortion is usually polymicrobial and may include E. coli, Bacteroides, anaerobic gram-negative rods, group B streptococci, Staphylococcus species, and sexually transmitted organisms such as gonorrhea and Chlamydia. Mastitis is most commonly caused by Staphylococcus aureus, followed by streptococci and gram-negative organisms.
Patients typically present with fever and chills, abdominal or uterine tenderness, and foul-smelling lochia in cases of endometritis. Septic abortion may resemble endometritis but can progress to shock, acute respiratory distress syndrome, or disseminated intravascular coagulation. Mastitis presents with fever, unilateral breast pain, engorgement, erythema, and tenderness. Other infection sources include wound infections with redness and swelling, and urinary tract infections with dysuria, frequency, flank pain, and costovertebral angle tenderness. A careful birth history should assess mode of delivery, duration of labor, rupture of membranes, instrumentation, exposure to sexually transmitted infections, and immunocompromised status.
Evaluation includes abdominal and pelvic examination, cervical cultures for Chlamydia, and endometrial cultures when indicated. Laboratory testing should include complete blood count, urinalysis and urine culture, and blood cultures. Imaging with CT or MRI is useful for suspected ovarian vein thrombosis, while ultrasound can identify abscess or retained products of conception. Plain radiographs may reveal retained foreign bodies or free air in septic abortion.
Management begins with airway, breathing, and circulation stabilization, particularly in patients with signs of sepsis or shock. Intravenous access, crystalloid resuscitation, supplemental oxygen, and cardiac monitoring are essential. Broad-spectrum intravenous antibiotics should be initiated promptly. Endometritis is commonly treated with regimens such as cefoxitin, cefotetan, piperacillin–tazobactam, ampicillin–sulbactam, or clindamycin plus gentamicin. Septic abortion requires broad triple antibiotic coverage targeting gram-positive, gram-negative, and anaerobic organisms, along with prompt dilation and curettage to remove retained tissue. Mastitis is treated with oral antibiotics such as dicloxacillin, cephalexin, clindamycin, or erythromycin, with vancomycin reserved for suspected or confirmed MRSA. Inpatient urinary tract infections or pyelonephritis may be treated with intravenous ciprofloxacin, ceftriaxone, or piperacillin–tazobactam.
Septic pelvic thrombophlebitis may require anticoagulation with heparin in addition to antibiotics. Infected wounds or abscesses require drainage, and necrotizing fasciitis mandates urgent surgical debridement with broad-spectrum antibiotics and possible adjunctive hyperbaric oxygen therapy. Continuous monitoring for hemodynamic instability, respiratory compromise, and progression to sepsis is critical.
Patients with endometritis, septic abortion, or suspected septic pelvic thrombophlebitis require hospital admission. Mild, nontoxic patients may be considered for outpatient management only with close obstetric consultation and follow-up. All patients should receive close follow-up with obstetrics or primary care to ensure clinical resolution and to monitor for complications. Early recognition, prompt antimicrobial therapy, and aggressive supportive care are essential to prevent morbidity and mortality in postpartum infections.
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Emergency And Acute Medicine – Preeclampsia/Eclampsia
Hypertensive disorders of pregnancy complicate approximately 1% of all pregnancies and account for 16% of maternal deaths. Gestational hypertension (GH) is defined as new-onset hypertension after 20 weeks of gestation that resolves with delivery and occurs in 6–7% of pregnancies. Preeclampsia is gestational hypertension accompanied by proteinuria and affects 2.2–6.3% of pregnancies. Eclampsia is defined as preeclampsia with the occurrence of seizures. Postpartum preeclampsia develops within 6 weeks of delivery, often without prior history of hypertension, and occurs in approximately 5% of patients, most commonly in African American women. HELLP syndrome—characterized by hemolysis, elevated liver enzymes, and low platelets—may occur in women with preeclampsia or eclampsia. Superimposed preeclampsia refers to preeclampsia developing in a woman with chronic hypertension and complicates up to 25% of such pregnancies.
Preeclampsia is thought to result from incomplete placental implantation leading to placental underperfusion, decreased angiogenic growth factors, and increased placental debris in the maternal circulation. Eclampsia may develop even in patients without prior documented hypertension; approximately one-third of patients who seize have no preceding hypertensive diagnosis. Risk factors include extremes of reproductive age, nulliparity, multiple gestations, molar pregnancy, obesity, diabetes, collagen vascular disease, chronic hypertension, renal disease, smoking, and prior history of preeclampsia.
Gestational hypertension is diagnosed when systolic blood pressure (SBP) exceeds 140 mm Hg or diastolic blood pressure (DBP) exceeds 90 mm Hg on two separate measurements after 20 weeks of gestation in a previously normotensive patient. Severe hypertension is defined as SBP greater than 160 mm Hg or DBP greater than 110 mm Hg. Preeclampsia requires the presence of hypertension and proteinuria, defined as ≥300 mg protein on 24-hour urine collection or ≥1+ protein on urinalysis. Mild preeclampsia presents with SBP <160 mm hg and dbp <110 hg, normal platelets liver function tests, absence of neurologic symptoms. severe preeclampsia includes sbp>160 mm Hg or DBP >110 mm Hg, heavy proteinuria, oliguria, thrombocytopenia, right upper quadrant pain, impaired liver function, cerebral symptoms, visual disturbances, pulmonary edema, or evidence of intrauterine growth restriction. HELLP syndrome may present with pulmonary edema, renal or liver failure, sepsis, stroke, or other systemic complications.
Patients commonly report headache, visual disturbances, abdominal pain (especially right upper quadrant), nausea, vomiting, weight gain, edema, shortness of breath, or neurologic symptoms. A history of prior preeclampsia, chronic hypertension, or renal disease increases suspicion. Physical examination should include serial blood pressure measurements, careful abdominal palpation for right upper quadrant tenderness, evaluation for edema, and detailed neurologic assessment including mental status and deep tendon reflexes.
Evaluation requires serial blood pressure monitoring and urinalysis. Laboratory studies include complete blood count, liver function tests, blood urea nitrogen, creatinine, uric acid, lactate dehydrogenase, coagulation studies, fibrinogen, and d-dimer levels. Proteinuria greater than 1+ on dipstick warrants 24-hour urine collection. Obstetric ultrasound assesses gestational age, fetal growth, viability, and amniotic fluid volume. Fetal monitoring and nonstress testing are indicated. Head CT should be performed when neurologic deficits or severe symptoms raise concern for intracranial hemorrhage or mass. Lumbar puncture may be necessary if infection or subarachnoid hemorrhage is suspected. Urine toxicology should be considered to exclude cocaine or methamphetamine use.
Management begins with stabilization of airway, breathing, and circulation. Patients should receive 100% oxygen and be placed in the left lateral decubitus position to reduce inferior vena cava compression and improve cardiac output. Continuous maternal cardiopulmonary and fetal monitoring is essential. Magnesium sulfate (MgSO₄) is the first-line agent for seizure prophylaxis and treatment. A typical regimen includes a 4 g IV loading dose (or 10 g IM) followed by a continuous infusion of 1–2 g/hour, with a target serum magnesium level of 4–7 mEq/L. The infusion rate should not exceed 1 g/min during bolus administration. Signs of magnesium toxicity include hypotension, loss of patellar reflexes, respiratory depression, decreased urine output, and elevated creatinine; calcium gluconate 1 g IV is the antidote.
Blood pressure control is achieved with intravenous hydralazine (5–20 mg IV) or labetalol (initial 10 mg IV, followed by incremental dosing). The goal is to reduce blood pressure by approximately 25% initially, then gradually to <160 />00 mm Hg over several hours. If seizures persist despite magnesium, second-line therapy includes diazepam, fosphenytoin, or phenytoin. Intubation is required for airway protection, refractory seizures, or hypoxia.
Delivery is the definitive treatment for preeclampsia and eclampsia. Obstetric consultation is mandatory in all cases. Expectant management may be considered in select patients less than 30 weeks’ gestation with stable disease, but delivery is recommended beyond 30 weeks or in the presence of severe features. Emergent induction or cesarean section is indicated for maternal or fetal instability.
All patients with preeclampsia, eclampsia, or HELLP syndrome require admission, often to intensive care or labor and delivery units. Patients with isolated hypertension who have negative evaluation for preeclampsia and are asymptomatic may be discharged with close obstetric follow-up. Patients should return immediately for headache, visual changes, abdominal pain, dyspnea, leg swelling, or decreased urine output.
Clinicians must remember that preeclampsia and eclampsia can occur up to 30 days postpartum and should be considered in any postpartum patient presenting with edema, headache, shortness of breath, or seizure. Airway management may be challenging due to airway edema and engorgement; smaller-diameter endotracheal tubes and fiberoptic techniques may be required. Early recognition, aggressive stabilization, and timely delivery are critical to reducing maternal and fetal morbidity and mortality.
Hypertensive disorders of pregnancy complicate approximately 1% of all pregnancies and account for 16% of maternal deaths. Gestational hypertension (GH) is defined as new-onset hypertension after 20 weeks of gestation that resolves with delivery and occurs in 6–7% of pregnancies. Preeclampsia is gestational hypertension accompanied by proteinuria and affects 2.2–6.3% of pregnancies. Eclampsia is defined as preeclampsia with the occurrence of seizures. Postpartum preeclampsia develops within 6 weeks of delivery, often without prior history of hypertension, and occurs in approximately 5% of patients, most commonly in African American women. HELLP syndrome—characterized by hemolysis, elevated liver enzymes, and low platelets—may occur in women with preeclampsia or eclampsia. Superimposed preeclampsia refers to preeclampsia developing in a woman with chronic hypertension and complicates up to 25% of such pregnancies.
Preeclampsia is thought to result from incomplete placental implantation leading to placental underperfusion, decreased angiogenic growth factors, and increased placental debris in the maternal circulation. Eclampsia may develop even in patients without prior documented hypertension; approximately one-third of patients who seize have no preceding hypertensive diagnosis. Risk factors include extremes of reproductive age, nulliparity, multiple gestations, molar pregnancy, obesity, diabetes, collagen vascular disease, chronic hypertension, renal disease, smoking, and prior history of preeclampsia.
Gestational hypertension is diagnosed when systolic blood pressure (SBP) exceeds 140 mm Hg or diastolic blood pressure (DBP) exceeds 90 mm Hg on two separate measurements after 20 weeks of gestation in a previously normotensive patient. Severe hypertension is defined as SBP greater than 160 mm Hg or DBP greater than 110 mm Hg. Preeclampsia requires the presence of hypertension and proteinuria, defined as ≥300 mg protein on 24-hour urine collection or ≥1+ protein on urinalysis. Mild preeclampsia presents with SBP <160 mm hg and dbp <110 hg, normal platelets liver function tests, absence of neurologic symptoms. severe preeclampsia includes sbp>160 mm Hg or DBP >110 mm Hg, heavy proteinuria, oliguria, thrombocytopenia, right upper quadrant pain, impaired liver function, cerebral symptoms, visual disturbances, pulmonary edema, or evidence of intrauterine growth restriction. HELLP syndrome may present with pulmonary edema, renal or liver failure, sepsis, stroke, or other systemic complications.
Patients commonly report headache, visual disturbances, abdominal pain (especially right upper quadrant), nausea, vomiting, weight gain, edema, shortness of breath, or neurologic symptoms. A history of prior preeclampsia, chronic hypertension, or renal disease increases suspicion. Physical examination should include serial blood pressure measurements, careful abdominal palpation for right upper quadrant tenderness, evaluation for edema, and detailed neurologic assessment including mental status and deep tendon reflexes.
Evaluation requires serial blood pressure monitoring and urinalysis. Laboratory studies include complete blood count, liver function tests, blood urea nitrogen, creatinine, uric acid, lactate dehydrogenase, coagulation studies, fibrinogen, and d-dimer levels. Proteinuria greater than 1+ on dipstick warrants 24-hour urine collection. Obstetric ultrasound assesses gestational age, fetal growth, viability, and amniotic fluid volume. Fetal monitoring and nonstress testing are indicated. Head CT should be performed when neurologic deficits or severe symptoms raise concern for intracranial hemorrhage or mass. Lumbar puncture may be necessary if infection or subarachnoid hemorrhage is suspected. Urine toxicology should be considered to exclude cocaine or methamphetamine use.
Management begins with stabilization of airway, breathing, and circulation. Patients should receive 100% oxygen and be placed in the left lateral decubitus position to reduce inferior vena cava compression and improve cardiac output. Continuous maternal cardiopulmonary and fetal monitoring is essential. Magnesium sulfate (MgSO₄) is the first-line agent for seizure prophylaxis and treatment. A typical regimen includes a 4 g IV loading dose (or 10 g IM) followed by a continuous infusion of 1–2 g/hour, with a target serum magnesium level of 4–7 mEq/L. The infusion rate should not exceed 1 g/min during bolus administration. Signs of magnesium toxicity include hypotension, loss of patellar reflexes, respiratory depression, decreased urine output, and elevated creatinine; calcium gluconate 1 g IV is the antidote.
Blood pressure control is achieved with intravenous hydralazine (5–20 mg IV) or labetalol (initial 10 mg IV, followed by incremental dosing). The goal is to reduce blood pressure by approximately 25% initially, then gradually to <160 />00 mm Hg over several hours. If seizures persist despite magnesium, second-line therapy includes diazepam, fosphenytoin, or phenytoin. Intubation is required for airway protection, refractory seizures, or hypoxia.
Delivery is the definitive treatment for preeclampsia and eclampsia. Obstetric consultation is mandatory in all cases. Expectant management may be considered in select patients less than 30 weeks’ gestation with stable disease, but delivery is recommended beyond 30 weeks or in the presence of severe features. Emergent induction or cesarean section is indicated for maternal or fetal instability.
All patients with preeclampsia, eclampsia, or HELLP syndrome require admission, often to intensive care or labor and delivery units. Patients with isolated hypertension who have negative evaluation for preeclampsia and are asymptomatic may be discharged with close obstetric follow-up. Patients should return immediately for headache, visual changes, abdominal pain, dyspnea, leg swelling, or decreased urine output.
Clinicians must remember that preeclampsia and eclampsia can occur up to 30 days postpartum and should be considered in any postpartum patient presenting with edema, headache, shortness of breath, or seizure. Airway management may be challenging due to airway edema and engorgement; smaller-diameter endotracheal tubes and fiberoptic techniques may be required. Early recognition, aggressive stabilization, and timely delivery are critical to reducing maternal and fetal morbidity and mortality.
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Emergency And Acute Medicine – Pregnancy, Trauma In
Trauma complicates approximately 7% of all pregnancies and is the most common cause of nonobstetric maternal morbidity and mortality. Fetal loss ranges from 3.4–38% depending on injury severity. After the first trimester, trauma increases fetal loss but does not significantly increase maternal mortality. The likelihood of fetal injury rises with the severity of maternal insult. Physiologic hypervolemia in pregnancy may mask blood loss, and clinical shock may not be apparent until 30% of maternal blood volume is lost. Abdominal findings are often subtle in gravid patients. Even minor trauma accounts for at least 50% of fetal losses, and an Injury Severity Score greater than 9 is associated with worse outcomes. Pelvic fractures carry increased maternal and fetal morbidity due to engorged pelvic organs and vasculature.
Fetal and uterine complications include placental abruption, fetomaternal hemorrhage (FMH), premature labor, uterine contusion or rupture, premature rupture of membranes, fetal hypoxia, direct fetal injury, and fetal demise. Placental abruption occurs in up to 60% of severe trauma and 1–5% of minor injuries, accounting for up to 50% of fetal losses. It may occur without external bleeding in 20% of cases and is characterized by uterine contractions, abdominal pain, and vaginal bleeding. Uterine rupture, more common in patients with prior cesarean section, carries nearly universal fetal mortality and approximately 10% maternal mortality. FMH occurs in more than 30% of severe trauma and can cause isoimmunization in Rh-negative mothers with as little as 0.03 mL of fetal blood. Falls, which affect one in four pregnant women, significantly increase risks of preterm birth, abruption, fetal distress, and fetal hypoxia. Burns involving more than 40% total body surface area approach 100% maternal and fetal mortality. Domestic violence, electrocution, penetrating trauma, and motor vehicle accidents are major contributors.
Motor vehicle accidents account for 48–84% of traumatic events in pregnancy, followed by domestic violence, falls, direct abdominal trauma, penetrating injuries, burns, and electrical injuries. Trauma occurs more frequently in younger women and is often associated with substance abuse or suicidal behavior.
Evaluation begins with a focused history including mechanism of injury, gestational age, last menstrual period, abdominal pain, uterine contractions, vaginal bleeding, leakage of fluid, prior cesarean sections, and substance use. Examination should follow primary, secondary, and tertiary trauma surveys with the patient positioned in the left lateral recumbent position when feasible. Findings suggestive of placental abruption include uterine tenderness and contractions. Uterine rupture may present with abnormal uterine contour and palpable fetal parts. Gestational age estimation is critical for assessing viability; after 16 weeks, fundal height in centimeters approximates gestational age in weeks.
Initial management prioritizes maternal stabilization with airway management and resuscitation as indicated. Spinal immobilization should be maintained. Oxygen, cardiac monitoring, pulse oximetry, and intravenous access are essential. The patient or backboard should be tilted 15–30 degrees to the left to prevent supine hypotension. Lactated Ringer solution is preferred; blood loss should be replaced in a 3:1 crystalloid-to-blood ratio. If severe hemorrhage occurs, balanced transfusion with packed red blood cells, plasma, and platelets in a 1:1:1 ratio reduces coagulopathy. O-negative blood should be used if type-specific blood is unavailable. Nasogastric decompression reduces aspiration risk, and Foley catheterization monitors urine output. Rapid sequence intubation is safe and preferred when needed.
Fetal assessment includes Doppler fetal heart tones and continuous fetal monitoring for viable fetuses, generally beyond 24 weeks’ gestation. Monitoring should continue for at least 4–6 hours. Absence of contractions during the first 4 hours makes abruption unlikely. More than eight contractions per hour or persistent contractions increase the risk of adverse outcomes. Fetal bradycardia, poor variability, or late decelerations indicate distress. A normal tracing with normal maternal examination has a near 100% negative predictive value for adverse outcomes.
Laboratory evaluation includes complete blood count, blood gas and electrolytes, urinalysis, blood type and Rh status, and Kleihauer–Betke testing to quantify FMH. Rh-negative patients should receive Rho(D) immune globulin within 72 hours: 50 μg before 12 weeks and 300 μg after 12 weeks, with repeat dosing if significant FMH is detected. Imaging studies necessary for maternal evaluation should not be withheld; shielding is recommended when possible. Radiation doses under 1 rad (10 mGy) carry minimal risk, while malformation risk increases at 5–10 rad. FAST ultrasound evaluates hemoperitoneum, fetal viability, gestational age, and amniotic fluid but may miss placental abruption.
Tocolytic therapy may be considered in hemodynamically stable patients with persistent contractions lasting more than 4 hours, typically using magnesium sulfate 4 g IV. Tocolytics are contraindicated with cervical dilation greater than 4 cm or when abruption or FMH is suspected. Perimortem cesarean delivery should be considered within 4–5 minutes of maternal cardiac arrest in viable pregnancies. In minor trauma beyond 20 weeks, monitoring is best conducted in a labor and delivery setting.
Admission is required for vaginal bleeding, amniotic fluid leakage, abdominal pain, uterine contractions, FMH, fetal distress, placental abruption, or evidence of internal injury. Discharge may be considered only after at least 4 hours of monitoring without contractions, bleeding, tenderness, or fetal distress, and only in consultation with obstetrics. Clear return precautions and prompt obstetric follow-up are mandatory.
Minor trauma can result in significant maternal or fetal morbidity and mortality. Stabilization of the mother is always the first priority, as maternal resuscitation optimizes fetal outcome. Clinicians must remember that signs of maternal shock may not appear until 1,500–2,000 mL of blood loss has occurred.
Trauma complicates approximately 7% of all pregnancies and is the most common cause of nonobstetric maternal morbidity and mortality. Fetal loss ranges from 3.4–38% depending on injury severity. After the first trimester, trauma increases fetal loss but does not significantly increase maternal mortality. The likelihood of fetal injury rises with the severity of maternal insult. Physiologic hypervolemia in pregnancy may mask blood loss, and clinical shock may not be apparent until 30% of maternal blood volume is lost. Abdominal findings are often subtle in gravid patients. Even minor trauma accounts for at least 50% of fetal losses, and an Injury Severity Score greater than 9 is associated with worse outcomes. Pelvic fractures carry increased maternal and fetal morbidity due to engorged pelvic organs and vasculature.
Fetal and uterine complications include placental abruption, fetomaternal hemorrhage (FMH), premature labor, uterine contusion or rupture, premature rupture of membranes, fetal hypoxia, direct fetal injury, and fetal demise. Placental abruption occurs in up to 60% of severe trauma and 1–5% of minor injuries, accounting for up to 50% of fetal losses. It may occur without external bleeding in 20% of cases and is characterized by uterine contractions, abdominal pain, and vaginal bleeding. Uterine rupture, more common in patients with prior cesarean section, carries nearly universal fetal mortality and approximately 10% maternal mortality. FMH occurs in more than 30% of severe trauma and can cause isoimmunization in Rh-negative mothers with as little as 0.03 mL of fetal blood. Falls, which affect one in four pregnant women, significantly increase risks of preterm birth, abruption, fetal distress, and fetal hypoxia. Burns involving more than 40% total body surface area approach 100% maternal and fetal mortality. Domestic violence, electrocution, penetrating trauma, and motor vehicle accidents are major contributors.
Motor vehicle accidents account for 48–84% of traumatic events in pregnancy, followed by domestic violence, falls, direct abdominal trauma, penetrating injuries, burns, and electrical injuries. Trauma occurs more frequently in younger women and is often associated with substance abuse or suicidal behavior.
Evaluation begins with a focused history including mechanism of injury, gestational age, last menstrual period, abdominal pain, uterine contractions, vaginal bleeding, leakage of fluid, prior cesarean sections, and substance use. Examination should follow primary, secondary, and tertiary trauma surveys with the patient positioned in the left lateral recumbent position when feasible. Findings suggestive of placental abruption include uterine tenderness and contractions. Uterine rupture may present with abnormal uterine contour and palpable fetal parts. Gestational age estimation is critical for assessing viability; after 16 weeks, fundal height in centimeters approximates gestational age in weeks.
Initial management prioritizes maternal stabilization with airway management and resuscitation as indicated. Spinal immobilization should be maintained. Oxygen, cardiac monitoring, pulse oximetry, and intravenous access are essential. The patient or backboard should be tilted 15–30 degrees to the left to prevent supine hypotension. Lactated Ringer solution is preferred; blood loss should be replaced in a 3:1 crystalloid-to-blood ratio. If severe hemorrhage occurs, balanced transfusion with packed red blood cells, plasma, and platelets in a 1:1:1 ratio reduces coagulopathy. O-negative blood should be used if type-specific blood is unavailable. Nasogastric decompression reduces aspiration risk, and Foley catheterization monitors urine output. Rapid sequence intubation is safe and preferred when needed.
Fetal assessment includes Doppler fetal heart tones and continuous fetal monitoring for viable fetuses, generally beyond 24 weeks’ gestation. Monitoring should continue for at least 4–6 hours. Absence of contractions during the first 4 hours makes abruption unlikely. More than eight contractions per hour or persistent contractions increase the risk of adverse outcomes. Fetal bradycardia, poor variability, or late decelerations indicate distress. A normal tracing with normal maternal examination has a near 100% negative predictive value for adverse outcomes.
Laboratory evaluation includes complete blood count, blood gas and electrolytes, urinalysis, blood type and Rh status, and Kleihauer–Betke testing to quantify FMH. Rh-negative patients should receive Rho(D) immune globulin within 72 hours: 50 μg before 12 weeks and 300 μg after 12 weeks, with repeat dosing if significant FMH is detected. Imaging studies necessary for maternal evaluation should not be withheld; shielding is recommended when possible. Radiation doses under 1 rad (10 mGy) carry minimal risk, while malformation risk increases at 5–10 rad. FAST ultrasound evaluates hemoperitoneum, fetal viability, gestational age, and amniotic fluid but may miss placental abruption.
Tocolytic therapy may be considered in hemodynamically stable patients with persistent contractions lasting more than 4 hours, typically using magnesium sulfate 4 g IV. Tocolytics are contraindicated with cervical dilation greater than 4 cm or when abruption or FMH is suspected. Perimortem cesarean delivery should be considered within 4–5 minutes of maternal cardiac arrest in viable pregnancies. In minor trauma beyond 20 weeks, monitoring is best conducted in a labor and delivery setting.
Admission is required for vaginal bleeding, amniotic fluid leakage, abdominal pain, uterine contractions, FMH, fetal distress, placental abruption, or evidence of internal injury. Discharge may be considered only after at least 4 hours of monitoring without contractions, bleeding, tenderness, or fetal distress, and only in consultation with obstetrics. Clear return precautions and prompt obstetric follow-up are mandatory.
Minor trauma can result in significant maternal or fetal morbidity and mortality. Stabilization of the mother is always the first priority, as maternal resuscitation optimizes fetal outcome. Clinicians must remember that signs of maternal shock may not appear until 1,500–2,000 mL of blood loss has occurred.
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Emergency And Acute Medicine – Pseudotumor Cerebri (Idiopathic Intracranial Hypertension)
Pseudotumor cerebri, also known as idiopathic intracranial hypertension, is characterized by elevated cerebrospinal fluid (CSF) pressure without an identifiable mass lesion or other clear cause. Proposed mechanisms include impaired venous drainage from intracranial venous stenosis or increased intra-abdominal pressure, as well as arachnoid granulation dysfunction possibly related to excess vitamin A levels. The condition is strongly associated with obesity, has an average onset around 30 years of age, shows a marked female predominance (approximately 7:1), and is relatively uncommon, with an incidence of about 1–5 cases per 100,000.
Risk factors and associated conditions include obesity, recent weight gain, intracranial venous outflow obstruction, hypervitaminosis A, steroid use or withdrawal, tetracycline antibiotics, oral contraceptive use, hypertension, and chronic carbon dioxide retention. Certain medications should be reviewed carefully when evaluating suspected cases.
Patients typically present with a constant, bilateral, pressure-like headache that is worse in the morning and exacerbated by Valsalva maneuvers. Nausea, vomiting, pulsatile tinnitus, diplopia, dizziness, transient visual obscurations, scotomas, blind spots, and progressive constriction of peripheral vision are common. Visual field defects occur in up to 90% of patients, often affecting the inferior nasal field. Papilledema is a hallmark finding. Sixth cranial nerve palsy may be present, leading to horizontal diplopia, and rarely seventh nerve palsy may occur. Aside from visual findings and abducens palsy, the neurologic examination is typically normal. In children, presentation may differ, with strabismus more common than headache.
Evaluation requires a thorough neurologic and fundoscopic examination. Neuroimaging with head CT or MRI must be performed before lumbar puncture to exclude mass lesions. Classically, CT may show slitlike ventricles. MRI is recommended for comprehensive evaluation and to assess for features suggestive of raised intracranial pressure. Cerebral venous thrombosis can closely mimic pseudotumor cerebri and must be excluded, often with MR venography. Lumbar puncture is diagnostic and therapeutic. Opening pressure is elevated, typically greater than 25 cm H2O (or greater than 20 cm H2O in a nonobese, relaxed patient), with otherwise normal CSF composition. Measurement must be performed in the lateral decubitus position with the neck and legs extended to ensure accuracy. Symptomatic improvement after lumbar puncture supports the diagnosis. The Modified Dandy criteria include symptoms of raised intracranial pressure, absence of focal neurologic deficits except sixth nerve palsy, normal neuroimaging without thrombosis, and elevated opening pressure with normal CSF studies.
Differential diagnoses include primary headache disorders such as migraine, tension, or cluster headache; hypertensive headache; subarachnoid hemorrhage; meningitis; intracranial tumors; subdural or epidural hematoma; cerebral venous thrombosis; glaucoma; optic neuritis; and other causes of papilledema or visual disturbance.
Initial management in the emergency setting focuses on pain control and stabilization. Large-volume lumbar puncture removing 20–30 mL of CSF may provide temporary relief if imaging confirms no obstructive pathology and open cisterns. Acetazolamide is first-line therapy and reduces CSF production. NSAIDs may be used for headache control. In cases of severe visual symptoms, a short course of corticosteroids may be considered. Additional agents such as furosemide or topiramate may be used in selected cases. Weight loss is strongly recommended. Any potentially causative medications should be discontinued.
Urgent consultation with neurology and ophthalmology is essential. Neurosurgical evaluation is required for acute or impending visual loss not responsive to medical therapy, as procedures such as optic nerve sheath fenestration, lumboperitoneal shunting, or venous sinus stenting (when stenosis is present) may be necessary.
Admission is indicated for patients with acute or worsening visual loss. Stable patients may be discharged with close follow-up if pain is controlled, oral diuretics are tolerated, and specialist consultation has been arranged. Patients must be instructed to return immediately for worsening headache, new focal neurologic deficits, or any visual deterioration.
Clinicians should consider this diagnosis in younger patients—particularly women with obesity—who present with chronic headache and visual complaints. Opening pressure should be measured whenever lumbar puncture is performed for unexplained headache. Visual symptoms may precede permanent visual loss, making early recognition and treatment critical.
Pseudotumor cerebri, also known as idiopathic intracranial hypertension, is characterized by elevated cerebrospinal fluid (CSF) pressure without an identifiable mass lesion or other clear cause. Proposed mechanisms include impaired venous drainage from intracranial venous stenosis or increased intra-abdominal pressure, as well as arachnoid granulation dysfunction possibly related to excess vitamin A levels. The condition is strongly associated with obesity, has an average onset around 30 years of age, shows a marked female predominance (approximately 7:1), and is relatively uncommon, with an incidence of about 1–5 cases per 100,000.
Risk factors and associated conditions include obesity, recent weight gain, intracranial venous outflow obstruction, hypervitaminosis A, steroid use or withdrawal, tetracycline antibiotics, oral contraceptive use, hypertension, and chronic carbon dioxide retention. Certain medications should be reviewed carefully when evaluating suspected cases.
Patients typically present with a constant, bilateral, pressure-like headache that is worse in the morning and exacerbated by Valsalva maneuvers. Nausea, vomiting, pulsatile tinnitus, diplopia, dizziness, transient visual obscurations, scotomas, blind spots, and progressive constriction of peripheral vision are common. Visual field defects occur in up to 90% of patients, often affecting the inferior nasal field. Papilledema is a hallmark finding. Sixth cranial nerve palsy may be present, leading to horizontal diplopia, and rarely seventh nerve palsy may occur. Aside from visual findings and abducens palsy, the neurologic examination is typically normal. In children, presentation may differ, with strabismus more common than headache.
Evaluation requires a thorough neurologic and fundoscopic examination. Neuroimaging with head CT or MRI must be performed before lumbar puncture to exclude mass lesions. Classically, CT may show slitlike ventricles. MRI is recommended for comprehensive evaluation and to assess for features suggestive of raised intracranial pressure. Cerebral venous thrombosis can closely mimic pseudotumor cerebri and must be excluded, often with MR venography. Lumbar puncture is diagnostic and therapeutic. Opening pressure is elevated, typically greater than 25 cm H2O (or greater than 20 cm H2O in a nonobese, relaxed patient), with otherwise normal CSF composition. Measurement must be performed in the lateral decubitus position with the neck and legs extended to ensure accuracy. Symptomatic improvement after lumbar puncture supports the diagnosis. The Modified Dandy criteria include symptoms of raised intracranial pressure, absence of focal neurologic deficits except sixth nerve palsy, normal neuroimaging without thrombosis, and elevated opening pressure with normal CSF studies.
Differential diagnoses include primary headache disorders such as migraine, tension, or cluster headache; hypertensive headache; subarachnoid hemorrhage; meningitis; intracranial tumors; subdural or epidural hematoma; cerebral venous thrombosis; glaucoma; optic neuritis; and other causes of papilledema or visual disturbance.
Initial management in the emergency setting focuses on pain control and stabilization. Large-volume lumbar puncture removing 20–30 mL of CSF may provide temporary relief if imaging confirms no obstructive pathology and open cisterns. Acetazolamide is first-line therapy and reduces CSF production. NSAIDs may be used for headache control. In cases of severe visual symptoms, a short course of corticosteroids may be considered. Additional agents such as furosemide or topiramate may be used in selected cases. Weight loss is strongly recommended. Any potentially causative medications should be discontinued.
Urgent consultation with neurology and ophthalmology is essential. Neurosurgical evaluation is required for acute or impending visual loss not responsive to medical therapy, as procedures such as optic nerve sheath fenestration, lumboperitoneal shunting, or venous sinus stenting (when stenosis is present) may be necessary.
Admission is indicated for patients with acute or worsening visual loss. Stable patients may be discharged with close follow-up if pain is controlled, oral diuretics are tolerated, and specialist consultation has been arranged. Patients must be instructed to return immediately for worsening headache, new focal neurologic deficits, or any visual deterioration.
Clinicians should consider this diagnosis in younger patients—particularly women with obesity—who present with chronic headache and visual complaints. Opening pressure should be measured whenever lumbar puncture is performed for unexplained headache. Visual symptoms may precede permanent visual loss, making early recognition and treatment critical.
- Published on
Emergency And Acute Medicine – Psychosis: Medical vs. Psychiatric
Psychosis is a mental derangement characterized by hallucinations, delusions, or grossly disorganized behavior resulting in loss of contact with reality. Its pathophysiology is complex and not fully understood, though excess dopaminergic signaling is thought to contribute. Psychosis can range from mild thought disturbance to severe states such as catatonia. Central nervous system impairment leading to psychosis may arise from neurologic disease, metabolic disturbances, toxins or medications, infections, or primary psychiatric illness. Distinguishing medical from psychiatric causes is critical in emergency care.
Certain features increase suspicion for a primary psychiatric disorder: onset in late adolescence or early adulthood, preserved orientation, and hallucinations incorporated into a structured delusional system. In contrast, features suggesting a medical cause include middle- or late-life onset, acute presentation, fluctuating course, abnormal vital signs, disorientation, distractibility, recent memory loss, substance use history, absence of prior psychiatric or family history, and presence of underlying medical illness. Visual hallucinations in particular are more commonly associated with medical etiologies such as delirium, dementia, migraines, dopaminergic therapy, posterior cerebral infarcts, or narcolepsy.
Medical causes of psychosis span multiple systems. Neurologic conditions include head trauma, tumors, stroke, seizures, hydrocephalus, and neurodegenerative disorders such as Parkinson, Huntington, Alzheimer, Pick, and Wilson disease. Infectious causes include urinary tract infection or pneumonia in the elderly, HIV, neurosyphilis, encephalitis, Lyme neuroborreliosis, and parasitic infections such as cerebral malaria or toxoplasmosis. Metabolic derangements include electrolyte abnormalities, hypoglycemia, hypoxia, porphyria, and withdrawal syndromes. Endocrine disorders (thyroid, parathyroid, adrenal, pituitary), organ failure (renal, hepatic, cardiac), nutritional deficiencies (B12 deficiency, Wernicke–Korsakoff syndrome, pellagra), autoimmune disease (SLE, sarcoidosis), demyelinating disease, and postoperative delirium may also present with psychosis. Intoxicants (alcohol, stimulants, hallucinogens, opioids, cannabis), toxins (carbon monoxide, heavy metals, organophosphates), and numerous medications—including corticosteroids, anticholinergics, sedative–hypnotics, antiparkinsonian agents, antibiotics, cardiac drugs, and over-the-counter sympathomimetics—must be considered. Primary psychiatric causes include schizophrenia spectrum disorders, mood disorders with psychotic features, delusional disorder, stress-related disorders, and postpartum psychosis.
Clinically, psychosis involves impaired reality testing, inappropriate affect, and poor impulse control. Hallucinations are sensory perceptions without external stimuli, while delusions are fixed false beliefs held with certainty and incorrigibility. Thought process abnormalities may include loose associations or disorganization. Affective features such as mania, depression, or catatonia may coexist. History should assess time course (acute vs. chronic), medication adherence, substance use, recent surgery or trauma, systemic symptoms (fever, weight loss), and family history. Collateral information is often essential. Physical examination must include vital signs and a focused neurologic and cognitive assessment, particularly attention and orientation.
A detailed history and exam guide the workup. In patients with known psychiatric illness, benign history, and normal exam, the likelihood of significant laboratory abnormalities is low. First-line laboratory studies often include CBC, electrolytes (including calcium), renal function, glucose, liver function tests, thyroid function tests, B12 and folate levels, urinalysis, and toxicology screening. Second-line tests are guided by suspicion and may include ammonia, HIV testing, fluorescent treponemal antibody absorption (for neurosyphilis), ceruloplasmin (for Wilson disease), heavy metal screening, ESR, CRP, or autoimmune markers. Neuroimaging is indicated when history or examination suggests neurologic disease, or in first-episode psychosis in patients over age 50. CT or MRI may be used; routine imaging without clinical indication has limited value. ECG is recommended before neuroleptic administration to assess QT interval. Lumbar puncture and EEG are not recommended for routine screening but may be appropriate when specific concerns arise.
Management begins with ensuring safety of the patient, staff, and bystanders. Vital signs, oxygen saturation, and serum glucose should be checked promptly. If the patient is uncooperative and dangerous, behavioral control may be necessary. When a medical cause is identified, treatment should target the underlying condition. For behavioral control, haloperidol combined with lorazepam is commonly used and minimally interferes with ongoing medical evaluation. Atypical antipsychotics such as olanzapine or ziprasidone may be administered IM; dissolving oral preparations of olanzapine and risperidone are available. IM lorazepam should not be given concurrently with IM olanzapine due to risk of respiratory depression. QT interval should be assessed before administering neuroleptics.
First-line pharmacologic management often includes haloperidol 2–10 mg IM or IV combined with lorazepam 0.5–2 mg IM or IV. Second-line options include olanzapine 5–10 mg PO/SL/IM, risperidone 1–2 mg PO/SL, quetiapine 25–100 mg PO, or diazepam 5–10 mg IV. In geriatric patients, antipsychotics carry increased mortality risk; lower starting doses are recommended, and benzodiazepines should be used cautiously, particularly in delirium. In pregnancy, first-generation antipsychotics such as haloperidol have the strongest safety data.
Disposition depends on etiology and risk. Patients with medical causes require admission to the appropriate medical service. Patients with primary psychiatric causes may require psychiatric hospitalization if they pose danger to themselves or others, cannot care for themselves, or have severely disorganized thought processes. Laws governing involuntary hospitalization vary by jurisdiction. Discharge is appropriate only when the patient is medically stable, not suicidal or homicidal, able to care for themselves, and capable of medical decision-making, with follow-up arranged within one to two weeks.
A key principle is to maintain high suspicion for organic causes before attributing psychosis solely to psychiatric illness. Collateral history is essential, as psychotic patients may not provide reliable accounts. Careful assessment and systematic evaluation are critical to prevent missing reversible medical causes.
Psychosis is a mental derangement characterized by hallucinations, delusions, or grossly disorganized behavior resulting in loss of contact with reality. Its pathophysiology is complex and not fully understood, though excess dopaminergic signaling is thought to contribute. Psychosis can range from mild thought disturbance to severe states such as catatonia. Central nervous system impairment leading to psychosis may arise from neurologic disease, metabolic disturbances, toxins or medications, infections, or primary psychiatric illness. Distinguishing medical from psychiatric causes is critical in emergency care.
Certain features increase suspicion for a primary psychiatric disorder: onset in late adolescence or early adulthood, preserved orientation, and hallucinations incorporated into a structured delusional system. In contrast, features suggesting a medical cause include middle- or late-life onset, acute presentation, fluctuating course, abnormal vital signs, disorientation, distractibility, recent memory loss, substance use history, absence of prior psychiatric or family history, and presence of underlying medical illness. Visual hallucinations in particular are more commonly associated with medical etiologies such as delirium, dementia, migraines, dopaminergic therapy, posterior cerebral infarcts, or narcolepsy.
Medical causes of psychosis span multiple systems. Neurologic conditions include head trauma, tumors, stroke, seizures, hydrocephalus, and neurodegenerative disorders such as Parkinson, Huntington, Alzheimer, Pick, and Wilson disease. Infectious causes include urinary tract infection or pneumonia in the elderly, HIV, neurosyphilis, encephalitis, Lyme neuroborreliosis, and parasitic infections such as cerebral malaria or toxoplasmosis. Metabolic derangements include electrolyte abnormalities, hypoglycemia, hypoxia, porphyria, and withdrawal syndromes. Endocrine disorders (thyroid, parathyroid, adrenal, pituitary), organ failure (renal, hepatic, cardiac), nutritional deficiencies (B12 deficiency, Wernicke–Korsakoff syndrome, pellagra), autoimmune disease (SLE, sarcoidosis), demyelinating disease, and postoperative delirium may also present with psychosis. Intoxicants (alcohol, stimulants, hallucinogens, opioids, cannabis), toxins (carbon monoxide, heavy metals, organophosphates), and numerous medications—including corticosteroids, anticholinergics, sedative–hypnotics, antiparkinsonian agents, antibiotics, cardiac drugs, and over-the-counter sympathomimetics—must be considered. Primary psychiatric causes include schizophrenia spectrum disorders, mood disorders with psychotic features, delusional disorder, stress-related disorders, and postpartum psychosis.
Clinically, psychosis involves impaired reality testing, inappropriate affect, and poor impulse control. Hallucinations are sensory perceptions without external stimuli, while delusions are fixed false beliefs held with certainty and incorrigibility. Thought process abnormalities may include loose associations or disorganization. Affective features such as mania, depression, or catatonia may coexist. History should assess time course (acute vs. chronic), medication adherence, substance use, recent surgery or trauma, systemic symptoms (fever, weight loss), and family history. Collateral information is often essential. Physical examination must include vital signs and a focused neurologic and cognitive assessment, particularly attention and orientation.
A detailed history and exam guide the workup. In patients with known psychiatric illness, benign history, and normal exam, the likelihood of significant laboratory abnormalities is low. First-line laboratory studies often include CBC, electrolytes (including calcium), renal function, glucose, liver function tests, thyroid function tests, B12 and folate levels, urinalysis, and toxicology screening. Second-line tests are guided by suspicion and may include ammonia, HIV testing, fluorescent treponemal antibody absorption (for neurosyphilis), ceruloplasmin (for Wilson disease), heavy metal screening, ESR, CRP, or autoimmune markers. Neuroimaging is indicated when history or examination suggests neurologic disease, or in first-episode psychosis in patients over age 50. CT or MRI may be used; routine imaging without clinical indication has limited value. ECG is recommended before neuroleptic administration to assess QT interval. Lumbar puncture and EEG are not recommended for routine screening but may be appropriate when specific concerns arise.
Management begins with ensuring safety of the patient, staff, and bystanders. Vital signs, oxygen saturation, and serum glucose should be checked promptly. If the patient is uncooperative and dangerous, behavioral control may be necessary. When a medical cause is identified, treatment should target the underlying condition. For behavioral control, haloperidol combined with lorazepam is commonly used and minimally interferes with ongoing medical evaluation. Atypical antipsychotics such as olanzapine or ziprasidone may be administered IM; dissolving oral preparations of olanzapine and risperidone are available. IM lorazepam should not be given concurrently with IM olanzapine due to risk of respiratory depression. QT interval should be assessed before administering neuroleptics.
First-line pharmacologic management often includes haloperidol 2–10 mg IM or IV combined with lorazepam 0.5–2 mg IM or IV. Second-line options include olanzapine 5–10 mg PO/SL/IM, risperidone 1–2 mg PO/SL, quetiapine 25–100 mg PO, or diazepam 5–10 mg IV. In geriatric patients, antipsychotics carry increased mortality risk; lower starting doses are recommended, and benzodiazepines should be used cautiously, particularly in delirium. In pregnancy, first-generation antipsychotics such as haloperidol have the strongest safety data.
Disposition depends on etiology and risk. Patients with medical causes require admission to the appropriate medical service. Patients with primary psychiatric causes may require psychiatric hospitalization if they pose danger to themselves or others, cannot care for themselves, or have severely disorganized thought processes. Laws governing involuntary hospitalization vary by jurisdiction. Discharge is appropriate only when the patient is medically stable, not suicidal or homicidal, able to care for themselves, and capable of medical decision-making, with follow-up arranged within one to two weeks.
A key principle is to maintain high suspicion for organic causes before attributing psychosis solely to psychiatric illness. Collateral history is essential, as psychotic patients may not provide reliable accounts. Careful assessment and systematic evaluation are critical to prevent missing reversible medical causes.
- Published on
Emergency And Acute Medicine – Psychiatric Commitment
Psychiatric “civil commitment” is the state-sanctioned involuntary hospitalization of a mentally disordered individual. Voluntary psychiatric hospitalization is the admission of a competent adult who agrees to hospitalization. Commitment criteria vary by jurisdiction, but commonly require that the individual is mentally ill (often excluding intellectual disability, antisocial behavior, purely medical illness, and substance use alone) and that there is a likelihood of serious harm. Serious harm is typically defined as a substantial risk of physical harm to self, a substantial risk of physical harm to others, or being “gravely disabled,” meaning unable to meet basic needs such as food, clothing, shelter, medical care, or safety. Commitment also generally requires that no less-restrictive alternative would adequately reduce the risk. The process often occurs in two stages: an emergency detention/hold (commonly around 72 hours with minimal legal process) and longer-term commitment, which requires judicial review with an adversarial process and potential legal representation for the patient.
The etiology of conditions leading to commitment often includes an underlying biologic or genetic predisposition to psychiatric illness, with psychosocial stressors triggering onset or worsening of symptoms. Substance use can worsen psychiatric symptoms or contribute to disinhibition and increased safety risk.
Evaluation begins with careful history and assessment of commitment criteria. Important historical elements include recent changes in behavior or thinking; psychotic symptoms such as hallucinations, delusions, or disorganized thought; mood symptoms including depression, anxiety, agitation, or mania; and evidence of risk such as actual or threatened self-harm, violence toward others, or inability to care for oneself. Past psychiatric history, hospitalizations, medication adherence, substance use (type, amount, timing), and access to weapons are critical. Physical examination should screen for intoxication, withdrawal syndromes, toxidromes, and signs of self-injury. A focused mental status exam assesses mood, thought process, hallucinations or delusions, cognition, and the presence of suicidal or homicidal ideation, including intent and plan.
Workup requires both medical and psychiatric evaluation. A medical assessment is important to rule out medical causes of altered thinking or behavior, such as delirium, infection, metabolic derangements, head injury, or neurologic disease. Laboratory testing is guided by presentation and may include electrolytes, renal function, glucose, liver function tests, CBC, toxicology screens, medication levels, urinalysis, and thyroid studies. Imaging such as head CT or MRI is considered if trauma or structural CNS pathology is suspected. EEG may be indicated for possible seizure or postictal states, and lumbar puncture is considered with fever, nuchal rigidity, or seizures.
The differential diagnosis includes intoxication or withdrawal, delirium, dementia, traumatic brain injury, temporal lobe seizures, encephalitis, meningitis, and malingering or antisocial behavior. Because causes can overlap, especially with substance use and psychiatric illness, evaluation should remain broad until medical contributors are excluded.
Management prioritizes safety of the patient and staff. This includes removing potential weapons or dangerous items, using a hazard-free room, constant observation to prevent elopement, and ensuring appropriate legal documentation for an emergency hold when applicable. Treatment includes medical stabilization, management of overdose or withdrawal, and psychiatric consultation when available. Restraint (verbal de-escalation, security presence, medications, and physical restraints) should use the least restrictive method necessary to maintain safety. Confirmed home psychiatric medications may be continued when appropriate. Symptomatic medications for agitation, anxiety, psychosis, and sleep may be used, and withdrawal syndromes must be treated promptly.
Medication options described include olanzapine 5–10 mg PO/IM as a first-line agent for agitation, or haloperidol 5 mg IM with lorazepam 2 mg IM and benztropine 1 mg IM. For alcohol or benzodiazepine withdrawal, diazepam 5–10 mg PO hourly as needed with standardized monitoring (e.g., CIWA) is first line. For delirium not due to alcohol withdrawal or anticholinergic excess, haloperidol 1–2 mg PO/IM/IV is suggested. For agitation not associated with psychosis, delirium, or alcohol withdrawal, lorazepam 1 mg PO/IM/IV may be used.
Admission is indicated when there is danger to self, danger to others, or severe disability preventing adequate self-care or safety, following the commitment process specific to the jurisdiction. Discharge may be appropriate after medical and psychiatric evaluation if the patient can care for themselves and risk is manageable in a less-restrictive setting such as crisis stabilization, partial hospitalization, or outpatient care with close follow-up. Patients discharged should receive clear return precautions for worsening symptoms or feeling unsafe, and referrals for timely outpatient psychiatric follow-up, crisis services, or structured programs as needed.
Psychiatric “civil commitment” is the state-sanctioned involuntary hospitalization of a mentally disordered individual. Voluntary psychiatric hospitalization is the admission of a competent adult who agrees to hospitalization. Commitment criteria vary by jurisdiction, but commonly require that the individual is mentally ill (often excluding intellectual disability, antisocial behavior, purely medical illness, and substance use alone) and that there is a likelihood of serious harm. Serious harm is typically defined as a substantial risk of physical harm to self, a substantial risk of physical harm to others, or being “gravely disabled,” meaning unable to meet basic needs such as food, clothing, shelter, medical care, or safety. Commitment also generally requires that no less-restrictive alternative would adequately reduce the risk. The process often occurs in two stages: an emergency detention/hold (commonly around 72 hours with minimal legal process) and longer-term commitment, which requires judicial review with an adversarial process and potential legal representation for the patient.
The etiology of conditions leading to commitment often includes an underlying biologic or genetic predisposition to psychiatric illness, with psychosocial stressors triggering onset or worsening of symptoms. Substance use can worsen psychiatric symptoms or contribute to disinhibition and increased safety risk.
Evaluation begins with careful history and assessment of commitment criteria. Important historical elements include recent changes in behavior or thinking; psychotic symptoms such as hallucinations, delusions, or disorganized thought; mood symptoms including depression, anxiety, agitation, or mania; and evidence of risk such as actual or threatened self-harm, violence toward others, or inability to care for oneself. Past psychiatric history, hospitalizations, medication adherence, substance use (type, amount, timing), and access to weapons are critical. Physical examination should screen for intoxication, withdrawal syndromes, toxidromes, and signs of self-injury. A focused mental status exam assesses mood, thought process, hallucinations or delusions, cognition, and the presence of suicidal or homicidal ideation, including intent and plan.
Workup requires both medical and psychiatric evaluation. A medical assessment is important to rule out medical causes of altered thinking or behavior, such as delirium, infection, metabolic derangements, head injury, or neurologic disease. Laboratory testing is guided by presentation and may include electrolytes, renal function, glucose, liver function tests, CBC, toxicology screens, medication levels, urinalysis, and thyroid studies. Imaging such as head CT or MRI is considered if trauma or structural CNS pathology is suspected. EEG may be indicated for possible seizure or postictal states, and lumbar puncture is considered with fever, nuchal rigidity, or seizures.
The differential diagnosis includes intoxication or withdrawal, delirium, dementia, traumatic brain injury, temporal lobe seizures, encephalitis, meningitis, and malingering or antisocial behavior. Because causes can overlap, especially with substance use and psychiatric illness, evaluation should remain broad until medical contributors are excluded.
Management prioritizes safety of the patient and staff. This includes removing potential weapons or dangerous items, using a hazard-free room, constant observation to prevent elopement, and ensuring appropriate legal documentation for an emergency hold when applicable. Treatment includes medical stabilization, management of overdose or withdrawal, and psychiatric consultation when available. Restraint (verbal de-escalation, security presence, medications, and physical restraints) should use the least restrictive method necessary to maintain safety. Confirmed home psychiatric medications may be continued when appropriate. Symptomatic medications for agitation, anxiety, psychosis, and sleep may be used, and withdrawal syndromes must be treated promptly.
Medication options described include olanzapine 5–10 mg PO/IM as a first-line agent for agitation, or haloperidol 5 mg IM with lorazepam 2 mg IM and benztropine 1 mg IM. For alcohol or benzodiazepine withdrawal, diazepam 5–10 mg PO hourly as needed with standardized monitoring (e.g., CIWA) is first line. For delirium not due to alcohol withdrawal or anticholinergic excess, haloperidol 1–2 mg PO/IM/IV is suggested. For agitation not associated with psychosis, delirium, or alcohol withdrawal, lorazepam 1 mg PO/IM/IV may be used.
Admission is indicated when there is danger to self, danger to others, or severe disability preventing adequate self-care or safety, following the commitment process specific to the jurisdiction. Discharge may be appropriate after medical and psychiatric evaluation if the patient can care for themselves and risk is manageable in a less-restrictive setting such as crisis stabilization, partial hospitalization, or outpatient care with close follow-up. Patients discharged should receive clear return precautions for worsening symptoms or feeling unsafe, and referrals for timely outpatient psychiatric follow-up, crisis services, or structured programs as needed.
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Emergency And Acute Medicine – Acute Psychosis
Acute psychosis is a disorder of brain function characterized by loss of contact with reality, abnormal perceptions, and disorganization of thought, emotion, and behavior. Dopaminergic pathways are strongly implicated in its pathophysiology. Psychosis may arise from primary psychiatric disorders or from medical, neurologic, metabolic, infectious, toxicologic, or pharmacologic causes. Because many medical conditions can mimic or precipitate psychosis, evaluation in the emergency setting must remain broad.
Medical and nonpsychiatric causes include neurologic disorders such as head injury, dementia, stroke, seizures, brain tumors, hydrocephalus, demyelinating disease, and neurodegenerative conditions. Infections such as urinary tract infection, pneumonia, HIV, neurosyphilis, Lyme disease, meningitis, encephalitis, and fungal infections may precipitate psychosis. Metabolic disturbances—including electrolyte imbalance, hypoglycemia, hypoxia, hypercarbia, porphyria, and organ failure (hepatic, renal, or cardiac)—must be considered. Endocrine abnormalities (thyroid, parathyroid, adrenal disorders), nutritional deficiencies (thiamine, niacin, B12, folate), autoimmune conditions, and paraneoplastic syndromes are also implicated. Numerous medications, including steroids, anticholinergics, dopaminergic agents, antibiotics, antivirals, chemotherapeutics, and sedative–hypnotics, may cause psychosis. Intoxication or withdrawal from alcohol, stimulants, opioids, hallucinogens, cannabis, benzodiazepines, or other substances is common. Primary psychiatric causes include brief psychotic disorder, schizophrenia spectrum disorders, mood disorders with psychotic features, schizoaffective disorder, and postpartum psychosis.
Core features of psychosis include delusions—fixed false beliefs not amenable to logic—often persecutory, religious, or somatic in nature. Hallucinations are sensory perceptions without external stimuli, most commonly auditory or visual. Thought disorder may manifest as loose associations, tangentiality, neologisms, or word salad. Disorganized or catatonic behavior may be present. Negative symptoms include flat affect, apathy, anhedonia, and social withdrawal. Features suggesting a medical rather than primary psychiatric etiology include sudden onset in patients over age 30, fluctuating course, abnormal vital signs, focal neurologic deficits, altered orientation or attention, and prominent visual, olfactory, gustatory, or tactile hallucinations.
History should assess onset, duration, triggers, and symptom content, including suicidal or homicidal ideation. Inquiry into recent medication changes, substance use or withdrawal, past psychiatric and medical history, and ability to care for self is essential. Collateral information from family or caregivers is often invaluable. Physical examination must include vital signs, general medical assessment, focused neurologic and cognitive evaluation, and careful screening for delirium.
The workup is guided by clinical suspicion. Basic laboratory studies often include electrolytes, renal function, glucose, calcium, CBC, thyroid-stimulating hormone, and toxicology screening. Urinalysis may identify infection. Further studies are tailored to suspected etiologies. Neuroimaging should be considered in new-onset psychosis of unclear cause, especially when focal neurologic findings are present. Lumbar puncture, EEG, or ECG (for QT monitoring) may be indicated depending on presentation.
Management prioritizes safety of the patient and staff. A calm environment, verbal de-escalation, removal of dangerous objects, and constant observation are first-line interventions. If agitation persists or safety is compromised, pharmacologic or physical restraints may be necessary. When a medical cause is suspected, the underlying condition must be identified and treated. If a primary psychiatric etiology is likely, psychiatric consultation should be obtained.
Antipsychotic medications are first-line for acute agitation associated with psychosis. Haloperidol 2–10 mg PO/IM/IV may be repeated as needed and is often combined with lorazepam for rapid tranquilization. Second-generation antipsychotics such as olanzapine, risperidone, aripiprazole, quetiapine, chlorpromazine, or ziprasidone may be used depending on clinical context. Ziprasidone requires QT monitoring. Concurrent use of IM olanzapine with IV benzodiazepines should be avoided due to risk of cardiopulmonary collapse. Benzodiazepines such as lorazepam 1–2 mg PO/IM/IV may augment sedation. Clinicians must monitor for extrapyramidal symptoms and neuroleptic malignant syndrome, characterized by hyperthermia, rigidity, autonomic instability, and altered mental status. Elderly patients with dementia-related psychosis have increased mortality risk when treated with antipsychotics.
Disposition depends on etiology and risk assessment. Patients with medical causes require admission to an appropriate medical service. Patients with psychiatric causes may require psychiatric hospitalization if they are a danger to themselves or others, are gravely disabled, or have new-onset psychosis after medical causes are excluded. Discharge may be appropriate if symptoms resolve, the patient is medically stable, not dangerous, and able to care for themselves, with prompt outpatient psychiatric follow-up arranged.
Psychosis should never be presumed to be purely psychiatric without appropriate evaluation for reversible medical causes, even in patients with known psychiatric illness. Visual or multisensory hallucinations, fluctuating mental status, or abnormal vital signs warrant thorough medical assessment. Early identification and treatment of reversible causes can significantly improve outcomes.
Acute psychosis is a disorder of brain function characterized by loss of contact with reality, abnormal perceptions, and disorganization of thought, emotion, and behavior. Dopaminergic pathways are strongly implicated in its pathophysiology. Psychosis may arise from primary psychiatric disorders or from medical, neurologic, metabolic, infectious, toxicologic, or pharmacologic causes. Because many medical conditions can mimic or precipitate psychosis, evaluation in the emergency setting must remain broad.
Medical and nonpsychiatric causes include neurologic disorders such as head injury, dementia, stroke, seizures, brain tumors, hydrocephalus, demyelinating disease, and neurodegenerative conditions. Infections such as urinary tract infection, pneumonia, HIV, neurosyphilis, Lyme disease, meningitis, encephalitis, and fungal infections may precipitate psychosis. Metabolic disturbances—including electrolyte imbalance, hypoglycemia, hypoxia, hypercarbia, porphyria, and organ failure (hepatic, renal, or cardiac)—must be considered. Endocrine abnormalities (thyroid, parathyroid, adrenal disorders), nutritional deficiencies (thiamine, niacin, B12, folate), autoimmune conditions, and paraneoplastic syndromes are also implicated. Numerous medications, including steroids, anticholinergics, dopaminergic agents, antibiotics, antivirals, chemotherapeutics, and sedative–hypnotics, may cause psychosis. Intoxication or withdrawal from alcohol, stimulants, opioids, hallucinogens, cannabis, benzodiazepines, or other substances is common. Primary psychiatric causes include brief psychotic disorder, schizophrenia spectrum disorders, mood disorders with psychotic features, schizoaffective disorder, and postpartum psychosis.
Core features of psychosis include delusions—fixed false beliefs not amenable to logic—often persecutory, religious, or somatic in nature. Hallucinations are sensory perceptions without external stimuli, most commonly auditory or visual. Thought disorder may manifest as loose associations, tangentiality, neologisms, or word salad. Disorganized or catatonic behavior may be present. Negative symptoms include flat affect, apathy, anhedonia, and social withdrawal. Features suggesting a medical rather than primary psychiatric etiology include sudden onset in patients over age 30, fluctuating course, abnormal vital signs, focal neurologic deficits, altered orientation or attention, and prominent visual, olfactory, gustatory, or tactile hallucinations.
History should assess onset, duration, triggers, and symptom content, including suicidal or homicidal ideation. Inquiry into recent medication changes, substance use or withdrawal, past psychiatric and medical history, and ability to care for self is essential. Collateral information from family or caregivers is often invaluable. Physical examination must include vital signs, general medical assessment, focused neurologic and cognitive evaluation, and careful screening for delirium.
The workup is guided by clinical suspicion. Basic laboratory studies often include electrolytes, renal function, glucose, calcium, CBC, thyroid-stimulating hormone, and toxicology screening. Urinalysis may identify infection. Further studies are tailored to suspected etiologies. Neuroimaging should be considered in new-onset psychosis of unclear cause, especially when focal neurologic findings are present. Lumbar puncture, EEG, or ECG (for QT monitoring) may be indicated depending on presentation.
Management prioritizes safety of the patient and staff. A calm environment, verbal de-escalation, removal of dangerous objects, and constant observation are first-line interventions. If agitation persists or safety is compromised, pharmacologic or physical restraints may be necessary. When a medical cause is suspected, the underlying condition must be identified and treated. If a primary psychiatric etiology is likely, psychiatric consultation should be obtained.
Antipsychotic medications are first-line for acute agitation associated with psychosis. Haloperidol 2–10 mg PO/IM/IV may be repeated as needed and is often combined with lorazepam for rapid tranquilization. Second-generation antipsychotics such as olanzapine, risperidone, aripiprazole, quetiapine, chlorpromazine, or ziprasidone may be used depending on clinical context. Ziprasidone requires QT monitoring. Concurrent use of IM olanzapine with IV benzodiazepines should be avoided due to risk of cardiopulmonary collapse. Benzodiazepines such as lorazepam 1–2 mg PO/IM/IV may augment sedation. Clinicians must monitor for extrapyramidal symptoms and neuroleptic malignant syndrome, characterized by hyperthermia, rigidity, autonomic instability, and altered mental status. Elderly patients with dementia-related psychosis have increased mortality risk when treated with antipsychotics.
Disposition depends on etiology and risk assessment. Patients with medical causes require admission to an appropriate medical service. Patients with psychiatric causes may require psychiatric hospitalization if they are a danger to themselves or others, are gravely disabled, or have new-onset psychosis after medical causes are excluded. Discharge may be appropriate if symptoms resolve, the patient is medically stable, not dangerous, and able to care for themselves, with prompt outpatient psychiatric follow-up arranged.
Psychosis should never be presumed to be purely psychiatric without appropriate evaluation for reversible medical causes, even in patients with known psychiatric illness. Visual or multisensory hallucinations, fluctuating mental status, or abnormal vital signs warrant thorough medical assessment. Early identification and treatment of reversible causes can significantly improve outcomes.
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Emergency And Acute Medicine – Procedural Sedation
Procedural sedation involves the administration of sedative agents with or without analgesics to facilitate diagnostic or therapeutic procedures while minimizing pain and anxiety and maintaining cardiorespiratory function. Informed consent should be obtained prior to sedation. Preparation includes ensuring availability of airway equipment such as bag-valve masks, oral and nasal airways, laryngoscopes, endotracheal tubes, suction, and a defibrillator. An emergency cart with resuscitation medications, including naloxone and flumazenil, must be accessible. Continuous monitoring with cardiac monitor, pulse oximetry, and blood pressure measurement is required. Oxygen should be administered to maintain saturation above 95%. All medications should be clearly labeled and prepared at the bedside. Patients must be observed throughout the procedure and recovery period until they are awake, alert, and have returned to baseline function.
Pre-sedation assessment includes a focused history of past medical problems, prior anesthesia complications, medications, allergies, and time of last oral intake. Physical examination should include vital signs, cardiopulmonary and neurologic assessment, and airway evaluation. Risk factors for difficult ventilation include beards, abnormal facial anatomy, obesity, edentulous state, and underlying pulmonary or cardiac disease. Difficult airway predictors include short neck, large tongue, small mandible, high Mallampati score, and signs of airway obstruction such as stridor, drooling, or dysphagia.
Sedative and analgesic medications may cause dose-dependent respiratory depression, and combining agents increases the risk of hypoxia and apnea. For painless procedures, single agents such as methohexital, chloral hydrate (in children), etomidate, pentobarbital, midazolam, or ketamine may be used. Painful procedures typically require agents with analgesic properties such as ketamine, fentanyl with midazolam, propofol with fentanyl, etomidate with fentanyl, nitrous oxide, dexmedetomidine, or ketamine–propofol combinations.
Methohexital is a short-acting barbiturate producing unconsciousness and amnesia without analgesia. It has rapid onset and short duration but may cause respiratory depression and hypotension. Pentobarbital is used primarily for painless diagnostic procedures and may cause central nervous system and respiratory depression. Midazolam, a benzodiazepine, provides anxiolysis and amnesia but no analgesia; it has rapid onset and short duration when given intravenously. Its effects are potentiated by opioids and may be reversed with flumazenil. Chloral hydrate is used in young children for painless procedures but has prolonged effects and risk of respiratory depression. Dexmedetomidine provides sedation, anxiolysis, and some analgesia, with predictable reductions in heart rate and blood pressure.
Etomidate provides rapid sedation and amnesia with minimal cardiovascular effects but lacks analgesia and may cause myoclonus, nausea, and transient adrenal suppression. Ketamine produces dissociative anesthesia with analgesia and preservation of airway reflexes. It may increase heart rate, blood pressure, intracranial pressure, and secretions, and can cause emergence reactions, particularly in adults. Nitrous oxide offers rapid-onset analgesia and anxiolysis for short procedures but is contraindicated in pregnancy, pneumothorax, and bowel obstruction. Fentanyl and remifentanil are short-acting opioids providing analgesia with risk of respiratory depression, hypotension, and rarely chest wall rigidity. Propofol provides rapid-onset sedation and amnesia but no analgesia; it may cause significant respiratory depression and hypotension.
Reversal agents include naloxone for opioid-induced respiratory depression and flumazenil for benzodiazepine reversal. Naloxone may precipitate acute withdrawal in opioid-dependent patients. Flumazenil may provoke seizures or withdrawal in patients dependent on benzodiazepines. Both agents have shorter durations of action than many sedatives, requiring continued monitoring for recurrent sedation.
Patients may be discharged once they are awake, alert, hemodynamically stable, ambulatory, able to tolerate oral intake, and have a responsible adult for supervision and transport. Admission is indicated for post-procedural complications, inability to ambulate, persistent sedation, or lack of appropriate supervision.
Key principles include continuous cardiorespiratory monitoring during and after sedation, readiness with airway adjuncts and resuscitation equipment, cautious dosing—especially when combining medications—and careful observation through recovery to minimize complications.
Procedural sedation involves the administration of sedative agents with or without analgesics to facilitate diagnostic or therapeutic procedures while minimizing pain and anxiety and maintaining cardiorespiratory function. Informed consent should be obtained prior to sedation. Preparation includes ensuring availability of airway equipment such as bag-valve masks, oral and nasal airways, laryngoscopes, endotracheal tubes, suction, and a defibrillator. An emergency cart with resuscitation medications, including naloxone and flumazenil, must be accessible. Continuous monitoring with cardiac monitor, pulse oximetry, and blood pressure measurement is required. Oxygen should be administered to maintain saturation above 95%. All medications should be clearly labeled and prepared at the bedside. Patients must be observed throughout the procedure and recovery period until they are awake, alert, and have returned to baseline function.
Pre-sedation assessment includes a focused history of past medical problems, prior anesthesia complications, medications, allergies, and time of last oral intake. Physical examination should include vital signs, cardiopulmonary and neurologic assessment, and airway evaluation. Risk factors for difficult ventilation include beards, abnormal facial anatomy, obesity, edentulous state, and underlying pulmonary or cardiac disease. Difficult airway predictors include short neck, large tongue, small mandible, high Mallampati score, and signs of airway obstruction such as stridor, drooling, or dysphagia.
Sedative and analgesic medications may cause dose-dependent respiratory depression, and combining agents increases the risk of hypoxia and apnea. For painless procedures, single agents such as methohexital, chloral hydrate (in children), etomidate, pentobarbital, midazolam, or ketamine may be used. Painful procedures typically require agents with analgesic properties such as ketamine, fentanyl with midazolam, propofol with fentanyl, etomidate with fentanyl, nitrous oxide, dexmedetomidine, or ketamine–propofol combinations.
Methohexital is a short-acting barbiturate producing unconsciousness and amnesia without analgesia. It has rapid onset and short duration but may cause respiratory depression and hypotension. Pentobarbital is used primarily for painless diagnostic procedures and may cause central nervous system and respiratory depression. Midazolam, a benzodiazepine, provides anxiolysis and amnesia but no analgesia; it has rapid onset and short duration when given intravenously. Its effects are potentiated by opioids and may be reversed with flumazenil. Chloral hydrate is used in young children for painless procedures but has prolonged effects and risk of respiratory depression. Dexmedetomidine provides sedation, anxiolysis, and some analgesia, with predictable reductions in heart rate and blood pressure.
Etomidate provides rapid sedation and amnesia with minimal cardiovascular effects but lacks analgesia and may cause myoclonus, nausea, and transient adrenal suppression. Ketamine produces dissociative anesthesia with analgesia and preservation of airway reflexes. It may increase heart rate, blood pressure, intracranial pressure, and secretions, and can cause emergence reactions, particularly in adults. Nitrous oxide offers rapid-onset analgesia and anxiolysis for short procedures but is contraindicated in pregnancy, pneumothorax, and bowel obstruction. Fentanyl and remifentanil are short-acting opioids providing analgesia with risk of respiratory depression, hypotension, and rarely chest wall rigidity. Propofol provides rapid-onset sedation and amnesia but no analgesia; it may cause significant respiratory depression and hypotension.
Reversal agents include naloxone for opioid-induced respiratory depression and flumazenil for benzodiazepine reversal. Naloxone may precipitate acute withdrawal in opioid-dependent patients. Flumazenil may provoke seizures or withdrawal in patients dependent on benzodiazepines. Both agents have shorter durations of action than many sedatives, requiring continued monitoring for recurrent sedation.
Patients may be discharged once they are awake, alert, hemodynamically stable, ambulatory, able to tolerate oral intake, and have a responsible adult for supervision and transport. Admission is indicated for post-procedural complications, inability to ambulate, persistent sedation, or lack of appropriate supervision.
Key principles include continuous cardiorespiratory monitoring during and after sedation, readiness with airway adjuncts and resuscitation equipment, cautious dosing—especially when combining medications—and careful observation through recovery to minimize complications.
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Emergency And Acute Medicine – Pulmonary Contusion
Pulmonary contusion results from transfer of kinetic energy to the lung, causing direct injury to the lung parenchyma with hemorrhage and edema in the absence of a pulmonary laceration. It is most commonly associated with blunt thoracic trauma but may also occur with penetrating injury. Mortality ranges from 10–25% and pulmonary contusion is an independent risk factor for acute respiratory distress syndrome (ARDS), pneumonia, and long-term respiratory dysfunction.
The pathophysiology develops in two stages. The first stage is due to direct injury, which disrupts the alveolocapillary membrane and leads to extravasation of blood into the interstitial and alveolar spaces. The second stage reflects indirect worsening of injury during resuscitation, particularly from intravenous fluid administration, which increases interstitial pulmonary edema. These processes result in increased intrapulmonary shunting, increased airway resistance, decreased lung compliance, increased work of breathing, hypoxemia, acidosis, and potentially respiratory failure.
Etiologies include blunt or penetrating thoracic trauma from motor vehicle collisions, falls from height, assaults, sudden deceleration–compression injuries, and missile injuries. Mechanism of injury is critical in raising suspicion.
Patients typically present after thoracic trauma with chest pain, dyspnea, and occasionally hemoptysis. Historical clues include seat belt use, steering wheel damage, and airbag deployment. Physical examination findings may initially be minimal, with normal or diminished breath sounds, but can progress to crackles, rales, or absent breath sounds. Chest wall ecchymosis (including the “seat belt sign”), localized tenderness, rib fractures, crepitus, paradoxical movement with flail chest, splinting respirations, cyanosis, tachycardia, hypotension, and tachypnea may be present. A key feature is the insidious progression of symptoms, often worsening 6–12 hours after injury.
Initial evaluation includes chest radiography, though radiographic findings may be delayed for 6–12 hours. Findings range from patchy alveolar infiltrates to consolidation. Associated injuries such as rib fractures, pneumothorax, hemothorax, or mediastinal widening should be assessed. Arterial blood gas analysis may reveal hypoxemia with an elevated alveolar–arterial gradient. The percentage of lung involvement on imaging can help predict severity: contusion involving less than 18% of lung volume rarely requires intubation, whereas involvement greater than 28% frequently necessitates ventilatory support. Thoracic CT is more sensitive than chest radiography and can quantify injury; involvement of more than 20% of total lung volume predicts need for assisted ventilation. Ultrasound has also been studied as a rapid diagnostic modality. Differential diagnosis includes ARDS, congestive heart failure, hemothorax, pneumonia, noncardiogenic pulmonary edema, pneumothorax, pulmonary laceration, infarction, or embolism.
Management begins with standard trauma principles. Patients with significant thoracic trauma or pre-existing lung disease should be transported to a trauma center. Airway management and resuscitation are priorities. Supplemental oxygen, intravenous access, cardiac monitoring, and pulse oximetry are required. Indications for endotracheal intubation include severe hypoxemia (PaO₂ <60 mm hg on room air or <80 oxygen), significant underlying lung disease, impending respiratory failure. early intubation with positive end-expiratory pressure (peep) can improve oxygenation, reduce work of breathing, and correct acidosis.< />pan>
In alert patients, oxygen via face mask is first-line therapy. If adequate oxygenation (PaO₂ >80 mm Hg) cannot be maintained on high-flow oxygen, noninvasive ventilation such as CPAP or BiPAP may be attempted in cooperative patients. However, noninvasive ventilation should not delay intubation in deteriorating patients. In cases of severe unilateral injury with significant hemoptysis or air leaks, selective bronchial intubation may be considered. Excessive intravenous fluid administration should be avoided, as it can worsen pulmonary edema; fluid resuscitation must be balanced carefully. Frequent reassessment and serial chest radiographs are necessary due to the risk of delayed deterioration.
Adequate pain control is essential to allow effective ventilation and prevent atelectasis. Steroids have not shown proven benefit, and prophylactic antibiotics are not indicated. In pediatric patients, increased chest wall pliability predisposes to pulmonary contusions even without rib fractures. In geriatric patients, reduced cardiopulmonary reserve and aggressive fluid resuscitation increase the risk of respiratory failure; pulmonary contusion in the elderly is associated with worse outcomes.
All patients with confirmed pulmonary contusion should be admitted for observation due to the risk of delayed respiratory compromise. Discharge may be considered only in patients with minimal trauma, normal respiratory rate and oxygen saturation, negative chest radiograph, and no evidence of hypoxemia or distress, with strict return precautions for worsening shortness of breath, hemoptysis, increasing pain, or cough.
Pulmonary contusion severity should not be underestimated based on an initially normal chest radiograph. Failure to recognize and monitor this injury can result in unexpected deterioration. Careful monitoring, cautious fluid management, and early airway intervention when indicated are essential to improving outcomes.
Pulmonary contusion results from transfer of kinetic energy to the lung, causing direct injury to the lung parenchyma with hemorrhage and edema in the absence of a pulmonary laceration. It is most commonly associated with blunt thoracic trauma but may also occur with penetrating injury. Mortality ranges from 10–25% and pulmonary contusion is an independent risk factor for acute respiratory distress syndrome (ARDS), pneumonia, and long-term respiratory dysfunction.
The pathophysiology develops in two stages. The first stage is due to direct injury, which disrupts the alveolocapillary membrane and leads to extravasation of blood into the interstitial and alveolar spaces. The second stage reflects indirect worsening of injury during resuscitation, particularly from intravenous fluid administration, which increases interstitial pulmonary edema. These processes result in increased intrapulmonary shunting, increased airway resistance, decreased lung compliance, increased work of breathing, hypoxemia, acidosis, and potentially respiratory failure.
Etiologies include blunt or penetrating thoracic trauma from motor vehicle collisions, falls from height, assaults, sudden deceleration–compression injuries, and missile injuries. Mechanism of injury is critical in raising suspicion.
Patients typically present after thoracic trauma with chest pain, dyspnea, and occasionally hemoptysis. Historical clues include seat belt use, steering wheel damage, and airbag deployment. Physical examination findings may initially be minimal, with normal or diminished breath sounds, but can progress to crackles, rales, or absent breath sounds. Chest wall ecchymosis (including the “seat belt sign”), localized tenderness, rib fractures, crepitus, paradoxical movement with flail chest, splinting respirations, cyanosis, tachycardia, hypotension, and tachypnea may be present. A key feature is the insidious progression of symptoms, often worsening 6–12 hours after injury.
Initial evaluation includes chest radiography, though radiographic findings may be delayed for 6–12 hours. Findings range from patchy alveolar infiltrates to consolidation. Associated injuries such as rib fractures, pneumothorax, hemothorax, or mediastinal widening should be assessed. Arterial blood gas analysis may reveal hypoxemia with an elevated alveolar–arterial gradient. The percentage of lung involvement on imaging can help predict severity: contusion involving less than 18% of lung volume rarely requires intubation, whereas involvement greater than 28% frequently necessitates ventilatory support. Thoracic CT is more sensitive than chest radiography and can quantify injury; involvement of more than 20% of total lung volume predicts need for assisted ventilation. Ultrasound has also been studied as a rapid diagnostic modality. Differential diagnosis includes ARDS, congestive heart failure, hemothorax, pneumonia, noncardiogenic pulmonary edema, pneumothorax, pulmonary laceration, infarction, or embolism.
Management begins with standard trauma principles. Patients with significant thoracic trauma or pre-existing lung disease should be transported to a trauma center. Airway management and resuscitation are priorities. Supplemental oxygen, intravenous access, cardiac monitoring, and pulse oximetry are required. Indications for endotracheal intubation include severe hypoxemia (PaO₂ <60 mm hg on room air or <80 oxygen), significant underlying lung disease, impending respiratory failure. early intubation with positive end-expiratory pressure (peep) can improve oxygenation, reduce work of breathing, and correct acidosis.< />pan>
In alert patients, oxygen via face mask is first-line therapy. If adequate oxygenation (PaO₂ >80 mm Hg) cannot be maintained on high-flow oxygen, noninvasive ventilation such as CPAP or BiPAP may be attempted in cooperative patients. However, noninvasive ventilation should not delay intubation in deteriorating patients. In cases of severe unilateral injury with significant hemoptysis or air leaks, selective bronchial intubation may be considered. Excessive intravenous fluid administration should be avoided, as it can worsen pulmonary edema; fluid resuscitation must be balanced carefully. Frequent reassessment and serial chest radiographs are necessary due to the risk of delayed deterioration.
Adequate pain control is essential to allow effective ventilation and prevent atelectasis. Steroids have not shown proven benefit, and prophylactic antibiotics are not indicated. In pediatric patients, increased chest wall pliability predisposes to pulmonary contusions even without rib fractures. In geriatric patients, reduced cardiopulmonary reserve and aggressive fluid resuscitation increase the risk of respiratory failure; pulmonary contusion in the elderly is associated with worse outcomes.
All patients with confirmed pulmonary contusion should be admitted for observation due to the risk of delayed respiratory compromise. Discharge may be considered only in patients with minimal trauma, normal respiratory rate and oxygen saturation, negative chest radiograph, and no evidence of hypoxemia or distress, with strict return precautions for worsening shortness of breath, hemoptysis, increasing pain, or cough.
Pulmonary contusion severity should not be underestimated based on an initially normal chest radiograph. Failure to recognize and monitor this injury can result in unexpected deterioration. Careful monitoring, cautious fluid management, and early airway intervention when indicated are essential to improving outcomes.
