- Published on
Emergency And Acute Medicine – Priapism
Priapism is a prolonged penile erection involving engorgement of the corpora cavernosa that occurs in the absence of sexual arousal and is often painful. It is classified into low-flow (ischemic) and high-flow (nonischemic) types. Low-flow priapism is the most common and results from impaired venous outflow, leading to stagnant, hypoxic blood within the corpora cavernosa. It is typically painful and constitutes a urologic emergency because ischemia and thrombosis can occur within hours, with subsequent fibrosis and permanent erectile dysfunction as late complications. High-flow priapism is rare and results from arterial laceration, usually following trauma, causing uncontrolled arterial inflow. It is typically painless, presents later, and is less likely to result in ischemia or erectile dysfunction.
The etiology of priapism includes idiopathic causes, medications, hematologic disorders, trauma, and systemic disease. Intracavernosal agents used for erectile dysfunction—such as prostaglandin E1, papaverine, and phentolamine—are common pharmacologic causes. Psychotropic medications including phenothiazines, butyrophenones, trazodone, sedative–hypnotics, and selective serotonin reuptake inhibitors are implicated, as are antihypertensives such as prazosin and hydralazine. Phosphodiesterase inhibitors such as sildenafil, tadalafil, and vardenafil are rarely associated. Recreational drugs including cocaine, marijuana, and ethanol, as well as toxins such as Black Widow or scorpion venom, have also been reported. Hematologic disorders that increase blood viscosity—particularly sickle cell anemia (the most common cause overall and in children), leukemia, multiple myeloma, and polycythemia—predispose to low-flow priapism. Penile or perineal trauma may lead to high-flow priapism, while spinal trauma can disrupt inhibitory adrenergic tone. Rare causes include pelvic tumors, infiltrative diseases, dialysis, and parenteral nutrition containing fat emulsions.
Diagnosis is clinical. Low-flow priapism presents with a painful, rigid erection and often a history of medication use or hematologic disease. High-flow priapism is typically painless and associated with penile trauma. Examination should assess for penile implants, signs of trauma including urethral or rectal injury, and urinary retention. Laboratory and imaging studies should not delay urgent urologic consultation. Laboratory evaluation may include complete blood count, coagulation studies, and sickle cell testing when indicated. Duplex Doppler ultrasound can help identify arterial injury in high-flow priapism, and angiography can localize and treat arterial lacerations. Intracavernosal blood gas analysis differentiates the types: low-flow priapism shows acidosis and hypoxia (pH <7.25, po₂ <30 mm hg), whereas high-flow priapism demonstrates near-normal values.< />pan>
Initial management includes oxygen, analgesia, sedation, and intravenous hydration. Urgent urologic consultation is required. Underlying causes should be addressed concurrently. In sickle cell disease, treatment may include hydration, oxygenation, and packed red blood cell transfusion or exchange transfusion. Leukemia requires oncologic management. High-flow priapism from arterial injury may be managed expectantly or with angiographic embolization.
Low-flow priapism often requires intracavernosal aspiration and sympathomimetic injection. If specialty care is unavailable, the emergency physician may perform the procedure using sterile technique. After local anesthesia or penile nerve block, a 19-gauge butterfly needle is inserted laterally into the corpus cavernosum at the 2- or 10-o’clock position to avoid the urethra and dorsal neurovascular bundle. Blood is aspirated slowly while milking the shaft until brighter arterial blood appears, often requiring removal of 30–50 mL. Saline irrigation may be used. Phenylephrine is the preferred agent for intracavernosal injection due to fewer systemic effects; it should be diluted and administered in small boluses with cardiac and blood pressure monitoring. Injections may be repeated every 5–15 minutes for up to one hour. Epinephrine may be used as a second-line agent. Terbutaline may be administered subcutaneously or orally as adjunctive therapy but is often insufficient alone. Surgical shunting may be required if conservative measures fail.
Admission is indicated for persistent priapism despite initial treatment or for patients with serious underlying conditions such as sickle cell disease or leukemia. Patients may be discharged after complete detumescence and several hours of observation without recurrence, provided urologic consultation has occurred. All patients require short-term urologic follow-up, evaluation of underlying conditions, and discontinuation of offending medications. They should be advised to return immediately if erection recurs.
Timely intervention is critical to reduce the risk of permanent erectile dysfunction. Management of underlying conditions should not delay definitive penile decompression. Intracavernosal vasoactive medications should not be injected during partial tumescence due to risk of systemic absorption and hypertensive complications. Even with prompt treatment, patients must be counseled about the possibility of future erectile dysfunction and this discussion should be documented carefully.
Priapism is a prolonged penile erection involving engorgement of the corpora cavernosa that occurs in the absence of sexual arousal and is often painful. It is classified into low-flow (ischemic) and high-flow (nonischemic) types. Low-flow priapism is the most common and results from impaired venous outflow, leading to stagnant, hypoxic blood within the corpora cavernosa. It is typically painful and constitutes a urologic emergency because ischemia and thrombosis can occur within hours, with subsequent fibrosis and permanent erectile dysfunction as late complications. High-flow priapism is rare and results from arterial laceration, usually following trauma, causing uncontrolled arterial inflow. It is typically painless, presents later, and is less likely to result in ischemia or erectile dysfunction.
The etiology of priapism includes idiopathic causes, medications, hematologic disorders, trauma, and systemic disease. Intracavernosal agents used for erectile dysfunction—such as prostaglandin E1, papaverine, and phentolamine—are common pharmacologic causes. Psychotropic medications including phenothiazines, butyrophenones, trazodone, sedative–hypnotics, and selective serotonin reuptake inhibitors are implicated, as are antihypertensives such as prazosin and hydralazine. Phosphodiesterase inhibitors such as sildenafil, tadalafil, and vardenafil are rarely associated. Recreational drugs including cocaine, marijuana, and ethanol, as well as toxins such as Black Widow or scorpion venom, have also been reported. Hematologic disorders that increase blood viscosity—particularly sickle cell anemia (the most common cause overall and in children), leukemia, multiple myeloma, and polycythemia—predispose to low-flow priapism. Penile or perineal trauma may lead to high-flow priapism, while spinal trauma can disrupt inhibitory adrenergic tone. Rare causes include pelvic tumors, infiltrative diseases, dialysis, and parenteral nutrition containing fat emulsions.
Diagnosis is clinical. Low-flow priapism presents with a painful, rigid erection and often a history of medication use or hematologic disease. High-flow priapism is typically painless and associated with penile trauma. Examination should assess for penile implants, signs of trauma including urethral or rectal injury, and urinary retention. Laboratory and imaging studies should not delay urgent urologic consultation. Laboratory evaluation may include complete blood count, coagulation studies, and sickle cell testing when indicated. Duplex Doppler ultrasound can help identify arterial injury in high-flow priapism, and angiography can localize and treat arterial lacerations. Intracavernosal blood gas analysis differentiates the types: low-flow priapism shows acidosis and hypoxia (pH <7.25, po₂ <30 mm hg), whereas high-flow priapism demonstrates near-normal values.< />pan>
Initial management includes oxygen, analgesia, sedation, and intravenous hydration. Urgent urologic consultation is required. Underlying causes should be addressed concurrently. In sickle cell disease, treatment may include hydration, oxygenation, and packed red blood cell transfusion or exchange transfusion. Leukemia requires oncologic management. High-flow priapism from arterial injury may be managed expectantly or with angiographic embolization.
Low-flow priapism often requires intracavernosal aspiration and sympathomimetic injection. If specialty care is unavailable, the emergency physician may perform the procedure using sterile technique. After local anesthesia or penile nerve block, a 19-gauge butterfly needle is inserted laterally into the corpus cavernosum at the 2- or 10-o’clock position to avoid the urethra and dorsal neurovascular bundle. Blood is aspirated slowly while milking the shaft until brighter arterial blood appears, often requiring removal of 30–50 mL. Saline irrigation may be used. Phenylephrine is the preferred agent for intracavernosal injection due to fewer systemic effects; it should be diluted and administered in small boluses with cardiac and blood pressure monitoring. Injections may be repeated every 5–15 minutes for up to one hour. Epinephrine may be used as a second-line agent. Terbutaline may be administered subcutaneously or orally as adjunctive therapy but is often insufficient alone. Surgical shunting may be required if conservative measures fail.
Admission is indicated for persistent priapism despite initial treatment or for patients with serious underlying conditions such as sickle cell disease or leukemia. Patients may be discharged after complete detumescence and several hours of observation without recurrence, provided urologic consultation has occurred. All patients require short-term urologic follow-up, evaluation of underlying conditions, and discontinuation of offending medications. They should be advised to return immediately if erection recurs.
Timely intervention is critical to reduce the risk of permanent erectile dysfunction. Management of underlying conditions should not delay definitive penile decompression. Intracavernosal vasoactive medications should not be injected during partial tumescence due to risk of systemic absorption and hypertensive complications. Even with prompt treatment, patients must be counseled about the possibility of future erectile dysfunction and this discussion should be documented carefully.
- Published on
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.
- Published on
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.
- Published on
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.
- Published on
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.
- Published on
Emergency And Acute Medicine – Polycythemia
Polycythemia is defined as an increase in hemoglobin above the normal range, typically hemoglobin >17.5 g/dL or hematocrit >52% in men and hemoglobin >16 g/dL or hematocrit >48% in women. Symptoms are largely related to increased blood viscosity, which rises exponentially when the hematocrit exceeds 60%, predisposing patients to thrombotic and hyperviscosity complications.
Polycythemia may be relative, primary, or secondary. Relative (apparent) polycythemia results from decreased plasma volume rather than true red blood cell mass increase. Acute causes include dehydration, while chronic forms include Gaisbock syndrome, commonly seen in obese, hypertensive, middle-aged smokers. Primary erythrocytosis refers to polycythemia vera, a stem cell disorder characterized by panhyperplasia of bone marrow elements with increased red blood cells, leukocytes, and platelets. Most cases involve a JAK2 mutation, rendering hematopoietic cells hypersensitive to erythropoietin. It typically affects older adults, may progress to myelofibrosis or acute leukemia, and carries a high thrombotic risk. Secondary polycythemia results from increased erythropoietin production, often due to chronic hypoxia (such as chronic lung disease, sleep apnea, obesity hypoventilation syndrome, congenital heart disease, high altitude, or chronic carbon monoxide exposure) or renal and neoplastic causes that stimulate erythropoietin production. Drug-related causes include androgen use, recombinant erythropoietin abuse, and blood doping. Genetic disorders and certain infections may also contribute.
Clinical manifestations reflect hyperviscosity and thrombosis. Patients may report headache, dizziness, fatigue, dyspnea, visual disturbances, and paresthesias. Pruritus, especially after warm bathing, and erythromelalgia characterized by burning pain, redness, and warmth of the extremities are classic features of polycythemia vera. Thrombotic events are common and may involve arterial or venous systems, including stroke, myocardial infarction, deep vein thrombosis, pulmonary embolism, and unusual sites such as hepatic or cerebral veins. Hemorrhagic manifestations such as epistaxis and gingival bleeding may occur due to platelet dysfunction. Splenomegaly and hepatomegaly are common in polycythemia vera.
Evaluation begins with a complete blood count and assessment of volume status to distinguish relative from true erythrocytosis. Pulse oximetry, erythropoietin levels, carboxyhemoglobin levels, and appropriate imaging help identify secondary causes. A low erythropoietin level strongly suggests polycythemia vera. Detection of a JAK2 mutation by PCR is diagnostic in most cases. Elevated platelet count, leukocytosis, elevated vitamin B12, and splenomegaly further support the diagnosis.
In the emergency setting, management focuses on complications of hyperviscosity and thrombosis. Patients with hematocrit greater than 60% or symptoms of hyperviscosity require fluid resuscitation unless contraindicated by heart failure, followed by therapeutic phlebotomy with careful replacement using isotonic saline. The goal is gradual reduction of hematocrit to safer levels, generally around 45%. Aspirin may be administered in thrombocytosis without bleeding risk. Long-term management includes periodic phlebotomy to maintain target hematocrit, low-dose aspirin, and cytoreductive therapy such as hydroxyurea in high-risk patients.
Patients with new diagnosis, hematocrit above 60%, symptoms of hyperviscosity, or unstable comorbid conditions should be admitted. Asymptomatic patients with stable vital signs and controlled hematocrit may be discharged with close hematology follow-up. It is essential to distinguish polycythemia vera from secondary causes because of the significantly higher risk of thrombotic complications associated with the primary disorder.
Polycythemia is defined as an increase in hemoglobin above the normal range, typically hemoglobin >17.5 g/dL or hematocrit >52% in men and hemoglobin >16 g/dL or hematocrit >48% in women. Symptoms are largely related to increased blood viscosity, which rises exponentially when the hematocrit exceeds 60%, predisposing patients to thrombotic and hyperviscosity complications.
Polycythemia may be relative, primary, or secondary. Relative (apparent) polycythemia results from decreased plasma volume rather than true red blood cell mass increase. Acute causes include dehydration, while chronic forms include Gaisbock syndrome, commonly seen in obese, hypertensive, middle-aged smokers. Primary erythrocytosis refers to polycythemia vera, a stem cell disorder characterized by panhyperplasia of bone marrow elements with increased red blood cells, leukocytes, and platelets. Most cases involve a JAK2 mutation, rendering hematopoietic cells hypersensitive to erythropoietin. It typically affects older adults, may progress to myelofibrosis or acute leukemia, and carries a high thrombotic risk. Secondary polycythemia results from increased erythropoietin production, often due to chronic hypoxia (such as chronic lung disease, sleep apnea, obesity hypoventilation syndrome, congenital heart disease, high altitude, or chronic carbon monoxide exposure) or renal and neoplastic causes that stimulate erythropoietin production. Drug-related causes include androgen use, recombinant erythropoietin abuse, and blood doping. Genetic disorders and certain infections may also contribute.
Clinical manifestations reflect hyperviscosity and thrombosis. Patients may report headache, dizziness, fatigue, dyspnea, visual disturbances, and paresthesias. Pruritus, especially after warm bathing, and erythromelalgia characterized by burning pain, redness, and warmth of the extremities are classic features of polycythemia vera. Thrombotic events are common and may involve arterial or venous systems, including stroke, myocardial infarction, deep vein thrombosis, pulmonary embolism, and unusual sites such as hepatic or cerebral veins. Hemorrhagic manifestations such as epistaxis and gingival bleeding may occur due to platelet dysfunction. Splenomegaly and hepatomegaly are common in polycythemia vera.
Evaluation begins with a complete blood count and assessment of volume status to distinguish relative from true erythrocytosis. Pulse oximetry, erythropoietin levels, carboxyhemoglobin levels, and appropriate imaging help identify secondary causes. A low erythropoietin level strongly suggests polycythemia vera. Detection of a JAK2 mutation by PCR is diagnostic in most cases. Elevated platelet count, leukocytosis, elevated vitamin B12, and splenomegaly further support the diagnosis.
In the emergency setting, management focuses on complications of hyperviscosity and thrombosis. Patients with hematocrit greater than 60% or symptoms of hyperviscosity require fluid resuscitation unless contraindicated by heart failure, followed by therapeutic phlebotomy with careful replacement using isotonic saline. The goal is gradual reduction of hematocrit to safer levels, generally around 45%. Aspirin may be administered in thrombocytosis without bleeding risk. Long-term management includes periodic phlebotomy to maintain target hematocrit, low-dose aspirin, and cytoreductive therapy such as hydroxyurea in high-risk patients.
Patients with new diagnosis, hematocrit above 60%, symptoms of hyperviscosity, or unstable comorbid conditions should be admitted. Asymptomatic patients with stable vital signs and controlled hematocrit may be discharged with close hematology follow-up. It is essential to distinguish polycythemia vera from secondary causes because of the significantly higher risk of thrombotic complications associated with the primary disorder.
- Published on
Emergency And Acute Medicine – Poisoning, Gastric Decontamination
Gastric decontamination refers to techniques used to reduce gastrointestinal absorption of ingested toxins. The role of these interventions has decreased over time, and most poisoned patients are managed with supportive care and selected use of activated charcoal.
Ipecac is contraindicated in the prehospital ambulance setting and is not recommended for routine home use. In extremely rare circumstances, such as prolonged transit time with a protected airway, ipecac should only be considered after consultation with a regional poison control center. In general, it has no role in emergency department management.
Initial stabilization follows standard airway, breathing, and circulation principles. The airway must be secured in patients with decreased mental status or inability to protect their airway. Intravenous access and cardiac monitoring should be established. In patients with altered mental status due to suspected overdose, administer naloxone, thiamine, and dextrose as indicated.
Activated charcoal is the mainstay of gastric decontamination. It is produced from treated wood pulp, creating a large surface area that binds many toxins. It is most effective when administered within one hour of ingestion of a charcoal-adsorbable toxin in a patient with a protected airway. The recommended dose is 1–2 g/kg (or a charcoal-to-drug ratio of approximately 10:1), given orally or via nasogastric tube. Adverse effects include vomiting, constipation, and risk of aspiration with subsequent pneumonitis. It is contraindicated in caustic ingestions, unprotected airway, bowel obstruction, or ileus. Substances poorly adsorbed by charcoal include metals (iron, lithium, bromide, borates), alcohols, potassium, hydrocarbons, caustics, and potassium cyanide. In children, charcoal may be mixed with a palatable beverage or administered via gastric tube. Randomized trials suggest limited benefit in asymptomatic patients and a small increased risk of complications.
Multiple-dose activated charcoal may be used for toxins that undergo enterohepatic circulation or prolonged absorption. Typical dosing is 1 g/kg initially, followed by 0.5 g/kg every 2–6 hours. It is considered for salicylate and theophylline poisoning and may reduce serum concentrations of phenobarbital, phenytoin, and carbamazepine, though outcome benefit is unproven. Cathartics must never be used with multiple-dose charcoal.
Cathartics such as sorbitol, magnesium citrate, or magnesium sulfate have been used with charcoal to enhance gastrointestinal transit. Evidence does not demonstrate improved toxin elimination, and harm has been reported. Cathartics alone have no proven benefit and should be avoided. Sorbitol may be added only to the first charcoal dose. Adverse effects include dehydration, diarrhea, abdominal discomfort, and hypermagnesemia. They are contraindicated in dehydration, renal disease, and in children.
Whole-bowel irrigation involves administration of polyethylene glycol electrolyte solution to flush the gastrointestinal tract. It is indicated for toxins not well adsorbed by charcoal (such as iron or lithium), ingestion of sustained-release products, and body packers without signs of perforation. Adults receive approximately 2 L/hour and children 0.5 L/hour via nasogastric tube until rectal effluent is clear. Adverse effects include bloating, rectal irritation, and frequent bowel movements. It is contraindicated in bowel obstruction, ileus, hypotension, intestinal perforation, and unprotected airway.
Orogastric lavage involves placement of a large-bore gastric tube (32F–36F) to remove stomach contents. Its effectiveness depends on time from ingestion and the substance involved. A protected airway is mandatory prior to the procedure. Indications are rare and limited to patients presenting within one hour of a potentially lethal ingestion without a known antidote, particularly if intubated. Complications include aspiration, esophageal or gastric perforation, and patient discomfort. It is contraindicated in caustic or hydrocarbon ingestion, ingestion of large pills that cannot pass through the tube, rapidly sedating agents, or unprotected airway. In children, lavage is generally avoided due to low efficacy and increased aspiration risk. Randomized trials have shown no benefit when lavage plus charcoal is compared with charcoal alone.
Ipecac syrup, derived from Cephaelis acuminata, induces vomiting through gastric irritation and central stimulation. It delays charcoal administration and provides no benefit over charcoal alone when both are potentially effective. It has no role in emergency department care. It is contraindicated in caustic or hydrocarbon ingestion, rapidly sedating agents, and actively vomiting patients.
Key clinical considerations include avoiding ipecac in the emergency department, administering activated charcoal early in appropriate patients with a protected airway, and never combining repeated cathartics with multiple-dose activated charcoal.
Gastric decontamination refers to techniques used to reduce gastrointestinal absorption of ingested toxins. The role of these interventions has decreased over time, and most poisoned patients are managed with supportive care and selected use of activated charcoal.
Ipecac is contraindicated in the prehospital ambulance setting and is not recommended for routine home use. In extremely rare circumstances, such as prolonged transit time with a protected airway, ipecac should only be considered after consultation with a regional poison control center. In general, it has no role in emergency department management.
Initial stabilization follows standard airway, breathing, and circulation principles. The airway must be secured in patients with decreased mental status or inability to protect their airway. Intravenous access and cardiac monitoring should be established. In patients with altered mental status due to suspected overdose, administer naloxone, thiamine, and dextrose as indicated.
Activated charcoal is the mainstay of gastric decontamination. It is produced from treated wood pulp, creating a large surface area that binds many toxins. It is most effective when administered within one hour of ingestion of a charcoal-adsorbable toxin in a patient with a protected airway. The recommended dose is 1–2 g/kg (or a charcoal-to-drug ratio of approximately 10:1), given orally or via nasogastric tube. Adverse effects include vomiting, constipation, and risk of aspiration with subsequent pneumonitis. It is contraindicated in caustic ingestions, unprotected airway, bowel obstruction, or ileus. Substances poorly adsorbed by charcoal include metals (iron, lithium, bromide, borates), alcohols, potassium, hydrocarbons, caustics, and potassium cyanide. In children, charcoal may be mixed with a palatable beverage or administered via gastric tube. Randomized trials suggest limited benefit in asymptomatic patients and a small increased risk of complications.
Multiple-dose activated charcoal may be used for toxins that undergo enterohepatic circulation or prolonged absorption. Typical dosing is 1 g/kg initially, followed by 0.5 g/kg every 2–6 hours. It is considered for salicylate and theophylline poisoning and may reduce serum concentrations of phenobarbital, phenytoin, and carbamazepine, though outcome benefit is unproven. Cathartics must never be used with multiple-dose charcoal.
Cathartics such as sorbitol, magnesium citrate, or magnesium sulfate have been used with charcoal to enhance gastrointestinal transit. Evidence does not demonstrate improved toxin elimination, and harm has been reported. Cathartics alone have no proven benefit and should be avoided. Sorbitol may be added only to the first charcoal dose. Adverse effects include dehydration, diarrhea, abdominal discomfort, and hypermagnesemia. They are contraindicated in dehydration, renal disease, and in children.
Whole-bowel irrigation involves administration of polyethylene glycol electrolyte solution to flush the gastrointestinal tract. It is indicated for toxins not well adsorbed by charcoal (such as iron or lithium), ingestion of sustained-release products, and body packers without signs of perforation. Adults receive approximately 2 L/hour and children 0.5 L/hour via nasogastric tube until rectal effluent is clear. Adverse effects include bloating, rectal irritation, and frequent bowel movements. It is contraindicated in bowel obstruction, ileus, hypotension, intestinal perforation, and unprotected airway.
Orogastric lavage involves placement of a large-bore gastric tube (32F–36F) to remove stomach contents. Its effectiveness depends on time from ingestion and the substance involved. A protected airway is mandatory prior to the procedure. Indications are rare and limited to patients presenting within one hour of a potentially lethal ingestion without a known antidote, particularly if intubated. Complications include aspiration, esophageal or gastric perforation, and patient discomfort. It is contraindicated in caustic or hydrocarbon ingestion, ingestion of large pills that cannot pass through the tube, rapidly sedating agents, or unprotected airway. In children, lavage is generally avoided due to low efficacy and increased aspiration risk. Randomized trials have shown no benefit when lavage plus charcoal is compared with charcoal alone.
Ipecac syrup, derived from Cephaelis acuminata, induces vomiting through gastric irritation and central stimulation. It delays charcoal administration and provides no benefit over charcoal alone when both are potentially effective. It has no role in emergency department care. It is contraindicated in caustic or hydrocarbon ingestion, rapidly sedating agents, and actively vomiting patients.
Key clinical considerations include avoiding ipecac in the emergency department, administering activated charcoal early in appropriate patients with a protected airway, and never combining repeated cathartics with multiple-dose activated charcoal.
- Published on
Emergency And Acute Medicine – Poisoning, Toxidromes
A toxidrome is a recognizable constellation of signs and symptoms produced by a specific class of toxins. Identification of a toxidrome helps guide rapid diagnosis and empiric management when the exact substance is unknown. The clinical presentation depends on the toxin’s mechanism of action and receptor targets.
Several major toxidromes are commonly encountered in emergency practice: anticholinergic, cholinergic, sympathomimetic, hallucinogenic, opioid, sedative–hypnotic, withdrawal syndromes, serotonin syndrome, and neuroleptic malignant syndrome.
The anticholinergic toxidrome is classically remembered as “blind as a bat, mad as a hatter, red as a beet, hot as a hare, dry as a bone, the bowel and bladder lose their tone, and the heart runs alone.” Patients present with hyperthermia, dry flushed skin, mydriasis, delirium, tachycardia, hypertension, urinary retention, decreased bowel sounds, and possible seizures or somnolence.
The cholinergic toxidrome is summarized by the mnemonic DUMBELS for muscarinic effects: diarrhea and diaphoresis, urination, miosis, bradycardia with bronchorrhea and bronchospasm (the “killer Bs”), emesis, lacrimation, and salivation. Nicotinic findings include tachycardia, hypertension, weakness, fasciculations, and occasionally mydriasis.
The sympathomimetic toxidrome resembles anticholinergic toxicity but is distinguished by diaphoresis and increased bowel sounds. Patients exhibit tachycardia, hypertension, hyperthermia, mydriasis, agitation, seizures, and increased peristalsis.
Hallucinogenic toxicity may overlap with sympathomimetic features. Patients may present with disorientation, hallucinations, anxiety, panic, and seizures. Substances such as LSD, psilocybin, mescaline, and MDMA may produce these effects.
The opioid toxidrome is characterized by the classic triad of miosis, hypoventilation, and coma. Additional findings include bradycardia, hypotension, hypothermia, and decreased bowel sounds.
Sedative–hypnotic and alcohol toxicity present with sedation, confusion, slurred speech, ataxia, nystagmus, blurred vision, and delirium. In contrast, withdrawal from alcohol, benzodiazepines, or barbiturates produces tachycardia, hypertension, hyperthermia, tremor, diaphoresis, agitation, hallucinations, and seizures. Opioid withdrawal presents with mydriasis, piloerection, nausea, vomiting, diarrhea, abdominal cramps, tachycardia, lacrimation, salivation, yawning, and hypertension.
Neuroleptic malignant syndrome occurs after initiation or dose increase of antipsychotics and may develop hours to weeks after exposure. It presents with hyperthermia, muscular rigidity, diaphoresis, altered mental status, blood pressure instability, tremor, sialorrhea, leukocytosis, elevated creatine phosphokinase, and metabolic acidosis.
Serotonin syndrome typically develops shortly after an increase or addition of serotonergic agents. Common features include agitation, confusion, hyperthermia, diaphoresis, tachycardia, hypertension, mydriasis, tremor, hyperreflexia, clonus, myoclonus, muscle rigidity, and seizures.
Vital sign abnormalities may suggest specific toxin classes. Bradycardia may be seen with β-blockers, calcium channel blockers, clonidine, digoxin, cholinergics, and opioids. Tachycardia occurs with sympathomimetics, anticholinergics, tricyclic antidepressants, methylxanthines, and withdrawal states. Hyperthermia may result from anticholinergics, sympathomimetics, serotonin syndrome, neuroleptic malignant syndrome, salicylates, and withdrawal. Hypothermia is associated with opioids, ethanol, sedative–hypnotics, carbon monoxide, and α2-agonists. Hypertension is common with sympathomimetics, anticholinergics, nicotine, and phencyclidine. Hypotension may occur with β-blockers, calcium channel blockers, opioids, sedative–hypnotics, tricyclic antidepressants, and nitrates.
Pupillary changes are diagnostically useful. Miosis suggests opioids, cholinergics, clonidine, and certain antipsychotics. Mydriasis is seen with anticholinergics, sympathomimetics, and withdrawal states. Toxic seizures may be remembered by the mnemonic OTIS CAMPBELL, which includes organophosphates, tricyclic antidepressants, isoniazid, sympathomimetics, camphor, cocaine, amphetamines, methylxanthines, phencyclidine, benzodiazepine withdrawal, bupropion, ethanol withdrawal, lithium, lidocaine, and lead.
Dermatologic clues may assist diagnosis. Mees lines may suggest arsenic or thallium exposure. Bullae may be seen with barbiturates or carbon monoxide. Flushing can occur with anticholinergics, niacin, disulfiram reactions, scombroid poisoning, or vancomycin. Blue or cyanotic skin may indicate methemoglobinemia from nitrites, dapsone, aniline dyes, benzocaine, or chloroquine, whereas pseudocyanosis may occur with amiodarone, minocycline, silver, or gold.
Essential evaluation depends on the suspected toxin but commonly includes complete blood count, electrolytes, renal function, glucose, urinalysis, arterial or venous blood gas, carboxyhemoglobin and methemoglobin levels, toxicology screening, acetaminophen and salicylate levels, prothrombin time, and liver function tests.
An elevated anion gap metabolic acidosis may be remembered by the mnemonic A CAT MUD PILES, which includes alcohol ketoacidosis, carbon monoxide or cyanide, acetaminophen (late), toluene, methanol, uremia, diabetic ketoacidosis, paraldehyde or metformin, iron or isoniazid, lactic acidosis, ethylene glycol, and salicylates. An increased osmolar gap suggests methanol, ethylene glycol, isopropyl alcohol, ethanol, acetone, glycerol, mannitol, or glycine.
Initial management focuses on airway, breathing, and circulation. Further emergency department management depends on the identified or suspected toxidrome and may include antidotes, supportive care, and consultation with a poison control center or medical toxicologist.
Key clinical principles include recognizing characteristic patterns, obtaining appropriate laboratory studies early, and using toxidrome identification to guide timely and targeted therapy.
- Published on
Emergency And Acute Medicine – Polio
Polio is caused by infection with poliovirus. The incubation period is typically 7–14 days, and the duration of acute illness is usually less than 1 week. Clinical manifestations vary widely. Approximately 90–95% of infections are subclinical and not clinically apparent. Abortive poliomyelitis accounts for 4–8% of cases and presents as a nonspecific viral illness with fever, myalgias, and malaise; it is often recognized as polio only during outbreaks. Nonparalytic poliomyelitis occurs in 1–2% of cases and resembles aseptic meningitis, with meningeal irritation and a similar clinical course. Paralytic poliomyelitis occurs in about 0.1% of infections and is subdivided into spinal, bulbar, and mixed bulbospinal forms. Spinal paralytic poliomyelitis causes asymmetric flaccid paralysis, more prominent in the lower extremities. Bulbar involvement, seen in about 10% of paralytic cases, affects cranial nerve–innervated muscles and may compromise respiratory and circulatory centers, resulting in high mortality. Postpoliomyelitis syndrome is characterized by new-onset weakness, pain, and atrophy occurring 8–70 years after the initial illness, usually in previously affected limbs, and progresses gradually.
Poliovirus is a small, nonenveloped RNA virus in the enterovirus genus of the Picornavirus family. There are three subtypes (1, 2, and 3). Transmission occurs via the fecal–oral route. The virus enters through the oral cavity and replicates in the pharynx, gastrointestinal tract, and lymphatic tissue. Humans are the only natural host and reservoir. The virus selectively destroys motor and autonomic neurons. Wild-type poliovirus has been eliminated in the United States since 1979. In the United States, prior cases were associated with the oral poliovirus vaccine (OPV), which could rarely undergo neurovirulent conversion, resulting in vaccine-associated paralytic poliomyelitis (VAP). With the widespread use of inactivated poliovirus vaccine (IPV), VAP has markedly decreased. OPV remains in use in some regions as part of global eradication efforts.
Most infections are asymptomatic. Symptomatic cases may present with fever, headache, malaise, sore throat, fatigue, nausea, and vomiting. Nonparalytic disease manifests with stiff neck and back pain consistent with aseptic meningitis. Paralytic disease is characterized by progressive weakness lasting less than one week, sometimes accompanied by dysphagia and dysarthria in bulbar involvement. In children, a biphasic course is more common, with an initial viral prodrome lasting 1–2 days, followed by a symptom-free interval of 2–5 days, and then abrupt onset of major neurologic illness.
History should include vaccination status, prior polio infection, recent exposure to individuals vaccinated with OPV, recent travel to endemic areas such as Nigeria, Pakistan, India, or Afghanistan, and comorbid immunocompromising conditions, particularly B-cell disorders. On physical examination, patients may have low-grade fever, headache, photophobia, and nuchal rigidity. Neurologic findings include severe muscle soreness progressing to flaccid weakness and asymmetric paralysis, typically greater in the lower extremities. Reflexes may be initially hyperactive and later absent. Sensory function remains intact. Urinary retention occurs in approximately half of paralytic cases. Patients may appear apprehensive and irritable.
Diagnosis is primarily clinical and requires differentiation from other causes of acute flaccid paralysis. Public health authorities must be notified when polio is suspected. Laboratory findings may show normal or mildly elevated white blood cell count. Confirmation is achieved by demonstrating a rise in antibody titers between acute and convalescent sera or by isolating the virus from blood, cerebrospinal fluid, stool, or throat secretions during the first week of infection. Cerebrospinal fluid analysis typically shows findings consistent with aseptic meningitis, including lymphocytic pleocytosis and elevated protein, although the virus is rarely isolated from CSF. Electrodiagnostic studies demonstrate motor involvement with preserved sensory function.
The differential diagnosis depends on the clinical form. Abortive disease resembles other viral illnesses. Nonparalytic disease is indistinguishable from other causes of aseptic meningitis. Paralytic disease must be differentiated from Guillain–Barré syndrome, acute transverse myelitis, spinal cord compression or infarction, multiple sclerosis, amyotrophic lateral sclerosis, rhabdomyolysis, acute intermittent porphyria, West Nile virus infection, diphtheria, botulism, tick paralysis, and encephalitis.
Management is supportive. Fatal cases are usually due to respiratory insufficiency, which requires prompt recognition and ventilatory support. Aggressive pulmonary toilet and early intubation are indicated when respiratory compromise develops. Treatment includes bed rest to reduce risk of worsening paralysis and analgesics for severe muscle pain and spasm. Unnecessary intramuscular injections or tissue injury should be avoided, as paralysis may localize to recently traumatized limbs. There are no effective antiviral agents.
Prevention is achieved through vaccination. Inactivated poliovirus vaccine is currently used in the United States and does not cause vaccine-associated disease. Oral poliovirus vaccine, though no longer used in the United States, remains part of global eradication programs because of its ability to confer community immunity through fecal–oral spread.
All patients with acute-phase paralytic poliomyelitis require hospital admission for strict bed rest and close monitoring for respiratory involvement. Isolation from unvaccinated individuals is necessary. Patients without nervous system involvement and without risk of contact transmission may be discharged. Physical therapy is essential during recovery, although only about one-third of patients with acute flaccid paralysis regain full strength. Postpolio syndrome may occur decades later with progressive neuromuscular symptoms.
Key clinical points include the wide spectrum of presentation from asymptomatic infection to acute flaccid paralysis, the importance of vaccination history and travel exposure, the need for early respiratory monitoring in paralytic cases, and the primarily supportive nature of treatment.
- Published on
Emergency And Acute Medicine – Polyneuropathy
Polyneuropathy is a peripheral nerve disorder in which multiple nerves throughout the body malfunction simultaneously. It may present acutely or chronically and may involve sensory, motor, autonomic, or mixed dysfunction. Acute causes include infections (such as toxin-producing bacteria and viruses), autoimmune conditions like Guillain–Barré syndrome, toxic exposures including heavy metals such as lead and mercury, medications such as phenytoin, chloramphenicol, nitrofurantoin, sulfonamides, vincristine, vinblastine, and certain sedatives, as well as malignancies like multiple myeloma. Chronic polyneuropathy is most commonly caused by diabetes mellitus, but may also result from chronic alcohol use, nutritional deficiencies (particularly thiamine and vitamin B12), hypothyroidism, liver failure, kidney failure, lung cancer, and chronic inflammatory demyelinating polyneuropathy (CIDP).
Polyneuropathy affects approximately 2% of the general U.S. population and up to 8% of individuals over age 55. Diabetes is the most common cause in the United States and occurs in roughly half of insulin-dependent diabetics. Pathophysiologically, polyneuropathy may result from myelin dysfunction, vascular compromise to the vasa nervorum, or primary axonal injury. Myelin dysfunction is often immune-mediated, triggered by infections such as Campylobacter, diphtheria, influenza, or HIV, and may follow vaccination. Guillain–Barré syndrome presents acutely with rapidly progressive weakness and may lead to respiratory failure, whereas CIDP follows a more chronic or relapsing course. Vascular compromise from atherosclerosis, vasculitis, infection, or hypercoagulable states may cause ischemic nerve injury. Axonal injury is most commonly due to toxic-metabolic conditions such as diabetes, nutritional deficiencies, or drug and chemical exposure.
Clinically, polyneuropathy usually begins distally in the lower extremities and progresses proximally in a symmetrical “stocking-glove” distribution. Patients often report numbness, burning, tingling, weakness, and difficulty walking. Autonomic symptoms may include constipation, urinary retention or incontinence, sexual dysfunction, orthostatic dizziness, dry skin, and decreased sweating. On examination, findings are typically bilateral and symmetrical, including decreased sensation, impaired vibration and position sense, diminished motor strength, reduced reflexes, muscle atrophy, and sometimes fasciculations or paralysis. In demyelinating disorders such as Guillain–Barré syndrome and CIDP, weakness may be disproportionate to atrophy and reflexes are markedly diminished. Ischemic neuropathies often cause painful burning sensations with preserved reflexes and distal involvement. Toxic-metabolic axonopathies are typically painful and distally symmetric.
Evaluation begins with a thorough history and physical examination. Initial laboratory testing should include complete blood count, electrolytes, glucose, renal and liver function tests, thyroid-stimulating hormone, erythrocyte sedimentation rate, antinuclear antibody, vitamin B12, folate, rapid plasma reagin, HIV, hepatitis B and C serologies, Lyme testing, creatine phosphokinase, and serum protein electrophoresis. Additional tests such as heavy metal levels, genetic studies, or immune-mediated antibody testing are guided by clinical suspicion. Electromyography and nerve conduction studies are essential diagnostic tools. Lumbar puncture demonstrating elevated cerebrospinal fluid protein with normal cell count supports Guillain–Barré syndrome or CIDP. Nerve or skin biopsy may be considered in selected cases.
Emergency management focuses on airway, breathing, and circulation. Respiratory compromise is a critical concern in acute demyelinating neuropathies; measurement of negative inspiratory force (normal approximately −60 cm H₂O) helps assess impending respiratory failure. Patients with respiratory weakness require prompt ventilatory support. Pain management may include narcotics, tricyclic antidepressants such as amitriptyline, and anticonvulsants such as gabapentin. Plasma exchange or intravenous immunoglobulin is indicated for acute demyelinating neuropathies, while corticosteroids or other immunosuppressive agents are used in chronic demyelinating conditions. Supportive care, including intravenous fluids and vasopressors, may be necessary for autonomic instability.
Admission is warranted for patients with respiratory failure, blood pressure instability, inability to ambulate or care for themselves, inadequate pain control, rapidly progressive symptoms, or poorly controlled underlying disease. Stable patients without respiratory or autonomic compromise who can manage self-care and have adequate outpatient follow-up may be discharged. All patients require referral to primary care and neurology for ongoing evaluation and management, and many benefit from physical therapy. Recognizing potentially reversible causes and identifying patients at risk for respiratory failure or autonomic instability are essential priorities in emergency and acute care.
Polyneuropathy is a peripheral nerve disorder in which multiple nerves throughout the body malfunction simultaneously. It may present acutely or chronically and may involve sensory, motor, autonomic, or mixed dysfunction. Acute causes include infections (such as toxin-producing bacteria and viruses), autoimmune conditions like Guillain–Barré syndrome, toxic exposures including heavy metals such as lead and mercury, medications such as phenytoin, chloramphenicol, nitrofurantoin, sulfonamides, vincristine, vinblastine, and certain sedatives, as well as malignancies like multiple myeloma. Chronic polyneuropathy is most commonly caused by diabetes mellitus, but may also result from chronic alcohol use, nutritional deficiencies (particularly thiamine and vitamin B12), hypothyroidism, liver failure, kidney failure, lung cancer, and chronic inflammatory demyelinating polyneuropathy (CIDP).
Polyneuropathy affects approximately 2% of the general U.S. population and up to 8% of individuals over age 55. Diabetes is the most common cause in the United States and occurs in roughly half of insulin-dependent diabetics. Pathophysiologically, polyneuropathy may result from myelin dysfunction, vascular compromise to the vasa nervorum, or primary axonal injury. Myelin dysfunction is often immune-mediated, triggered by infections such as Campylobacter, diphtheria, influenza, or HIV, and may follow vaccination. Guillain–Barré syndrome presents acutely with rapidly progressive weakness and may lead to respiratory failure, whereas CIDP follows a more chronic or relapsing course. Vascular compromise from atherosclerosis, vasculitis, infection, or hypercoagulable states may cause ischemic nerve injury. Axonal injury is most commonly due to toxic-metabolic conditions such as diabetes, nutritional deficiencies, or drug and chemical exposure.
Clinically, polyneuropathy usually begins distally in the lower extremities and progresses proximally in a symmetrical “stocking-glove” distribution. Patients often report numbness, burning, tingling, weakness, and difficulty walking. Autonomic symptoms may include constipation, urinary retention or incontinence, sexual dysfunction, orthostatic dizziness, dry skin, and decreased sweating. On examination, findings are typically bilateral and symmetrical, including decreased sensation, impaired vibration and position sense, diminished motor strength, reduced reflexes, muscle atrophy, and sometimes fasciculations or paralysis. In demyelinating disorders such as Guillain–Barré syndrome and CIDP, weakness may be disproportionate to atrophy and reflexes are markedly diminished. Ischemic neuropathies often cause painful burning sensations with preserved reflexes and distal involvement. Toxic-metabolic axonopathies are typically painful and distally symmetric.
Evaluation begins with a thorough history and physical examination. Initial laboratory testing should include complete blood count, electrolytes, glucose, renal and liver function tests, thyroid-stimulating hormone, erythrocyte sedimentation rate, antinuclear antibody, vitamin B12, folate, rapid plasma reagin, HIV, hepatitis B and C serologies, Lyme testing, creatine phosphokinase, and serum protein electrophoresis. Additional tests such as heavy metal levels, genetic studies, or immune-mediated antibody testing are guided by clinical suspicion. Electromyography and nerve conduction studies are essential diagnostic tools. Lumbar puncture demonstrating elevated cerebrospinal fluid protein with normal cell count supports Guillain–Barré syndrome or CIDP. Nerve or skin biopsy may be considered in selected cases.
Emergency management focuses on airway, breathing, and circulation. Respiratory compromise is a critical concern in acute demyelinating neuropathies; measurement of negative inspiratory force (normal approximately −60 cm H₂O) helps assess impending respiratory failure. Patients with respiratory weakness require prompt ventilatory support. Pain management may include narcotics, tricyclic antidepressants such as amitriptyline, and anticonvulsants such as gabapentin. Plasma exchange or intravenous immunoglobulin is indicated for acute demyelinating neuropathies, while corticosteroids or other immunosuppressive agents are used in chronic demyelinating conditions. Supportive care, including intravenous fluids and vasopressors, may be necessary for autonomic instability.
Admission is warranted for patients with respiratory failure, blood pressure instability, inability to ambulate or care for themselves, inadequate pain control, rapidly progressive symptoms, or poorly controlled underlying disease. Stable patients without respiratory or autonomic compromise who can manage self-care and have adequate outpatient follow-up may be discharged. All patients require referral to primary care and neurology for ongoing evaluation and management, and many benefit from physical therapy. Recognizing potentially reversible causes and identifying patients at risk for respiratory failure or autonomic instability are essential priorities in emergency and acute care.
