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Emergency And Acute Medicine – Diaphragmatic Trauma
Basics
Description Diaphragmatic trauma results from either penetrating or blunt mechanisms. Penetrating injury involves violation of the diaphragm by an object, most commonly stab or gunshot wounds. Any portion of the diaphragm may be involved, and defects are usually smaller than those from blunt injury, making them more likely to be missed. Blunt injury occurs when a sudden increase in intra-abdominal or intrathoracic pressure is transmitted to the diaphragm, leading to rupture, most often due to motor vehicle crashes. Injuries are more commonly left-sided because the left hemidiaphragm has a posterolateral embryologic point of weakness, whereas the right hemidiaphragm is relatively protected by the liver. Blunt injuries tend to be larger, frequently measuring 5–15 cm. Diaphragmatic defects do not heal spontaneously because the pleuroperitoneal pressure gradient, which may exceed 100 cm H₂O during maximal respiratory effort, promotes progressive herniation of abdominal contents into the chest.
Epidemiology
Incidence Diaphragmatic injury is uncommon, accounting for less than 1% of all traumatic injuries.
Etiology Lateral torso impact is approximately three times more likely to cause ipsilateral diaphragmatic rupture than frontal impact. Diaphragmatic injury should be suspected in penetrating trauma to the thoracoabdominal region and in injuries that cross the plane of the diaphragm.
Diagnosis
Alert In the acute phase, abdominal visceral herniation may be absent, and the injury can be missed even during initial laparotomy or laparoscopy.
Signs And Symptoms Clinical presentation varies depending on whether the phase is acute, latent, or obstructive.
Acute phase Patients may present with tachypnea, hypotension, absent or diminished breath sounds, abdominal distention, or bowel sounds heard in the chest.
Latent phase Symptoms include intermittent abdominal discomfort from herniation of abdominal contents into the thorax, postprandial abdominal pain, worsening pain when supine, left shoulder pain, nausea, vomiting, or belching.
Obstructive phase Patients develop severe abdominal pain, obstipation, nausea, vomiting, and abdominal distention. Strangulated abdominal organs may perforate, spilling contents into the chest and leading to respiratory compromise, sepsis, and death. Obstructive presentations are often delayed.
Essential Workup Chest radiography may reveal herniated bowel loops or abdominal viscera in the thorax. A nasogastric tube visualized above the diaphragm is pathognomonic. More commonly, findings are nonspecific and include elevated hemidiaphragm, irregular diaphragmatic contour, mediastinal shift away from the affected side, unilateral pleural thickening or effusion, basal atelectasis or consolidation, or small hemothorax or pneumothorax. Up to 50% of initial chest radiographs may be normal. Diagnosis is particularly challenging in the latent phase due to intermittent herniation. Contrast gastrointestinal studies may be helpful.
Diagnosis Tests And Interpretation
Lab No laboratory study definitively confirms or excludes diaphragmatic injury. If diagnostic peritoneal lavage is performed after penetrating trauma, a red blood cell count of ≥1,000 RBC/mm³ is considered positive, though false-negative results occur in up to 40% of isolated injuries.
Imaging Chest radiography is diagnostic in up to 90% of cases when herniation is present but has limited sensitivity without acute hernia. Gastrointestinal contrast studies are most useful for diagnosing chronic herniation. Ultrasound may aid diagnosis, particularly on the right side with hepatic herniation. Conventional CT has poor sensitivity, whereas helical and multidetector CT significantly improve detection of subtle injuries. MRI visualizes the diaphragm well but is impractical in acute trauma.
Diagnostic procedures or surgery Diagnostic pneumoperitoneography involves injecting air through a diagnostic peritoneal lavage catheter; pneumothorax on subsequent chest radiograph confirms diaphragmatic injury. This technique is poorly tolerated in unstable patients and may necessitate chest tube placement. Thoracoscopic or laparoscopic exploration may be indicated when suspicion remains high despite negative imaging and allows minimally invasive repair.
Differential Diagnosis Atelectasis, hemothorax, pneumothorax, pulmonary contusion, gastric dilation, intra-abdominal fluid, traumatic pneumatocele, subdiaphragmatic abscess, intrathoracic cyst, empyema, and congenital eventration of the diaphragm.
Treatment
Alert Herniation of abdominal contents into the chest may mimic hemothorax or tension pneumothorax. Bowel sounds in the chest can help differentiate. Be cautious with needle or tube thoracostomy in patients with lateral chest compression; fecal thorax has been reported after bowel rupture.
Initial stabilization and therapy Follow advanced trauma life support protocols. In patients with respiratory distress, immediate nasogastric tube placement may decompress herniated abdominal contents.
Emergency department treatment and procedures Palpate the chest cavity for visceral organs before chest tube insertion. Patients with visceral perforation are septic and require aggressive resuscitation and empiric broad-spectrum antibiotics. Early surgical intervention is critical, and minimally invasive repair may be feasible in selected cases.
Medication Empiric antimicrobial coverage for perforated viscera includes agents targeting gram-negative aerobes and anaerobes. Options include gentamicin, clindamycin, metronidazole, ampicillin–sulbactam, cefotetan, cefoxitin, or ticarcillin–clavulanate, with pediatric dosing adjusted appropriately.
Follow-Up Disposition
Admission criteria Any patient with confirmed or suspected diaphragmatic injury must be admitted to trauma surgery, typically to a monitored unit or intensive care setting.
Discharge criteria Patients with diaphragmatic injury or significant suspicion for it should not be discharged from the emergency department.
Follow-Up Recommendations Patients who undergo diaphragmatic repair require follow-up with a trauma surgeon to monitor for recurrence.
Pediatric Considerations Pediatric anatomic features predispose children to diaphragmatic injury from less severe mechanisms, including a thinner abdominal wall, more horizontal diaphragm, and greater cartilaginous rib composition. Right- and left-sided injuries occur with equal frequency and are more likely to be isolated.
Pearls And Pitfalls Overall mortality ranges from 18% to 40%, depending on mechanism, and is highly associated with concomitant injuries to the spleen, liver, lungs, and pelvis. Maintain a high index of suspicion with left-sided upper abdominal or lower thoracic penetrating trauma. Delayed diagnosis increases the risk of herniation and strangulation of abdominal organs. Chest imaging should always be obtained.
Basics
Description Diaphragmatic trauma results from either penetrating or blunt mechanisms. Penetrating injury involves violation of the diaphragm by an object, most commonly stab or gunshot wounds. Any portion of the diaphragm may be involved, and defects are usually smaller than those from blunt injury, making them more likely to be missed. Blunt injury occurs when a sudden increase in intra-abdominal or intrathoracic pressure is transmitted to the diaphragm, leading to rupture, most often due to motor vehicle crashes. Injuries are more commonly left-sided because the left hemidiaphragm has a posterolateral embryologic point of weakness, whereas the right hemidiaphragm is relatively protected by the liver. Blunt injuries tend to be larger, frequently measuring 5–15 cm. Diaphragmatic defects do not heal spontaneously because the pleuroperitoneal pressure gradient, which may exceed 100 cm H₂O during maximal respiratory effort, promotes progressive herniation of abdominal contents into the chest.
Epidemiology
Incidence Diaphragmatic injury is uncommon, accounting for less than 1% of all traumatic injuries.
Etiology Lateral torso impact is approximately three times more likely to cause ipsilateral diaphragmatic rupture than frontal impact. Diaphragmatic injury should be suspected in penetrating trauma to the thoracoabdominal region and in injuries that cross the plane of the diaphragm.
Diagnosis
Alert In the acute phase, abdominal visceral herniation may be absent, and the injury can be missed even during initial laparotomy or laparoscopy.
Signs And Symptoms Clinical presentation varies depending on whether the phase is acute, latent, or obstructive.
Acute phase Patients may present with tachypnea, hypotension, absent or diminished breath sounds, abdominal distention, or bowel sounds heard in the chest.
Latent phase Symptoms include intermittent abdominal discomfort from herniation of abdominal contents into the thorax, postprandial abdominal pain, worsening pain when supine, left shoulder pain, nausea, vomiting, or belching.
Obstructive phase Patients develop severe abdominal pain, obstipation, nausea, vomiting, and abdominal distention. Strangulated abdominal organs may perforate, spilling contents into the chest and leading to respiratory compromise, sepsis, and death. Obstructive presentations are often delayed.
Essential Workup Chest radiography may reveal herniated bowel loops or abdominal viscera in the thorax. A nasogastric tube visualized above the diaphragm is pathognomonic. More commonly, findings are nonspecific and include elevated hemidiaphragm, irregular diaphragmatic contour, mediastinal shift away from the affected side, unilateral pleural thickening or effusion, basal atelectasis or consolidation, or small hemothorax or pneumothorax. Up to 50% of initial chest radiographs may be normal. Diagnosis is particularly challenging in the latent phase due to intermittent herniation. Contrast gastrointestinal studies may be helpful.
Diagnosis Tests And Interpretation
Lab No laboratory study definitively confirms or excludes diaphragmatic injury. If diagnostic peritoneal lavage is performed after penetrating trauma, a red blood cell count of ≥1,000 RBC/mm³ is considered positive, though false-negative results occur in up to 40% of isolated injuries.
Imaging Chest radiography is diagnostic in up to 90% of cases when herniation is present but has limited sensitivity without acute hernia. Gastrointestinal contrast studies are most useful for diagnosing chronic herniation. Ultrasound may aid diagnosis, particularly on the right side with hepatic herniation. Conventional CT has poor sensitivity, whereas helical and multidetector CT significantly improve detection of subtle injuries. MRI visualizes the diaphragm well but is impractical in acute trauma.
Diagnostic procedures or surgery Diagnostic pneumoperitoneography involves injecting air through a diagnostic peritoneal lavage catheter; pneumothorax on subsequent chest radiograph confirms diaphragmatic injury. This technique is poorly tolerated in unstable patients and may necessitate chest tube placement. Thoracoscopic or laparoscopic exploration may be indicated when suspicion remains high despite negative imaging and allows minimally invasive repair.
Differential Diagnosis Atelectasis, hemothorax, pneumothorax, pulmonary contusion, gastric dilation, intra-abdominal fluid, traumatic pneumatocele, subdiaphragmatic abscess, intrathoracic cyst, empyema, and congenital eventration of the diaphragm.
Treatment
Alert Herniation of abdominal contents into the chest may mimic hemothorax or tension pneumothorax. Bowel sounds in the chest can help differentiate. Be cautious with needle or tube thoracostomy in patients with lateral chest compression; fecal thorax has been reported after bowel rupture.
Initial stabilization and therapy Follow advanced trauma life support protocols. In patients with respiratory distress, immediate nasogastric tube placement may decompress herniated abdominal contents.
Emergency department treatment and procedures Palpate the chest cavity for visceral organs before chest tube insertion. Patients with visceral perforation are septic and require aggressive resuscitation and empiric broad-spectrum antibiotics. Early surgical intervention is critical, and minimally invasive repair may be feasible in selected cases.
Medication Empiric antimicrobial coverage for perforated viscera includes agents targeting gram-negative aerobes and anaerobes. Options include gentamicin, clindamycin, metronidazole, ampicillin–sulbactam, cefotetan, cefoxitin, or ticarcillin–clavulanate, with pediatric dosing adjusted appropriately.
Follow-Up Disposition
Admission criteria Any patient with confirmed or suspected diaphragmatic injury must be admitted to trauma surgery, typically to a monitored unit or intensive care setting.
Discharge criteria Patients with diaphragmatic injury or significant suspicion for it should not be discharged from the emergency department.
Follow-Up Recommendations Patients who undergo diaphragmatic repair require follow-up with a trauma surgeon to monitor for recurrence.
Pediatric Considerations Pediatric anatomic features predispose children to diaphragmatic injury from less severe mechanisms, including a thinner abdominal wall, more horizontal diaphragm, and greater cartilaginous rib composition. Right- and left-sided injuries occur with equal frequency and are more likely to be isolated.
Pearls And Pitfalls Overall mortality ranges from 18% to 40%, depending on mechanism, and is highly associated with concomitant injuries to the spleen, liver, lungs, and pelvis. Maintain a high index of suspicion with left-sided upper abdominal or lower thoracic penetrating trauma. Delayed diagnosis increases the risk of herniation and strangulation of abdominal organs. Chest imaging should always be obtained.
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Emergency and Acute Medicine - Juvenile Diabetes Mellitus
Basics
Description Decrease in effective circulating insulin. Increase in counter regulatory hormones including glucagon, catecholamines, cortisol, and growth hormone. Hyperglycemia owing to: Decreased peripheral glucose utilization. Increased hepatic gluconeogenesis. Hyperosmolality and osmotic diuresis due to hyperglycemia. Ketoacidosis produced by increased lipolysis, with ketone body (β-hydroxybutyrate, acetoacetate) production, causes ketonemia and metabolic acidosis, which is augmented with lactic acidosis from poor tissue perfusion. Potassium deficit: Intracellular shifts into extracellular space owing to hydrogen ion exchange. Loss from osmotic diuresis.
Etiology
Mechanism: Immune-mediated pancreatic islet β-cell destruction. The overall incidence has been increased worldwide by 2–5% over the past 20 yr. Precipitating events leading to diabetic ketoacidosis (DKA): Infection, often minor acute illness such as virus, group A streptococcal pharyngitis, or UTI. Stress. Endocrine: Pregnancy, puberty, hyperthyroidism. Psychiatric disorders, including eating disorders. Medication noncompliance, inappropriate interruption of insulin pump therapy, or treatment error. Risk factors for cerebral edema: Attenuated rise in measured serum sodium during DKA therapy (unrelated to the volume or sodium content of IV fluid or rate of change in serum glucose). Bicarbonate treatment for acidosis correction. Hypocapnia. Increased serum urea nitrogen. No association with degree of hyperglycemia. Demographic factors that have been associated with an increased risk of cerebral edema include younger age, longer duration of symptoms, and new onset diabetes mellitus. These factors are also associated with increased risk of severe DKA.
Diagnosis
Signs and symptoms Polydipsia. Polyuria (may have good urine output despite dehydration). Nocturia. Polyphagia. Malaise, weight loss. DKA: Initial presentation in 20-40% of patients. Often associated with tachypnea (Kussmaul respiration), tachycardia, orthostatic BP changes. Nausea. Vomiting. Abdominal pain, often resolving with reduction in ketosis/acidosis. Hyperpnea. Fruity breath secondary to ketones. Rapid onset of DKA can occur within 7-8 hr with the use of insulin pump therapy if there is an infusion set or insulin delivery malfunction. This is due secondary to lack of long acting insulin to provide a safety net (more commonly seen in female >10 yr of age). Findings with more advanced disease: Dehydration, drowsiness, altered mental status, and ultimately, late stage coma and shock. Cerebral edema: The incidence ranges from 0.87–1.1%. Cerebral edema accounts for 57–87% of all DKA deaths. It typically occurs 4–12 hr after treatment is initiated, but can be presenting (subclinical) before treatment has started. Headache. Change in neurologic status, such as drowsiness, irritability, or specific neurologic deficit, such as pupillary responses or cranial nerve palsies. Inappropriate slowing in pulse rate. Increase in BP. Hyperglycemic hyperosmolar nonketotic coma: Glucose level of 800–1,200 mg/dL. Rare in children; more common in adults.
Essential workup
For DKA: The International Society for Pediatric and Adolescent Diabetes (ISPAD) defines DKA as blood bicarbonate level <15 mmol /> or venous pH <7.3 and hyperglycemia (>200 mg/dL) with related ketonemia or ketonuria. DKA classification: Mild DKA: Venous pH <7.2–7.3 or hco3 <10–15 mmol />. Moderate DKA: Venous pH <7.1–7.2 or hco3 <5–10 mmol />. Severe DKA: Venous pH <7.1 or hco3 <5 mmol />. Hourly vital signs and neurologic checks. Frequent blood chemistries. ECG monitoring (in severe DKA) to assess T-waves for evidence of hyperkalemia or hypokalemia. Accurate fluid input and output. Consider urinary catheterization in patients with impaired level of consciousness.
Diagnosis tests & interpretation
Lab For DKA: Glucose, serum: Hyperglycemia. Urinalysis: Glycosuria. Ketonuria. Exclude UTI. Blood chemistries every 2–4 hr until acidosis has resolved (more frequent as clinically indicated in the more severe cases). Electrolytes and venous pH. Anion gap metabolic acidosis: Potassium—high or normal (artifactual owing to extracellular shift). Serum potassium rises 0.5 mEqL for each 0.1 decrease in pH. Sodium—low or normal (may be artifactual owing to hyperglycemia). Corrected Na (mEq/L) = [measured serum Na (mEqL) + plasma glucose (mg/dL) – 100] × 0.016. Bicarbonate—low. Calculation: Na – (Cl + HCO3). Serum ketones—elevated. β-hydroxybutyrate (BHOB) is a quantitative test that is available to replace the classic nitroprusside test for serum ketones. Serum osmolality. CBC: WBC often elevated owing to stress or infection. Calcium. Phosphate. Cultures as indicated: Group A streptococcal pharyngeal swab, urine, etc. Pregnancy test if indicated. ECG if potassium markedly abnormal. Imaging: CXR if any suggestion of pneumonia. Head CT if there are concerns about cerebral edema.
Differential diagnosis
Infection (may precipitate): UTI. Gastroenteritis. Appendicitis. Sepsis. Ingestion (salicylates, alcohols, glycols). Diabetes insipidus.
Treatment
Pre hospital For DKA: ABCs. Airway protection. Establish IV access and initiate fluid therapy.
Initial stabilization/therapy For DKA: Oxygen. Cardiac monitor. IV access and volume resuscitation.
Ed treatment/procedures For DKA: Fluid replacement: Assume fluid deficit of 10% of body weight. Initial volume expansion with 10-20 mL/kg of 0.9% NaCl or lactated Ringer; may repeat to achieve hemodynamic stability. Correct 50% of fluid deficit over 1st 8 hr, remainder over 24-48 hr. Do not give >3 L/m2 over 1st 24 hr. Begin IV insulin infusion after ketoacidosis confirmed: Initial rate of continuous infusion (regular insulin) 0.1 U/kg/h IV. Adjust rate to drop serum glucose 50–100 mg/dL/h. Add dextrose to infusion fluid when serum glucose <300 mg />L. Change to SC insulin when no longer significantly acidotic and able to eat. Some clinicians prefer IM route, commonly initially using regular insulin at a dose of 0.1–0.2 U/kg/h. Replace potassium and phosphate losses: Verify adequate urine output. Add to fluids as K-acetate (or KCl if acetate not available) and K3PO4 in equal amounts. Large doses of K+ may be necessary; guide therapy by frequent monitoring of K+. Monitor serum sodium: Risk for cerebral edema if Na+ fails to rise as glucose falls. Bicarbonate therapy: Not recommended in most cases since generally it does not alter outcome and it increases risk for cerebral edema with its use. Use it with caution in patients with severe acidosis (pH <6.9) in whom peripheral vasodilation and decreased cardiac contractility may further impair tissue perfusion potentially life-threatening hyperkalemia. cerebral edema: treat edema as soon the condition is suspected due to its high mortality morbidity rates: 21–25% 10–26%, respectively. decrease fluid administration rate. mannitol (0.25–1 g />g over 20 min): No large studies to date demonstrate definitive beneficial or detrimental effects. Consider its use in patients with signs of cerebral edema before impeding respiratory failure. Dose can be repeated in 2 hr if there is no initial response. Endotracheal intubation and ventilation: Avoid aggressive hyperventilation since it has been associated with poor outcome in DKA-related cerebral edema (similar to that found in head trauma).
Medication
Insulin drip: Start regular insulin 0.1 U/kg/h IV (some clinicians prefer the IM dosing and route). Mannitol: 0.25–1 g/kg IV.
Follow-up disposition
Admission criteria For DKA: ICU: Altered mental status. Shock or cardiac dysrhythmia. Initial glucose >700 mg/dL. Initial pH <7. risk factors for cerebral edema (age <5 yr, prolonged symptoms, high bun). inpatient unit: stable new-onset diabetic patients requiring intensive education. with ketoacidosis not meeting requirements icu care. compliance concerns or other social issues. discharge criteria known who respond well to therapy normalization of glucose, ph, and ketosis. tolerating oral fluids. reliable parents. follow-up within 24 hr including appropriate issues referral critically ill. persistent abnormal mental status. poorly controlled diabetes.< />pan>
Follow-up recommendations
Close follow-up with the primary care physician is important even after the resolution of DKA to ensure appropriate management of the patient’s diabetes to prevent further occurrence of DKA. Many children with diabetes are followed at comprehensive diabetes centers in collaboration with primary care physician.
Pearls and pitfalls
Mortality from DKA is predominately related to the occurrence of cerebral edema. Therefore, early and appropriate treatment is of most importance in managing children with DKA. In children, avoid using an insulin bolus since it increase the risk of cerebral edema. Recently, some data suggest that starting insulin drip at 0.05 U/kg/h may reduce the risk for rapid fluid shifts and theoretically for cerebral edema.
Basics
Description Decrease in effective circulating insulin. Increase in counter regulatory hormones including glucagon, catecholamines, cortisol, and growth hormone. Hyperglycemia owing to: Decreased peripheral glucose utilization. Increased hepatic gluconeogenesis. Hyperosmolality and osmotic diuresis due to hyperglycemia. Ketoacidosis produced by increased lipolysis, with ketone body (β-hydroxybutyrate, acetoacetate) production, causes ketonemia and metabolic acidosis, which is augmented with lactic acidosis from poor tissue perfusion. Potassium deficit: Intracellular shifts into extracellular space owing to hydrogen ion exchange. Loss from osmotic diuresis.
Etiology
Mechanism: Immune-mediated pancreatic islet β-cell destruction. The overall incidence has been increased worldwide by 2–5% over the past 20 yr. Precipitating events leading to diabetic ketoacidosis (DKA): Infection, often minor acute illness such as virus, group A streptococcal pharyngitis, or UTI. Stress. Endocrine: Pregnancy, puberty, hyperthyroidism. Psychiatric disorders, including eating disorders. Medication noncompliance, inappropriate interruption of insulin pump therapy, or treatment error. Risk factors for cerebral edema: Attenuated rise in measured serum sodium during DKA therapy (unrelated to the volume or sodium content of IV fluid or rate of change in serum glucose). Bicarbonate treatment for acidosis correction. Hypocapnia. Increased serum urea nitrogen. No association with degree of hyperglycemia. Demographic factors that have been associated with an increased risk of cerebral edema include younger age, longer duration of symptoms, and new onset diabetes mellitus. These factors are also associated with increased risk of severe DKA.
Diagnosis
Signs and symptoms Polydipsia. Polyuria (may have good urine output despite dehydration). Nocturia. Polyphagia. Malaise, weight loss. DKA: Initial presentation in 20-40% of patients. Often associated with tachypnea (Kussmaul respiration), tachycardia, orthostatic BP changes. Nausea. Vomiting. Abdominal pain, often resolving with reduction in ketosis/acidosis. Hyperpnea. Fruity breath secondary to ketones. Rapid onset of DKA can occur within 7-8 hr with the use of insulin pump therapy if there is an infusion set or insulin delivery malfunction. This is due secondary to lack of long acting insulin to provide a safety net (more commonly seen in female >10 yr of age). Findings with more advanced disease: Dehydration, drowsiness, altered mental status, and ultimately, late stage coma and shock. Cerebral edema: The incidence ranges from 0.87–1.1%. Cerebral edema accounts for 57–87% of all DKA deaths. It typically occurs 4–12 hr after treatment is initiated, but can be presenting (subclinical) before treatment has started. Headache. Change in neurologic status, such as drowsiness, irritability, or specific neurologic deficit, such as pupillary responses or cranial nerve palsies. Inappropriate slowing in pulse rate. Increase in BP. Hyperglycemic hyperosmolar nonketotic coma: Glucose level of 800–1,200 mg/dL. Rare in children; more common in adults.
Essential workup
For DKA: The International Society for Pediatric and Adolescent Diabetes (ISPAD) defines DKA as blood bicarbonate level <15 mmol /> or venous pH <7.3 and hyperglycemia (>200 mg/dL) with related ketonemia or ketonuria. DKA classification: Mild DKA: Venous pH <7.2–7.3 or hco3 <10–15 mmol />. Moderate DKA: Venous pH <7.1–7.2 or hco3 <5–10 mmol />. Severe DKA: Venous pH <7.1 or hco3 <5 mmol />. Hourly vital signs and neurologic checks. Frequent blood chemistries. ECG monitoring (in severe DKA) to assess T-waves for evidence of hyperkalemia or hypokalemia. Accurate fluid input and output. Consider urinary catheterization in patients with impaired level of consciousness.
Diagnosis tests & interpretation
Lab For DKA: Glucose, serum: Hyperglycemia. Urinalysis: Glycosuria. Ketonuria. Exclude UTI. Blood chemistries every 2–4 hr until acidosis has resolved (more frequent as clinically indicated in the more severe cases). Electrolytes and venous pH. Anion gap metabolic acidosis: Potassium—high or normal (artifactual owing to extracellular shift). Serum potassium rises 0.5 mEqL for each 0.1 decrease in pH. Sodium—low or normal (may be artifactual owing to hyperglycemia). Corrected Na (mEq/L) = [measured serum Na (mEqL) + plasma glucose (mg/dL) – 100] × 0.016. Bicarbonate—low. Calculation: Na – (Cl + HCO3). Serum ketones—elevated. β-hydroxybutyrate (BHOB) is a quantitative test that is available to replace the classic nitroprusside test for serum ketones. Serum osmolality. CBC: WBC often elevated owing to stress or infection. Calcium. Phosphate. Cultures as indicated: Group A streptococcal pharyngeal swab, urine, etc. Pregnancy test if indicated. ECG if potassium markedly abnormal. Imaging: CXR if any suggestion of pneumonia. Head CT if there are concerns about cerebral edema.
Differential diagnosis
Infection (may precipitate): UTI. Gastroenteritis. Appendicitis. Sepsis. Ingestion (salicylates, alcohols, glycols). Diabetes insipidus.
Treatment
Pre hospital For DKA: ABCs. Airway protection. Establish IV access and initiate fluid therapy.
Initial stabilization/therapy For DKA: Oxygen. Cardiac monitor. IV access and volume resuscitation.
Ed treatment/procedures For DKA: Fluid replacement: Assume fluid deficit of 10% of body weight. Initial volume expansion with 10-20 mL/kg of 0.9% NaCl or lactated Ringer; may repeat to achieve hemodynamic stability. Correct 50% of fluid deficit over 1st 8 hr, remainder over 24-48 hr. Do not give >3 L/m2 over 1st 24 hr. Begin IV insulin infusion after ketoacidosis confirmed: Initial rate of continuous infusion (regular insulin) 0.1 U/kg/h IV. Adjust rate to drop serum glucose 50–100 mg/dL/h. Add dextrose to infusion fluid when serum glucose <300 mg />L. Change to SC insulin when no longer significantly acidotic and able to eat. Some clinicians prefer IM route, commonly initially using regular insulin at a dose of 0.1–0.2 U/kg/h. Replace potassium and phosphate losses: Verify adequate urine output. Add to fluids as K-acetate (or KCl if acetate not available) and K3PO4 in equal amounts. Large doses of K+ may be necessary; guide therapy by frequent monitoring of K+. Monitor serum sodium: Risk for cerebral edema if Na+ fails to rise as glucose falls. Bicarbonate therapy: Not recommended in most cases since generally it does not alter outcome and it increases risk for cerebral edema with its use. Use it with caution in patients with severe acidosis (pH <6.9) in whom peripheral vasodilation and decreased cardiac contractility may further impair tissue perfusion potentially life-threatening hyperkalemia. cerebral edema: treat edema as soon the condition is suspected due to its high mortality morbidity rates: 21–25% 10–26%, respectively. decrease fluid administration rate. mannitol (0.25–1 g />g over 20 min): No large studies to date demonstrate definitive beneficial or detrimental effects. Consider its use in patients with signs of cerebral edema before impeding respiratory failure. Dose can be repeated in 2 hr if there is no initial response. Endotracheal intubation and ventilation: Avoid aggressive hyperventilation since it has been associated with poor outcome in DKA-related cerebral edema (similar to that found in head trauma).
Medication
Insulin drip: Start regular insulin 0.1 U/kg/h IV (some clinicians prefer the IM dosing and route). Mannitol: 0.25–1 g/kg IV.
Follow-up disposition
Admission criteria For DKA: ICU: Altered mental status. Shock or cardiac dysrhythmia. Initial glucose >700 mg/dL. Initial pH <7. risk factors for cerebral edema (age <5 yr, prolonged symptoms, high bun). inpatient unit: stable new-onset diabetic patients requiring intensive education. with ketoacidosis not meeting requirements icu care. compliance concerns or other social issues. discharge criteria known who respond well to therapy normalization of glucose, ph, and ketosis. tolerating oral fluids. reliable parents. follow-up within 24 hr including appropriate issues referral critically ill. persistent abnormal mental status. poorly controlled diabetes.< />pan>
Follow-up recommendations
Close follow-up with the primary care physician is important even after the resolution of DKA to ensure appropriate management of the patient’s diabetes to prevent further occurrence of DKA. Many children with diabetes are followed at comprehensive diabetes centers in collaboration with primary care physician.
Pearls and pitfalls
Mortality from DKA is predominately related to the occurrence of cerebral edema. Therefore, early and appropriate treatment is of most importance in managing children with DKA. In children, avoid using an insulin bolus since it increase the risk of cerebral edema. Recently, some data suggest that starting insulin drip at 0.05 U/kg/h may reduce the risk for rapid fluid shifts and theoretically for cerebral edema.
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Emergency And Acute Medicine – Adult Diarrhea
Basics
Description Diarrhea is defined as frequent bowel movements (>3/day) that are loose and watery, most commonly due to infectious agents or toxin exposure.
Etiology
Viruses Account for 50–70% of cases.
Invasive bacteria
Campylobacter: Contaminated food or water, wilderness water, birds, animals; most common bacterial cause; gross or occult blood in 60–90%.
Salmonella: Contaminated water, eggs, poultry, dairy; Salmonella typhi causes typhoid fever with sustained fever, abdominal pain, rose spots, splenomegaly, and bradycardia.
Shigella: Fecal–oral transmission.
Vibrio parahaemolyticus: Raw or undercooked seafood.
Yersinia: Contaminated pork, water, milk; may mimic appendicitis or present as mesenteric adenitis.
Bacterial toxin–mediated
Escherichia coli: Major cause of traveler’s diarrhea; fecal contamination of food or water.
Staphylococcus aureus: Most common toxin-related illness; symptoms 1–6 hr after ingestion.
Bacillus cereus: Classically from reheated fried rice; symptoms within 1–36 hr.
Clostridium difficile: Antibiotic-associated enteritis and pseudomembranous colitis; onset within 10 days of antibiotic exposure.
Aeromonas hydrophila: Aquatic exposure; typically affects children <3 yr; fecal leukocytes absent.< />pan>
Cholera (Vibrio cholerae): Enterotoxin-mediated; profuse “rice-water” stools.
Protozoa
Giardia lamblia: Most common parasitic cause in North America; associated with travel, daycare, institutions, men who have sex with men, and untreated mountain water.
Cryptosporidium parvum: Common in patients with AIDS.
Entamoeba histolytica: May cause extraintestinal disease, including hepatic amebic abscess.
Pediatric considerations Most cases are viral and self-limited; rotavirus accounts for ~50%. Shigella may be associated with seizures. Assessment should focus on hydration status.
Diagnosis
Signs And Symptoms
History Loose or watery stools, bloody stools with mucus, abdominal cramps, tenesmus, flatulence, fever, headache, myalgias, nausea, vomiting, dehydration, lethargy, or stupor.
Physical exam Dry mucous membranes, abdominal tenderness, perianal inflammation, fissures, or fistulae.
Essential Workup Digital rectal exam for gross or occult blood. Fecal leukocytes suggest invasive bacterial infection and are absent in viral, protozoal, or toxin-mediated diarrhea.
Diagnosis Tests And Interpretation
Lab
CBC for significant blood loss or systemic toxicity.
Electrolytes, glucose, BUN, creatinine for lethargy, dehydration, toxicity, altered mental status, diuretic use, or chronic liver/renal disease.
Stool culture if fecal leukocytes present or in immunocompromised patients, travelers, men who have sex with men, food handlers, healthcare workers, daycare workers, or institutionalized patients.
Blood cultures if bacteremia suspected, patient requires admission, or is immunocompromised, elderly, or an infant.
Imaging Abdominal radiographs only if obstruction or toxic megacolon is suspected.
Differential Diagnosis Ulcerative colitis, Crohn disease, mesenteric ischemia, diverticulitis, anal fissures, hemorrhoids, irritable bowel syndrome, food allergies, malrotation with volvulus, Meckel diverticulum, intussusception, appendicitis, drugs and toxins (mannitol, sorbitol, magnesium antacids, quinidine, colchicine), mushrooms, mercury poisoning.
Treatment
Prehospital Establish IV access if severe dehydration; avoid exposure to contaminated body fluids.
Initial stabilization and therapy Assess airway, breathing, circulation. Begin IV 0.9% normal saline for severe dehydration.
Emergency department treatment and procedures
Oral rehydration for mild dehydration (oral rehydration solutions).
IV fluids for hypotension, persistent vomiting, obtundation, metabolic acidosis, or severe electrolyte abnormalities.
Bismuth subsalicylate for symptomatic relief.
Kaolin-pectin reduces stool liquidity but does not alter disease course.
Antimotility agents (loperamide, diphenoxylate) may be used cautiously in noninfectious diarrhea; avoid prolonged use in infectious diarrhea due to risk of toxic megacolon and bacteremia.
Targeted antibiotics for confirmed or strongly suspected bacterial or protozoal infections.
Medication
Ampicillin, TMP-SMX, ceftriaxone, ciprofloxacin, doxycycline, erythromycin, iodoquinol, metronidazole, quinacrine, tetracycline, or oral vancomycin as indicated by organism and patient factors.
Follow-Up Disposition
Admission criteria Hypotension refractory to fluids, significant bleeding, sepsis or toxicity, intractable vomiting or abdominal pain, severe electrolyte imbalance, metabolic acidosis, altered mental status, or children with >10–15% dehydration.
Discharge criteria Mild disease with adequate oral intake or dehydration responsive to IV fluids.
Issues for referral Prolonged or recurrent diarrhea may require gastroenterology evaluation.
Follow-Up Recommendations Most cases are self-limited; routine follow-up is optional unless symptoms persist.
Pearls And Pitfalls Avoid prolonged antimotility therapy in infectious diarrhea. TMP-SMX, ciprofloxacin, doxycycline, and tetracycline are contraindicated in pregnancy; metronidazole may be used in the third trimester. Healthcare workers and food handlers with infectious diarrhea may require public health clearance before returning to work. Clostridioides difficile infection is increasingly common, particularly in nursing home populations.
Basics
Description Diarrhea is defined as frequent bowel movements (>3/day) that are loose and watery, most commonly due to infectious agents or toxin exposure.
Etiology
Viruses Account for 50–70% of cases.
Invasive bacteria
Campylobacter: Contaminated food or water, wilderness water, birds, animals; most common bacterial cause; gross or occult blood in 60–90%.
Salmonella: Contaminated water, eggs, poultry, dairy; Salmonella typhi causes typhoid fever with sustained fever, abdominal pain, rose spots, splenomegaly, and bradycardia.
Shigella: Fecal–oral transmission.
Vibrio parahaemolyticus: Raw or undercooked seafood.
Yersinia: Contaminated pork, water, milk; may mimic appendicitis or present as mesenteric adenitis.
Bacterial toxin–mediated
Escherichia coli: Major cause of traveler’s diarrhea; fecal contamination of food or water.
Staphylococcus aureus: Most common toxin-related illness; symptoms 1–6 hr after ingestion.
Bacillus cereus: Classically from reheated fried rice; symptoms within 1–36 hr.
Clostridium difficile: Antibiotic-associated enteritis and pseudomembranous colitis; onset within 10 days of antibiotic exposure.
Aeromonas hydrophila: Aquatic exposure; typically affects children <3 yr; fecal leukocytes absent.< />pan>
Cholera (Vibrio cholerae): Enterotoxin-mediated; profuse “rice-water” stools.
Protozoa
Giardia lamblia: Most common parasitic cause in North America; associated with travel, daycare, institutions, men who have sex with men, and untreated mountain water.
Cryptosporidium parvum: Common in patients with AIDS.
Entamoeba histolytica: May cause extraintestinal disease, including hepatic amebic abscess.
Pediatric considerations Most cases are viral and self-limited; rotavirus accounts for ~50%. Shigella may be associated with seizures. Assessment should focus on hydration status.
Diagnosis
Signs And Symptoms
History Loose or watery stools, bloody stools with mucus, abdominal cramps, tenesmus, flatulence, fever, headache, myalgias, nausea, vomiting, dehydration, lethargy, or stupor.
Physical exam Dry mucous membranes, abdominal tenderness, perianal inflammation, fissures, or fistulae.
Essential Workup Digital rectal exam for gross or occult blood. Fecal leukocytes suggest invasive bacterial infection and are absent in viral, protozoal, or toxin-mediated diarrhea.
Diagnosis Tests And Interpretation
Lab
CBC for significant blood loss or systemic toxicity.
Electrolytes, glucose, BUN, creatinine for lethargy, dehydration, toxicity, altered mental status, diuretic use, or chronic liver/renal disease.
Stool culture if fecal leukocytes present or in immunocompromised patients, travelers, men who have sex with men, food handlers, healthcare workers, daycare workers, or institutionalized patients.
Blood cultures if bacteremia suspected, patient requires admission, or is immunocompromised, elderly, or an infant.
Imaging Abdominal radiographs only if obstruction or toxic megacolon is suspected.
Differential Diagnosis Ulcerative colitis, Crohn disease, mesenteric ischemia, diverticulitis, anal fissures, hemorrhoids, irritable bowel syndrome, food allergies, malrotation with volvulus, Meckel diverticulum, intussusception, appendicitis, drugs and toxins (mannitol, sorbitol, magnesium antacids, quinidine, colchicine), mushrooms, mercury poisoning.
Treatment
Prehospital Establish IV access if severe dehydration; avoid exposure to contaminated body fluids.
Initial stabilization and therapy Assess airway, breathing, circulation. Begin IV 0.9% normal saline for severe dehydration.
Emergency department treatment and procedures
Oral rehydration for mild dehydration (oral rehydration solutions).
IV fluids for hypotension, persistent vomiting, obtundation, metabolic acidosis, or severe electrolyte abnormalities.
Bismuth subsalicylate for symptomatic relief.
Kaolin-pectin reduces stool liquidity but does not alter disease course.
Antimotility agents (loperamide, diphenoxylate) may be used cautiously in noninfectious diarrhea; avoid prolonged use in infectious diarrhea due to risk of toxic megacolon and bacteremia.
Targeted antibiotics for confirmed or strongly suspected bacterial or protozoal infections.
Medication
Ampicillin, TMP-SMX, ceftriaxone, ciprofloxacin, doxycycline, erythromycin, iodoquinol, metronidazole, quinacrine, tetracycline, or oral vancomycin as indicated by organism and patient factors.
Follow-Up Disposition
Admission criteria Hypotension refractory to fluids, significant bleeding, sepsis or toxicity, intractable vomiting or abdominal pain, severe electrolyte imbalance, metabolic acidosis, altered mental status, or children with >10–15% dehydration.
Discharge criteria Mild disease with adequate oral intake or dehydration responsive to IV fluids.
Issues for referral Prolonged or recurrent diarrhea may require gastroenterology evaluation.
Follow-Up Recommendations Most cases are self-limited; routine follow-up is optional unless symptoms persist.
Pearls And Pitfalls Avoid prolonged antimotility therapy in infectious diarrhea. TMP-SMX, ciprofloxacin, doxycycline, and tetracycline are contraindicated in pregnancy; metronidazole may be used in the third trimester. Healthcare workers and food handlers with infectious diarrhea may require public health clearance before returning to work. Clostridioides difficile infection is increasingly common, particularly in nursing home populations.
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Emergency And Acute Medicine – Diarrhea, Pediatric
Rajender Gattu • Richard Lichenstein
Basics
Description Pediatric diarrhea is one of the most common emergency department complaints, second only to respiratory infections. It is a leading cause of childhood illness and mortality worldwide. Acute infectious enteritis presents with vomiting and diarrhea, most often in children under 5 years of age, who typically experience about two episodes annually. Diarrhea is defined as an acute change in normal bowel habits with increased stool frequency or volume lasting less than 7 days; three or more loose or watery stools per day meet the World Health Organization definition. Diarrhea persisting longer than 2 weeks is considered chronic.
Etiology
Acute enteritis
Infectious causes predominate. Viruses account for 70–80% of cases, most commonly rotavirus, followed by enteric adenovirus and norovirus, particularly in foodborne outbreaks. Bacterial causes account for 10–20% and include Escherichia coli, Salmonella, Shigella, Campylobacter, Yersinia, Vibrio, Clostridioides difficile, and Aeromonas. Parasitic causes represent about 5% and include Giardia lamblia and Cryptosporidium, often waterborne.
Noninfectious causes include postinfectious diarrhea, food allergy or intolerance (cow’s milk protein, soy protein, lactose intolerance), methylxanthines, chemotherapy- or radiation-induced injury, drug-induced diarrhea from antibiotics, laxatives, or antacids, ingestion of heavy metals or toxic plants, vitamin deficiencies (niacin, folate), vitamin excess (vitamin C), and diarrhea associated with other infections such as otitis media, urinary tract infection, pneumonia, meningitis, or appendicitis.
Chronic diarrhea
Dietary excess of sorbitol or fructose, enteric infections in immunocompromised hosts, malnutrition, endocrine disorders such as thyrotoxicosis or pheochromocytoma, inflammatory bowel disease, malabsorption syndromes including cystic fibrosis and celiac disease, and irritable bowel syndrome.
Diagnosis
Signs And Symptoms Frequent loose stools that may be watery, bloody, or mucoid, with possible abdominal pain, fever, anorexia, and tenesmus. Dehydration severity reflects total body water loss and is classified as mild (<5%), moderate (5-10%), or severe (>15%). Severe dehydration is associated with altered mental status, poor muscle tone, dry mucous membranes, decreased skin turgor, depressed fontanelle, hypotension, tachycardia, prolonged capillary refill, decreased urine output, sunken eyes, absent tears, and intense thirst.
History Focus on onset, duration, stool characteristics, urine output, feeding, recent antibiotic use, travel, possible ingestions, immunodeficiency, and underlying intestinal disease.
Physical exam Key findings include abnormal respiratory pattern, decreased skin turgor, and prolonged capillary refill, which together are the most reliable indicators of dehydration.
Essential Workup Most children with acute diarrhea require no laboratory testing. Evaluation is indicated for high fever, systemic illness, bloody diarrhea, symptoms lasting more than 2 weeks, tenesmus, or dehydration beyond mild severity requiring parenteral therapy.
Diagnosis Tests And Interpretation
Lab CBC, blood culture, urinalysis, and urine culture if systemic infection is suspected. Serum electrolytes, BUN, creatinine, and bicarbonate are useful in children requiring IV fluids; low bicarbonate is a sensitive marker of moderate dehydration. Stool pH <5.5 or positive reducing substances suggest lactose intolerance. stool microscopy showing>5 fecal leukocytes per high-power field suggests invasive bacterial infection. Stool cultures are reserved for cases with bloody stools or high likelihood of bacterial pathogens.
Imaging Generally not indicated; abdominal radiography or ultrasound may be useful if intussusception, appendicitis, or ileus is suspected.
Differential Diagnosis Postinfectious diarrhea, milk allergy, malrotation with volvulus, inflammatory bowel disease, intussusception, malabsorption syndromes, extraintestinal infections, and medication-induced diarrhea.
Treatment
Initial stabilization and therapy Severely dehydrated children in shock require IV or intraosseous access with 20 mL/kg of 0.9% normal saline; administer dextrose if hypoglycemic. Pulse oximetry and airway support are used as needed.
Emergency department treatment and procedures Mild to moderate dehydration is treated with oral rehydration therapy at 50–100 mL/kg over 4 hours, with additional 10 mL/kg for each stool. Oral rehydration solutions should be low osmolarity with appropriate glucose and sodium content. Moderate to severe dehydration requires IV fluids to replace maintenance and deficit needs. Antibiotics are reserved for defined invasive or severe infections or high-risk patients. Antidiarrheal agents are not recommended. Probiotics such as Lactobacillus GG may reduce duration of illness. Age-appropriate feeding should continue during rehydration, emphasizing complex carbohydrates, lean proteins, fruits, vegetables, yogurt, and avoidance of fatty or high-sugar foods.
Medication Antibiotic selection depends on identified pathogens and includes agents such as TMP-SMX, erythromycin, metronidazole, vancomycin, ceftriaxone, or doxycycline when indicated. Zinc supplementation is recommended for young children.
Follow-Up Disposition
Admission criteria Surgical abdomen, inability to tolerate oral fluids, dehydration ≥10%, toxic appearance, or suspected complicated bacterial enteritis.
Discharge criteria Clinical improvement, adequate hydration, and caregivers capable of providing oral rehydration and recognizing dehydration signs.
Issues for referral Immunocompromised children, seizure-associated illness, or underlying bowel disease.
Follow-Up Recommendations Uncomplicated diarrhea usually requires no routine follow-up. Neonates and high-risk children require close outpatient reassessment.
Pearls And Pitfalls History and physical examination are key to distinguishing benign diarrhea from serious disease. Most children do not need extensive laboratory testing. Antibiotics and antidiarrheal agents have limited roles. Always consider alternative diagnoses such as appendicitis, intussusception, urinary tract infection, and sepsis.
Rajender Gattu • Richard Lichenstein
Basics
Description Pediatric diarrhea is one of the most common emergency department complaints, second only to respiratory infections. It is a leading cause of childhood illness and mortality worldwide. Acute infectious enteritis presents with vomiting and diarrhea, most often in children under 5 years of age, who typically experience about two episodes annually. Diarrhea is defined as an acute change in normal bowel habits with increased stool frequency or volume lasting less than 7 days; three or more loose or watery stools per day meet the World Health Organization definition. Diarrhea persisting longer than 2 weeks is considered chronic.
Etiology
Acute enteritis
Infectious causes predominate. Viruses account for 70–80% of cases, most commonly rotavirus, followed by enteric adenovirus and norovirus, particularly in foodborne outbreaks. Bacterial causes account for 10–20% and include Escherichia coli, Salmonella, Shigella, Campylobacter, Yersinia, Vibrio, Clostridioides difficile, and Aeromonas. Parasitic causes represent about 5% and include Giardia lamblia and Cryptosporidium, often waterborne.
Noninfectious causes include postinfectious diarrhea, food allergy or intolerance (cow’s milk protein, soy protein, lactose intolerance), methylxanthines, chemotherapy- or radiation-induced injury, drug-induced diarrhea from antibiotics, laxatives, or antacids, ingestion of heavy metals or toxic plants, vitamin deficiencies (niacin, folate), vitamin excess (vitamin C), and diarrhea associated with other infections such as otitis media, urinary tract infection, pneumonia, meningitis, or appendicitis.
Chronic diarrhea
Dietary excess of sorbitol or fructose, enteric infections in immunocompromised hosts, malnutrition, endocrine disorders such as thyrotoxicosis or pheochromocytoma, inflammatory bowel disease, malabsorption syndromes including cystic fibrosis and celiac disease, and irritable bowel syndrome.
Diagnosis
Signs And Symptoms Frequent loose stools that may be watery, bloody, or mucoid, with possible abdominal pain, fever, anorexia, and tenesmus. Dehydration severity reflects total body water loss and is classified as mild (<5%), moderate (5-10%), or severe (>15%). Severe dehydration is associated with altered mental status, poor muscle tone, dry mucous membranes, decreased skin turgor, depressed fontanelle, hypotension, tachycardia, prolonged capillary refill, decreased urine output, sunken eyes, absent tears, and intense thirst.
History Focus on onset, duration, stool characteristics, urine output, feeding, recent antibiotic use, travel, possible ingestions, immunodeficiency, and underlying intestinal disease.
Physical exam Key findings include abnormal respiratory pattern, decreased skin turgor, and prolonged capillary refill, which together are the most reliable indicators of dehydration.
Essential Workup Most children with acute diarrhea require no laboratory testing. Evaluation is indicated for high fever, systemic illness, bloody diarrhea, symptoms lasting more than 2 weeks, tenesmus, or dehydration beyond mild severity requiring parenteral therapy.
Diagnosis Tests And Interpretation
Lab CBC, blood culture, urinalysis, and urine culture if systemic infection is suspected. Serum electrolytes, BUN, creatinine, and bicarbonate are useful in children requiring IV fluids; low bicarbonate is a sensitive marker of moderate dehydration. Stool pH <5.5 or positive reducing substances suggest lactose intolerance. stool microscopy showing>5 fecal leukocytes per high-power field suggests invasive bacterial infection. Stool cultures are reserved for cases with bloody stools or high likelihood of bacterial pathogens.
Imaging Generally not indicated; abdominal radiography or ultrasound may be useful if intussusception, appendicitis, or ileus is suspected.
Differential Diagnosis Postinfectious diarrhea, milk allergy, malrotation with volvulus, inflammatory bowel disease, intussusception, malabsorption syndromes, extraintestinal infections, and medication-induced diarrhea.
Treatment
Initial stabilization and therapy Severely dehydrated children in shock require IV or intraosseous access with 20 mL/kg of 0.9% normal saline; administer dextrose if hypoglycemic. Pulse oximetry and airway support are used as needed.
Emergency department treatment and procedures Mild to moderate dehydration is treated with oral rehydration therapy at 50–100 mL/kg over 4 hours, with additional 10 mL/kg for each stool. Oral rehydration solutions should be low osmolarity with appropriate glucose and sodium content. Moderate to severe dehydration requires IV fluids to replace maintenance and deficit needs. Antibiotics are reserved for defined invasive or severe infections or high-risk patients. Antidiarrheal agents are not recommended. Probiotics such as Lactobacillus GG may reduce duration of illness. Age-appropriate feeding should continue during rehydration, emphasizing complex carbohydrates, lean proteins, fruits, vegetables, yogurt, and avoidance of fatty or high-sugar foods.
Medication Antibiotic selection depends on identified pathogens and includes agents such as TMP-SMX, erythromycin, metronidazole, vancomycin, ceftriaxone, or doxycycline when indicated. Zinc supplementation is recommended for young children.
Follow-Up Disposition
Admission criteria Surgical abdomen, inability to tolerate oral fluids, dehydration ≥10%, toxic appearance, or suspected complicated bacterial enteritis.
Discharge criteria Clinical improvement, adequate hydration, and caregivers capable of providing oral rehydration and recognizing dehydration signs.
Issues for referral Immunocompromised children, seizure-associated illness, or underlying bowel disease.
Follow-Up Recommendations Uncomplicated diarrhea usually requires no routine follow-up. Neonates and high-risk children require close outpatient reassessment.
Pearls And Pitfalls History and physical examination are key to distinguishing benign diarrhea from serious disease. Most children do not need extensive laboratory testing. Antibiotics and antidiarrheal agents have limited roles. Always consider alternative diagnoses such as appendicitis, intussusception, urinary tract infection, and sepsis.
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Emergency And Acute Medicine – Congestive Heart Failure
Description
Congestive heart failure is a clinical syndrome in which the heart is unable to maintain adequate circulation to meet metabolic demands. It is characterized by chronic debility, episodes of acute decompensation, and high mortality. Acute decompensated heart failure is a rapidly progressive state developing over hours to days and is a common reason for emergency department presentation, often triggered by a precipitating event that exceeds the heart’s compensatory reserve. Chronic heart failure is a progressive condition evolving over months to years, marked by cardiac remodeling and neurohormonal activation. Subtypes include systolic heart failure with impaired contractility and reduced ejection fraction, diastolic heart failure with impaired ventricular relaxation and filling, low-output failure, high-output failure in which cardiac output is normal or increased but insufficient for metabolic needs, left-sided failure with pulmonary congestion, and right-sided failure characterized by hepatic enlargement, jugular venous distention, and dependent edema. Congestive heart failure affects approximately 5.8 million Americans and represents a major cause of hospitalization and healthcare expenditure.
Etiology
Heart failure results from underlying cardiac disease and acute precipitants. Causes include reduced myocardial contractility from ischemia or infarction, cardiomyopathies, myocarditis, and dysrhythmias; reduced contractile efficiency from medications or metabolic disorders; pressure overload from hypertension, valvular disease, congenital heart disease, pulmonary embolism, or pulmonary hypertension; restricted cardiac output due to infiltrative myocardial disease; volume overload from dietary sodium excess, transfusions, intravenous fluids, or sodium-retaining medications; and high-demand states such as hyperthyroidism, pregnancy, anemia, arteriovenous fistula, beriberi, and Paget disease. Pediatric causes vary by age and include congenital shunt lesions in infancy and acquired myocardial dysfunction in older children and adolescents.
Clinical Features
Symptoms reflect poor perfusion and congestion. Poor perfusion manifests as fatigue, somnolence, lightheadedness, palpitations, cool extremities, worsening renal function, and dyspnea. Congestion presents with exertional dyspnea, cough, orthopnea, paroxysmal nocturnal dyspnea, decreased exercise tolerance, elevated jugular venous pressure, dependent edema, rales or wheezing, pleural effusions, third or fourth heart sounds, displaced apical impulse, hepatic enlargement, nausea, and ascites. Acute decompensated heart failure with hemodynamic instability may cause confusion, anxiety, syncope, tachypnea, tachycardia, hypotension, cool or cyanotic extremities, narrow pulse pressure, pulsus alternans, and Cheyne–Stokes respirations.
Essential Diagnostic Evaluation
Chest radiography is central to confirming the diagnosis and assessing severity, although radiographic changes may lag behind symptom onset and persist after clinical improvement. Continuous reassessment is required.
Diagnostic Tests And Interpretation
Laboratory studies include electrolytes and renal function to establish baseline and guide therapy, complete blood count to assess anemia or infection, liver function tests for hepatic congestion or ischemia, thyroid function tests in older patients or those with atrial fibrillation, and cardiac enzymes to evaluate ischemia. B-type natriuretic peptide is useful for differentiating cardiac from pulmonary causes of dyspnea, with high values supporting heart failure and low values making it unlikely, though interpretation must consider age, obesity, and comorbidities. NT-proBNP may also aid diagnosis. Imaging with chest radiography may reveal cardiomegaly, vascular redistribution, interstitial or alveolar edema, pleural effusions, and classic perihilar patterns. Electrocardiography evaluates ischemia, dysrhythmias, hypertrophy, and conduction abnormalities. Echocardiography provides assessment of ejection fraction, ventricular size, valvular pathology, regional wall motion abnormalities, and pericardial disease.
Differential Diagnosis
Left-sided heart failure must be distinguished from acute exacerbations of chronic obstructive pulmonary disease, asthma, pneumonia, acute respiratory distress syndrome, constrictive pericarditis, anemia, malnutrition, pericardial tamponade, and coarctation of the aorta. Right-sided failure may mimic nephrotic syndrome, chronic renal failure, cirrhosis, pulmonary embolism, sleep-disordered breathing, or venous stasis.
Initial Stabilization And Therapy
Management begins with airway assessment, supplemental oxygen, intravenous access, cardiac monitoring, and electrocardiography. Elevating the head of the bed reduces venous return. Noninvasive positive pressure ventilation is often beneficial to reduce work of breathing and improve oxygenation, while intubation is reserved for impending respiratory failure.
Emergency Department Management
Treatment focuses on optimizing oxygenation, ventilation, and hemodynamics while addressing the underlying cause. In patients with congestion and adequate perfusion, preload reduction with nitrates and cautious diuretic therapy is appropriate, particularly in acute pulmonary edema. Afterload reduction must be used carefully and avoided in hypotension, acute renal failure, or hyperkalemia. In patients with poor perfusion and hypotension, inotropic support with agents such as dobutamine, dopamine, or milrinone is indicated, with diuretics added after stabilization. Vasodilators should be avoided in shock states. Venous thromboembolism prophylaxis should be considered when appropriate. Pediatric management varies by age and may require prostaglandin infusion in ductal-dependent lesions.
Medications
Common agents include loop diuretics, nitrates, inotropes, vasodilators, angiotensin-converting enzyme inhibitors when appropriate, and adjunctive therapies based on etiology. Medication selection and dosing should be individualized based on hemodynamic status and comorbidities.
Disposition And Follow-Up
Admission to the intensive care unit is required for pulmonary edema, cardiogenic shock, or concomitant ischemia. Medical ward admission is indicated for new-onset heart failure or symptoms refractory to emergency treatment. Discharge may be considered in mild exacerbations that respond well to therapy, provided close follow-up is arranged.
Follow-Up Recommendations
Patients require close outpatient follow-up within one week, education on medication adherence and dietary sodium restriction, monitoring of body weight, and regular assessment of renal function and electrolytes.
Clinical Pearls And Pitfalls
B-type natriuretic peptide is helpful when the diagnosis is uncertain but should not be used in isolation. Early use of noninvasive ventilation can prevent respiratory deterioration. Identifying and treating the precipitating cause of decompensation, such as ischemia, arrhythmia, pulmonary embolism, or valvular disease, is essential to successful management.
Description
Congestive heart failure is a clinical syndrome in which the heart is unable to maintain adequate circulation to meet metabolic demands. It is characterized by chronic debility, episodes of acute decompensation, and high mortality. Acute decompensated heart failure is a rapidly progressive state developing over hours to days and is a common reason for emergency department presentation, often triggered by a precipitating event that exceeds the heart’s compensatory reserve. Chronic heart failure is a progressive condition evolving over months to years, marked by cardiac remodeling and neurohormonal activation. Subtypes include systolic heart failure with impaired contractility and reduced ejection fraction, diastolic heart failure with impaired ventricular relaxation and filling, low-output failure, high-output failure in which cardiac output is normal or increased but insufficient for metabolic needs, left-sided failure with pulmonary congestion, and right-sided failure characterized by hepatic enlargement, jugular venous distention, and dependent edema. Congestive heart failure affects approximately 5.8 million Americans and represents a major cause of hospitalization and healthcare expenditure.
Etiology
Heart failure results from underlying cardiac disease and acute precipitants. Causes include reduced myocardial contractility from ischemia or infarction, cardiomyopathies, myocarditis, and dysrhythmias; reduced contractile efficiency from medications or metabolic disorders; pressure overload from hypertension, valvular disease, congenital heart disease, pulmonary embolism, or pulmonary hypertension; restricted cardiac output due to infiltrative myocardial disease; volume overload from dietary sodium excess, transfusions, intravenous fluids, or sodium-retaining medications; and high-demand states such as hyperthyroidism, pregnancy, anemia, arteriovenous fistula, beriberi, and Paget disease. Pediatric causes vary by age and include congenital shunt lesions in infancy and acquired myocardial dysfunction in older children and adolescents.
Clinical Features
Symptoms reflect poor perfusion and congestion. Poor perfusion manifests as fatigue, somnolence, lightheadedness, palpitations, cool extremities, worsening renal function, and dyspnea. Congestion presents with exertional dyspnea, cough, orthopnea, paroxysmal nocturnal dyspnea, decreased exercise tolerance, elevated jugular venous pressure, dependent edema, rales or wheezing, pleural effusions, third or fourth heart sounds, displaced apical impulse, hepatic enlargement, nausea, and ascites. Acute decompensated heart failure with hemodynamic instability may cause confusion, anxiety, syncope, tachypnea, tachycardia, hypotension, cool or cyanotic extremities, narrow pulse pressure, pulsus alternans, and Cheyne–Stokes respirations.
Essential Diagnostic Evaluation
Chest radiography is central to confirming the diagnosis and assessing severity, although radiographic changes may lag behind symptom onset and persist after clinical improvement. Continuous reassessment is required.
Diagnostic Tests And Interpretation
Laboratory studies include electrolytes and renal function to establish baseline and guide therapy, complete blood count to assess anemia or infection, liver function tests for hepatic congestion or ischemia, thyroid function tests in older patients or those with atrial fibrillation, and cardiac enzymes to evaluate ischemia. B-type natriuretic peptide is useful for differentiating cardiac from pulmonary causes of dyspnea, with high values supporting heart failure and low values making it unlikely, though interpretation must consider age, obesity, and comorbidities. NT-proBNP may also aid diagnosis. Imaging with chest radiography may reveal cardiomegaly, vascular redistribution, interstitial or alveolar edema, pleural effusions, and classic perihilar patterns. Electrocardiography evaluates ischemia, dysrhythmias, hypertrophy, and conduction abnormalities. Echocardiography provides assessment of ejection fraction, ventricular size, valvular pathology, regional wall motion abnormalities, and pericardial disease.
Differential Diagnosis
Left-sided heart failure must be distinguished from acute exacerbations of chronic obstructive pulmonary disease, asthma, pneumonia, acute respiratory distress syndrome, constrictive pericarditis, anemia, malnutrition, pericardial tamponade, and coarctation of the aorta. Right-sided failure may mimic nephrotic syndrome, chronic renal failure, cirrhosis, pulmonary embolism, sleep-disordered breathing, or venous stasis.
Initial Stabilization And Therapy
Management begins with airway assessment, supplemental oxygen, intravenous access, cardiac monitoring, and electrocardiography. Elevating the head of the bed reduces venous return. Noninvasive positive pressure ventilation is often beneficial to reduce work of breathing and improve oxygenation, while intubation is reserved for impending respiratory failure.
Emergency Department Management
Treatment focuses on optimizing oxygenation, ventilation, and hemodynamics while addressing the underlying cause. In patients with congestion and adequate perfusion, preload reduction with nitrates and cautious diuretic therapy is appropriate, particularly in acute pulmonary edema. Afterload reduction must be used carefully and avoided in hypotension, acute renal failure, or hyperkalemia. In patients with poor perfusion and hypotension, inotropic support with agents such as dobutamine, dopamine, or milrinone is indicated, with diuretics added after stabilization. Vasodilators should be avoided in shock states. Venous thromboembolism prophylaxis should be considered when appropriate. Pediatric management varies by age and may require prostaglandin infusion in ductal-dependent lesions.
Medications
Common agents include loop diuretics, nitrates, inotropes, vasodilators, angiotensin-converting enzyme inhibitors when appropriate, and adjunctive therapies based on etiology. Medication selection and dosing should be individualized based on hemodynamic status and comorbidities.
Disposition And Follow-Up
Admission to the intensive care unit is required for pulmonary edema, cardiogenic shock, or concomitant ischemia. Medical ward admission is indicated for new-onset heart failure or symptoms refractory to emergency treatment. Discharge may be considered in mild exacerbations that respond well to therapy, provided close follow-up is arranged.
Follow-Up Recommendations
Patients require close outpatient follow-up within one week, education on medication adherence and dietary sodium restriction, monitoring of body weight, and regular assessment of renal function and electrolytes.
Clinical Pearls And Pitfalls
B-type natriuretic peptide is helpful when the diagnosis is uncertain but should not be used in isolation. Early use of noninvasive ventilation can prevent respiratory deterioration. Identifying and treating the precipitating cause of decompensation, such as ischemia, arrhythmia, pulmonary embolism, or valvular disease, is essential to successful management.
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Emergency And Acute Medicine – Clavicle Fracture
Description And Classification
Clavicle fractures account for approximately 5% of all fractures across all age groups. The majority involve the middle third of the clavicle (about 80%), followed by distal-third fractures (15%) and medial-third fractures (5%). Fractures are classified anatomically into middle-third fractures (Group I), distal-third fractures (Group II), and medial-third fractures (Group III). Distal-third fractures are further subdivided based on ligament involvement: type I fractures have intact coracoclavicular ligaments and are nondisplaced, type II fractures involve disruption of the coracoclavicular ligaments, and type III fractures extend into the acromioclavicular joint.
Etiology And Risk Factors
Clavicle fractures most commonly result from direct trauma to the clavicle, a fall onto the lateral shoulder, or a fall onto an outstretched hand. In children, clavicle fracture is the most common pediatric fracture and may also occur in newborns as a result of birth trauma. In older adults, these injuries may significantly impair activities of daily living, making assessment of social support and home safety essential. In pregnant patients, clavicle fractures are caused by trauma, and evaluation must include assessment for associated injuries and fetal monitoring, as even minor trauma can affect fetal well-being.
Clinical Presentation
Patients typically present with localized pain, tenderness, and swelling over the clavicle. Crepitus is common because of the subcutaneous position of the bone. The affected arm is often held adducted against the chest wall with limited range of motion, and the shoulder may appear displaced anteriorly and inferiorly. Physical examination should include careful palpation of the clavicle and assessment of the shoulder and humerus for associated fractures, dislocations, or subluxations. It is essential to determine whether the fracture is open or closed and to evaluate for associated injuries, including cervical spine trauma, first-rib fractures with possible aortic injury, and sternoclavicular or acromioclavicular joint injuries.
Diagnostic Evaluation
Imaging is essential for diagnosis and assessment of associated injuries. Anteroposterior radiographs of both clavicles are mandatory and should include views of the upper humerus, shoulder girdle, and upper lung fields to exclude pneumothorax. Oblique and apical lordotic views may help visualize medial or distal fractures not clearly seen on standard views. Stress views are no longer routinely recommended for distal clavicle fractures. Angiography should be obtained if there is any concern for vascular injury, particularly involving the subclavian vessels.
Differential Diagnosis
Distal clavicle fractures should be differentiated from acromioclavicular joint separations, while medial fractures may mimic sternoclavicular joint injuries. Shoulder fracture–dislocations should also be considered.
Initial And Emergency Management
Prehospital care includes application of ice, pain control with nonsteroidal anti-inflammatory drugs or narcotics, and immobilization of the affected arm in a sling. Initial emergency department management focuses on airway stabilization and resuscitation as needed. Open clavicle fractures are uncommon but require immediate orthopedic consultation for surgical debridement and internal fixation. Closed fractures are managed based on fracture location and displacement. Nondisplaced middle-third fractures are typically treated with a sling or shoulder immobilizer. Although closed reduction may be attempted for displaced fractures, alignment is often difficult to maintain regardless of splinting technique. Distal-third fractures generally require immobilization, analgesia, and orthopedic follow-up, with type II and III fractures more likely to need operative repair. Medial-third fractures are treated with sling immobilization, pain control, and close orthopedic follow-up. Neurovascular status must be reassessed after immobilization.
Medication And Pain Control
Pain management may include acetaminophen or ibuprofen, with opioid analgesics reserved for adults with severe pain. Care must be taken to avoid excessive acetaminophen dosing, and opioid-containing medications should generally be avoided in pediatric patients.
Disposition And Follow-Up
Admission is indicated for open fractures or when associated life-threatening injuries are present. Patients with isolated, closed clavicle fractures may be discharged if pain is controlled, adequate home support is available, and orthopedic follow-up is arranged. Immediate orthopedic referral is required for open fractures, complex injuries, or any signs of neurovascular compromise.
Clinical Pearls And Pitfalls
Always maintain a high index of suspicion for associated life-threatening injuries, including cervical spine, aortic, and cardiopulmonary trauma. A careful neurologic and vascular examination is essential in all patients with clavicle fractures, as these associated injuries may be subtle on initial presentation.
Description And Classification
Clavicle fractures account for approximately 5% of all fractures across all age groups. The majority involve the middle third of the clavicle (about 80%), followed by distal-third fractures (15%) and medial-third fractures (5%). Fractures are classified anatomically into middle-third fractures (Group I), distal-third fractures (Group II), and medial-third fractures (Group III). Distal-third fractures are further subdivided based on ligament involvement: type I fractures have intact coracoclavicular ligaments and are nondisplaced, type II fractures involve disruption of the coracoclavicular ligaments, and type III fractures extend into the acromioclavicular joint.
Etiology And Risk Factors
Clavicle fractures most commonly result from direct trauma to the clavicle, a fall onto the lateral shoulder, or a fall onto an outstretched hand. In children, clavicle fracture is the most common pediatric fracture and may also occur in newborns as a result of birth trauma. In older adults, these injuries may significantly impair activities of daily living, making assessment of social support and home safety essential. In pregnant patients, clavicle fractures are caused by trauma, and evaluation must include assessment for associated injuries and fetal monitoring, as even minor trauma can affect fetal well-being.
Clinical Presentation
Patients typically present with localized pain, tenderness, and swelling over the clavicle. Crepitus is common because of the subcutaneous position of the bone. The affected arm is often held adducted against the chest wall with limited range of motion, and the shoulder may appear displaced anteriorly and inferiorly. Physical examination should include careful palpation of the clavicle and assessment of the shoulder and humerus for associated fractures, dislocations, or subluxations. It is essential to determine whether the fracture is open or closed and to evaluate for associated injuries, including cervical spine trauma, first-rib fractures with possible aortic injury, and sternoclavicular or acromioclavicular joint injuries.
Diagnostic Evaluation
Imaging is essential for diagnosis and assessment of associated injuries. Anteroposterior radiographs of both clavicles are mandatory and should include views of the upper humerus, shoulder girdle, and upper lung fields to exclude pneumothorax. Oblique and apical lordotic views may help visualize medial or distal fractures not clearly seen on standard views. Stress views are no longer routinely recommended for distal clavicle fractures. Angiography should be obtained if there is any concern for vascular injury, particularly involving the subclavian vessels.
Differential Diagnosis
Distal clavicle fractures should be differentiated from acromioclavicular joint separations, while medial fractures may mimic sternoclavicular joint injuries. Shoulder fracture–dislocations should also be considered.
Initial And Emergency Management
Prehospital care includes application of ice, pain control with nonsteroidal anti-inflammatory drugs or narcotics, and immobilization of the affected arm in a sling. Initial emergency department management focuses on airway stabilization and resuscitation as needed. Open clavicle fractures are uncommon but require immediate orthopedic consultation for surgical debridement and internal fixation. Closed fractures are managed based on fracture location and displacement. Nondisplaced middle-third fractures are typically treated with a sling or shoulder immobilizer. Although closed reduction may be attempted for displaced fractures, alignment is often difficult to maintain regardless of splinting technique. Distal-third fractures generally require immobilization, analgesia, and orthopedic follow-up, with type II and III fractures more likely to need operative repair. Medial-third fractures are treated with sling immobilization, pain control, and close orthopedic follow-up. Neurovascular status must be reassessed after immobilization.
Medication And Pain Control
Pain management may include acetaminophen or ibuprofen, with opioid analgesics reserved for adults with severe pain. Care must be taken to avoid excessive acetaminophen dosing, and opioid-containing medications should generally be avoided in pediatric patients.
Disposition And Follow-Up
Admission is indicated for open fractures or when associated life-threatening injuries are present. Patients with isolated, closed clavicle fractures may be discharged if pain is controlled, adequate home support is available, and orthopedic follow-up is arranged. Immediate orthopedic referral is required for open fractures, complex injuries, or any signs of neurovascular compromise.
Clinical Pearls And Pitfalls
Always maintain a high index of suspicion for associated life-threatening injuries, including cervical spine, aortic, and cardiopulmonary trauma. A careful neurologic and vascular examination is essential in all patients with clavicle fractures, as these associated injuries may be subtle on initial presentation.
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Emergency And Acute Medicine – Delirium
Basics And Description
Delirium is an acute clinical syndrome marked by sudden changes in awareness, cognition, and perception, with a fluctuating, waxing-and-waning course. It is not a primary disease but a manifestation of an underlying medical condition. The exact pathophysiology is unknown, though it is thought to involve diffuse cerebral dysfunction and disturbances in neurotransmitters, particularly decreased cerebral acetylcholine and altered dopamine, γ-aminobutyric acid (GABA), and serotonin activity. Delirium is frequently overlooked in the emergency department because patients often present with atypical or vague complaints. It is associated with increased inpatient mortality and longer hospital stays.
Etiology
Neurologic causes include meningitis, encephalitis, seizures, Wernicke encephalopathy, hypoxia or hypoperfusion of the brain, and intracranial hemorrhage or mass lesions. Pulmonary causes include pneumonia and other conditions leading to hypoxia. Cardiovascular etiologies include hypertensive crisis, acute coronary syndromes, and arrhythmias. Gastrointestinal causes include hepatic encephalopathy and dehydration. Renal causes include urinary tract infection and acute renal failure. Endocrine disorders include hypoglycemia, hyperglycemia, and hypothyroidism. Rheumatologic causes include collagen vascular diseases. Toxicologic causes include environmental toxins, medications, and withdrawal from alcohol or barbiturates. Other causes include electrolyte abnormalities, vitamin deficiencies, hypothermia, hyperthermia, and trauma.
Geriatric Considerations
Delirium is common in older emergency department patients, with up to 10% affected. Presentations are often subtle, with complaints such as falls, dizziness, or a general sense of not feeling well. Symptoms frequently fluctuate, and the underlying cause may be a life-threatening condition.
Diagnosis – Signs And Symptoms
Disturbances of consciousness may be hyperactive, hypoactive, or mixed. Hyperactive delirium presents with agitation and combativeness, while hypoactive delirium presents with lethargy, stupor, or coma. Mixed states may rapidly alternate between the two. Cognitive changes include disorientation, impaired memory, disorganized thinking and speech, reduced environmental awareness, misperceptions, illusions, delusions, and hallucinations. Inattention is a key feature, with difficulty focusing, sustaining, or shifting attention. Patients may also demonstrate restlessness, distractibility, and emotional lability.
History
Collateral history from caregivers is essential. Key elements include the time course, typically hours to days, and a fluctuating pattern. A thorough medication history is critical, including prescribed, over-the-counter, and illicit substances, recent medication changes, and withdrawals. Associated symptoms and pre-existing medical conditions may point toward the underlying etiology.
Physical Examination
Vital signs should be carefully assessed. A complete neurologic examination is essential, with attention to mental status, orientation, focal deficits, and hallucinations. A psychiatric assessment and cardiovascular, pulmonary, and gastrointestinal examinations should be performed to identify potential sources of infection, sepsis, or other systemic illness.
Screening Tools
Several tools can aid in identifying delirium. The Confusion Assessment Method includes four features: acute onset or fluctuating course, inattention, disorganized thinking, and altered level of consciousness. Delirium is diagnosed when features one and two are present along with either three or four. The Mini-Mental State Examination may be used serially, though patient cooperation can limit its utility in the emergency setting.
Essential Workup
Recognizing delirium as a syndrome is critical. The diagnostic approach should be broad and guided by history, physical examination, and clinical suspicion to identify the underlying organic cause.
Diagnosis Tests And Interpretation
Initial laboratory testing should include electrolytes, calcium, renal function, hepatic function, glucose, complete blood count, urinalysis with culture, and toxicology screening. Additional tests may include arterial blood gas analysis, thyroid-stimulating hormone, and cardiac enzymes. Imaging studies often include ECG, chest radiograph, and head CT. Further imaging is guided by clinical findings. Diagnostic procedures such as lumbar puncture or EEG are performed when indicated, particularly if infection or seizure activity is suspected.
Differential Diagnosis
Delirium must be distinguished from psychiatric illness, which typically lacks fluctuating consciousness and is more often associated with auditory hallucinations. Dementia is characterized by a slow, progressive decline without acute fluctuation or changes in consciousness. Once delirium is identified, the differential diagnosis for its underlying cause remains extensive.
Treatment – Prehospital Care
Establish IV access and monitor oxygen saturation and cardiac rhythm. Check blood glucose. Administer naloxone if respiratory insufficiency is suspected. Provide advanced life support transport as needed. Look for clues to the underlying cause, such as medications or medical alert identification, and document a baseline neurologic examination including Glasgow Coma Scale score, pupillary response, and extremity movement.
Emergency Department Treatment And Procedures
Management focuses on identifying and treating the underlying cause. Provide IV access, supplemental oxygen if hypoxic, and continuous cardiac, pulse oximetry, and blood pressure monitoring. Administer thiamine to alcoholic or malnourished patients. In severely agitated patients, short-term pharmacologic control may be necessary to allow safe evaluation and treatment.
Medication Management
Treatment is directed at the underlying etiology. Benzodiazepines are first-line therapy for alcohol or benzodiazepine withdrawal but should be avoided in most other causes of delirium if possible. Before administering antipsychotics, assess for prolonged QT interval. Haloperidol 5–10 mg IV or IM may be used, with lower doses recommended for elderly patients. Atypical antipsychotics may be equally effective. Thiamine 100 mg IV, IM, or PO should be given when indicated. Second-line agents include alprazolam 0.25–0.5 mg PO or lorazepam 0.5–2 mg IV, IM, or PO.
Follow-Up And Disposition
Admission is indicated when the cause of delirium is unclear or symptoms persist. Discharge may be considered if a treatable cause is identified and corrected, mental status returns to baseline in the emergency department, reliable caregivers are available, and follow-up is assured.
Follow-Up Recommendations
Follow-up depends on the underlying condition. If delirium resolves during the emergency visit, close follow-up with a primary care provider is recommended, ideally within two days. Patients and caregivers must receive clear return precautions, as any recurrence of delirium warrants immediate reevaluation.
Key Clinical Lessons And Common Errors
Prompt identification of the underlying cause is essential. Delirium is frequently missed in the emergency department, and maintaining awareness of delirium as a medical syndrome is critical, as it may signal a life-threatening condition.
Basics And Description
Delirium is an acute clinical syndrome marked by sudden changes in awareness, cognition, and perception, with a fluctuating, waxing-and-waning course. It is not a primary disease but a manifestation of an underlying medical condition. The exact pathophysiology is unknown, though it is thought to involve diffuse cerebral dysfunction and disturbances in neurotransmitters, particularly decreased cerebral acetylcholine and altered dopamine, γ-aminobutyric acid (GABA), and serotonin activity. Delirium is frequently overlooked in the emergency department because patients often present with atypical or vague complaints. It is associated with increased inpatient mortality and longer hospital stays.
Etiology
Neurologic causes include meningitis, encephalitis, seizures, Wernicke encephalopathy, hypoxia or hypoperfusion of the brain, and intracranial hemorrhage or mass lesions. Pulmonary causes include pneumonia and other conditions leading to hypoxia. Cardiovascular etiologies include hypertensive crisis, acute coronary syndromes, and arrhythmias. Gastrointestinal causes include hepatic encephalopathy and dehydration. Renal causes include urinary tract infection and acute renal failure. Endocrine disorders include hypoglycemia, hyperglycemia, and hypothyroidism. Rheumatologic causes include collagen vascular diseases. Toxicologic causes include environmental toxins, medications, and withdrawal from alcohol or barbiturates. Other causes include electrolyte abnormalities, vitamin deficiencies, hypothermia, hyperthermia, and trauma.
Geriatric Considerations
Delirium is common in older emergency department patients, with up to 10% affected. Presentations are often subtle, with complaints such as falls, dizziness, or a general sense of not feeling well. Symptoms frequently fluctuate, and the underlying cause may be a life-threatening condition.
Diagnosis – Signs And Symptoms
Disturbances of consciousness may be hyperactive, hypoactive, or mixed. Hyperactive delirium presents with agitation and combativeness, while hypoactive delirium presents with lethargy, stupor, or coma. Mixed states may rapidly alternate between the two. Cognitive changes include disorientation, impaired memory, disorganized thinking and speech, reduced environmental awareness, misperceptions, illusions, delusions, and hallucinations. Inattention is a key feature, with difficulty focusing, sustaining, or shifting attention. Patients may also demonstrate restlessness, distractibility, and emotional lability.
History
Collateral history from caregivers is essential. Key elements include the time course, typically hours to days, and a fluctuating pattern. A thorough medication history is critical, including prescribed, over-the-counter, and illicit substances, recent medication changes, and withdrawals. Associated symptoms and pre-existing medical conditions may point toward the underlying etiology.
Physical Examination
Vital signs should be carefully assessed. A complete neurologic examination is essential, with attention to mental status, orientation, focal deficits, and hallucinations. A psychiatric assessment and cardiovascular, pulmonary, and gastrointestinal examinations should be performed to identify potential sources of infection, sepsis, or other systemic illness.
Screening Tools
Several tools can aid in identifying delirium. The Confusion Assessment Method includes four features: acute onset or fluctuating course, inattention, disorganized thinking, and altered level of consciousness. Delirium is diagnosed when features one and two are present along with either three or four. The Mini-Mental State Examination may be used serially, though patient cooperation can limit its utility in the emergency setting.
Essential Workup
Recognizing delirium as a syndrome is critical. The diagnostic approach should be broad and guided by history, physical examination, and clinical suspicion to identify the underlying organic cause.
Diagnosis Tests And Interpretation
Initial laboratory testing should include electrolytes, calcium, renal function, hepatic function, glucose, complete blood count, urinalysis with culture, and toxicology screening. Additional tests may include arterial blood gas analysis, thyroid-stimulating hormone, and cardiac enzymes. Imaging studies often include ECG, chest radiograph, and head CT. Further imaging is guided by clinical findings. Diagnostic procedures such as lumbar puncture or EEG are performed when indicated, particularly if infection or seizure activity is suspected.
Differential Diagnosis
Delirium must be distinguished from psychiatric illness, which typically lacks fluctuating consciousness and is more often associated with auditory hallucinations. Dementia is characterized by a slow, progressive decline without acute fluctuation or changes in consciousness. Once delirium is identified, the differential diagnosis for its underlying cause remains extensive.
Treatment – Prehospital Care
Establish IV access and monitor oxygen saturation and cardiac rhythm. Check blood glucose. Administer naloxone if respiratory insufficiency is suspected. Provide advanced life support transport as needed. Look for clues to the underlying cause, such as medications or medical alert identification, and document a baseline neurologic examination including Glasgow Coma Scale score, pupillary response, and extremity movement.
Emergency Department Treatment And Procedures
Management focuses on identifying and treating the underlying cause. Provide IV access, supplemental oxygen if hypoxic, and continuous cardiac, pulse oximetry, and blood pressure monitoring. Administer thiamine to alcoholic or malnourished patients. In severely agitated patients, short-term pharmacologic control may be necessary to allow safe evaluation and treatment.
Medication Management
Treatment is directed at the underlying etiology. Benzodiazepines are first-line therapy for alcohol or benzodiazepine withdrawal but should be avoided in most other causes of delirium if possible. Before administering antipsychotics, assess for prolonged QT interval. Haloperidol 5–10 mg IV or IM may be used, with lower doses recommended for elderly patients. Atypical antipsychotics may be equally effective. Thiamine 100 mg IV, IM, or PO should be given when indicated. Second-line agents include alprazolam 0.25–0.5 mg PO or lorazepam 0.5–2 mg IV, IM, or PO.
Follow-Up And Disposition
Admission is indicated when the cause of delirium is unclear or symptoms persist. Discharge may be considered if a treatable cause is identified and corrected, mental status returns to baseline in the emergency department, reliable caregivers are available, and follow-up is assured.
Follow-Up Recommendations
Follow-up depends on the underlying condition. If delirium resolves during the emergency visit, close follow-up with a primary care provider is recommended, ideally within two days. Patients and caregivers must receive clear return precautions, as any recurrence of delirium warrants immediate reevaluation.
Key Clinical Lessons And Common Errors
Prompt identification of the underlying cause is essential. Delirium is frequently missed in the emergency department, and maintaining awareness of delirium as a medical syndrome is critical, as it may signal a life-threatening condition.
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Emergency and Acute Medicine -Cocaine Poisoning
Description And Pharmacology
Cocaine poisoning results from exposure to a potent sympathomimetic agent that inhibits neurotransmitter reuptake at presynaptic nerve terminals. This leads to excessive stimulation of adrenergic, dopaminergic, and serotonergic pathways. Cocaine is metabolized through hepatic degradation, nonenzymatic hydrolysis, and cholinesterase-mediated pathways, producing both active and inactive metabolites.
Etiology And Routes Of Exposure
Cocaine may be administered intravenously, intranasally, or orally. Oral ingestion is particularly important in the context of illicit drug transport. Body stuffers ingest hastily wrapped packets, often poorly sealed, in an attempt to evade law enforcement. Body packers deliberately ingest or insert carefully wrapped packets containing large quantities of cocaine into oral, rectal, or vaginal cavities for smuggling purposes, placing them at high risk for massive toxicity if a packet ruptures.
Clinical Features And Symptomatology
Patients typically present with a classic sympathomimetic toxidrome. Cardiovascular manifestations include hypertension, tachycardia, and chest pain consistent with angina or myocardial ischemia. Respiratory findings may include tachypnea, pleuritic chest pain, pneumomediastinum, pneumothorax, bronchitis, pulmonary infarction, or cough. Neurologic effects range from agitation and tremulousness to seizures, coma, and stroke. Additional findings may include hyperthermia, which is a poor prognostic sign, limb ischemia from inadvertent intra-arterial injection, corneal ulcerations in heavy crack smokers, and rhabdomyolysis.
History And Physical Examination
A focused history is critical, particularly in suspected body packers or stuffers, and should include time since ingestion, route of exposure, number of packets, and packing material. On examination, patients often demonstrate hypertension, tachycardia, tachypnea, hyperthermia, diaphoresis, mydriasis, and neuromuscular hyperactivity consistent with sympathomimetic toxicity.
Initial Clinical Assessment And Toxidrome Recognition
Recognition of the sympathomimetic toxidrome is essential and should be distinguished from anticholinergic toxicity. Sympathomimetic poisoning is characterized by tachycardia, elevated blood pressure, moist skin, increased bowel sounds, elevated temperature, and absence of urinary retention, whereas anticholinergic toxicity presents with dry skin, decreased bowel sounds, and urinary retention.
Diagnostic Evaluation And Testing
Laboratory evaluation includes complete blood count, electrolytes, renal function, glucose, urinalysis for myoglobin, creatine phosphokinase, and cardiac enzymes in patients with chest pain or ECG abnormalities. Imaging studies include ECG for ischemia or dysrhythmias, chest radiography for chest pain or dyspnea to evaluate for pneumothorax or pneumomediastinum, and abdominal radiography for suspected body packers. Computed tomography of the abdomen with contrast may be required if suspicion remains high despite negative radiographs. CT brain imaging is indicated for altered mental status or severe headache to evaluate for ischemic or hemorrhagic stroke.
Differential Diagnosis
The differential diagnosis includes other causes of sympathomimetic toxicity such as amphetamines, caffeine, theophylline, albuterol, tricyclic antidepressants, antihistamines, phencyclidine, hallucinogens, thyrotoxicosis, and neuroleptic malignant syndrome.
Prehospital And Initial Stabilization
Early management includes establishment of intravenous access, cardiac monitoring, and administration of benzodiazepines to control agitation and autonomic excess. In cases of combined opioid and cocaine use, naloxone should be administered incrementally to reverse opioid-induced coma. Initial stabilization in the emergency department follows standard airway, breathing, and circulation principles, with consideration of dextrose, thiamine, and naloxone for altered mental status.
Emergency Department Management
Supportive care is the cornerstone of treatment. Benzodiazepines are first-line therapy for agitation, seizures, hypertension, and tachycardia. Active cooling using evaporative and convective methods is essential for hyperthermia. Rhabdomyolysis is treated with aggressive intravenous hydration and urine alkalinization in severe cases. Cocaine-associated chest pain is managed with aspirin, nitrates, oxygen, and opiates, while avoiding beta-blockers due to the risk of unopposed alpha-adrenergic stimulation. Severe hypertension may require vasodilators such as nitroglycerin or nitroprusside, or alpha-blockade with phentolamine.
Management Of Body Packers And Stuffers
Asymptomatic or minimally symptomatic body stuffers may receive a single dose of activated charcoal. Whole-bowel irrigation with polyethylene glycol may be considered, though efficacy is uncertain. Symptomatic body packers and stuffers require surgical consultation, and operative removal of packets is indicated when toxicity cannot be controlled with medical therapy.
Disposition And Follow-Up
Admission is indicated for patients with altered mental status, abnormal vital signs, hyperthermia, cocaine-induced myocardial ischemia, or confirmed body packing. Moderate to severe toxicity warrants ICU admission. Patients may be discharged after adequate observation if mental status and vital signs normalize and no complications are identified, with longer observation required for body stuffers until packet passage is confirmed.
Clinical Pearls And Pitfalls
Benzodiazepines are the primary treatment for cocaine-induced sympathomimetic toxicity. Beta-blockers should generally be avoided due to the risk of worsening hypertension. Cocaine-associated chest pain requires a broad differential, including myocardial infarction. Abdominal radiographs are useful for body packers but unreliable for body stuffers.
Description And Pharmacology
Cocaine poisoning results from exposure to a potent sympathomimetic agent that inhibits neurotransmitter reuptake at presynaptic nerve terminals. This leads to excessive stimulation of adrenergic, dopaminergic, and serotonergic pathways. Cocaine is metabolized through hepatic degradation, nonenzymatic hydrolysis, and cholinesterase-mediated pathways, producing both active and inactive metabolites.
Etiology And Routes Of Exposure
Cocaine may be administered intravenously, intranasally, or orally. Oral ingestion is particularly important in the context of illicit drug transport. Body stuffers ingest hastily wrapped packets, often poorly sealed, in an attempt to evade law enforcement. Body packers deliberately ingest or insert carefully wrapped packets containing large quantities of cocaine into oral, rectal, or vaginal cavities for smuggling purposes, placing them at high risk for massive toxicity if a packet ruptures.
Clinical Features And Symptomatology
Patients typically present with a classic sympathomimetic toxidrome. Cardiovascular manifestations include hypertension, tachycardia, and chest pain consistent with angina or myocardial ischemia. Respiratory findings may include tachypnea, pleuritic chest pain, pneumomediastinum, pneumothorax, bronchitis, pulmonary infarction, or cough. Neurologic effects range from agitation and tremulousness to seizures, coma, and stroke. Additional findings may include hyperthermia, which is a poor prognostic sign, limb ischemia from inadvertent intra-arterial injection, corneal ulcerations in heavy crack smokers, and rhabdomyolysis.
History And Physical Examination
A focused history is critical, particularly in suspected body packers or stuffers, and should include time since ingestion, route of exposure, number of packets, and packing material. On examination, patients often demonstrate hypertension, tachycardia, tachypnea, hyperthermia, diaphoresis, mydriasis, and neuromuscular hyperactivity consistent with sympathomimetic toxicity.
Initial Clinical Assessment And Toxidrome Recognition
Recognition of the sympathomimetic toxidrome is essential and should be distinguished from anticholinergic toxicity. Sympathomimetic poisoning is characterized by tachycardia, elevated blood pressure, moist skin, increased bowel sounds, elevated temperature, and absence of urinary retention, whereas anticholinergic toxicity presents with dry skin, decreased bowel sounds, and urinary retention.
Diagnostic Evaluation And Testing
Laboratory evaluation includes complete blood count, electrolytes, renal function, glucose, urinalysis for myoglobin, creatine phosphokinase, and cardiac enzymes in patients with chest pain or ECG abnormalities. Imaging studies include ECG for ischemia or dysrhythmias, chest radiography for chest pain or dyspnea to evaluate for pneumothorax or pneumomediastinum, and abdominal radiography for suspected body packers. Computed tomography of the abdomen with contrast may be required if suspicion remains high despite negative radiographs. CT brain imaging is indicated for altered mental status or severe headache to evaluate for ischemic or hemorrhagic stroke.
Differential Diagnosis
The differential diagnosis includes other causes of sympathomimetic toxicity such as amphetamines, caffeine, theophylline, albuterol, tricyclic antidepressants, antihistamines, phencyclidine, hallucinogens, thyrotoxicosis, and neuroleptic malignant syndrome.
Prehospital And Initial Stabilization
Early management includes establishment of intravenous access, cardiac monitoring, and administration of benzodiazepines to control agitation and autonomic excess. In cases of combined opioid and cocaine use, naloxone should be administered incrementally to reverse opioid-induced coma. Initial stabilization in the emergency department follows standard airway, breathing, and circulation principles, with consideration of dextrose, thiamine, and naloxone for altered mental status.
Emergency Department Management
Supportive care is the cornerstone of treatment. Benzodiazepines are first-line therapy for agitation, seizures, hypertension, and tachycardia. Active cooling using evaporative and convective methods is essential for hyperthermia. Rhabdomyolysis is treated with aggressive intravenous hydration and urine alkalinization in severe cases. Cocaine-associated chest pain is managed with aspirin, nitrates, oxygen, and opiates, while avoiding beta-blockers due to the risk of unopposed alpha-adrenergic stimulation. Severe hypertension may require vasodilators such as nitroglycerin or nitroprusside, or alpha-blockade with phentolamine.
Management Of Body Packers And Stuffers
Asymptomatic or minimally symptomatic body stuffers may receive a single dose of activated charcoal. Whole-bowel irrigation with polyethylene glycol may be considered, though efficacy is uncertain. Symptomatic body packers and stuffers require surgical consultation, and operative removal of packets is indicated when toxicity cannot be controlled with medical therapy.
Disposition And Follow-Up
Admission is indicated for patients with altered mental status, abnormal vital signs, hyperthermia, cocaine-induced myocardial ischemia, or confirmed body packing. Moderate to severe toxicity warrants ICU admission. Patients may be discharged after adequate observation if mental status and vital signs normalize and no complications are identified, with longer observation required for body stuffers until packet passage is confirmed.
Clinical Pearls And Pitfalls
Benzodiazepines are the primary treatment for cocaine-induced sympathomimetic toxicity. Beta-blockers should generally be avoided due to the risk of worsening hypertension. Cocaine-associated chest pain requires a broad differential, including myocardial infarction. Abdominal radiographs are useful for body packers but unreliable for body stuffers.
