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Emergency And Acute Medicine: Hyponatremia
Basics
Description Hyponatremia is defined as serum sodium <136 meq /> and is the most common electrolyte disturbance, occurring in 1–4% of hospitalized patients.
Etiology
Pseudohyponatremia Low measured sodium with normal serum osmolality due to displacement of sodium in the aqueous phase; seen with hyperlipidemia or hyperproteinemia (e.g., multiple myeloma).
Hyponatremia With Normal Osmolarity And Fluid Overload Inappropriate water retention seen in CHF, cirrhosis, renal failure, and nephrotic syndrome.
Hyponatremia With Normal Osmolarity And Euvolemia Dilutional hyponatremia with increased total body water and minimal edema. Causes include hypothyroidism, stress, SIADH (pulmonary disease, CNS disorders, malignancy, HIV), water intoxication, postoperative states, beer potomania, MDMA use, and mineralocorticoid abnormalities.
Hyponatremia With Normal Osmolarity And Hypovolemia Total body sodium and water loss with sodium loss predominating; causes include GI losses, sweating, burns, cerebral salt wasting, cystic fibrosis, salt-wasting nephropathies, and diuretics.
Drug Induced ADH stimulation (amiodarone, carbamazepine, cyclophosphamide, opiates, vincristine), increased ADH sensitivity (chlorpropamide, NSAIDs), or increased thirst (SSRIs, antipsychotics, MDMA).
Hyponatremia With Hyperosmolarity Due to osmotically active substances, most commonly hyperglycemia. Corrected Na = measured Na + 0.016 × (glucose − 100). Also seen with mannitol, maltose, or glycine.
Pediatric Considerations Higher risk of water intoxication and iatrogenic hyponatremia.
Pregnancy Considerations Vasopressin antagonists are pregnancy class C.
Geriatric Considerations Increased symptom burden due to impaired free water excretion and low sodium intake.
Diagnosis
Signs And Symptoms Mild (Na >120): headache, nausea, vomiting, weakness, anorexia, cramps. Moderate (110–120): confusion, hallucinations, bizarre behavior, incontinence, gait disturbance. Severe (<110): seizures, coma, herniation signs, respiratory arrest. chronic hyponatremia may be asymptomatic.< />pan>
History And Exam Review medications and assess volume status. Perform full neurologic examination.
Essential Workup Confirm serum sodium level with repeat testing.
Diagnosis Tests And Interpretation
Lab Electrolytes, BUN, creatinine, glucose (correct sodium if hyperglycemic), serum and urine osmolality, urine sodium, thyroid and adrenal function, CPK if rhabdomyolysis suspected. Plasma osmolality = 2 × Na + glucose/18 + BUN/2.8.
Imaging CXR for CHF, infection, or malignancy. CT head if altered mental status.
Differential Diagnosis Pseudohyponatremia from hyperglycemia, hyperlipidemia, hyperproteinemia, or radiocontrast exposure.
Treatment
Prehospital Supportive care and IV access.
Initial Stabilization/Therapy ABCs, IV 0.9% NS, naloxone, thiamine, and D50W for altered mental status.
Emergency Department Treatment/Procedures Management depends on severity, chronicity, and cause. Chronic hyponatremia requires slow correction to prevent osmotic demyelination; limit correction to 10-12 mEq/L in 24 hr. Acute severe hyponatremia with seizures requires hypertonic saline to raise sodium 8-10 mEq/L over 4-6 hr or to >120–125 mEq/L, then slow or stop correction. Typical dose is 200–400 mL of 3% saline over 2 hr or 1–2 mL/kg/hr.
Hypovolemic Hyponatremia Restore volume with 0.9% NS.
Euvolemic Or Hypervolemic Hyponatremia Water restriction (<1 l />ay), high salt intake, or 0.9% NS with loop diuretics. Maximum correction rate 0.5 mEq/L/hr.
Medication
First Line 500 mL–1 L isotonic saline bolus.
Adjuncts Furosemide 20–40 mg IV.
Second Line Conivaptan IV or tolvaptan PO for euvolemic or hypervolemic hyponatremia only.
Follow-Up And Disposition
Admission Criteria Symptomatic hyponatremia, sodium <120 meq />, or comorbid risk factors.
Discharge Criteria Sodium >130 mEq/L and asymptomatic, or stable chronic mild hyponatremia with close follow-up.
Follow-Up Recommendations Repeat sodium within one week, especially if diuretic-related.
Pearls And Pitfalls Avoid rapid correction to prevent osmotic demyelination syndrome, especially in women, alcoholics, malnourished patients, those with hypokalemia, or liver transplant history. Perform serial neurologic exams. Beware of falsely low sodium from blood draws near hypotonic IV lines. Thiazide-induced hyponatremia may persist up to two weeks after discontinuation.
Basics
Description Hyponatremia is defined as serum sodium <136 meq /> and is the most common electrolyte disturbance, occurring in 1–4% of hospitalized patients.
Etiology
Pseudohyponatremia Low measured sodium with normal serum osmolality due to displacement of sodium in the aqueous phase; seen with hyperlipidemia or hyperproteinemia (e.g., multiple myeloma).
Hyponatremia With Normal Osmolarity And Fluid Overload Inappropriate water retention seen in CHF, cirrhosis, renal failure, and nephrotic syndrome.
Hyponatremia With Normal Osmolarity And Euvolemia Dilutional hyponatremia with increased total body water and minimal edema. Causes include hypothyroidism, stress, SIADH (pulmonary disease, CNS disorders, malignancy, HIV), water intoxication, postoperative states, beer potomania, MDMA use, and mineralocorticoid abnormalities.
Hyponatremia With Normal Osmolarity And Hypovolemia Total body sodium and water loss with sodium loss predominating; causes include GI losses, sweating, burns, cerebral salt wasting, cystic fibrosis, salt-wasting nephropathies, and diuretics.
Drug Induced ADH stimulation (amiodarone, carbamazepine, cyclophosphamide, opiates, vincristine), increased ADH sensitivity (chlorpropamide, NSAIDs), or increased thirst (SSRIs, antipsychotics, MDMA).
Hyponatremia With Hyperosmolarity Due to osmotically active substances, most commonly hyperglycemia. Corrected Na = measured Na + 0.016 × (glucose − 100). Also seen with mannitol, maltose, or glycine.
Pediatric Considerations Higher risk of water intoxication and iatrogenic hyponatremia.
Pregnancy Considerations Vasopressin antagonists are pregnancy class C.
Geriatric Considerations Increased symptom burden due to impaired free water excretion and low sodium intake.
Diagnosis
Signs And Symptoms Mild (Na >120): headache, nausea, vomiting, weakness, anorexia, cramps. Moderate (110–120): confusion, hallucinations, bizarre behavior, incontinence, gait disturbance. Severe (<110): seizures, coma, herniation signs, respiratory arrest. chronic hyponatremia may be asymptomatic.< />pan>
History And Exam Review medications and assess volume status. Perform full neurologic examination.
Essential Workup Confirm serum sodium level with repeat testing.
Diagnosis Tests And Interpretation
Lab Electrolytes, BUN, creatinine, glucose (correct sodium if hyperglycemic), serum and urine osmolality, urine sodium, thyroid and adrenal function, CPK if rhabdomyolysis suspected. Plasma osmolality = 2 × Na + glucose/18 + BUN/2.8.
Imaging CXR for CHF, infection, or malignancy. CT head if altered mental status.
Differential Diagnosis Pseudohyponatremia from hyperglycemia, hyperlipidemia, hyperproteinemia, or radiocontrast exposure.
Treatment
Prehospital Supportive care and IV access.
Initial Stabilization/Therapy ABCs, IV 0.9% NS, naloxone, thiamine, and D50W for altered mental status.
Emergency Department Treatment/Procedures Management depends on severity, chronicity, and cause. Chronic hyponatremia requires slow correction to prevent osmotic demyelination; limit correction to 10-12 mEq/L in 24 hr. Acute severe hyponatremia with seizures requires hypertonic saline to raise sodium 8-10 mEq/L over 4-6 hr or to >120–125 mEq/L, then slow or stop correction. Typical dose is 200–400 mL of 3% saline over 2 hr or 1–2 mL/kg/hr.
Hypovolemic Hyponatremia Restore volume with 0.9% NS.
Euvolemic Or Hypervolemic Hyponatremia Water restriction (<1 l />ay), high salt intake, or 0.9% NS with loop diuretics. Maximum correction rate 0.5 mEq/L/hr.
Medication
First Line 500 mL–1 L isotonic saline bolus.
Adjuncts Furosemide 20–40 mg IV.
Second Line Conivaptan IV or tolvaptan PO for euvolemic or hypervolemic hyponatremia only.
Follow-Up And Disposition
Admission Criteria Symptomatic hyponatremia, sodium <120 meq />, or comorbid risk factors.
Discharge Criteria Sodium >130 mEq/L and asymptomatic, or stable chronic mild hyponatremia with close follow-up.
Follow-Up Recommendations Repeat sodium within one week, especially if diuretic-related.
Pearls And Pitfalls Avoid rapid correction to prevent osmotic demyelination syndrome, especially in women, alcoholics, malnourished patients, those with hypokalemia, or liver transplant history. Perform serial neurologic exams. Beware of falsely low sodium from blood draws near hypotonic IV lines. Thiazide-induced hyponatremia may persist up to two weeks after discontinuation.
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KembaraXtra-Emergency and Acute Medicine: Hydatidiform Mole
Basics
Description Hydatidiform mole is a noninvasive, localized tumor arising from trophoblastic tissue and may be associated with malignancy. Twinning with a normal pregnancy is possible but carries a higher risk of persistent maternal disease and metastasis, although a normal infant may occasionally result. Complete mole occurs in ~1/1,500 pregnancies, with no fetal tissue, diffuse chorionic villi swelling, and diffuse trophoblastic hyperplasia; malignancy develops in 15–20% (commonly lung). Genetics are typically 46,XX (90%) or 46,XY (10%) with paternal-only DNA due to fertilization of an enucleated ovum by two sperm or duplication of a haploid sperm. Partial mole occurs in ~1/750 pregnancies, often with fetal or embryonic tissue, focal villous swelling, and focal trophoblastic hyperplasia; malignancy risk is 4–12%. Genetics are usually triploid (69XXX, 69XXY, rarely 69XYY) with both maternal and paternal DNA.
Etiology Largely unknown. Risk factors include extremes of maternal age (>35 years with 5–10× risk; <20 years), prior molar pregnancy (1–2% recurrence), higher prevalence in Asian and Latin American regions, dietary deficiency of animal fat and vitamin A, smoking (>15 cigarettes/day), maternal blood types AB/A/B, infertility or nulliparity, and occurrence in ~1 of 600 therapeutic abortions.
Diagnosis
Signs and symptoms Usually exaggerated pregnancy symptoms. Complete mole commonly presents with painless vaginal bleeding (97%) described as “prune juice,” passage of grapelike vesicles, hyperemesis from high β-hCG, preeclampsia (27%), hyperthyroidism (7%), and acute respiratory distress (2%) from trophoblastic emboli or related cardiopulmonary effects. Partial mole often resembles threatened or spontaneous abortion with vaginal bleeding, possible fetal heart tones, and later presentation.
History Missed menses, positive pregnancy test, nausea, vomiting, vaginal bleeding.
Physical exam Uterine size–date discrepancy in 50–66% (larger in complete, smaller in partial). Ovarian enlargement with bilateral theca lutein cysts is common in complete moles.
Essential workup
Laboratory β-hCG (often >100,000 mIU/mL in complete moles; lower in partial; >40,000 mIU/mL indicates poorer prognosis), blood type/Rh and cross-match, CBC, coagulation profile, electrolytes with BUN/creatinine, LFTs, TSH/free T4 if hyperthyroidism suspected, urinalysis for proteinuria.
Imaging
Ultrasound shows a “snowstorm” pattern with absent fetus and no amniotic fluid in complete moles and a “Swiss-cheese” placental appearance with possible fetus in partial moles. Chest X-ray assesses pulmonary edema and metastatic disease.
Pathology
All products of conception require histology. Complete moles show edematous villi with diffuse trophoblastic hyperplasia; partial moles show fetal tissue, vessels, amnion, and edematous villi.
Differential diagnosis
Threatened, missed, or incomplete abortion; ectopic pregnancy; hyperthyroidism; hyperemesis gravidarum; hypertension and preeclampsia.
Treatment
Prehospital Secure airway, provide oxygen, establish IV access, treat seizures with benzodiazepines, and save passed tissue.
Initial stabilization IV access, cardiac monitoring, and blood preparation if evacuation is planned.
Emergency department management Intubate for respiratory distress; give β-blockers before evacuation for hyperthyroidism; manage preeclampsia/eclampsia with benzodiazepines and magnesium sulfate and control blood pressure with hydralazine or labetalol; transfuse blood products for coagulopathy; administer Rho(D) immune globulin; perform suction curettage (fertility-sparing and curative in ~80%) with oxytocin; consider chemoprophylaxis only in selected high-risk cases with reliable follow-up; consider hysterectomy for older patients, those not desiring fertility, or high-risk disease.
Follow-up and disposition
Admission criteria Uterine size >16 weeks, clinical preeclampsia/hyperthyroidism/respiratory distress, hemodynamic instability, partial mole, or hysterectomy.
Discharge criteria Uncomplicated curettage of a small, low-risk mole with reliable follow-up.
Follow-up recommendations Close OB-GYN follow-up with serial β-hCG weekly for ≥4 weeks then monthly until undetectable; any rise prompts evaluation for metastasis. Use contraception and avoid pregnancy for 12 months; perform early ultrasound in future pregnancies. Recurrence risk is 1–1.5% after one mole and up to 20% after two.
Pearls and pitfalls Diagnosis may be missed with apparent normal pregnancy, preeclampsia before 24 weeks, or severe hyperemesis. Strict β-hCG follow-up is essential; up to 20% may develop malignancy if not monitored.
Basics
Description Hydatidiform mole is a noninvasive, localized tumor arising from trophoblastic tissue and may be associated with malignancy. Twinning with a normal pregnancy is possible but carries a higher risk of persistent maternal disease and metastasis, although a normal infant may occasionally result. Complete mole occurs in ~1/1,500 pregnancies, with no fetal tissue, diffuse chorionic villi swelling, and diffuse trophoblastic hyperplasia; malignancy develops in 15–20% (commonly lung). Genetics are typically 46,XX (90%) or 46,XY (10%) with paternal-only DNA due to fertilization of an enucleated ovum by two sperm or duplication of a haploid sperm. Partial mole occurs in ~1/750 pregnancies, often with fetal or embryonic tissue, focal villous swelling, and focal trophoblastic hyperplasia; malignancy risk is 4–12%. Genetics are usually triploid (69XXX, 69XXY, rarely 69XYY) with both maternal and paternal DNA.
Etiology Largely unknown. Risk factors include extremes of maternal age (>35 years with 5–10× risk; <20 years), prior molar pregnancy (1–2% recurrence), higher prevalence in Asian and Latin American regions, dietary deficiency of animal fat and vitamin A, smoking (>15 cigarettes/day), maternal blood types AB/A/B, infertility or nulliparity, and occurrence in ~1 of 600 therapeutic abortions.
Diagnosis
Signs and symptoms Usually exaggerated pregnancy symptoms. Complete mole commonly presents with painless vaginal bleeding (97%) described as “prune juice,” passage of grapelike vesicles, hyperemesis from high β-hCG, preeclampsia (27%), hyperthyroidism (7%), and acute respiratory distress (2%) from trophoblastic emboli or related cardiopulmonary effects. Partial mole often resembles threatened or spontaneous abortion with vaginal bleeding, possible fetal heart tones, and later presentation.
History Missed menses, positive pregnancy test, nausea, vomiting, vaginal bleeding.
Physical exam Uterine size–date discrepancy in 50–66% (larger in complete, smaller in partial). Ovarian enlargement with bilateral theca lutein cysts is common in complete moles.
Essential workup
Laboratory β-hCG (often >100,000 mIU/mL in complete moles; lower in partial; >40,000 mIU/mL indicates poorer prognosis), blood type/Rh and cross-match, CBC, coagulation profile, electrolytes with BUN/creatinine, LFTs, TSH/free T4 if hyperthyroidism suspected, urinalysis for proteinuria.
Imaging
Ultrasound shows a “snowstorm” pattern with absent fetus and no amniotic fluid in complete moles and a “Swiss-cheese” placental appearance with possible fetus in partial moles. Chest X-ray assesses pulmonary edema and metastatic disease.
Pathology
All products of conception require histology. Complete moles show edematous villi with diffuse trophoblastic hyperplasia; partial moles show fetal tissue, vessels, amnion, and edematous villi.
Differential diagnosis
Threatened, missed, or incomplete abortion; ectopic pregnancy; hyperthyroidism; hyperemesis gravidarum; hypertension and preeclampsia.
Treatment
Prehospital Secure airway, provide oxygen, establish IV access, treat seizures with benzodiazepines, and save passed tissue.
Initial stabilization IV access, cardiac monitoring, and blood preparation if evacuation is planned.
Emergency department management Intubate for respiratory distress; give β-blockers before evacuation for hyperthyroidism; manage preeclampsia/eclampsia with benzodiazepines and magnesium sulfate and control blood pressure with hydralazine or labetalol; transfuse blood products for coagulopathy; administer Rho(D) immune globulin; perform suction curettage (fertility-sparing and curative in ~80%) with oxytocin; consider chemoprophylaxis only in selected high-risk cases with reliable follow-up; consider hysterectomy for older patients, those not desiring fertility, or high-risk disease.
Follow-up and disposition
Admission criteria Uterine size >16 weeks, clinical preeclampsia/hyperthyroidism/respiratory distress, hemodynamic instability, partial mole, or hysterectomy.
Discharge criteria Uncomplicated curettage of a small, low-risk mole with reliable follow-up.
Follow-up recommendations Close OB-GYN follow-up with serial β-hCG weekly for ≥4 weeks then monthly until undetectable; any rise prompts evaluation for metastasis. Use contraception and avoid pregnancy for 12 months; perform early ultrasound in future pregnancies. Recurrence risk is 1–1.5% after one mole and up to 20% after two.
Pearls and pitfalls Diagnosis may be missed with apparent normal pregnancy, preeclampsia before 24 weeks, or severe hyperemesis. Strict β-hCG follow-up is essential; up to 20% may develop malignancy if not monitored.
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KembaraXtra-Emergency And Acute Medicine: Hydrocele
Basics
Description Hydrocele is the most common cause of painless scrotal swelling and is classified as congenital or acquired. Congenital hydrocele results from a patent processus vaginalis with communication between the tunica vaginalis and peritoneal cavity; most close spontaneously by 2 years of age. Acquired (secondary) hydrocele occurs due to intrascrotal infection, neoplasm, inguinal or scrotal surgery, or regional or systemic disease. Communicating hydrocele involves a patent processus vaginalis, with scrotal size fluctuating based on position and intra-abdominal pressure. Noncommunicating hydrocele results from excess serous fluid production or impaired absorption within the scrotum.
Etiology Hydrocele results from an imbalance between fluid production and resorption between the tunica vaginalis and tunica albuginea. Causes of adult noncommunicating hydrocele include epididymitis, trauma, mumps, tuberculosis, hypoalbuminemia, and spermatic vein ligation. In the developing world, filarial infections such as Wuchereria bancrofti or Loa loa are the most common causes worldwide. Rare causes include testicular malignancy or lymphoma and abdominoscrotal hydrocele, which may compress adjacent structures causing hydroureter or unilateral limb edema; ultrasound shows a single sac extending through the deep inguinal ring.
Pediatric considerations Congenital hydrocele occurs in approximately 6% of newborn boys and is commonly diagnosed in the newborn period. It is caused by a patent processus vaginalis, which remains open in most newborns. Size may vary with position or crying, and the mass may intermittently resolve. Most close spontaneously by age 2 years.
Diagnosis
Signs and symptoms Painless scrotal swelling with a sensation of heaviness, pulling, or dragging.
History Focus on onset, progression, variability in size, and exclusion of testicular torsion.
Physical exam The mass may feel soft and doughy or firm depending on fluid volume. Transillumination may show homogeneous light transmission but is increasingly replaced by bedside ultrasound.
Essential workup Bedside ultrasound is the diagnostic test of choice, allowing visualization of the hydrocele and testicle and helping identify underlying masses. In adults, the entire testicle must be palpated because hydrocele may obscure a primary neoplasm.
Diagnosis tests and interpretation
Laboratory No routine laboratory testing is required unless evaluating an underlying cause (e.g., urinalysis, AFP, β-hCG).
Imaging Ultrasound demonstrates a large anechoic fluid-filled collection surrounding the anterolateral aspect of the testicle.
Differential diagnosis Epididymitis, indirect inguinal hernia, orchitis, testicular neoplasm, testicular torsion, varicocele.
Treatment
Initial stabilization/therapy Address and stabilize any underlying cause such as trauma or infection.
Emergency department management Perform thorough testicular examination to exclude neoplasm and arrange appropriate referral.
Medication Treat underlying pathology if identified.
Follow-up and disposition
Admission criteria Secondary hydrocele with concern for underlying pathology such as trauma or malignancy.
Discharge criteria Otherwise healthy patients may be discharged with urology referral. Hydrocele repair is elective and performed for discomfort or cosmetic reasons. Options include surgical hydrocelectomy or aspiration with sclerotherapy.
Pediatric considerations Most infant hydroceles resolve spontaneously by 12 months; observation and referral are appropriate. Persistent hydroceles after 12–18 months should be referred for surgical repair due to associated inguinal hernia risk.
Follow-up recommendations Urology follow-up is recommended.
Key points Hydroceles may not transilluminate if the tunica vaginalis is thickened. Bedside ultrasound should always confirm both the fluid collection and normal testicular anatomy to avoid missing serious pathology.
Basics
Description Hydrocele is the most common cause of painless scrotal swelling and is classified as congenital or acquired. Congenital hydrocele results from a patent processus vaginalis with communication between the tunica vaginalis and peritoneal cavity; most close spontaneously by 2 years of age. Acquired (secondary) hydrocele occurs due to intrascrotal infection, neoplasm, inguinal or scrotal surgery, or regional or systemic disease. Communicating hydrocele involves a patent processus vaginalis, with scrotal size fluctuating based on position and intra-abdominal pressure. Noncommunicating hydrocele results from excess serous fluid production or impaired absorption within the scrotum.
Etiology Hydrocele results from an imbalance between fluid production and resorption between the tunica vaginalis and tunica albuginea. Causes of adult noncommunicating hydrocele include epididymitis, trauma, mumps, tuberculosis, hypoalbuminemia, and spermatic vein ligation. In the developing world, filarial infections such as Wuchereria bancrofti or Loa loa are the most common causes worldwide. Rare causes include testicular malignancy or lymphoma and abdominoscrotal hydrocele, which may compress adjacent structures causing hydroureter or unilateral limb edema; ultrasound shows a single sac extending through the deep inguinal ring.
Pediatric considerations Congenital hydrocele occurs in approximately 6% of newborn boys and is commonly diagnosed in the newborn period. It is caused by a patent processus vaginalis, which remains open in most newborns. Size may vary with position or crying, and the mass may intermittently resolve. Most close spontaneously by age 2 years.
Diagnosis
Signs and symptoms Painless scrotal swelling with a sensation of heaviness, pulling, or dragging.
History Focus on onset, progression, variability in size, and exclusion of testicular torsion.
Physical exam The mass may feel soft and doughy or firm depending on fluid volume. Transillumination may show homogeneous light transmission but is increasingly replaced by bedside ultrasound.
Essential workup Bedside ultrasound is the diagnostic test of choice, allowing visualization of the hydrocele and testicle and helping identify underlying masses. In adults, the entire testicle must be palpated because hydrocele may obscure a primary neoplasm.
Diagnosis tests and interpretation
Laboratory No routine laboratory testing is required unless evaluating an underlying cause (e.g., urinalysis, AFP, β-hCG).
Imaging Ultrasound demonstrates a large anechoic fluid-filled collection surrounding the anterolateral aspect of the testicle.
Differential diagnosis Epididymitis, indirect inguinal hernia, orchitis, testicular neoplasm, testicular torsion, varicocele.
Treatment
Initial stabilization/therapy Address and stabilize any underlying cause such as trauma or infection.
Emergency department management Perform thorough testicular examination to exclude neoplasm and arrange appropriate referral.
Medication Treat underlying pathology if identified.
Follow-up and disposition
Admission criteria Secondary hydrocele with concern for underlying pathology such as trauma or malignancy.
Discharge criteria Otherwise healthy patients may be discharged with urology referral. Hydrocele repair is elective and performed for discomfort or cosmetic reasons. Options include surgical hydrocelectomy or aspiration with sclerotherapy.
Pediatric considerations Most infant hydroceles resolve spontaneously by 12 months; observation and referral are appropriate. Persistent hydroceles after 12–18 months should be referred for surgical repair due to associated inguinal hernia risk.
Follow-up recommendations Urology follow-up is recommended.
Key points Hydroceles may not transilluminate if the tunica vaginalis is thickened. Bedside ultrasound should always confirm both the fluid collection and normal testicular anatomy to avoid missing serious pathology.
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Infectious Diseases and Microbiology: Low Back Pain and Fever
Basics
Description
Back pain refers to acute or chronic pain arising from the spine or paraspinal structures. The combination of back pain and fever requires careful evaluation for nonmechanical causes. History should specifically assess weight loss, pain worse when lying down, morning stiffness, and sudden severe or colicky pain. Serial spinal and neurologic examinations are crucial, and any spinal tenderness or focal pain warrants full diagnostic assessment. Vertebral osteomyelitis is commonly suggested by pain worsened by movement and not relieved by rest, focal vertebral tenderness, and elevated erythrocyte sedimentation rate. Pain from neoplastic nerve infiltration is typically constant, progressively worse, and persists at night without relief, whereas mechanical low back pain usually improves with rest. Work-up often begins with plain radiography followed by bone scintigraphy, MRI, CT, laboratory testing, and biopsy based on abnormal findings.
Epidemiology
A definitive pain source is difficult to establish and is identified in fewer than one-quarter of cases. Mechanical causes account for about 97% of low back pain, with degenerative disk disease and lumbar sprain/strain comprising most cases. The spine is a frequent site of bone metastasis. Vertebral osteomyelitis is uncommon at roughly 1 per 100,000 persons annually, with rising rates attributed to vascular devices and intravenous drug use; it occurs more often in early childhood and in adults over 50. Spinal epidural abscess occurs in about 1 per 10,000 hospital admissions per year, and MRSA-related vertebral osteomyelitis and epidural abscess are increasingly reported. Despite global increases in tuberculosis, the rate of extrapulmonary spinal disease remains relatively stable; Pott disease, typically involving the lower thoracic vertebrae, is the most common musculoskeletal extrapulmonary manifestation. Improved survival in sickle cell disease has been accompanied by more Salmonella vertebral osteomyelitis.
Risk Factors
Infectious complications can follow bites from many animals, often linked to occupational exposure (farmers, laboratory workers, veterinarians) or recreation (hunters, campers, exotic pet owners). Systemic infection after animal or human bites is more likely with extremity edema or impaired lymphatic drainage and in immunocompromised hosts. Fever after a dog bite in an immunosuppressed patient should prompt concern for invasive Capnocytophaga canimorsus infection.
Etiology
Infectious sources of back pain with fever include biliary tract infection, chronic prostatitis, herpes zoster, pyelonephritis, retroperitoneal abscess, spinal epidural abscess, and vertebral osteomyelitis. Noninfectious causes include colonic cancer, pancreatic disease, histiocytosis X, metastatic malignancy (breast, lung, prostate, thyroid, kidney, gastrointestinal tract), multiple myeloma, neoplastic invasion of pelvic nerves, lymphoma, pregnancy, vertebral fracture, renal artery or vein thrombosis, renal stones, retroperitoneal hemorrhage or tumors, and tumors of the posterior stomach or duodenum. Staphylococcus aureus is the leading cause of spinal epidural abscess, accounting for most reported cases, with additional pathogens including Actinomyces israelii, Aspergillus, Blastomyces, Brucella, Cryptococcus, Haemophilus parainfluenzae, Mycobacterium tuberculosis, and Streptococcus milleri. Vertebral osteomyelitis is most often due to staphylococci but may be caused by other bacteria or tuberculosis; one multicenter retrospective study from southern Spain reported a high proportion due to Brucella, with the remainder split between pyogenic and tuberculous disease.
Commonly Associated Conditions
Vertebral osteomyelitis and spinal epidural abscess are frequently associated with diabetes, injection drug use, chronic renal failure, alcohol use disorder, bacteremia or focal infections, and malignancy. Most epidural abscesses arise via hematogenous spread from skin or mucosal sources, though direct extension from adjacent infection is also recognized. Postoperative abscesses account for a substantial minority, and epidural catheter placement is another risk factor. Blunt trauma may precede symptoms and may lead to an epidural hematoma that later becomes infected.
Diagnosis
Spinal epidural abscess classically presents with fever, spinal pain and tenderness, and radicular pain progressing to limb weakness, with pain being the most consistent feature. Early on, spinal pain with or without fever may be the only findings before sudden neurologic decline. When sepsis dominates or when patients are bedbound, neurologic deficits may be missed. Fever is absent in a notable minority of pyogenic vertebral osteomyelitis cases and is even more commonly absent in tuberculous vertebral osteomyelitis.
History
Key elements include age; systemic symptoms such as fever, weakness, weight loss, and night sweats; prior trauma, infection, or cancer; pain characteristics; immune status; glycemic control in diabetes; and injection drug use. Screen for neurologic complaints including weakness, paresthesias, numbness, and bowel, bladder, or sexual dysfunction. Risk is higher in patients over 50, those using steroids, individuals with HIV, those on immunosuppressants, and those with prior surgery.
Physical Examination
Assess general appearance, vital signs, peripheral pulses, and perform a focused cardiopulmonary and abdominal evaluation in unstable patients. Look for referred pain by examining potential primary sources of tenderness. Perform a complete neurologic examination to evaluate for spinal cord compromise and localize deficits; lesions below T12 can produce lower motor neuron findings, and cauda equina syndrome may include bowel or bladder incontinence. In older adults, fever may be low-grade and does not reliably indicate severity. Percussion of spinous processes may reveal focal vertebral tenderness due to trauma, malignancy, or infection. Examine for signs of endocarditis and septic emboli.
Diagnostic Tests and Interpretation
Laboratory Studies
Routine blood tests are often nonspecific for vertebral osteomyelitis, but leukocytosis, neutrophilia, and markedly elevated ESR and C-reactive protein support pyogenic disease. Blood cultures are the most useful routine test and identify the organism in about half of pyogenic and Brucella vertebral osteomyelitis cases. Bone biopsy is often required to confirm the diagnosis, especially in tuberculous disease.
Imaging
Plain spinal radiographs may be normal early in vertebral osteomyelitis. MRI best defines the extent and location of spinal epidural abscess. MRI or CT myelography is preferred when spinal metastasis is suspected.
Diagnostic Procedures/Other
CT-guided needle biopsy reliably diagnoses carcinoma but is less dependable for lymphoma, though performance has improved with CT guidance, immunophenotyping, and larger needles; false-negative rates remain significant. Establishing an etiologic diagnosis of vertebral osteomyelitis often requires percutaneous or surgical vertebral biopsy.
Differential Diagnosis
Tuberculosis may appear early as an opportunistic infection in AIDS and can be AIDS-defining, while Mycobacterium avium complex typically occurs later with very low CD4 counts. Pertussis should be considered when cough is the predominant symptom, particularly with paroxysms, inspiratory whoop, posttussive vomiting, sleep-disrupting cough, or exposure to similar illness.
Treatment
Medications
Suspected vertebral osteomyelitis or epidural abscess warrants empiric vancomycin to cover MRSA, with addition of a third- or fourth-generation cephalosporin when gram-negative bacteremia is suspected, especially with concurrent pyelonephritis. Therapy should be narrowed once the pathogen is identified; for methicillin-sensitive S. aureus, options include nafcillin, oxacillin, or cefazolin. Typical duration is at least six weeks. Management of tuberculous, brucellar, and salmonella bone disease follows their respective regimens. Corticosteroids may help in acute spinal cord compression. NSAIDs provide symptomatic analgesia, and bisphosphonates may be used for fractures related to breast cancer metastases.
Additional Treatment
Prompt diagnosis with targeted therapy is essential. Epidural abscess requires urgent surgical management with early decompression plus antibiotics. Spinal cord compression is a neurosurgical emergency, and decompression via surgery or radiotherapy within 24 hours of symptom onset is needed to reduce permanent neurologic injury. In suspected spinal or paraspinal infection, bactericidal empiric antibiotics should be started immediately.
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Ongoing Care and Follow-Up
If symptoms persist beyond six weeks, repeat laboratory testing and imaging are recommended. After six weeks of antibiotics for osteomyelitis or epidural abscess, reassessment is needed to determine whether treatment should continue. Ongoing monitoring for medication toxicity is important, particularly in older adults who are more susceptible to adverse drug effects.
Basics
Description
Back pain refers to acute or chronic pain arising from the spine or paraspinal structures. The combination of back pain and fever requires careful evaluation for nonmechanical causes. History should specifically assess weight loss, pain worse when lying down, morning stiffness, and sudden severe or colicky pain. Serial spinal and neurologic examinations are crucial, and any spinal tenderness or focal pain warrants full diagnostic assessment. Vertebral osteomyelitis is commonly suggested by pain worsened by movement and not relieved by rest, focal vertebral tenderness, and elevated erythrocyte sedimentation rate. Pain from neoplastic nerve infiltration is typically constant, progressively worse, and persists at night without relief, whereas mechanical low back pain usually improves with rest. Work-up often begins with plain radiography followed by bone scintigraphy, MRI, CT, laboratory testing, and biopsy based on abnormal findings.
Epidemiology
A definitive pain source is difficult to establish and is identified in fewer than one-quarter of cases. Mechanical causes account for about 97% of low back pain, with degenerative disk disease and lumbar sprain/strain comprising most cases. The spine is a frequent site of bone metastasis. Vertebral osteomyelitis is uncommon at roughly 1 per 100,000 persons annually, with rising rates attributed to vascular devices and intravenous drug use; it occurs more often in early childhood and in adults over 50. Spinal epidural abscess occurs in about 1 per 10,000 hospital admissions per year, and MRSA-related vertebral osteomyelitis and epidural abscess are increasingly reported. Despite global increases in tuberculosis, the rate of extrapulmonary spinal disease remains relatively stable; Pott disease, typically involving the lower thoracic vertebrae, is the most common musculoskeletal extrapulmonary manifestation. Improved survival in sickle cell disease has been accompanied by more Salmonella vertebral osteomyelitis.
Risk Factors
Infectious complications can follow bites from many animals, often linked to occupational exposure (farmers, laboratory workers, veterinarians) or recreation (hunters, campers, exotic pet owners). Systemic infection after animal or human bites is more likely with extremity edema or impaired lymphatic drainage and in immunocompromised hosts. Fever after a dog bite in an immunosuppressed patient should prompt concern for invasive Capnocytophaga canimorsus infection.
Etiology
Infectious sources of back pain with fever include biliary tract infection, chronic prostatitis, herpes zoster, pyelonephritis, retroperitoneal abscess, spinal epidural abscess, and vertebral osteomyelitis. Noninfectious causes include colonic cancer, pancreatic disease, histiocytosis X, metastatic malignancy (breast, lung, prostate, thyroid, kidney, gastrointestinal tract), multiple myeloma, neoplastic invasion of pelvic nerves, lymphoma, pregnancy, vertebral fracture, renal artery or vein thrombosis, renal stones, retroperitoneal hemorrhage or tumors, and tumors of the posterior stomach or duodenum. Staphylococcus aureus is the leading cause of spinal epidural abscess, accounting for most reported cases, with additional pathogens including Actinomyces israelii, Aspergillus, Blastomyces, Brucella, Cryptococcus, Haemophilus parainfluenzae, Mycobacterium tuberculosis, and Streptococcus milleri. Vertebral osteomyelitis is most often due to staphylococci but may be caused by other bacteria or tuberculosis; one multicenter retrospective study from southern Spain reported a high proportion due to Brucella, with the remainder split between pyogenic and tuberculous disease.
Commonly Associated Conditions
Vertebral osteomyelitis and spinal epidural abscess are frequently associated with diabetes, injection drug use, chronic renal failure, alcohol use disorder, bacteremia or focal infections, and malignancy. Most epidural abscesses arise via hematogenous spread from skin or mucosal sources, though direct extension from adjacent infection is also recognized. Postoperative abscesses account for a substantial minority, and epidural catheter placement is another risk factor. Blunt trauma may precede symptoms and may lead to an epidural hematoma that later becomes infected.
Diagnosis
Spinal epidural abscess classically presents with fever, spinal pain and tenderness, and radicular pain progressing to limb weakness, with pain being the most consistent feature. Early on, spinal pain with or without fever may be the only findings before sudden neurologic decline. When sepsis dominates or when patients are bedbound, neurologic deficits may be missed. Fever is absent in a notable minority of pyogenic vertebral osteomyelitis cases and is even more commonly absent in tuberculous vertebral osteomyelitis.
History
Key elements include age; systemic symptoms such as fever, weakness, weight loss, and night sweats; prior trauma, infection, or cancer; pain characteristics; immune status; glycemic control in diabetes; and injection drug use. Screen for neurologic complaints including weakness, paresthesias, numbness, and bowel, bladder, or sexual dysfunction. Risk is higher in patients over 50, those using steroids, individuals with HIV, those on immunosuppressants, and those with prior surgery.
Physical Examination
Assess general appearance, vital signs, peripheral pulses, and perform a focused cardiopulmonary and abdominal evaluation in unstable patients. Look for referred pain by examining potential primary sources of tenderness. Perform a complete neurologic examination to evaluate for spinal cord compromise and localize deficits; lesions below T12 can produce lower motor neuron findings, and cauda equina syndrome may include bowel or bladder incontinence. In older adults, fever may be low-grade and does not reliably indicate severity. Percussion of spinous processes may reveal focal vertebral tenderness due to trauma, malignancy, or infection. Examine for signs of endocarditis and septic emboli.
Diagnostic Tests and Interpretation
Laboratory Studies
Routine blood tests are often nonspecific for vertebral osteomyelitis, but leukocytosis, neutrophilia, and markedly elevated ESR and C-reactive protein support pyogenic disease. Blood cultures are the most useful routine test and identify the organism in about half of pyogenic and Brucella vertebral osteomyelitis cases. Bone biopsy is often required to confirm the diagnosis, especially in tuberculous disease.
Imaging
Plain spinal radiographs may be normal early in vertebral osteomyelitis. MRI best defines the extent and location of spinal epidural abscess. MRI or CT myelography is preferred when spinal metastasis is suspected.
Diagnostic Procedures/Other
CT-guided needle biopsy reliably diagnoses carcinoma but is less dependable for lymphoma, though performance has improved with CT guidance, immunophenotyping, and larger needles; false-negative rates remain significant. Establishing an etiologic diagnosis of vertebral osteomyelitis often requires percutaneous or surgical vertebral biopsy.
Differential Diagnosis
Tuberculosis may appear early as an opportunistic infection in AIDS and can be AIDS-defining, while Mycobacterium avium complex typically occurs later with very low CD4 counts. Pertussis should be considered when cough is the predominant symptom, particularly with paroxysms, inspiratory whoop, posttussive vomiting, sleep-disrupting cough, or exposure to similar illness.
Treatment
Medications
Suspected vertebral osteomyelitis or epidural abscess warrants empiric vancomycin to cover MRSA, with addition of a third- or fourth-generation cephalosporin when gram-negative bacteremia is suspected, especially with concurrent pyelonephritis. Therapy should be narrowed once the pathogen is identified; for methicillin-sensitive S. aureus, options include nafcillin, oxacillin, or cefazolin. Typical duration is at least six weeks. Management of tuberculous, brucellar, and salmonella bone disease follows their respective regimens. Corticosteroids may help in acute spinal cord compression. NSAIDs provide symptomatic analgesia, and bisphosphonates may be used for fractures related to breast cancer metastases.
Additional Treatment
Prompt diagnosis with targeted therapy is essential. Epidural abscess requires urgent surgical management with early decompression plus antibiotics. Spinal cord compression is a neurosurgical emergency, and decompression via surgery or radiotherapy within 24 hours of symptom onset is needed to reduce permanent neurologic injury. In suspected spinal or paraspinal infection, bactericidal empiric antibiotics should be started immediately.
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Ongoing Care and Follow-Up
If symptoms persist beyond six weeks, repeat laboratory testing and imaging are recommended. After six weeks of antibiotics for osteomyelitis or epidural abscess, reassessment is needed to determine whether treatment should continue. Ongoing monitoring for medication toxicity is important, particularly in older adults who are more susceptible to adverse drug effects.
- Published on
Infectious Diseases and Microbiology: Cough and Fever
Basics
Description
Cough is a forceful expiratory reflex that helps clear secretions and foreign material from the tracheobronchial tree. Fever is typically defined as a temperature rise of about 2°F above baseline or a measured temperature above 100.4°F and commonly reflects an immune-mediated increase in the hypothalamic set point. Cough duration is classified as acute (<3 weeks), subacute (3-8 or chronic (≥8 though in high-tuberculosis-burden settings, “chronic cough” is often considered>2–3 weeks.
Epidemiology
Cough is one of the most frequent outpatient complaints. The combination of cough and fever commonly indicates respiratory illness but may also occur with nonrespiratory conditions.
Risk Factors
Risk increases with immunodeficiency, smoking, asthma, or COPD. Pneumonia risk is highest at the extremes of age. Aspiration risk rises with swallowing dysfunction from neurologic disease (including stroke and Parkinson disease) and after surgery or radiation involving the oral cavity, pharynx, or esophagus. Specific environmental or occupational exposures point to particular infections, including unpasteurized dairy (brucellosis), birds (psittacosis due to Chlamydia psittaci), residence or travel to the U.S. Southwest (coccidioidomycosis), rodents (hantavirus), bat guano (histoplasmosis), aerosolized water sources (legionellosis), and water contaminated with animal urine (leptospirosis). Unusually severe pneumonia in a previously healthy person or clustered cases should raise concern for inhalational anthrax, tularemia, plague, other high-consequence infections, pandemic influenza, or SARS, including possible bioterrorism scenarios.
General Prevention
Maintain current vaccination against influenza and Streptococcus pneumoniae, ensure pertussis and Haemophilus influenzae type b immunization in children, and encourage smoking cessation.
Pathophysiology
Cough is triggered as a protective reflex by airway irritation from inhaled substances such as smoke, dust, or fumes, or by aspirated material such as upper-airway secretions, gastric contents, or foreign bodies.
Etiology
Acute cough with fever is most often due to viral nasopharyngitis, including influenza, parainfluenza, respiratory syncytial virus, rhinovirus, coronavirus, and adenovirus. In adults with typical “common cold” syndromes, only mild temperature elevation is expected, and higher fever is atypical. Other acute causes include upper respiratory infections such as acute sinusitis and bronchitis, which are frequently viral and in which cough predominates, and lower respiratory infections such as pneumonia of bacterial, viral, fungal, or aspiration origin, bronchiectasis exacerbations, and lung abscess, as well as mediastinitis, endocarditis, malaria, and pulmonary embolism; several of these may also cause chronic cough with intermittent fever. Subacute cough may result from bacterial sinusitis or be postinfectious; even with minimal fever, pertussis must be considered because it can be mild or atypical after immunization yet remains highly contagious and dangerous to infants. Chronic cough with fever suggests tuberculosis in at-risk populations such as those with homelessness, HIV/AIDS, or exposure in endemic regions, and may also reflect chronic sinusitis, chronic melioidosis due to Burkholderia pseudomallei in Southeast Asia, endobronchial sarcoidosis, Kaposi sarcoma, lymphoma, airway-infiltrating tumors such as bronchogenic carcinoma or carcinoid, pulmonary embolism, or inflammatory pseudotumor. Cough and fever may also represent unrelated processes when their onsets differ, and chronic cough may stem from noninfectious causes such as gastroesophageal reflux, postnasal drip, ACE-inhibitor effect, or asthma.
Commonly Associated Conditions
HIV/AIDS and other immunodeficiency states are frequently linked to cough with fever and broaden the infectious and noninfectious differential.
Diagnosis
History
Because severe febrile respiratory syndromes can rapidly progress to respiratory failure, the first step is to identify life-threatening illness or systemic toxicity, including bacterial pneumonia, influenza, SARS-like syndromes, high-consequence or bioterrorism-related infections, and pulmonary embolism. Assess for dyspnea, hemoptysis, sputum production, other infectious symptoms, and immunodeficiency. A detailed exposure and travel history is essential, and history may also point toward noninfectious causes such as pulmonary embolism after prolonged immobility or malignancy suggested by smoking, weight loss, and hemoptysis without tuberculosis risk factors.
Physical Examination
Examine lungs plus upper airway structures (mouth, throat, nose, sinuses) and ears, and judge overall appearance for severity, fatigue, and impending respiratory compromise. Evaluate for tachycardia (>100/min), tachypnea (>24/min), and impaired oxygenation. Focal rales and egophony support lower respiratory infection, but examination alone often cannot confirm pneumonia.
Diagnostic Tests and Interpretation
Laboratory Studies
Purulent sputum suggests chronic bronchitis, bronchiectasis, pneumonia, or lung abscess, while hemoptysis can occur in these disorders and may also indicate an endobronchial tumor. Sputum microscopy and Gram stain can sometimes identify pathogens and guide antibiotics, but overall yield is limited by variability in collection and interpretation and by inability of many pneumonia patients to produce sputum. For chronic cough in high–tuberculosis-prevalence settings, obtain sputum smears and cultures for acid-fast bacilli and a chest radiograph.
Imaging
Chest radiography helps distinguish upper versus lower respiratory involvement, detect pneumonia, and identify intrathoracic masses. Patients with a syndrome consistent with acute bronchitis who have normal vital signs and a normal lung exam generally do not need chest radiography because pneumonia likelihood is low. Radiographic infiltrate patterns can suggest but do not confirm specific causes: lobar consolidation, cavitation, and large pleural effusions favor bacterial infection; bilateral diffuse involvement may occur with Pneumocystis jirovecii, Legionella, viral infections, or Mycoplasma pneumoniae; necrotizing pneumonia with cavitation and empyema suggests aspiration, gram-negative organisms, or staphylococci; nodular or cavitary patterns may reflect lung abscess or infections such as Nocardia, actinomycosis, atypical mycobacteria, cryptococcosis, or aspergillosis; and focal infiltrates are common with bacteria (including Nocardia), mycobacteria, Cryptococcus, and Aspergillus. High-resolution CT is preferred to demonstrate airway dilation and confirm bronchiectasis, and chest CT helps assess infections not responding to therapy, delineate lung abscess, and evaluate postobstructive pneumonia due to a mass. If the diagnosis remains unclear, consider sinus imaging and otolaryngology evaluation, and assess for extrapulmonary spread such as brain abscess when neurologic or other systemic findings are present.
Diagnostic Procedures/Other
Fiberoptic bronchoscopy assists with specimen collection and histopathologic evaluation of suspected endobronchial tumors and can help define organism susceptibilities in pneumonia unresponsive to therapy using protected sampling techniques. Pleural fluid analysis and pleural biopsy can support diagnosis of tuberculosis or malignancy.
Treatment
Medications
Management depends on identifying the underlying cause and treating it specifically. Antibiotics are generally unnecessary for acute viral upper respiratory infection, and when bacterial sinusitis cannot be distinguished from viral URI at presentation, delaying antibiotics for about seven days is appropriate. Antibiotics are indicated for pneumonia, tuberculosis, and pertussis. Irritative nonproductive cough can be suppressed with antitussives that raise cough threshold such as codeine 15 mg four times daily or dextromethorphan 15 mg four times daily. Additional agents that may reduce cough include NSAIDs such as naproxen, sedating antihistamines for common-cold–related cough (with newer nonsedating antihistamines generally ineffective), and inhaled ipratropium 2–4 puffs four times daily in chronic bronchitis. Productive cough with substantial sputum should usually not be suppressed because secretion retention can worsen ventilation, impair aeration, and reduce host defense. Hydration and expectorants such as guaifenesin may help thin mucus and improve clearance. Inflammatory pseudotumors, though typically resected, have also responded to antibiotics, radiation, or corticosteroids, and may occasionally regress spontaneously.
Additional Treatment
Maintain hydration and support smoking cessation.
In-Patient Considerations
Initial Stabilization
Consider intubation and positive-pressure ventilation for respiratory fatigue or severe oxygenation/ventilation failure based on arterial blood gases. Implement infection control measures, including isolation and airborne precautions, when severe febrile respiratory illness occurs with epidemiologic features suggesting transmissible high-consequence infection, relevant travel, animal or laboratory exposure, or potential bioterrorism.
Admission Criteria
Tools such as the Pneumonia Severity Index, though developed for pneumonia, can help guide disposition in febrile respiratory illness. Advanced age, significant comorbidities, and abnormal vital signs such as tachypnea, tachycardia, hypotension, and altered physiology indicate higher risk of morbidity and mortality.
Ongoing Care and Follow-Up
Reinforce smoking cessation.
Prognosis
Community-acquired pneumonia carries an approximate mortality of 13%.
Complications
Severe coughing paroxysms can trigger syncope. Patients with tuberculosis and cough are infectious and can transmit disease.
Basics
Description
Cough is a forceful expiratory reflex that helps clear secretions and foreign material from the tracheobronchial tree. Fever is typically defined as a temperature rise of about 2°F above baseline or a measured temperature above 100.4°F and commonly reflects an immune-mediated increase in the hypothalamic set point. Cough duration is classified as acute (<3 weeks), subacute (3-8 or chronic (≥8 though in high-tuberculosis-burden settings, “chronic cough” is often considered>2–3 weeks.
Epidemiology
Cough is one of the most frequent outpatient complaints. The combination of cough and fever commonly indicates respiratory illness but may also occur with nonrespiratory conditions.
Risk Factors
Risk increases with immunodeficiency, smoking, asthma, or COPD. Pneumonia risk is highest at the extremes of age. Aspiration risk rises with swallowing dysfunction from neurologic disease (including stroke and Parkinson disease) and after surgery or radiation involving the oral cavity, pharynx, or esophagus. Specific environmental or occupational exposures point to particular infections, including unpasteurized dairy (brucellosis), birds (psittacosis due to Chlamydia psittaci), residence or travel to the U.S. Southwest (coccidioidomycosis), rodents (hantavirus), bat guano (histoplasmosis), aerosolized water sources (legionellosis), and water contaminated with animal urine (leptospirosis). Unusually severe pneumonia in a previously healthy person or clustered cases should raise concern for inhalational anthrax, tularemia, plague, other high-consequence infections, pandemic influenza, or SARS, including possible bioterrorism scenarios.
General Prevention
Maintain current vaccination against influenza and Streptococcus pneumoniae, ensure pertussis and Haemophilus influenzae type b immunization in children, and encourage smoking cessation.
Pathophysiology
Cough is triggered as a protective reflex by airway irritation from inhaled substances such as smoke, dust, or fumes, or by aspirated material such as upper-airway secretions, gastric contents, or foreign bodies.
Etiology
Acute cough with fever is most often due to viral nasopharyngitis, including influenza, parainfluenza, respiratory syncytial virus, rhinovirus, coronavirus, and adenovirus. In adults with typical “common cold” syndromes, only mild temperature elevation is expected, and higher fever is atypical. Other acute causes include upper respiratory infections such as acute sinusitis and bronchitis, which are frequently viral and in which cough predominates, and lower respiratory infections such as pneumonia of bacterial, viral, fungal, or aspiration origin, bronchiectasis exacerbations, and lung abscess, as well as mediastinitis, endocarditis, malaria, and pulmonary embolism; several of these may also cause chronic cough with intermittent fever. Subacute cough may result from bacterial sinusitis or be postinfectious; even with minimal fever, pertussis must be considered because it can be mild or atypical after immunization yet remains highly contagious and dangerous to infants. Chronic cough with fever suggests tuberculosis in at-risk populations such as those with homelessness, HIV/AIDS, or exposure in endemic regions, and may also reflect chronic sinusitis, chronic melioidosis due to Burkholderia pseudomallei in Southeast Asia, endobronchial sarcoidosis, Kaposi sarcoma, lymphoma, airway-infiltrating tumors such as bronchogenic carcinoma or carcinoid, pulmonary embolism, or inflammatory pseudotumor. Cough and fever may also represent unrelated processes when their onsets differ, and chronic cough may stem from noninfectious causes such as gastroesophageal reflux, postnasal drip, ACE-inhibitor effect, or asthma.
Commonly Associated Conditions
HIV/AIDS and other immunodeficiency states are frequently linked to cough with fever and broaden the infectious and noninfectious differential.
Diagnosis
History
Because severe febrile respiratory syndromes can rapidly progress to respiratory failure, the first step is to identify life-threatening illness or systemic toxicity, including bacterial pneumonia, influenza, SARS-like syndromes, high-consequence or bioterrorism-related infections, and pulmonary embolism. Assess for dyspnea, hemoptysis, sputum production, other infectious symptoms, and immunodeficiency. A detailed exposure and travel history is essential, and history may also point toward noninfectious causes such as pulmonary embolism after prolonged immobility or malignancy suggested by smoking, weight loss, and hemoptysis without tuberculosis risk factors.
Physical Examination
Examine lungs plus upper airway structures (mouth, throat, nose, sinuses) and ears, and judge overall appearance for severity, fatigue, and impending respiratory compromise. Evaluate for tachycardia (>100/min), tachypnea (>24/min), and impaired oxygenation. Focal rales and egophony support lower respiratory infection, but examination alone often cannot confirm pneumonia.
Diagnostic Tests and Interpretation
Laboratory Studies
Purulent sputum suggests chronic bronchitis, bronchiectasis, pneumonia, or lung abscess, while hemoptysis can occur in these disorders and may also indicate an endobronchial tumor. Sputum microscopy and Gram stain can sometimes identify pathogens and guide antibiotics, but overall yield is limited by variability in collection and interpretation and by inability of many pneumonia patients to produce sputum. For chronic cough in high–tuberculosis-prevalence settings, obtain sputum smears and cultures for acid-fast bacilli and a chest radiograph.
Imaging
Chest radiography helps distinguish upper versus lower respiratory involvement, detect pneumonia, and identify intrathoracic masses. Patients with a syndrome consistent with acute bronchitis who have normal vital signs and a normal lung exam generally do not need chest radiography because pneumonia likelihood is low. Radiographic infiltrate patterns can suggest but do not confirm specific causes: lobar consolidation, cavitation, and large pleural effusions favor bacterial infection; bilateral diffuse involvement may occur with Pneumocystis jirovecii, Legionella, viral infections, or Mycoplasma pneumoniae; necrotizing pneumonia with cavitation and empyema suggests aspiration, gram-negative organisms, or staphylococci; nodular or cavitary patterns may reflect lung abscess or infections such as Nocardia, actinomycosis, atypical mycobacteria, cryptococcosis, or aspergillosis; and focal infiltrates are common with bacteria (including Nocardia), mycobacteria, Cryptococcus, and Aspergillus. High-resolution CT is preferred to demonstrate airway dilation and confirm bronchiectasis, and chest CT helps assess infections not responding to therapy, delineate lung abscess, and evaluate postobstructive pneumonia due to a mass. If the diagnosis remains unclear, consider sinus imaging and otolaryngology evaluation, and assess for extrapulmonary spread such as brain abscess when neurologic or other systemic findings are present.
Diagnostic Procedures/Other
Fiberoptic bronchoscopy assists with specimen collection and histopathologic evaluation of suspected endobronchial tumors and can help define organism susceptibilities in pneumonia unresponsive to therapy using protected sampling techniques. Pleural fluid analysis and pleural biopsy can support diagnosis of tuberculosis or malignancy.
Treatment
Medications
Management depends on identifying the underlying cause and treating it specifically. Antibiotics are generally unnecessary for acute viral upper respiratory infection, and when bacterial sinusitis cannot be distinguished from viral URI at presentation, delaying antibiotics for about seven days is appropriate. Antibiotics are indicated for pneumonia, tuberculosis, and pertussis. Irritative nonproductive cough can be suppressed with antitussives that raise cough threshold such as codeine 15 mg four times daily or dextromethorphan 15 mg four times daily. Additional agents that may reduce cough include NSAIDs such as naproxen, sedating antihistamines for common-cold–related cough (with newer nonsedating antihistamines generally ineffective), and inhaled ipratropium 2–4 puffs four times daily in chronic bronchitis. Productive cough with substantial sputum should usually not be suppressed because secretion retention can worsen ventilation, impair aeration, and reduce host defense. Hydration and expectorants such as guaifenesin may help thin mucus and improve clearance. Inflammatory pseudotumors, though typically resected, have also responded to antibiotics, radiation, or corticosteroids, and may occasionally regress spontaneously.
Additional Treatment
Maintain hydration and support smoking cessation.
In-Patient Considerations
Initial Stabilization
Consider intubation and positive-pressure ventilation for respiratory fatigue or severe oxygenation/ventilation failure based on arterial blood gases. Implement infection control measures, including isolation and airborne precautions, when severe febrile respiratory illness occurs with epidemiologic features suggesting transmissible high-consequence infection, relevant travel, animal or laboratory exposure, or potential bioterrorism.
Admission Criteria
Tools such as the Pneumonia Severity Index, though developed for pneumonia, can help guide disposition in febrile respiratory illness. Advanced age, significant comorbidities, and abnormal vital signs such as tachypnea, tachycardia, hypotension, and altered physiology indicate higher risk of morbidity and mortality.
Ongoing Care and Follow-Up
Reinforce smoking cessation.
Prognosis
Community-acquired pneumonia carries an approximate mortality of 13%.
Complications
Severe coughing paroxysms can trigger syncope. Patients with tuberculosis and cough are infectious and can transmit disease.
- Published on
Infectious Diseases and Microbiology: Diarrhea and Fever
Basics
Description
Diarrhea is defined as stool output exceeding 200 g/day and, in practice, as three or more loose stools daily. It is acute when <14 days and chronic when>4 weeks. Inflammatory diarrhea presents with frequent, small-volume stools that are mucoid and/or bloody and may include tenesmus, fever, or severe abdominal pain; stool leukocytes are a key feature. Noninflammatory diarrhea is typically watery, may be high volume (>1 L/day), and occurs without blood, pus, severe pain, or fever.
Epidemiology
Incidence
In the United States, acute diarrhea occurs hundreds of millions of times yearly, with tens of millions of episodes linked to identified pathogens, and foodborne spread accounting for a large proportion of known-pathogen disease. Surveillance data have identified non-typhoidal Salmonella, Campylobacter, Shigella, Cryptosporidium, and Shiga toxin–producing E. coli O157 as leading reported causes, with highest bacterial diarrhea rates from Salmonella, Campylobacter, and Yersinia in infants under one year. Post-diarrheal hemolytic uremic syndrome occurs infrequently overall but is most common in children under five. Traveler’s diarrhea affects a substantial fraction of international travelers.
Risk Factors
Risks include consuming undercooked eggs, meat, poultry, seafood, or unpasteurized dairy, and drinking untreated surface water. Greater severity or pathogen-specific risk occurs with HIV, immunosuppressive therapies (including glucocorticoids, TNF inhibitors, and chemotherapy), recent antibiotic exposure, liver disease, neutropenia, malnutrition, zinc deficiency, and IgA deficiency. Oral–anal sexual contact increases risk of enteric infection. Antibiotic exposure is a major risk factor for Clostridioides difficile–associated diarrhea.
General Prevention
Handwashing before eating or food preparation, avoiding undercooked animal products and unpasteurized dairy, and avoiding untreated stream or river water reduce risk. During travel in areas with unsafe water, avoid tap water and ice. Typhoid vaccination is available for travelers, and infant rotavirus vaccination is recommended in the United States; destination-based vaccine guidance is available through travel medicine resources.
Etiology
Bacterial causes include Campylobacter, Salmonella, Shigella, Yersinia enterocolitica, C. difficile, Vibrio cholerae, Vibrio parahaemolyticus, Aeromonas, Plesiomonas shigelloides, and multiple diarrheagenic E. coli pathotypes including ETEC, EPEC, EIEC, STEC (including O157:H7), and EAEC. Viral causes include rotavirus, human caliciviruses such as norovirus, adenovirus, and cytomegalovirus. Parasitic causes include Giardia intestinalis, Cryptosporidium parvum, Entamoeba histolytica, Cyclospora cayetanensis, Isospora belli, and Strongyloides stercoralis. Toxin-mediated syndromes include Staphylococcus aureus, Bacillus cereus, and Clostridium perfringens.
Diagnosis
History
Evaluation should define likely cause, illness severity, and complications. Ask about travel, diet, antibiotic use, sexual practices, day-care exposure, sick contacts, outbreaks, seasonality, and other illnesses, and characterize stool frequency, duration, and appearance. Infectious diarrhea may include fever, chills, vomiting, nausea, abdominal pain, and tenesmus. Dizziness, presyncope, or syncope suggests volume depletion. Dysentery points to invasive pathogens such as Shigella, Salmonella, Campylobacter, STEC (often without fever), or Yersinia. STEC commonly starts watery and becomes bloody and is frequently associated with contaminated beef or produce; fever is often absent. Yersinia and Salmonella may involve the terminal ileum and cecum, producing right lower quadrant pain that mimics appendicitis. Watery diarrhea alone is nonspecific. Enterotoxin-mediated food poisoning from S. aureus, B. cereus, or C. perfringens typically has a short incubation and brief course, with vomiting alone more typical of S. aureus or C. perfringens and watery diarrhea more typical of B. cereus or C. perfringens; fever is usually absent. Extraintestinal features such as arthritis, skin lesions, or eye symptoms suggest inflammatory bowel disease. With recent international travel, likely pathogens depend on location, setting, and season, commonly including ETEC, EAEC, Campylobacter, Salmonella, and norovirus, and travel medicine resources can guide evaluation.
Physical Examination
Assess blood pressure, heart rate, respiratory rate, temperature, and mental status to gauge severity. Look for dehydration signs such as dry mucous membranes, reduced skin turgor, sunken eyes, delayed capillary refill, low jugular venous pressure, and orthostatic hypotension. Examine for abdominal tenderness, peritoneal signs, hepatomegaly, and splenomegaly.
Diagnostic Tests and Interpretation
Laboratory Studies
Testing is indicated with fever, systemic toxicity, bloody stools, dehydration, suspected foodborne outbreak, recent international travel, immunosuppression, or recent antibiotic exposure. Send stool for culture, noting that routine processing commonly targets Shigella, Salmonella, and Campylobacter, so the laboratory should be alerted if suspicion is high for STEC or other E. coli pathotypes, Yersinia, Vibrio, or other organisms. Stool culture yield is generally low. For bloody diarrhea, culture for Salmonella, Shigella, Campylobacter, and STEC and obtain a Shiga toxin immunoassay; if E. coli is isolated, arrange serotyping via a reference laboratory. If there is recent antibiotic exposure, recent hospitalization, day-care exposure, or recent chemotherapy, test stool for C. difficile toxins. If diarrhea persists beyond seven days, submit multiple stools for ova and parasite examination with attention to Giardia, Cryptosporidium, Isospora, and Cyclospora and consider noninfectious causes; in AIDS or immunosuppression, also evaluate for microsporidia, Mycobacterium avium complex, and cytomegalovirus. Fecal polymorphonuclear cells support an inflammatory process. If dehydration or severe illness is present, obtain electrolytes, renal and liver function tests, complete blood count, and blood cultures.
Imaging
If the diagnosis remains unclear in critical illness, with prominent abdominal pain or peritoneal signs, consider CT abdomen with oral and intravenous contrast.
t
Diagnostic Procedures/Other
Further evaluation may require upper endoscopy or colonoscopy with biopsies
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Differential Diagnosis
Acute inflammatory diarrhea may be noninfectious, including ulcerative colitis, Crohn disease, radiation or ischemic colitis, partial obstruction, diverticulitis, laxative abuse, rectosigmoid abscess, Whipple disease, pernicious anemia, diabetes-related enteropathy, malabsorption disorders, scleroderma, or celiac disease. Fever and diarrhea can also result from infections outside the gut such as malaria or sepsis.
Treatment
Medications
Core management is rehydration with selective antibiotic use. Oral rehydration is effective and cost-efficient across settings, while intravenous fluids are indicated for severe dehydration or major electrolyte disturbances; rice-based oral solutions are superior for cholera in children and adults. Antibiotics are recommended for severe infection and for persistent gastroenteritis and are favored in adults over 65, immunocompromised patients, those with prosthetic material, and invasive infections, except when STEC is suspected or confirmed. Empiric therapy for febrile community-acquired invasive diarrhea or moderate to severe traveler’s diarrhea includes ciprofloxacin 500 mg twice daily or levofloxacin 500 mg daily while awaiting studies unless STEC is suspected; travel to Southeast Asia raises concern for fluoroquinolone-resistant Campylobacter. For suspected antibiotic-associated or nosocomial diarrhea, treat empirically with metronidazole or vancomycin while awaiting C. difficile testing. Pathogen-directed therapy includes treating non-typhoidal Salmonella in high-risk or severe disease with fluoroquinolones, TMP-SMX, or ceftriaxone for typical short courses and longer courses in immunocompromised patients, recognizing antibiotics may prolong shedding; treating Shigella with short-course fluoroquinolones or TMP-SMX when susceptible and longer courses for severe or immunocompromised cases; treating Campylobacter with erythromycin while acknowledging high fluoroquinolone resistance especially in Southeast Asia; avoiding antibiotics in STEC due to increased HUS risk and providing supportive care; treating ETEC/EPEC/EIEC similarly to traveler’s diarrhea regimens; usually avoiding antibiotics in Yersinia unless severe or immunocompromised, in which case doxycycline plus an aminoglycoside, fluoroquinolones, or TMP-SMX may be used; managing C. difficile by stopping unnecessary antibiotics and using metronidazole for milder disease or oral vancomycin for 10–14 days; prioritizing fluids in cholera with antibiotics guided by local resistance; treating amebiasis with metronidazole followed by a luminal agent such as paromomycin or iodoquinol; treating giardiasis with metronidazole or single-dose tinidazole; and treating Cyclospora or Isospora with TMP-SMX with extended therapy and possible suppression in immunocompromised hosts.
Additional Treatment
Most mild cases resolve without specific therapy; supportive care includes hydration and symptom control. Loperamide is preferred for adults with mild to moderate nonbloody diarrhea but is contraindicated in severe inflammatory diarrhea, bloody diarrhea, C. difficile infection, and in children under two. Bismuth subsalicylate can reduce stool volume in adults and children. Severe or persistent unexplained diarrhea warrants gastroenterology and/or infectious diseases consultation, and cases due to major reportable pathogens or suspected outbreaks should be reported to public health authorities.
In-Patient Considerations
Initial Stabilization
Severe acute inflammatory diarrhea with systemic toxicity requires rapid rehydration and empiric antibiotics.
Admission Criteria
Hospitalize patients with severe dehydration or inability to maintain oral intake.
IV Fluids
Use intravenous volume repletion for severe dehydration or altered mental status.
Discharge Criteria
Discharge is appropriate when fever has been absent for more than 24 hours, vital signs are stable, and the patient can maintain adequate oral fluids and nutrition.
Ongoing Care and Follow-Up
Evaluate and treat household members with similar symptoms when appropriate.
Diet
Resume food about four hours after starting rehydration, using small frequent meals of easily digestible foods, and avoid hyperosmolar fruit juices that can worsen diarrhea.
Patient Education
Counsel on food safety and strategies to prevent foodborne illness, especially during travel.
Prognosis
Gastrointestinal illness contributes to a large burden of hospitalization and death annually in the United States.
Complications
Potential complications include dehydration, electrolyte derangements, bacteremia and sepsis, malnutrition and vitamin loss, hemolytic uremic syndrome, and systemic amebiasis.
Basics
Description
Diarrhea is defined as stool output exceeding 200 g/day and, in practice, as three or more loose stools daily. It is acute when <14 days and chronic when>4 weeks. Inflammatory diarrhea presents with frequent, small-volume stools that are mucoid and/or bloody and may include tenesmus, fever, or severe abdominal pain; stool leukocytes are a key feature. Noninflammatory diarrhea is typically watery, may be high volume (>1 L/day), and occurs without blood, pus, severe pain, or fever.
Epidemiology
Incidence
In the United States, acute diarrhea occurs hundreds of millions of times yearly, with tens of millions of episodes linked to identified pathogens, and foodborne spread accounting for a large proportion of known-pathogen disease. Surveillance data have identified non-typhoidal Salmonella, Campylobacter, Shigella, Cryptosporidium, and Shiga toxin–producing E. coli O157 as leading reported causes, with highest bacterial diarrhea rates from Salmonella, Campylobacter, and Yersinia in infants under one year. Post-diarrheal hemolytic uremic syndrome occurs infrequently overall but is most common in children under five. Traveler’s diarrhea affects a substantial fraction of international travelers.
Risk Factors
Risks include consuming undercooked eggs, meat, poultry, seafood, or unpasteurized dairy, and drinking untreated surface water. Greater severity or pathogen-specific risk occurs with HIV, immunosuppressive therapies (including glucocorticoids, TNF inhibitors, and chemotherapy), recent antibiotic exposure, liver disease, neutropenia, malnutrition, zinc deficiency, and IgA deficiency. Oral–anal sexual contact increases risk of enteric infection. Antibiotic exposure is a major risk factor for Clostridioides difficile–associated diarrhea.
General Prevention
Handwashing before eating or food preparation, avoiding undercooked animal products and unpasteurized dairy, and avoiding untreated stream or river water reduce risk. During travel in areas with unsafe water, avoid tap water and ice. Typhoid vaccination is available for travelers, and infant rotavirus vaccination is recommended in the United States; destination-based vaccine guidance is available through travel medicine resources.
Etiology
Bacterial causes include Campylobacter, Salmonella, Shigella, Yersinia enterocolitica, C. difficile, Vibrio cholerae, Vibrio parahaemolyticus, Aeromonas, Plesiomonas shigelloides, and multiple diarrheagenic E. coli pathotypes including ETEC, EPEC, EIEC, STEC (including O157:H7), and EAEC. Viral causes include rotavirus, human caliciviruses such as norovirus, adenovirus, and cytomegalovirus. Parasitic causes include Giardia intestinalis, Cryptosporidium parvum, Entamoeba histolytica, Cyclospora cayetanensis, Isospora belli, and Strongyloides stercoralis. Toxin-mediated syndromes include Staphylococcus aureus, Bacillus cereus, and Clostridium perfringens.
Diagnosis
History
Evaluation should define likely cause, illness severity, and complications. Ask about travel, diet, antibiotic use, sexual practices, day-care exposure, sick contacts, outbreaks, seasonality, and other illnesses, and characterize stool frequency, duration, and appearance. Infectious diarrhea may include fever, chills, vomiting, nausea, abdominal pain, and tenesmus. Dizziness, presyncope, or syncope suggests volume depletion. Dysentery points to invasive pathogens such as Shigella, Salmonella, Campylobacter, STEC (often without fever), or Yersinia. STEC commonly starts watery and becomes bloody and is frequently associated with contaminated beef or produce; fever is often absent. Yersinia and Salmonella may involve the terminal ileum and cecum, producing right lower quadrant pain that mimics appendicitis. Watery diarrhea alone is nonspecific. Enterotoxin-mediated food poisoning from S. aureus, B. cereus, or C. perfringens typically has a short incubation and brief course, with vomiting alone more typical of S. aureus or C. perfringens and watery diarrhea more typical of B. cereus or C. perfringens; fever is usually absent. Extraintestinal features such as arthritis, skin lesions, or eye symptoms suggest inflammatory bowel disease. With recent international travel, likely pathogens depend on location, setting, and season, commonly including ETEC, EAEC, Campylobacter, Salmonella, and norovirus, and travel medicine resources can guide evaluation.
Physical Examination
Assess blood pressure, heart rate, respiratory rate, temperature, and mental status to gauge severity. Look for dehydration signs such as dry mucous membranes, reduced skin turgor, sunken eyes, delayed capillary refill, low jugular venous pressure, and orthostatic hypotension. Examine for abdominal tenderness, peritoneal signs, hepatomegaly, and splenomegaly.
Diagnostic Tests and Interpretation
Laboratory Studies
Testing is indicated with fever, systemic toxicity, bloody stools, dehydration, suspected foodborne outbreak, recent international travel, immunosuppression, or recent antibiotic exposure. Send stool for culture, noting that routine processing commonly targets Shigella, Salmonella, and Campylobacter, so the laboratory should be alerted if suspicion is high for STEC or other E. coli pathotypes, Yersinia, Vibrio, or other organisms. Stool culture yield is generally low. For bloody diarrhea, culture for Salmonella, Shigella, Campylobacter, and STEC and obtain a Shiga toxin immunoassay; if E. coli is isolated, arrange serotyping via a reference laboratory. If there is recent antibiotic exposure, recent hospitalization, day-care exposure, or recent chemotherapy, test stool for C. difficile toxins. If diarrhea persists beyond seven days, submit multiple stools for ova and parasite examination with attention to Giardia, Cryptosporidium, Isospora, and Cyclospora and consider noninfectious causes; in AIDS or immunosuppression, also evaluate for microsporidia, Mycobacterium avium complex, and cytomegalovirus. Fecal polymorphonuclear cells support an inflammatory process. If dehydration or severe illness is present, obtain electrolytes, renal and liver function tests, complete blood count, and blood cultures.
Imaging
If the diagnosis remains unclear in critical illness, with prominent abdominal pain or peritoneal signs, consider CT abdomen with oral and intravenous contrast.
t
Diagnostic Procedures/Other
Further evaluation may require upper endoscopy or colonoscopy with biopsies
.
Differential Diagnosis
Acute inflammatory diarrhea may be noninfectious, including ulcerative colitis, Crohn disease, radiation or ischemic colitis, partial obstruction, diverticulitis, laxative abuse, rectosigmoid abscess, Whipple disease, pernicious anemia, diabetes-related enteropathy, malabsorption disorders, scleroderma, or celiac disease. Fever and diarrhea can also result from infections outside the gut such as malaria or sepsis.
Treatment
Medications
Core management is rehydration with selective antibiotic use. Oral rehydration is effective and cost-efficient across settings, while intravenous fluids are indicated for severe dehydration or major electrolyte disturbances; rice-based oral solutions are superior for cholera in children and adults. Antibiotics are recommended for severe infection and for persistent gastroenteritis and are favored in adults over 65, immunocompromised patients, those with prosthetic material, and invasive infections, except when STEC is suspected or confirmed. Empiric therapy for febrile community-acquired invasive diarrhea or moderate to severe traveler’s diarrhea includes ciprofloxacin 500 mg twice daily or levofloxacin 500 mg daily while awaiting studies unless STEC is suspected; travel to Southeast Asia raises concern for fluoroquinolone-resistant Campylobacter. For suspected antibiotic-associated or nosocomial diarrhea, treat empirically with metronidazole or vancomycin while awaiting C. difficile testing. Pathogen-directed therapy includes treating non-typhoidal Salmonella in high-risk or severe disease with fluoroquinolones, TMP-SMX, or ceftriaxone for typical short courses and longer courses in immunocompromised patients, recognizing antibiotics may prolong shedding; treating Shigella with short-course fluoroquinolones or TMP-SMX when susceptible and longer courses for severe or immunocompromised cases; treating Campylobacter with erythromycin while acknowledging high fluoroquinolone resistance especially in Southeast Asia; avoiding antibiotics in STEC due to increased HUS risk and providing supportive care; treating ETEC/EPEC/EIEC similarly to traveler’s diarrhea regimens; usually avoiding antibiotics in Yersinia unless severe or immunocompromised, in which case doxycycline plus an aminoglycoside, fluoroquinolones, or TMP-SMX may be used; managing C. difficile by stopping unnecessary antibiotics and using metronidazole for milder disease or oral vancomycin for 10–14 days; prioritizing fluids in cholera with antibiotics guided by local resistance; treating amebiasis with metronidazole followed by a luminal agent such as paromomycin or iodoquinol; treating giardiasis with metronidazole or single-dose tinidazole; and treating Cyclospora or Isospora with TMP-SMX with extended therapy and possible suppression in immunocompromised hosts.
Additional Treatment
Most mild cases resolve without specific therapy; supportive care includes hydration and symptom control. Loperamide is preferred for adults with mild to moderate nonbloody diarrhea but is contraindicated in severe inflammatory diarrhea, bloody diarrhea, C. difficile infection, and in children under two. Bismuth subsalicylate can reduce stool volume in adults and children. Severe or persistent unexplained diarrhea warrants gastroenterology and/or infectious diseases consultation, and cases due to major reportable pathogens or suspected outbreaks should be reported to public health authorities.
In-Patient Considerations
Initial Stabilization
Severe acute inflammatory diarrhea with systemic toxicity requires rapid rehydration and empiric antibiotics.
Admission Criteria
Hospitalize patients with severe dehydration or inability to maintain oral intake.
IV Fluids
Use intravenous volume repletion for severe dehydration or altered mental status.
Discharge Criteria
Discharge is appropriate when fever has been absent for more than 24 hours, vital signs are stable, and the patient can maintain adequate oral fluids and nutrition.
Ongoing Care and Follow-Up
Evaluate and treat household members with similar symptoms when appropriate.
Diet
Resume food about four hours after starting rehydration, using small frequent meals of easily digestible foods, and avoid hyperosmolar fruit juices that can worsen diarrhea.
Patient Education
Counsel on food safety and strategies to prevent foodborne illness, especially during travel.
Prognosis
Gastrointestinal illness contributes to a large burden of hospitalization and death annually in the United States.
Complications
Potential complications include dehydration, electrolyte derangements, bacteremia and sepsis, malnutrition and vitamin loss, hemolytic uremic syndrome, and systemic amebiasis.
- Published on
Infectious Diseases and Microbiology: Dysuria and Fever
Basics
Description
Dysuria refers to painful urination. Acute urethral syndrome describes dysuria with urgency and frequency in the absence of significant bacteriuria.
Approach to the Patient
Irritation of urethral and bladder mucosa typically causes frequent, painful voiding of small urine volumes. Dysuria is often assumed to be a urinary tract infection and treated empirically, which can miss important diagnoses in some patients and lead to unnecessary antibiotics in others, so targeted evaluation is preferred. A focused history and examination, including pelvic and rectal examination when indicated, often clarifies the cause and enables directed therapy. Sexually transmitted infections including Chlamydia trachomatis, Neisseria gonorrhoeae, and herpes simplex virus can cause dysuria in any sex. Prostatitis is a key diagnosis in men because it is harder to eradicate and can recur. Fever is uncommon in cystitis but may occur with acute prostatitis; dysuria with fever should also raise concern for upper-tract infection such as pyelonephritis. Primary genital herpes can cause dysuria with fever, while chlamydia, gonorrhea, and nonspecific urethritis rarely cause fever unless complicated by pelvic inflammatory disease or Fitz-Hugh–Curtis syndrome. Dysuria with hematuria suggests infectious or noninfectious cystitis and also warrants consideration of tuberculous cystitis, bladder cancer, trauma, renal stones, and schistosomiasis. Dysuria with urethral or vaginal discharge suggests gonorrhea or chlamydia, nonspecific urethritis (with or without conjunctivitis and arthritis consistent with reactive arthritis), and prostatitis. Urinalysis and urine culture are standard initial tests, though young women with classic uncomplicated symptoms and no risk factors for complicated or recurrent infection may be treated empirically.
Epidemiology
Incidence
UTIs are among the most common infectious syndromes and carry substantial costs, including antibiotic expenditures exceeding one billion dollars annually in the United States. Most patients with primary symptomatic genital herpes experience dysuria, though dysuria is typically absent with recurrences. Sexual intercourse is linked to several dysuria etiologies, with symptom timing differing by syndrome: postcoital cystitis often appears within days, urethritis tends to appear after one to two weeks, and vaginitis may present weeks to months later. Pyelonephritis is a frequent cause of hospitalization, and UTIs account for over 100,000 U.S. admissions annually. Healthcare-associated infections are often UTIs, commonly catheter-related; bacteriuria develops in a substantial proportion of patients with prolonged catheterization with a daily incremental risk of infection, and even single catheterization can cause UTI. Escherichia coli causes most uncomplicated UTIs. In pregnancy, asymptomatic bacteriuria can progress to pyelonephritis and is associated with adverse obstetric outcomes including premature labor
.
Etiology
Beyond bacterial cystitis and pyelonephritis and sexually transmitted causes, dysuria may result from atrophic vaginitis, Candida-associated vaginitis, irritation from a distal urethral stone, chemical exposures, compression from an adnexal mass, radiation injury, and vaginal or urethral trauma including sexual abuse or foreign body insertion. Among women with acute dysuria and frequency, most have significant bacteriuria, and many without significant bacteriuria still have infections of the bladder, kidneys, or urethra. Ureaplasma urealyticum is often detected in symptomatic patients but is also found in asymptomatic individuals, and both U. urealyticum and Mycoplasma hominis have been identified in prostatic and renal tissues in patients with dysuria. Adenovirus can cause acute hemorrhagic cystitis in children and some young adults, sometimes in outbreaks, while other urinary viral isolates are generally not considered causes of infection in immunocompetent hosts.
Diagnosis
History
Dysuria with frequency, urgency, and suprapubic discomfort commonly reflects bladder or urethral inflammation. Prostatitis typically causes dysuria, frequency, and urgency and may be suggested by a boggy, tender prostate on rectal examination. Acute pyelonephritis usually evolves over hours to a day with fever, rigors, nausea, vomiting, and sometimes diarrhea; cystitis symptoms may be absent or present. Examination in pyelonephritis often shows fever, tachycardia, diffuse myalgias, and marked costovertebral angle tenderness. Evaluate predisposing factors for UTI or pyelonephritis, including atrophic vaginitis, which may present with reduced discharge, vaginal tenderness, postcoital spotting, and dyspareunia.
Physical Examination
Check vital signs and hydration, especially when pyelonephritis is possible. Suprapubic tenderness supports lower-tract infection, while flank tenderness suggests upper-tract involvement. Perform a genital examination when sexually transmitted infection is suspected, and perform a prostate examination in all men.
Diagnostic Tests and Interpretation
Laboratory Studies
Pyuria is the most sensitive indicator of UTI, and leukocyte esterase testing is highly sensitive for detecting infection-associated pyuria. Urine colony counts of 10^5 CFU/mL generally indicate infection, while lower thresholds (≥10^2 CFU/mL) can be diagnostic in symptomatic patients and in specimens obtained by suprapubic aspiration or catheterization. Most uropathogens convert nitrate to nitrite; nitrite positivity is highly specific but has low sensitivity. Rapid bacteriuria detection methods using techniques such as photometry or bioluminescence can yield results in one to two hours but may miss infections when lower colony counts are used as the comparison standard. Sterile pyuria suggests atypical infections such as chlamydia, ureaplasma, tuberculosis, or fungal infection and can also occur with prostatitis and noninfectious urologic conditions including stones, structural abnormalities, nephrocalcinosis, vesicoureteral reflux, interstitial nephritis, polycystic kidney disease, and related disorders.
Treatment
Therapy for acute urethritis depends on cause. Uncomplicated lower-tract infection in women is treated with short-course antibiotics (about 3–5 days), while men or those with upper-tract disease generally require longer courses (10–14 days). Suspected or confirmed prostatitis requires prolonged therapy, typically at least four weeks. Patients with acute dysuria and frequency who have negative urine cultures and no pyuria generally do not improve with antibiotics.
Ongoing Care and Follow-Up
Many women experience cystitis during their lifetime, and recurrent episodes are common. Most recurrent UTIs represent reinfections after at least one month without symptoms and are often related to vaginal and rectal colonization with uropathogens; anatomic abnormalities are uncommon in young women with recurrent cystitis.
Complications
Lower-tract infection can ascend and cause upper-tract disease.
Basics
Description
Dysuria refers to painful urination. Acute urethral syndrome describes dysuria with urgency and frequency in the absence of significant bacteriuria.
Approach to the Patient
Irritation of urethral and bladder mucosa typically causes frequent, painful voiding of small urine volumes. Dysuria is often assumed to be a urinary tract infection and treated empirically, which can miss important diagnoses in some patients and lead to unnecessary antibiotics in others, so targeted evaluation is preferred. A focused history and examination, including pelvic and rectal examination when indicated, often clarifies the cause and enables directed therapy. Sexually transmitted infections including Chlamydia trachomatis, Neisseria gonorrhoeae, and herpes simplex virus can cause dysuria in any sex. Prostatitis is a key diagnosis in men because it is harder to eradicate and can recur. Fever is uncommon in cystitis but may occur with acute prostatitis; dysuria with fever should also raise concern for upper-tract infection such as pyelonephritis. Primary genital herpes can cause dysuria with fever, while chlamydia, gonorrhea, and nonspecific urethritis rarely cause fever unless complicated by pelvic inflammatory disease or Fitz-Hugh–Curtis syndrome. Dysuria with hematuria suggests infectious or noninfectious cystitis and also warrants consideration of tuberculous cystitis, bladder cancer, trauma, renal stones, and schistosomiasis. Dysuria with urethral or vaginal discharge suggests gonorrhea or chlamydia, nonspecific urethritis (with or without conjunctivitis and arthritis consistent with reactive arthritis), and prostatitis. Urinalysis and urine culture are standard initial tests, though young women with classic uncomplicated symptoms and no risk factors for complicated or recurrent infection may be treated empirically.
Epidemiology
Incidence
UTIs are among the most common infectious syndromes and carry substantial costs, including antibiotic expenditures exceeding one billion dollars annually in the United States. Most patients with primary symptomatic genital herpes experience dysuria, though dysuria is typically absent with recurrences. Sexual intercourse is linked to several dysuria etiologies, with symptom timing differing by syndrome: postcoital cystitis often appears within days, urethritis tends to appear after one to two weeks, and vaginitis may present weeks to months later. Pyelonephritis is a frequent cause of hospitalization, and UTIs account for over 100,000 U.S. admissions annually. Healthcare-associated infections are often UTIs, commonly catheter-related; bacteriuria develops in a substantial proportion of patients with prolonged catheterization with a daily incremental risk of infection, and even single catheterization can cause UTI. Escherichia coli causes most uncomplicated UTIs. In pregnancy, asymptomatic bacteriuria can progress to pyelonephritis and is associated with adverse obstetric outcomes including premature labor
.
Etiology
Beyond bacterial cystitis and pyelonephritis and sexually transmitted causes, dysuria may result from atrophic vaginitis, Candida-associated vaginitis, irritation from a distal urethral stone, chemical exposures, compression from an adnexal mass, radiation injury, and vaginal or urethral trauma including sexual abuse or foreign body insertion. Among women with acute dysuria and frequency, most have significant bacteriuria, and many without significant bacteriuria still have infections of the bladder, kidneys, or urethra. Ureaplasma urealyticum is often detected in symptomatic patients but is also found in asymptomatic individuals, and both U. urealyticum and Mycoplasma hominis have been identified in prostatic and renal tissues in patients with dysuria. Adenovirus can cause acute hemorrhagic cystitis in children and some young adults, sometimes in outbreaks, while other urinary viral isolates are generally not considered causes of infection in immunocompetent hosts.
Diagnosis
History
Dysuria with frequency, urgency, and suprapubic discomfort commonly reflects bladder or urethral inflammation. Prostatitis typically causes dysuria, frequency, and urgency and may be suggested by a boggy, tender prostate on rectal examination. Acute pyelonephritis usually evolves over hours to a day with fever, rigors, nausea, vomiting, and sometimes diarrhea; cystitis symptoms may be absent or present. Examination in pyelonephritis often shows fever, tachycardia, diffuse myalgias, and marked costovertebral angle tenderness. Evaluate predisposing factors for UTI or pyelonephritis, including atrophic vaginitis, which may present with reduced discharge, vaginal tenderness, postcoital spotting, and dyspareunia.
Physical Examination
Check vital signs and hydration, especially when pyelonephritis is possible. Suprapubic tenderness supports lower-tract infection, while flank tenderness suggests upper-tract involvement. Perform a genital examination when sexually transmitted infection is suspected, and perform a prostate examination in all men.
Diagnostic Tests and Interpretation
Laboratory Studies
Pyuria is the most sensitive indicator of UTI, and leukocyte esterase testing is highly sensitive for detecting infection-associated pyuria. Urine colony counts of 10^5 CFU/mL generally indicate infection, while lower thresholds (≥10^2 CFU/mL) can be diagnostic in symptomatic patients and in specimens obtained by suprapubic aspiration or catheterization. Most uropathogens convert nitrate to nitrite; nitrite positivity is highly specific but has low sensitivity. Rapid bacteriuria detection methods using techniques such as photometry or bioluminescence can yield results in one to two hours but may miss infections when lower colony counts are used as the comparison standard. Sterile pyuria suggests atypical infections such as chlamydia, ureaplasma, tuberculosis, or fungal infection and can also occur with prostatitis and noninfectious urologic conditions including stones, structural abnormalities, nephrocalcinosis, vesicoureteral reflux, interstitial nephritis, polycystic kidney disease, and related disorders.
Treatment
Therapy for acute urethritis depends on cause. Uncomplicated lower-tract infection in women is treated with short-course antibiotics (about 3–5 days), while men or those with upper-tract disease generally require longer courses (10–14 days). Suspected or confirmed prostatitis requires prolonged therapy, typically at least four weeks. Patients with acute dysuria and frequency who have negative urine cultures and no pyuria generally do not improve with antibiotics.
Ongoing Care and Follow-Up
Many women experience cystitis during their lifetime, and recurrent episodes are common. Most recurrent UTIs represent reinfections after at least one month without symptoms and are often related to vaginal and rectal colonization with uropathogens; anatomic abnormalities are uncommon in young women with recurrent cystitis.
Complications
Lower-tract infection can ascend and cause upper-tract disease.
- Published on
KembaraXtra-Emergency And Acute Medicine: Hydrocephalus
Basics
Description Hydrocephalus is an abnormal increase in cerebrospinal fluid (CSF) volume within the cranial cavity. Cerebral atrophy may also increase CSF volume but without elevated CSF pressure. Obstructive hydrocephalus is the most common form and results from blockage within the ventricular system or subarachnoid space, potentially causing rapid rises in intracranial pressure (ICP) leading to death or permanent brain injury. Nonobstructive hydrocephalus produces subacute symptoms and represents a potentially reversible cause of dementia. Hydrocephalus is also classified as communicating, where CSF flow is blocked after exiting the ventricles, and noncommunicating, where flow is blocked within ventricular pathways.
Etiology Obstructive hydrocephalus results from blockage at specific anatomic sites. Aqueduct of Sylvius obstruction is most common, causing dilation of the lateral and third ventricles with sparing of the fourth ventricle; causes include congenital stenosis, tumor, subarachnoid hemorrhage, postmeningitic scarring, or idiopathic disease. Foramen of Monro obstruction leads to dilation of one or both lateral ventricles. Obstruction at the foramina of Luschka and Magendie causes fourth ventricle blockage with subsequent dilation of the entire ventricular system. Subarachnoid space obstruction around the brainstem may occur after infection or subarachnoid hemorrhage, producing global ventricular dilation. Acute presentations are often due to CSF shunt malfunction, subarachnoid hemorrhage, or severe head trauma. Nonobstructive hydrocephalus, including normal pressure hydrocephalus, involves impaired CSF absorption with ventricular enlargement but no sustained intracranial hypertension and is sometimes termed chronic hydrocephalus. Pediatric hydrocephalus may be congenital or acquired and is commonly related to neonatal hemorrhage, congenital malformations, or postinfectious scarring.
Diagnosis
Signs and symptoms Obstructive hydrocephalus presents with headache, nausea, vomiting, decreased consciousness, urinary incontinence, ocular palsies, papilledema, visual loss, pupillary dilation, and Cushing response with hypertension and bradycardia. Pediatric patients may show a full fontanelle, irritability, lethargy, and elevated blood pressure. Slowly progressive obstruction may resemble nonobstructive hydrocephalus. Nonobstructive hydrocephalus presents with insidious dementia, somnolence, gait disturbance, urinary incontinence, impaired upward gaze, generalized weakness, and lethargy, typically without headache or papilledema.
Pediatric considerations Gradual CSF accumulation may cause craniomegaly, developmental delay, prominent scalp veins, and impaired upward gaze (setting-sun sign).
History Assess symptom onset, presence of a CSF shunt, headache, nausea or vomiting, weakness, confusion, visual changes, and urinary incontinence.
Physical exam Perform a complete neurologic examination including motor, sensory, reflexes, gait, and cranial nerves. Assess mental status and look for papilledema. Palpate any CSF shunt; inability to compress suggests distal malfunction, and failure to refill suggests proximal obstruction. In children, evaluate the anterior fontanelle.
Essential workup Noncontrast CT of the head assesses ventricular size and symmetry and helps identify hemorrhage, mass lesions, or cerebral edema.
Diagnosis tests and interpretation
Laboratory Lumbar puncture is performed only after CT and only for suspected nonobstructive causes; opening pressure may be elevated. Send CSF for routine studies if infection is suspected.
Imaging MRI provides detailed assessment of ventricular anatomy and improved detection of masses compared with CT.
Diagnostic procedures Lumbar puncture may be diagnostic or therapeutic in selected nonobstructive cases.
Differential diagnosis Acute ischemic stroke, intracranial hemorrhage, CNS infection, mass effect from tumor or hematoma, other causes of dementia or delirium, and toxic or metabolic encephalopathies.
Pediatric considerations Consider congenital anomalies such as Dandy–Walker malformation, Arnold–Chiari malformation, meningomyelocele, choroid plexus papilloma, or arachnoid villi dysfunction, as well as infections (rubella, CMV, toxoplasmosis, syphilis, bacterial meningitis), tumors of the posterior fossa, and intraventricular or subarachnoid hemorrhage.
Treatment
Prehospital Hydrocephalus cannot be definitively diagnosed in the field. Provide supplemental oxygen and airway support as needed. Transport with the head elevated to approximately 30° unless hypotension is present, in which case prioritize cerebral perfusion with fluid resuscitation.
Initial stabilization/therapy For signs of impending herniation, perform rapid-sequence intubation using agents such as etomidate or thiopental. Maintain controlled ventilation with PaCO₂ around 35 mm Hg and systolic blood pressure above 100 mm Hg in adults. Administer mannitol as indicated. In patients with CSF shunts and impending herniation, shunt pumping or controlled CSF drainage may be attempted to reduce pressure.
Emergency department management ED intervention is required for acute shunt malfunction or impending herniation. Definitive therapy involves shunt placement or revision or treatment of the underlying cause such as tumor. Symptoms of normal pressure hydrocephalus may transiently improve after removal of 20–30 mL of CSF via lumbar puncture. Acute obstructive hydrocephalus from intraventricular hemorrhage may require ventriculostomy. Provide sedation for agitated or intubated patients, maintain head elevation unless hypotensive, consider mannitol, and use seizure prophylaxis when appropriate.
Medication Atropine 0.02 mg/kg IV (max 0.1 mg), etomidate 0.2–0.3 mg/kg IV, lidocaine 1 mg/kg IV, mannitol 0.5–1.5 g/kg IV, rocuronium 0.6 mg/kg IV, succinylcholine 1–1.5 mg/kg IV, vecuronium 0.1 mg/kg IV, fosphenytoin 15–20 mg/kg loading dose.
Follow-up and disposition
Admission criteria Evidence of increased ICP or suspected shunt malfunction.
Discharge criteria Selected patients with presumed normal pressure hydrocephalus and no acute findings may be discharged with close follow-up.
Issues for referral Early neurosurgical consultation is essential for acute obstructive hydrocephalus or shunt malfunction; transfer should be considered if neurosurgical care is unavailable, with airway secured when indicated.
Follow-up recommendations Stable patients require prompt follow-up with neurology and/or neurosurgery.
Key points Lumbar puncture is contraindicated in obstructive hydrocephalus due to herniation risk. Rapid head growth in children should prompt evaluation for hydrocephalus. Any neurologic complaint in a patient with a CSF shunt should raise concern for shunt malfunction.
Basics
Description Hydrocephalus is an abnormal increase in cerebrospinal fluid (CSF) volume within the cranial cavity. Cerebral atrophy may also increase CSF volume but without elevated CSF pressure. Obstructive hydrocephalus is the most common form and results from blockage within the ventricular system or subarachnoid space, potentially causing rapid rises in intracranial pressure (ICP) leading to death or permanent brain injury. Nonobstructive hydrocephalus produces subacute symptoms and represents a potentially reversible cause of dementia. Hydrocephalus is also classified as communicating, where CSF flow is blocked after exiting the ventricles, and noncommunicating, where flow is blocked within ventricular pathways.
Etiology Obstructive hydrocephalus results from blockage at specific anatomic sites. Aqueduct of Sylvius obstruction is most common, causing dilation of the lateral and third ventricles with sparing of the fourth ventricle; causes include congenital stenosis, tumor, subarachnoid hemorrhage, postmeningitic scarring, or idiopathic disease. Foramen of Monro obstruction leads to dilation of one or both lateral ventricles. Obstruction at the foramina of Luschka and Magendie causes fourth ventricle blockage with subsequent dilation of the entire ventricular system. Subarachnoid space obstruction around the brainstem may occur after infection or subarachnoid hemorrhage, producing global ventricular dilation. Acute presentations are often due to CSF shunt malfunction, subarachnoid hemorrhage, or severe head trauma. Nonobstructive hydrocephalus, including normal pressure hydrocephalus, involves impaired CSF absorption with ventricular enlargement but no sustained intracranial hypertension and is sometimes termed chronic hydrocephalus. Pediatric hydrocephalus may be congenital or acquired and is commonly related to neonatal hemorrhage, congenital malformations, or postinfectious scarring.
Diagnosis
Signs and symptoms Obstructive hydrocephalus presents with headache, nausea, vomiting, decreased consciousness, urinary incontinence, ocular palsies, papilledema, visual loss, pupillary dilation, and Cushing response with hypertension and bradycardia. Pediatric patients may show a full fontanelle, irritability, lethargy, and elevated blood pressure. Slowly progressive obstruction may resemble nonobstructive hydrocephalus. Nonobstructive hydrocephalus presents with insidious dementia, somnolence, gait disturbance, urinary incontinence, impaired upward gaze, generalized weakness, and lethargy, typically without headache or papilledema.
Pediatric considerations Gradual CSF accumulation may cause craniomegaly, developmental delay, prominent scalp veins, and impaired upward gaze (setting-sun sign).
History Assess symptom onset, presence of a CSF shunt, headache, nausea or vomiting, weakness, confusion, visual changes, and urinary incontinence.
Physical exam Perform a complete neurologic examination including motor, sensory, reflexes, gait, and cranial nerves. Assess mental status and look for papilledema. Palpate any CSF shunt; inability to compress suggests distal malfunction, and failure to refill suggests proximal obstruction. In children, evaluate the anterior fontanelle.
Essential workup Noncontrast CT of the head assesses ventricular size and symmetry and helps identify hemorrhage, mass lesions, or cerebral edema.
Diagnosis tests and interpretation
Laboratory Lumbar puncture is performed only after CT and only for suspected nonobstructive causes; opening pressure may be elevated. Send CSF for routine studies if infection is suspected.
Imaging MRI provides detailed assessment of ventricular anatomy and improved detection of masses compared with CT.
Diagnostic procedures Lumbar puncture may be diagnostic or therapeutic in selected nonobstructive cases.
Differential diagnosis Acute ischemic stroke, intracranial hemorrhage, CNS infection, mass effect from tumor or hematoma, other causes of dementia or delirium, and toxic or metabolic encephalopathies.
Pediatric considerations Consider congenital anomalies such as Dandy–Walker malformation, Arnold–Chiari malformation, meningomyelocele, choroid plexus papilloma, or arachnoid villi dysfunction, as well as infections (rubella, CMV, toxoplasmosis, syphilis, bacterial meningitis), tumors of the posterior fossa, and intraventricular or subarachnoid hemorrhage.
Treatment
Prehospital Hydrocephalus cannot be definitively diagnosed in the field. Provide supplemental oxygen and airway support as needed. Transport with the head elevated to approximately 30° unless hypotension is present, in which case prioritize cerebral perfusion with fluid resuscitation.
Initial stabilization/therapy For signs of impending herniation, perform rapid-sequence intubation using agents such as etomidate or thiopental. Maintain controlled ventilation with PaCO₂ around 35 mm Hg and systolic blood pressure above 100 mm Hg in adults. Administer mannitol as indicated. In patients with CSF shunts and impending herniation, shunt pumping or controlled CSF drainage may be attempted to reduce pressure.
Emergency department management ED intervention is required for acute shunt malfunction or impending herniation. Definitive therapy involves shunt placement or revision or treatment of the underlying cause such as tumor. Symptoms of normal pressure hydrocephalus may transiently improve after removal of 20–30 mL of CSF via lumbar puncture. Acute obstructive hydrocephalus from intraventricular hemorrhage may require ventriculostomy. Provide sedation for agitated or intubated patients, maintain head elevation unless hypotensive, consider mannitol, and use seizure prophylaxis when appropriate.
Medication Atropine 0.02 mg/kg IV (max 0.1 mg), etomidate 0.2–0.3 mg/kg IV, lidocaine 1 mg/kg IV, mannitol 0.5–1.5 g/kg IV, rocuronium 0.6 mg/kg IV, succinylcholine 1–1.5 mg/kg IV, vecuronium 0.1 mg/kg IV, fosphenytoin 15–20 mg/kg loading dose.
Follow-up and disposition
Admission criteria Evidence of increased ICP or suspected shunt malfunction.
Discharge criteria Selected patients with presumed normal pressure hydrocephalus and no acute findings may be discharged with close follow-up.
Issues for referral Early neurosurgical consultation is essential for acute obstructive hydrocephalus or shunt malfunction; transfer should be considered if neurosurgical care is unavailable, with airway secured when indicated.
Follow-up recommendations Stable patients require prompt follow-up with neurology and/or neurosurgery.
Key points Lumbar puncture is contraindicated in obstructive hydrocephalus due to herniation risk. Rapid head growth in children should prompt evaluation for hydrocephalus. Any neurologic complaint in a patient with a CSF shunt should raise concern for shunt malfunction.
- Published on
KembaraXtra-Emergency And Acute Medicine: Hydrocarbon Poisoning
Basics
Description The most serious complication of hydrocarbon exposure is aspiration, primarily affecting the respiratory and central nervous systems. Toxicity is influenced by physical properties. Viscosity: lower viscosity increases aspiration risk. Volatility: highly volatile substances displace alveolar oxygen, leading to hypoxia. Surface tension: low surface tension facilitates spread from the oropharynx into the trachea, increasing aspiration risk (e.g., mineral oil, seal oil). Volatile-substance abuse commonly involves solvents such as typewriter correction fluid, adhesives, gasoline, and lighter fluid. Methods include sniffing (direct inhalation), huffing (from a soaked rag), and bagging (from a bag). Major hydrocarbon classes include aliphatics (kerosene, mineral oil, gasoline, solvents, paint thinners) causing pulmonary toxicity via aspiration and asphyxiation from methane or butane; halogenated hydrocarbons (carbon tetrachloride, trichloroethane) used industrially, well absorbed, and associated with hepatic and renal failure; aromatic or cyclic hydrocarbons (toluene, xylene) that are highly volatile and systemically absorbed, with fatal benzene ingestion reported at ~15 mL; and terpenes or wood distillates (turpentine, pine oil) causing significant gastrointestinal absorption and CNS depression.
Etiology Accidental exposure is most common in young children, while inhalant abuse and intentional self-harm are more frequent in adolescents and adults.
Diagnosis
Signs and symptoms Patients may be asymptomatic initially and often have a hydrocarbon odor on the breath. Early effects include euphoria and disinhibition; later effects include dysphoria, ataxia, confusion, and hallucinations. Sudden sniffing death can occur in volatile-substance abusers due to malignant dysrhythmias from myocardial sensitization. Pulmonary manifestations range from mild respiratory distress to cyanosis and aspiration pneumonitis. CNS effects include intoxication, slurred speech, lethargy, and coma. Gastrointestinal findings include mucosal irritation, gastritis, and diarrhea. Cardiac effects include tachycardia and dysrhythmias. Dermal findings include erythema, maculopapular or vesicular eruptions, defatting dermatitis, and “huffer face” rash with chronic exposure.
History Assess route, substance, amount, timing, intent, possible coingestions, symptoms, and any prehospital interventions.
Physical exam Evaluate airway protection in patients with vomiting or decreased consciousness. Respiratory symptoms usually appear within 30 minutes but may be delayed. Monitor for hypoxia, hypotension, and dysrhythmias. Early fever suggests chemical pneumonitis, whereas fever after 48 hours suggests secondary infection.
Essential workup Identify the exact product, manufacturer, ingredients, exposure type, and estimated quantity; review MSDS when applicable.
Diagnosis tests and interpretation
Laboratory Obtain ECG in volatile-substance abusers. Use pulse oximetry and ABG if abnormal. Check electrolytes, BUN, creatinine, glucose, and liver function tests for halogenated or aromatic exposures; metabolic acidosis and hypokalemia may be present. Measure carboxyhemoglobin for methylene chloride exposure.
Imaging Chest radiograph abnormalities may appear from 20 minutes to 24 hours (typically by 6 hours) and include increased bronchovascular markings with bibasilar or perihilar infiltrates. Lobar consolidation is uncommon; pneumothorax, pneumomediastinum, pleural effusion, and pneumatoceles are rare. Repeat imaging if respiratory status worsens.
Differential diagnosis Caustic ingestion, pesticide poisoning, toxic alcohol ingestion, assessment of accidental versus intentional exposure (psychiatric evaluation), and possible child neglect.
Treatment
Prehospital Remove contaminated clothing and decontaminate exposed skin and hair. Do not induce emesis; ipecac is contraindicated. Keep volatile-substance abusers calm and minimize agitation. Selected asymptomatic patients with known products and reliable observation may be managed at home.
Initial stabilization Follow ABCs, establish IV access with fluids if needed, administer oxygen, monitor cardiac rhythm, and give naloxone, thiamine, and dextrose for altered mental status as indicated.
Emergency department management Provide supportive care. Treat bronchospasm with oxygen and nebulized albuterol; intubate and ventilate for respiratory failure. Steroids are not recommended. Avoid epinephrine in volatile-substance abusers due to dysrhythmia risk. Alert Gastric decontamination is generally not indicated because aspiration risk outweighs benefit. Avoid if spontaneous emesis occurred. Consider limited gastric aspiration only for select CHAMP ingestions (camphor, halogenated hydrocarbons, aromatic hydrocarbons, metals, pesticides) within 60 minutes, with airway protection if needed. Activated charcoal and cathartics are not recommended.
Medication Albuterol 2.5–5 mg nebulized (pediatrics 0.15–0.3 mg/kg). Dextrose D50W 25 g IV (pediatrics D25W 2–4 mL/kg). Naloxone 2 mg IV or IM (pediatrics 0.1 mg/kg). Thiamine 100 mg IV or IM (pediatrics 50 mg).
Follow-up and disposition
Admission criteria Symptomatic patients or those at risk for delayed organ toxicity.
Discharge criteria Observe for at least 6 hours; discharge asymptomatic patients with normal pulse oximetry and chest radiograph, or those asymptomatic with abnormal imaging but normal oxygenation if reliable follow-up is ensured. Observe volatile-substance abusers until mental status normalizes.
Follow-up recommendations Reassess within 24 hours for patients who remain asymptomatic after observation. Repeat chest radiograph in 24 hours for asymptomatic patients with initial abnormalities.
Key points Aspiration is the dominant hazard in hydrocarbon exposure, with risk rising as viscosity and surface tension decrease and volatility increases. Prompt external decontamination is essential. Gastric decontamination and induced emesis are rarely appropriate. All patients should be observed for at least 6 hours, with hospital admission for those who are symptomatic or at risk for delayed toxicity.
Basics
Description The most serious complication of hydrocarbon exposure is aspiration, primarily affecting the respiratory and central nervous systems. Toxicity is influenced by physical properties. Viscosity: lower viscosity increases aspiration risk. Volatility: highly volatile substances displace alveolar oxygen, leading to hypoxia. Surface tension: low surface tension facilitates spread from the oropharynx into the trachea, increasing aspiration risk (e.g., mineral oil, seal oil). Volatile-substance abuse commonly involves solvents such as typewriter correction fluid, adhesives, gasoline, and lighter fluid. Methods include sniffing (direct inhalation), huffing (from a soaked rag), and bagging (from a bag). Major hydrocarbon classes include aliphatics (kerosene, mineral oil, gasoline, solvents, paint thinners) causing pulmonary toxicity via aspiration and asphyxiation from methane or butane; halogenated hydrocarbons (carbon tetrachloride, trichloroethane) used industrially, well absorbed, and associated with hepatic and renal failure; aromatic or cyclic hydrocarbons (toluene, xylene) that are highly volatile and systemically absorbed, with fatal benzene ingestion reported at ~15 mL; and terpenes or wood distillates (turpentine, pine oil) causing significant gastrointestinal absorption and CNS depression.
Etiology Accidental exposure is most common in young children, while inhalant abuse and intentional self-harm are more frequent in adolescents and adults.
Diagnosis
Signs and symptoms Patients may be asymptomatic initially and often have a hydrocarbon odor on the breath. Early effects include euphoria and disinhibition; later effects include dysphoria, ataxia, confusion, and hallucinations. Sudden sniffing death can occur in volatile-substance abusers due to malignant dysrhythmias from myocardial sensitization. Pulmonary manifestations range from mild respiratory distress to cyanosis and aspiration pneumonitis. CNS effects include intoxication, slurred speech, lethargy, and coma. Gastrointestinal findings include mucosal irritation, gastritis, and diarrhea. Cardiac effects include tachycardia and dysrhythmias. Dermal findings include erythema, maculopapular or vesicular eruptions, defatting dermatitis, and “huffer face” rash with chronic exposure.
History Assess route, substance, amount, timing, intent, possible coingestions, symptoms, and any prehospital interventions.
Physical exam Evaluate airway protection in patients with vomiting or decreased consciousness. Respiratory symptoms usually appear within 30 minutes but may be delayed. Monitor for hypoxia, hypotension, and dysrhythmias. Early fever suggests chemical pneumonitis, whereas fever after 48 hours suggests secondary infection.
Essential workup Identify the exact product, manufacturer, ingredients, exposure type, and estimated quantity; review MSDS when applicable.
Diagnosis tests and interpretation
Laboratory Obtain ECG in volatile-substance abusers. Use pulse oximetry and ABG if abnormal. Check electrolytes, BUN, creatinine, glucose, and liver function tests for halogenated or aromatic exposures; metabolic acidosis and hypokalemia may be present. Measure carboxyhemoglobin for methylene chloride exposure.
Imaging Chest radiograph abnormalities may appear from 20 minutes to 24 hours (typically by 6 hours) and include increased bronchovascular markings with bibasilar or perihilar infiltrates. Lobar consolidation is uncommon; pneumothorax, pneumomediastinum, pleural effusion, and pneumatoceles are rare. Repeat imaging if respiratory status worsens.
Differential diagnosis Caustic ingestion, pesticide poisoning, toxic alcohol ingestion, assessment of accidental versus intentional exposure (psychiatric evaluation), and possible child neglect.
Treatment
Prehospital Remove contaminated clothing and decontaminate exposed skin and hair. Do not induce emesis; ipecac is contraindicated. Keep volatile-substance abusers calm and minimize agitation. Selected asymptomatic patients with known products and reliable observation may be managed at home.
Initial stabilization Follow ABCs, establish IV access with fluids if needed, administer oxygen, monitor cardiac rhythm, and give naloxone, thiamine, and dextrose for altered mental status as indicated.
Emergency department management Provide supportive care. Treat bronchospasm with oxygen and nebulized albuterol; intubate and ventilate for respiratory failure. Steroids are not recommended. Avoid epinephrine in volatile-substance abusers due to dysrhythmia risk. Alert Gastric decontamination is generally not indicated because aspiration risk outweighs benefit. Avoid if spontaneous emesis occurred. Consider limited gastric aspiration only for select CHAMP ingestions (camphor, halogenated hydrocarbons, aromatic hydrocarbons, metals, pesticides) within 60 minutes, with airway protection if needed. Activated charcoal and cathartics are not recommended.
Medication Albuterol 2.5–5 mg nebulized (pediatrics 0.15–0.3 mg/kg). Dextrose D50W 25 g IV (pediatrics D25W 2–4 mL/kg). Naloxone 2 mg IV or IM (pediatrics 0.1 mg/kg). Thiamine 100 mg IV or IM (pediatrics 50 mg).
Follow-up and disposition
Admission criteria Symptomatic patients or those at risk for delayed organ toxicity.
Discharge criteria Observe for at least 6 hours; discharge asymptomatic patients with normal pulse oximetry and chest radiograph, or those asymptomatic with abnormal imaging but normal oxygenation if reliable follow-up is ensured. Observe volatile-substance abusers until mental status normalizes.
Follow-up recommendations Reassess within 24 hours for patients who remain asymptomatic after observation. Repeat chest radiograph in 24 hours for asymptomatic patients with initial abnormalities.
Key points Aspiration is the dominant hazard in hydrocarbon exposure, with risk rising as viscosity and surface tension decrease and volatility increases. Prompt external decontamination is essential. Gastric decontamination and induced emesis are rarely appropriate. All patients should be observed for at least 6 hours, with hospital admission for those who are symptomatic or at risk for delayed toxicity.
- Published on
Emergency And Acute Medicine-Hypercalcemia
Basics
Description Hypercalcemia severity depends on the absolute calcium level and the rate of rise. It is detected in approximately 0.1–1% of routine screenings. Most cases are mild (<12 mg/dL) and asymptomatic. Hypercalcemic crisis, typically >14 mg/dL, causes severe and potentially life-threatening manifestations. Circulating calcium exists as ionized (45%, the only physiologically active form), protein-bound (40%, mainly albumin), and complexed to anions (15%).
Etiology The most common causes are primary hyperparathyroidism and malignancy, followed by miscellaneous conditions.
Diagnosis
Signs and symptoms Neurologic features include headache, fatigue, lethargy, weakness, impaired concentration, confusion, depression, paranoia, stupor, or coma. Renal manifestations include polyuria, polydipsia, dehydration, oliguria in renal failure, nephrolithiasis, nephrocalcinosis, and interstitial nephritis. Gastrointestinal symptoms include anorexia, nausea, vomiting, abdominal pain, constipation, peptic ulcer disease, and pancreatitis. Dermatologic findings include pruritus. Classic mnemonic: “stones, bones, groans, thrones, and psychiatric overtones,” where “thrones” refers to polyuria.
Pediatric considerations Failure to thrive, delayed development, and potential intellectual impairment.
Physical exam Neurologic findings include irritability, lethargy, hyporeflexia, and coma. Cardiovascular findings include hypotension from volume depletion or hypertension, sinus bradycardia, and rarely cardiac arrest. Renal signs reflect dehydration. Dermatologic findings include band keratopathy and ectopic calcifications. Pediatric findings may include characteristic facies (pug nose, broad nasal bridge, cupid’s-bow upper lip) and hypotonia.
Essential workup Measure total and ionized calcium and albumin. Normal total calcium is <10.5 mg/dL. Corrected calcium (mg/dL) = measured calcium + 0.8 × (4.0 − albumin [g/dL]). Obtain electrolytes, BUN/creatinine, and glucose. ECG may show shortened QT interval, PR prolongation, QRS widening, sinus bradycardia, conduction blocks, digoxin sensitivity, and rarely Osborn J-waves.
Diagnosis tests and interpretation
Laboratory Assess phosphate, protein, urinalysis, and parathyroid hormone (PTH). Elevated or high-normal PTH suggests primary hyperparathyroidism; PTH <20 pg/mL warrants evaluation for PTH-related peptide and vitamin D metabolites. Elevated 25-hydroxyvitamin D suggests exogenous intake; elevated 1,25-dihydroxyvitamin D suggests lymphoma or sarcoidosis. Check digoxin levels if applicable and thyroid studies if indicated.
Imaging CT head for altered mental status and chest imaging with malignancy workup if no clear cause.
Diagnostic procedures Parathyroidectomy is indicated for symptomatic or severe primary hyperparathyroidism and may be urgent.
Differential diagnosis Primary hyperparathyroidism (most common outpatient cause; adenoma most frequent) typically causes mild chronic elevations. Malignancy is the most common inpatient cause, often with rapid onset, higher calcium levels, and greater symptom burden, commonly due to PTH-related peptide or osteolytic disease (e.g., breast, lung, kidney, head and neck, multiple myeloma, lymphoma). Miscellaneous causes include granulomatous disease, excess calcium or vitamin D intake, thiazides, familial hypocalciuric hypercalcemia, vitamin A toxicity, milk-alkali syndrome, lithium therapy, renal transplantation, hyperthyroidism, and acute tubular necrosis.
Pediatric considerations Primary hyperparathyroidism is less common; consider infantile hypercalcemia, immobilization hypercalcemia in adolescents, and vitamin D sensitivity.
Treatment
Prehospital Routine stabilization.
Initial stabilization/therapy ABCs, IV access, oxygen, cardiac monitoring. Administer 0.9% saline (1 L bolus or 20 mL/kg) for hypotension or severe dehydration. Address altered mental status with glucose assessment and supportive measures.
Emergency department management Treat immediately if corrected calcium >14 mg/dL or if symptomatic. Mild, asymptomatic cases do not require emergency therapy. Volume repletion with isotonic saline at 200–300 mL/hr targeting urine output 100–150 mL/hr; total 2–5 L/day may be required with close monitoring for overload. Correct electrolyte abnormalities. Renal elimination with loop diuretics (furosemide) only after adequate volume expansion; avoid thiazides. Dialysis may be required in renal failure. Inhibit bone resorption with bisphosphonates (first-line) and calcitonin for rapid but modest effect. Consider hydrocortisone for vitamin D–mediated or granulomatous causes. Encourage ambulation when appropriate. Treat the underlying cause and discontinue offending agents.
Medication First line Calcitonin 4 IU/kg IM/SC q12h; pamidronate 60–90 mg IV over 2–24 hr; etidronate 7.5 mg/kg IV daily for 3–7 days; furosemide 10–40 mg IV q6–8h (pediatrics 1–2 mg/kg). Second line Gallium nitrate 200 mg/m²/day IV ×5 days; hydrocortisone 200–400 mg/day IV for 3–5 days; plicamycin 25 μg/kg/day IV.
Pediatric considerations Loop diuretics are rarely needed and may worsen renal function; bisphosphonates appear safe but data are limited.
Follow-up and disposition
Admission criteria Corrected calcium >13 mg/dL, symptoms attributable to hypercalcemia, ECG changes, or need for monitored care; ICU for levels >14 mg/dL or severe manifestations.
Discharge criteria Corrected calcium <13 mg/dL with no symptoms.
Issues for referral Arrange prompt evaluation to determine etiology and long-term management; consider endocrinology consultation.
Follow-up recommendations Maintain hydration and monitor for mental status changes.
Key points Base treatment decisions on symptoms and corrected calcium levels. All patients with calcium >14 mg/dL require treatment regardless of symptoms. Monitor ECG closely and balance aggressive hydration against the risk of fluid overload.
Basics
Description Hypercalcemia severity depends on the absolute calcium level and the rate of rise. It is detected in approximately 0.1–1% of routine screenings. Most cases are mild (<12 mg/dL) and asymptomatic. Hypercalcemic crisis, typically >14 mg/dL, causes severe and potentially life-threatening manifestations. Circulating calcium exists as ionized (45%, the only physiologically active form), protein-bound (40%, mainly albumin), and complexed to anions (15%).
Etiology The most common causes are primary hyperparathyroidism and malignancy, followed by miscellaneous conditions.
Diagnosis
Signs and symptoms Neurologic features include headache, fatigue, lethargy, weakness, impaired concentration, confusion, depression, paranoia, stupor, or coma. Renal manifestations include polyuria, polydipsia, dehydration, oliguria in renal failure, nephrolithiasis, nephrocalcinosis, and interstitial nephritis. Gastrointestinal symptoms include anorexia, nausea, vomiting, abdominal pain, constipation, peptic ulcer disease, and pancreatitis. Dermatologic findings include pruritus. Classic mnemonic: “stones, bones, groans, thrones, and psychiatric overtones,” where “thrones” refers to polyuria.
Pediatric considerations Failure to thrive, delayed development, and potential intellectual impairment.
Physical exam Neurologic findings include irritability, lethargy, hyporeflexia, and coma. Cardiovascular findings include hypotension from volume depletion or hypertension, sinus bradycardia, and rarely cardiac arrest. Renal signs reflect dehydration. Dermatologic findings include band keratopathy and ectopic calcifications. Pediatric findings may include characteristic facies (pug nose, broad nasal bridge, cupid’s-bow upper lip) and hypotonia.
Essential workup Measure total and ionized calcium and albumin. Normal total calcium is <10.5 mg/dL. Corrected calcium (mg/dL) = measured calcium + 0.8 × (4.0 − albumin [g/dL]). Obtain electrolytes, BUN/creatinine, and glucose. ECG may show shortened QT interval, PR prolongation, QRS widening, sinus bradycardia, conduction blocks, digoxin sensitivity, and rarely Osborn J-waves.
Diagnosis tests and interpretation
Laboratory Assess phosphate, protein, urinalysis, and parathyroid hormone (PTH). Elevated or high-normal PTH suggests primary hyperparathyroidism; PTH <20 pg/mL warrants evaluation for PTH-related peptide and vitamin D metabolites. Elevated 25-hydroxyvitamin D suggests exogenous intake; elevated 1,25-dihydroxyvitamin D suggests lymphoma or sarcoidosis. Check digoxin levels if applicable and thyroid studies if indicated.
Imaging CT head for altered mental status and chest imaging with malignancy workup if no clear cause.
Diagnostic procedures Parathyroidectomy is indicated for symptomatic or severe primary hyperparathyroidism and may be urgent.
Differential diagnosis Primary hyperparathyroidism (most common outpatient cause; adenoma most frequent) typically causes mild chronic elevations. Malignancy is the most common inpatient cause, often with rapid onset, higher calcium levels, and greater symptom burden, commonly due to PTH-related peptide or osteolytic disease (e.g., breast, lung, kidney, head and neck, multiple myeloma, lymphoma). Miscellaneous causes include granulomatous disease, excess calcium or vitamin D intake, thiazides, familial hypocalciuric hypercalcemia, vitamin A toxicity, milk-alkali syndrome, lithium therapy, renal transplantation, hyperthyroidism, and acute tubular necrosis.
Pediatric considerations Primary hyperparathyroidism is less common; consider infantile hypercalcemia, immobilization hypercalcemia in adolescents, and vitamin D sensitivity.
Treatment
Prehospital Routine stabilization.
Initial stabilization/therapy ABCs, IV access, oxygen, cardiac monitoring. Administer 0.9% saline (1 L bolus or 20 mL/kg) for hypotension or severe dehydration. Address altered mental status with glucose assessment and supportive measures.
Emergency department management Treat immediately if corrected calcium >14 mg/dL or if symptomatic. Mild, asymptomatic cases do not require emergency therapy. Volume repletion with isotonic saline at 200–300 mL/hr targeting urine output 100–150 mL/hr; total 2–5 L/day may be required with close monitoring for overload. Correct electrolyte abnormalities. Renal elimination with loop diuretics (furosemide) only after adequate volume expansion; avoid thiazides. Dialysis may be required in renal failure. Inhibit bone resorption with bisphosphonates (first-line) and calcitonin for rapid but modest effect. Consider hydrocortisone for vitamin D–mediated or granulomatous causes. Encourage ambulation when appropriate. Treat the underlying cause and discontinue offending agents.
Medication First line Calcitonin 4 IU/kg IM/SC q12h; pamidronate 60–90 mg IV over 2–24 hr; etidronate 7.5 mg/kg IV daily for 3–7 days; furosemide 10–40 mg IV q6–8h (pediatrics 1–2 mg/kg). Second line Gallium nitrate 200 mg/m²/day IV ×5 days; hydrocortisone 200–400 mg/day IV for 3–5 days; plicamycin 25 μg/kg/day IV.
Pediatric considerations Loop diuretics are rarely needed and may worsen renal function; bisphosphonates appear safe but data are limited.
Follow-up and disposition
Admission criteria Corrected calcium >13 mg/dL, symptoms attributable to hypercalcemia, ECG changes, or need for monitored care; ICU for levels >14 mg/dL or severe manifestations.
Discharge criteria Corrected calcium <13 mg/dL with no symptoms.
Issues for referral Arrange prompt evaluation to determine etiology and long-term management; consider endocrinology consultation.
Follow-up recommendations Maintain hydration and monitor for mental status changes.
Key points Base treatment decisions on symptoms and corrected calcium levels. All patients with calcium >14 mg/dL require treatment regardless of symptoms. Monitor ECG closely and balance aggressive hydration against the risk of fluid overload.
