- Published on
Emergency and Acute Medicine – Contact Dermatitis
Overview and Basic Description
Contact dermatitis is an inflammatory skin condition caused by direct exposure to external substances and is broadly classified into irritant, allergic, and photocontact forms. Irritant contact dermatitis is the most common type and presents as an immediate eczematous eruption resulting from a superficial inflammatory process that primarily involves the epidermis. In this condition, the triggering substance directly damages the skin, producing a non-immunologic inflammatory reaction manifested by erythema, dryness, cracking, or fissuring. It typically occurs due to repeated exposure to mild irritants such as water, soaps, heat, or friction. Symptoms often develop gradually and include itching or burning sensations, with lesions that have indistinct borders. The hands are most commonly affected, and the skin may appear dry, red, rough, and occasionally vesiculated or fissured. Frequent irritants include cement, hair dyes, wet diapers, rubber gloves, shampoos, and repeated handwashing.
Allergic contact dermatitis is a delayed type IV hypersensitivity reaction that requires prior sensitization. In this form, exposure to an allergen triggers an immune-mediated response, leading to localized edema, erythema, vesicles, pruritus, or burning. Lesions usually correspond exactly to the area of contact, such as beneath a watchband. In previously sensitized individuals, symptoms typically appear within 12–48 hours, whereas primary exposure may require 14–21 days before clinical manifestations develop. Common allergens include nickel, gold, neomycin, bacitracin, preservatives, fragrances, dyes, and poison ivy.
Photocontact dermatitis occurs when an otherwise harmless substance on the skin interacts with ultraviolet light, producing an inflammatory reaction. This type of dermatitis does not occur without sunlight exposure and is commonly associated with shaving lotions, sunscreens, sulfa-containing ointments, and perfumes.
Pediatric Considerations
Allergic contact dermatitis is less common in children, particularly infants, compared with adults. In pediatric patients, the major sources of contact allergy include metals, shoes, preservatives, and fragrances found in cosmetics, topical medications, and plants. Diaper dermatitis represents the prototype of irritant contact dermatitis in children and results from prolonged exposure to urine and feces. Circumoral dermatitis is seen in infants and young children and may be triggered by certain foods through either irritant or allergic mechanisms.
Etiology and Risk Factors
Irritant contact dermatitis accounts for approximately 80% of all cases and may be caused by soaps, solvents, chemicals, certain foods, urine, feces, diapers, and continuous or repeated exposure to moisture such as frequent handwashing. Physical irritants including coarse paper, glass fibers, and wool may also provoke dermatitis. Shoe dermatitis is a common presentation and is typically identified by lesions limited to the distal dorsal surface of the foot while sparing the interdigital spaces.
Allergic contact dermatitis may result from exposure to plants such as poison ivy, poison oak, and poison sumac, collectively referred to as rhus dermatitis, which is the most common form of allergic contact dermatitis in North America. The reaction is caused by oleoresin urushiol and may occur through direct contact with the plant or indirectly via contaminated pets, clothing, or smoke from burning leaves. Lesions may appear up to three days after exposure in sensitized individuals and may persist for as long as three weeks. The fluid contained within vesicles is not contagious and does not produce new lesions; however, urushiol oil on clothing or animal fur remains contagious until removed. Other allergic causes include cement, which may result in severe alkali burns with prolonged exposure, metals—especially nickel—solvents, epoxy, chemicals in rubber or leather, lotions, cosmetics, topical medications such as neomycin, hydrocortisone, benzocaine, and parabens, and certain foods. The ability to respond to specific antigens is likely influenced by genetic factors.
Photodermatitis represents an inflammatory reaction caused by exposure to an irritant, often plant sap, in combination with sunlight and typically does not occur in the absence of ultraviolet exposure.
Clinical Features and Diagnostic Evaluation
Assessment begins with a detailed history focusing on the date of onset, time course, pattern and distribution of lesions, relationship to occupational or work exposures, presence or absence of pruritus, mucosal involvement, and recent exposure to new products such as soaps, lotions, cosmetics, foods, medications, or jewelry. Physical examination should emphasize the morphology and distribution of the rash. Acute lesions are characterized by erythema and pruritus and may be accompanied by edema, papules, vesicles, bullae, serous discharge, or crusting. Subacute lesions demonstrate less prominent vesiculation, while chronic lesions may present with scaling, lichenification, pigmentation changes, or fissuring, often with little or no vesiculation and a characteristic distribution pattern.
There are no specific laboratory studies or imaging modalities that are routinely helpful in the emergency department for diagnosing contact dermatitis. Patch testing is generally not performed acutely and should be arranged through referral to an allergist or immunologist. When a fungal infection is suspected, a Wood lamp examination may be used to assess for fluorescence suggestive of tinea.
Differential Diagnosis
Conditions that may mimic contact dermatitis include atopic dermatitis, often associated with a family history of atopy; seborrheic dermatitis with greasy, scaly lesions; nummular dermatitis characterized by coin-shaped plaques; and intertrigo involving areas where skin surfaces are in apposition such as the axillae and groin. Other considerations include infectious eczematous dermatitis with secondary bacterial infection, usually due to Staphylococcus aureus; cellulitis presenting as a warm, painful, blanching lesion; impetigo with yellow crusting; scabies with intensely pruritic interdigital tracks; psoriasis with well-demarcated silvery plaques affecting extensor surfaces, scalp, or genital region; herpes simplex infection with painful grouped vesicles; herpes zoster following a dermatomal distribution; bullous pemphigoid with diffuse bullae; tinea with maximal involvement at the margins and Wood lamp fluorescence; pityriasis alba with asymptomatic hypopigmented lesions; urticaria with pruritic wheals and surrounding erythema; acrodermatitis enteropathica due to zinc deficiency, associated with failure to thrive, diarrhea, and alopecia; dyshidrotic eczema; drug-induced rashes; Stevens–Johnson syndrome; toxic epidermal necrolysis; and erythema nodosum.
Management in the Emergency Department
Initial stabilization is rarely required unless there is significant concomitant pathology. Treatment is primarily symptomatic and includes gentle cleansing of the affected area with mild soap and water, removal and avoidance of the offending agent, and washing of contaminated clothing. Cool, wet compresses are particularly effective during the acute blistering phase. Antipruritic therapy may include topical agents such as calamine lotion and topical corticosteroids, although corticosteroids do not penetrate intact blisters and benzocaine- or hydrocortisone-containing products should be avoided due to the risk of further sensitization. Systemic therapy may include antihistamines and corticosteroids when indicated. Aluminum acetate (Burrow solution) may be applied to weeping surfaces.
For irritant contact dermatitis, management focuses on removal of the offending agent, thorough washing with soap and warm water, reduction of wet–dry cycles such as frequent handwashing, and use of alcohol-based cleansers to decrease repetitive trauma. Bland emollients are recommended, and topical corticosteroids of medium to high potency, preferably in ointment form, may be used for severe cases on the hands twice daily for several weeks.
Allergic contact dermatitis is treated with topical corticosteroids applied twice daily for two to three weeks, with potency adjusted by location: low potency for the face, medium potency for the arms, legs, and trunk, and high potency for the hands and feet. Oral corticosteroids may be required for severe reactions. In rhus dermatitis, additional measures include washing all clothing and pets that may have come into contact with the plant, as the oil remains contagious. Oatmeal baths may provide symptomatic relief, and aseptic aspiration of tense bullae can reduce discomfort. Severe reactions involving more than 10% of total body surface area require systemic corticosteroids for two to three weeks with a gradual taper, as premature discontinuation may result in rapid rebound of symptoms. Shoe dermatitis management includes wearing open-toe, canvas, or vinyl shoes, controlling perspiration through frequent sock changes, and using absorbent powders. Diaper dermatitis management includes topical zinc oxide, petrolatum, or aquaphor and frequent diaper changes after each soiling.
Medications
Systemic therapy may include H1-receptor antagonists from both first- and second-generation antihistamines. Cetirizine may be given at 5–10 mg orally daily in adults and children older than six years, with pediatric dosing of 2.5 mg once or twice daily for ages two to six years. Diphenhydramine may be administered at 25–50 mg intravenously, intramuscularly, or orally every six hours as needed, with pediatric dosing of 5 mg/kg per 24 hours divided every six hours. Fexofenadine may be used at 60 mg orally twice daily or 180 mg once daily in adults, with pediatric dosing of 30 mg twice daily for children aged six to twelve years. Hydroxyzine may be given at 25–50 mg orally or intramuscularly up to four times daily, with weight-based pediatric dosing. Loratadine may be administered at 10 mg orally twice daily. For refractory pruritus, doxepin 75 mg orally daily may be effective.
Systemic corticosteroid therapy includes prednisone at 40–60 mg orally daily in adults, with pediatric dosing of 1–2 mg/kg per day to a maximum of 80 mg, administered once or divided twice daily. Topical therapies include aluminum acetate solution applied for 20 minutes three times daily until the skin is dry, calamine lotion every six hours as needed, and topical corticosteroids such as triamcinolone ointment, cream, or lotion at concentrations of 0.025% or 0.1% applied three to four times daily. Topical corticosteroids should not be applied to the face or eyelids. First-line therapy consists of topical corticosteroids and oral antihistamines, while oral corticosteroids are considered second-line treatment.
Disposition and Follow-Up
Hospital admission is rarely indicated and is generally reserved for patients with severe systemic reactions or significant secondary infections. Patients may be discharged once symptomatic relief is achieved and adequate outpatient follow-up is arranged. Follow-up with a primary care physician is recommended within two to three days for reassessment. Patients should be instructed to return to the emergency department if they develop facial swelling, difficulty breathing, or mucosal involvement that limits oral intake.
Clinical Pearls and Pitfalls
Effective management requires prompt removal of the offending agent. Clinicians should remain vigilant for progression to systemic anaphylaxis, particularly in cases involving latex exposure, and should monitor for concurrent bacterial infections. In rhus dermatitis, lesions are no longer contagious after washing with soap and water; however, all clothing and animals that may have been exposed must be thoroughly cleaned, as the oil remains contagious until removed.
Overview and Basic Description
Contact dermatitis is an inflammatory skin condition caused by direct exposure to external substances and is broadly classified into irritant, allergic, and photocontact forms. Irritant contact dermatitis is the most common type and presents as an immediate eczematous eruption resulting from a superficial inflammatory process that primarily involves the epidermis. In this condition, the triggering substance directly damages the skin, producing a non-immunologic inflammatory reaction manifested by erythema, dryness, cracking, or fissuring. It typically occurs due to repeated exposure to mild irritants such as water, soaps, heat, or friction. Symptoms often develop gradually and include itching or burning sensations, with lesions that have indistinct borders. The hands are most commonly affected, and the skin may appear dry, red, rough, and occasionally vesiculated or fissured. Frequent irritants include cement, hair dyes, wet diapers, rubber gloves, shampoos, and repeated handwashing.
Allergic contact dermatitis is a delayed type IV hypersensitivity reaction that requires prior sensitization. In this form, exposure to an allergen triggers an immune-mediated response, leading to localized edema, erythema, vesicles, pruritus, or burning. Lesions usually correspond exactly to the area of contact, such as beneath a watchband. In previously sensitized individuals, symptoms typically appear within 12–48 hours, whereas primary exposure may require 14–21 days before clinical manifestations develop. Common allergens include nickel, gold, neomycin, bacitracin, preservatives, fragrances, dyes, and poison ivy.
Photocontact dermatitis occurs when an otherwise harmless substance on the skin interacts with ultraviolet light, producing an inflammatory reaction. This type of dermatitis does not occur without sunlight exposure and is commonly associated with shaving lotions, sunscreens, sulfa-containing ointments, and perfumes.
Pediatric Considerations
Allergic contact dermatitis is less common in children, particularly infants, compared with adults. In pediatric patients, the major sources of contact allergy include metals, shoes, preservatives, and fragrances found in cosmetics, topical medications, and plants. Diaper dermatitis represents the prototype of irritant contact dermatitis in children and results from prolonged exposure to urine and feces. Circumoral dermatitis is seen in infants and young children and may be triggered by certain foods through either irritant or allergic mechanisms.
Etiology and Risk Factors
Irritant contact dermatitis accounts for approximately 80% of all cases and may be caused by soaps, solvents, chemicals, certain foods, urine, feces, diapers, and continuous or repeated exposure to moisture such as frequent handwashing. Physical irritants including coarse paper, glass fibers, and wool may also provoke dermatitis. Shoe dermatitis is a common presentation and is typically identified by lesions limited to the distal dorsal surface of the foot while sparing the interdigital spaces.
Allergic contact dermatitis may result from exposure to plants such as poison ivy, poison oak, and poison sumac, collectively referred to as rhus dermatitis, which is the most common form of allergic contact dermatitis in North America. The reaction is caused by oleoresin urushiol and may occur through direct contact with the plant or indirectly via contaminated pets, clothing, or smoke from burning leaves. Lesions may appear up to three days after exposure in sensitized individuals and may persist for as long as three weeks. The fluid contained within vesicles is not contagious and does not produce new lesions; however, urushiol oil on clothing or animal fur remains contagious until removed. Other allergic causes include cement, which may result in severe alkali burns with prolonged exposure, metals—especially nickel—solvents, epoxy, chemicals in rubber or leather, lotions, cosmetics, topical medications such as neomycin, hydrocortisone, benzocaine, and parabens, and certain foods. The ability to respond to specific antigens is likely influenced by genetic factors.
Photodermatitis represents an inflammatory reaction caused by exposure to an irritant, often plant sap, in combination with sunlight and typically does not occur in the absence of ultraviolet exposure.
Clinical Features and Diagnostic Evaluation
Assessment begins with a detailed history focusing on the date of onset, time course, pattern and distribution of lesions, relationship to occupational or work exposures, presence or absence of pruritus, mucosal involvement, and recent exposure to new products such as soaps, lotions, cosmetics, foods, medications, or jewelry. Physical examination should emphasize the morphology and distribution of the rash. Acute lesions are characterized by erythema and pruritus and may be accompanied by edema, papules, vesicles, bullae, serous discharge, or crusting. Subacute lesions demonstrate less prominent vesiculation, while chronic lesions may present with scaling, lichenification, pigmentation changes, or fissuring, often with little or no vesiculation and a characteristic distribution pattern.
There are no specific laboratory studies or imaging modalities that are routinely helpful in the emergency department for diagnosing contact dermatitis. Patch testing is generally not performed acutely and should be arranged through referral to an allergist or immunologist. When a fungal infection is suspected, a Wood lamp examination may be used to assess for fluorescence suggestive of tinea.
Differential Diagnosis
Conditions that may mimic contact dermatitis include atopic dermatitis, often associated with a family history of atopy; seborrheic dermatitis with greasy, scaly lesions; nummular dermatitis characterized by coin-shaped plaques; and intertrigo involving areas where skin surfaces are in apposition such as the axillae and groin. Other considerations include infectious eczematous dermatitis with secondary bacterial infection, usually due to Staphylococcus aureus; cellulitis presenting as a warm, painful, blanching lesion; impetigo with yellow crusting; scabies with intensely pruritic interdigital tracks; psoriasis with well-demarcated silvery plaques affecting extensor surfaces, scalp, or genital region; herpes simplex infection with painful grouped vesicles; herpes zoster following a dermatomal distribution; bullous pemphigoid with diffuse bullae; tinea with maximal involvement at the margins and Wood lamp fluorescence; pityriasis alba with asymptomatic hypopigmented lesions; urticaria with pruritic wheals and surrounding erythema; acrodermatitis enteropathica due to zinc deficiency, associated with failure to thrive, diarrhea, and alopecia; dyshidrotic eczema; drug-induced rashes; Stevens–Johnson syndrome; toxic epidermal necrolysis; and erythema nodosum.
Management in the Emergency Department
Initial stabilization is rarely required unless there is significant concomitant pathology. Treatment is primarily symptomatic and includes gentle cleansing of the affected area with mild soap and water, removal and avoidance of the offending agent, and washing of contaminated clothing. Cool, wet compresses are particularly effective during the acute blistering phase. Antipruritic therapy may include topical agents such as calamine lotion and topical corticosteroids, although corticosteroids do not penetrate intact blisters and benzocaine- or hydrocortisone-containing products should be avoided due to the risk of further sensitization. Systemic therapy may include antihistamines and corticosteroids when indicated. Aluminum acetate (Burrow solution) may be applied to weeping surfaces.
For irritant contact dermatitis, management focuses on removal of the offending agent, thorough washing with soap and warm water, reduction of wet–dry cycles such as frequent handwashing, and use of alcohol-based cleansers to decrease repetitive trauma. Bland emollients are recommended, and topical corticosteroids of medium to high potency, preferably in ointment form, may be used for severe cases on the hands twice daily for several weeks.
Allergic contact dermatitis is treated with topical corticosteroids applied twice daily for two to three weeks, with potency adjusted by location: low potency for the face, medium potency for the arms, legs, and trunk, and high potency for the hands and feet. Oral corticosteroids may be required for severe reactions. In rhus dermatitis, additional measures include washing all clothing and pets that may have come into contact with the plant, as the oil remains contagious. Oatmeal baths may provide symptomatic relief, and aseptic aspiration of tense bullae can reduce discomfort. Severe reactions involving more than 10% of total body surface area require systemic corticosteroids for two to three weeks with a gradual taper, as premature discontinuation may result in rapid rebound of symptoms. Shoe dermatitis management includes wearing open-toe, canvas, or vinyl shoes, controlling perspiration through frequent sock changes, and using absorbent powders. Diaper dermatitis management includes topical zinc oxide, petrolatum, or aquaphor and frequent diaper changes after each soiling.
Medications
Systemic therapy may include H1-receptor antagonists from both first- and second-generation antihistamines. Cetirizine may be given at 5–10 mg orally daily in adults and children older than six years, with pediatric dosing of 2.5 mg once or twice daily for ages two to six years. Diphenhydramine may be administered at 25–50 mg intravenously, intramuscularly, or orally every six hours as needed, with pediatric dosing of 5 mg/kg per 24 hours divided every six hours. Fexofenadine may be used at 60 mg orally twice daily or 180 mg once daily in adults, with pediatric dosing of 30 mg twice daily for children aged six to twelve years. Hydroxyzine may be given at 25–50 mg orally or intramuscularly up to four times daily, with weight-based pediatric dosing. Loratadine may be administered at 10 mg orally twice daily. For refractory pruritus, doxepin 75 mg orally daily may be effective.
Systemic corticosteroid therapy includes prednisone at 40–60 mg orally daily in adults, with pediatric dosing of 1–2 mg/kg per day to a maximum of 80 mg, administered once or divided twice daily. Topical therapies include aluminum acetate solution applied for 20 minutes three times daily until the skin is dry, calamine lotion every six hours as needed, and topical corticosteroids such as triamcinolone ointment, cream, or lotion at concentrations of 0.025% or 0.1% applied three to four times daily. Topical corticosteroids should not be applied to the face or eyelids. First-line therapy consists of topical corticosteroids and oral antihistamines, while oral corticosteroids are considered second-line treatment.
Disposition and Follow-Up
Hospital admission is rarely indicated and is generally reserved for patients with severe systemic reactions or significant secondary infections. Patients may be discharged once symptomatic relief is achieved and adequate outpatient follow-up is arranged. Follow-up with a primary care physician is recommended within two to three days for reassessment. Patients should be instructed to return to the emergency department if they develop facial swelling, difficulty breathing, or mucosal involvement that limits oral intake.
Clinical Pearls and Pitfalls
Effective management requires prompt removal of the offending agent. Clinicians should remain vigilant for progression to systemic anaphylaxis, particularly in cases involving latex exposure, and should monitor for concurrent bacterial infections. In rhus dermatitis, lesions are no longer contagious after washing with soap and water; however, all clothing and animals that may have been exposed must be thoroughly cleaned, as the oil remains contagious until removed.
- Published on
Emergency And Acute Medicine – Constipation
Description
Constipation is defined clinically using the Rome criteria, which require at least two of the following symptoms for a minimum of three months: straining during more than 25% of bowel movements, hard stools in more than 25% of bowel movements, a sensation of incomplete evacuation in more than 25% of bowel movements, or two or fewer bowel movements per week.
Pediatric Considerations
Defecation disorders account for approximately 3% of pediatric outpatient visits. Children with cerebral palsy are at increased risk of functional constipation. Pediatric constipation may be classified into anatomic causes, colonic neuromuscular disease such as Hirschsprung disease, and defecation disorders including functional constipation and nonretentive fecal soiling. Functional fecal retention is the most common cause and is often related to fear or pain with defecation, leading to irritability, abdominal cramping, decreased appetite, and early satiety.
Etiology
Metabolic and endocrine causes include diabetes, uremia, porphyria, hypothyroidism, hypercalcemia, pheochromocytoma, panhypopituitarism, and pregnancy. Functional and idiopathic causes include irritable bowel syndrome, diverticular disease, colonic inertia, megacolon or megarectum, pelvic intussusception, nonrelaxing puborectalis, rectocele, posthysterectomy syndrome, and descending perineum. Pharmacologic causes include analgesics, antacids, anticholinergics, anticonvulsants, antidepressants, antihypertensives, calcium channel blockers, diuretics, iron supplements, laxative abuse, monoamine oxidase inhibitors, opioids, paralytics, parasympatholytics, phenothiazines, and psychotropic medications. Neurologic causes include Parkinson disease, multiple sclerosis, cerebrovascular accidents, spinal cord injury, Hirschsprung disease, Chagas disease, neurofibromatosis, and autonomic neuropathy. Mechanical obstruction may result from neoplasm, stricture, hernia, or volvulus.
Clinical Features
Constipation represents a symptom rather than a primary diagnosis. Patients may report infrequent bowel movements, passage of hard stools, straining, abdominal distention or bloating, and difficulty with defecation. Liquid stool may pass around impacted feces, presenting as paradoxical diarrhea. Digital rectal examination may reveal firm stool or an empty rectal vault. History should include age at symptom onset, diet, exercise habits, stool characteristics, medication use, prior surgeries, use of laxatives or enemas, and symptoms suggestive of pelvic floor dysfunction. Physical examination may demonstrate abdominal masses from fecal loading and should include a focused rectal examination assessing sphincter tone, relaxation, stool consistency, and the presence of rectocele or cystocele.
Essential Evaluation
A detailed medical, surgical, and psychiatric history with careful physical examination is central to evaluation. The anorectal examination should assess for fissures, stenosis, neoplasm, sphincter tone abnormalities, perineal descent, tenderness, or spasm.
Diagnostic Tests And Interpretation
Laboratory testing is reserved for suspected metabolic or endocrine causes and may include a complete blood count, electrolytes, calcium, and thyroid function tests. Imaging is rarely required unless obstruction or other pathology is suspected. Abdominal radiographs may show fecal loading or colonic dilation. Computed tomography is indicated in elderly patients with abdominal pain or fever to exclude perforation. Contrast enemas may identify diverticulosis, megacolon, megarectum, Hirschsprung disease, or strictures.
Differential Diagnosis
The differential diagnosis includes bowel obstruction and secondary causes listed under etiology.
Initial Management
Intravenous access should be established in patients with significant abdominal pain or dehydration, and intravenous fluids administered as indicated.
Emergency Department Management
Initial treatment focuses on colonic evacuation using enemas, suppositories, or manual disimpaction when necessary. A long-term bowel regimen should be initiated, including increased noncaffeinated fluid intake, increased dietary fiber, regular exercise, stool softeners, and discontinuation or adjustment of constipating medications when possible.
Medications
Rectal therapies include sodium phosphate, mineral oil, and tap water enemas, as well as glycerin suppositories. Fiber supplements such as methylcellulose and psyllium may be used. Osmotic laxatives include lactulose, polyethylene glycol, and magnesium hydroxide. Stimulant laxatives include bisacodyl and senna. Stool softeners include docusate sodium and oral mineral oil.
Disposition And Follow-Up
Hospital admission is indicated for patients with severe abdominal pain, vomiting, bowel obstruction, peritonitis, or those unable to be adequately treated in the emergency department or home setting, particularly elderly or neurologically impaired patients. Patients may be discharged if pain free, adequately relieved of fecal burden, and without comorbid conditions requiring admission.
Follow-Up Recommendations
Primary care or gastroenterology follow-up is recommended for patients with chronic or recurrent constipation.
Practice Points And Common Errors
Patients should be counseled on dietary, fluid, and lifestyle modifications to reduce recurrence. A comprehensive history and physical examination are essential to avoid missing serious medical or surgical causes of constipation. Failure to consider secondary etiologies or medication-related causes is a common source of mismanagement.
Description
Constipation is defined clinically using the Rome criteria, which require at least two of the following symptoms for a minimum of three months: straining during more than 25% of bowel movements, hard stools in more than 25% of bowel movements, a sensation of incomplete evacuation in more than 25% of bowel movements, or two or fewer bowel movements per week.
Pediatric Considerations
Defecation disorders account for approximately 3% of pediatric outpatient visits. Children with cerebral palsy are at increased risk of functional constipation. Pediatric constipation may be classified into anatomic causes, colonic neuromuscular disease such as Hirschsprung disease, and defecation disorders including functional constipation and nonretentive fecal soiling. Functional fecal retention is the most common cause and is often related to fear or pain with defecation, leading to irritability, abdominal cramping, decreased appetite, and early satiety.
Etiology
Metabolic and endocrine causes include diabetes, uremia, porphyria, hypothyroidism, hypercalcemia, pheochromocytoma, panhypopituitarism, and pregnancy. Functional and idiopathic causes include irritable bowel syndrome, diverticular disease, colonic inertia, megacolon or megarectum, pelvic intussusception, nonrelaxing puborectalis, rectocele, posthysterectomy syndrome, and descending perineum. Pharmacologic causes include analgesics, antacids, anticholinergics, anticonvulsants, antidepressants, antihypertensives, calcium channel blockers, diuretics, iron supplements, laxative abuse, monoamine oxidase inhibitors, opioids, paralytics, parasympatholytics, phenothiazines, and psychotropic medications. Neurologic causes include Parkinson disease, multiple sclerosis, cerebrovascular accidents, spinal cord injury, Hirschsprung disease, Chagas disease, neurofibromatosis, and autonomic neuropathy. Mechanical obstruction may result from neoplasm, stricture, hernia, or volvulus.
Clinical Features
Constipation represents a symptom rather than a primary diagnosis. Patients may report infrequent bowel movements, passage of hard stools, straining, abdominal distention or bloating, and difficulty with defecation. Liquid stool may pass around impacted feces, presenting as paradoxical diarrhea. Digital rectal examination may reveal firm stool or an empty rectal vault. History should include age at symptom onset, diet, exercise habits, stool characteristics, medication use, prior surgeries, use of laxatives or enemas, and symptoms suggestive of pelvic floor dysfunction. Physical examination may demonstrate abdominal masses from fecal loading and should include a focused rectal examination assessing sphincter tone, relaxation, stool consistency, and the presence of rectocele or cystocele.
Essential Evaluation
A detailed medical, surgical, and psychiatric history with careful physical examination is central to evaluation. The anorectal examination should assess for fissures, stenosis, neoplasm, sphincter tone abnormalities, perineal descent, tenderness, or spasm.
Diagnostic Tests And Interpretation
Laboratory testing is reserved for suspected metabolic or endocrine causes and may include a complete blood count, electrolytes, calcium, and thyroid function tests. Imaging is rarely required unless obstruction or other pathology is suspected. Abdominal radiographs may show fecal loading or colonic dilation. Computed tomography is indicated in elderly patients with abdominal pain or fever to exclude perforation. Contrast enemas may identify diverticulosis, megacolon, megarectum, Hirschsprung disease, or strictures.
Differential Diagnosis
The differential diagnosis includes bowel obstruction and secondary causes listed under etiology.
Initial Management
Intravenous access should be established in patients with significant abdominal pain or dehydration, and intravenous fluids administered as indicated.
Emergency Department Management
Initial treatment focuses on colonic evacuation using enemas, suppositories, or manual disimpaction when necessary. A long-term bowel regimen should be initiated, including increased noncaffeinated fluid intake, increased dietary fiber, regular exercise, stool softeners, and discontinuation or adjustment of constipating medications when possible.
Medications
Rectal therapies include sodium phosphate, mineral oil, and tap water enemas, as well as glycerin suppositories. Fiber supplements such as methylcellulose and psyllium may be used. Osmotic laxatives include lactulose, polyethylene glycol, and magnesium hydroxide. Stimulant laxatives include bisacodyl and senna. Stool softeners include docusate sodium and oral mineral oil.
Disposition And Follow-Up
Hospital admission is indicated for patients with severe abdominal pain, vomiting, bowel obstruction, peritonitis, or those unable to be adequately treated in the emergency department or home setting, particularly elderly or neurologically impaired patients. Patients may be discharged if pain free, adequately relieved of fecal burden, and without comorbid conditions requiring admission.
Follow-Up Recommendations
Primary care or gastroenterology follow-up is recommended for patients with chronic or recurrent constipation.
Practice Points And Common Errors
Patients should be counseled on dietary, fluid, and lifestyle modifications to reduce recurrence. A comprehensive history and physical examination are essential to avoid missing serious medical or surgical causes of constipation. Failure to consider secondary etiologies or medication-related causes is a common source of mismanagement.
- Published on
Emergency And Acute Medicine – Conjunctivitis
Description
Conjunctivitis is inflammation of the conjunctiva caused by a wide range of infectious and noninfectious etiologies. It is commonly referred to as “pink eye” and is a frequent reason for emergency and primary care visits.
Etiology
Bacterial causes include Staphylococcus aureus, Streptococcus pneumoniae, and Haemophilus influenzae. Gonococcal conjunctivitis is an ophthalmic emergency because of rapid corneal invasion and risk of blindness. Chlamydial conjunctivitis occurs through autoinoculation from genital secretions and is common in newborns. Viral conjunctivitis is most often due to adenovirus, including epidemic keratoconjunctivitis, and is frequently associated with upper respiratory infections. Herpes simplex virus may cause recurrent ocular disease, and corticosteroids are contraindicated. Allergic conjunctivitis is associated with atopy and nasal symptoms. Contact-related conjunctivitis may result from chemical irritation or hypersensitivity, with Pseudomonas species commonly implicated in contact lens users.
Clinical Features
Patients typically present with red eye, burning or gritty sensation, foreign body sensation, discharge, eyelid sticking on awakening, chemosis, eyelid edema, tearing, and itching. Bacterial conjunctivitis produces mucopurulent discharge. Gonococcal infection causes hyperacute, copious purulent discharge within 12 hours, severe chemosis, and eyelid swelling. Chlamydial conjunctivitis presents with lacrimation, mucopurulent discharge, photophobia, and frequent concomitant genital infection. Viral conjunctivitis often causes watery discharge, preauricular lymphadenopathy, and spreads to the other eye within 24–48 hours. Epidemic keratoconjunctivitis may reduce vision due to corneal infiltrates. Allergic conjunctivitis is marked by intense itching and watery discharge. Contact-related disease may present acutely with corneal ulceration but normal visual acuity and intraocular pressure.
Essential Evaluation
History should assess onset, exposures, sick contacts, sexual history, medication or cosmetic use, and systemic disease. A careful eye examination including slit-lamp evaluation and fluorescein staining is essential.
Diagnostic Tests And Interpretation
Routine cultures are not required in uncomplicated cases. Indications for bacteriologic studies include ophthalmia neonatorum, suspected gonococcal infection, immunocompromised patients, systemic illness, or lack of improvement within 48–72 hours. Identification of gram-negative intracellular diplococci on Gram stain is sufficient to initiate gonococcal therapy. Serologic testing such as rapid plasma reagin may be indicated when sexually transmitted infection is suspected.
Differential Diagnosis
Conditions to exclude include acute angle-closure glaucoma, anterior uveitis, keratitis, corneal abrasion, foreign body, dry eye, scleritis, episcleritis, nasolacrimal obstruction, and subconjunctival hemorrhage.
Initial Management
Empiric treatment with broad-spectrum topical antibiotics is appropriate for most suspected bacterial cases. Systemic therapy is mandatory for gonococcal, chlamydial, meningococcal infections, ophthalmia neonatorum, and severe disease. Herpetic infections require ophthalmology consultation.
Emergency Department Management
Discharge should be gently cleaned from the eye, and contact lens wearers must discontinue lens use and discard contaminated lenses. Emphasize hand hygiene and avoidance of shared towels or cosmetics. Warm soaks help remove debris. Bacterial conjunctivitis is treated with topical antibiotics continued for 48 hours after symptom resolution. Failure to improve within 48–72 hours warrants culture and reevaluation. Viral conjunctivitis requires supportive care only. Allergic conjunctivitis is treated with antihistamine or mast cell stabilizer drops, artificial tears, and avoidance of triggers. Noninfectious irritation is managed with lubricating drops or ointments.
Medications
All contact lens wearers require antipseudomonal coverage. Common topical agents include ciprofloxacin, gentamicin, tobramycin, erythromycin, and sulfacetamide. Chlamydial infection requires systemic therapy with doxycycline or erythromycin. Gonococcal conjunctivitis requires parenteral ceftriaxone plus topical antibiotics. Viral conjunctivitis is managed with artificial tears and topical antihistamines. Herpetic disease is treated with antiviral ophthalmic agents. Allergic conjunctivitis responds to antihistamine, mast cell stabilizer, or NSAID drops.
Pediatric Considerations
In neonates, conjunctivitis often reflects systemic infection acquired during birth. Chemical conjunctivitis occurs within the first 36 hours of life. Ophthalmia neonatorum occurs within the first four weeks and is commonly caused by gonococcal, chlamydial, or herpetic infection. Ointments are preferred over drops in infants.
Disposition And Follow-Up
Hospital admission is required for known or suspected gonococcal infection at any age. Most patients can be discharged with close follow-up.
Follow-Up Recommendations
Ophthalmology follow-up is recommended for all bacterial conjunctivitis cases and is mandatory for epidemic keratoconjunctivitis or severe disease.
Key Clinical Insights And Common Errors
Conjunctivitis is highly contagious, particularly viral forms and epidemic keratoconjunctivitis, which may remain transmissible for up to two weeks. Strict hand hygiene and meticulous disinfection of examination equipment are essential to prevent spread. Corticosteroids should be used with extreme caution, as they can exacerbate unrecognized herpes simplex infection and worsen outcomes.
Description
Conjunctivitis is inflammation of the conjunctiva caused by a wide range of infectious and noninfectious etiologies. It is commonly referred to as “pink eye” and is a frequent reason for emergency and primary care visits.
Etiology
Bacterial causes include Staphylococcus aureus, Streptococcus pneumoniae, and Haemophilus influenzae. Gonococcal conjunctivitis is an ophthalmic emergency because of rapid corneal invasion and risk of blindness. Chlamydial conjunctivitis occurs through autoinoculation from genital secretions and is common in newborns. Viral conjunctivitis is most often due to adenovirus, including epidemic keratoconjunctivitis, and is frequently associated with upper respiratory infections. Herpes simplex virus may cause recurrent ocular disease, and corticosteroids are contraindicated. Allergic conjunctivitis is associated with atopy and nasal symptoms. Contact-related conjunctivitis may result from chemical irritation or hypersensitivity, with Pseudomonas species commonly implicated in contact lens users.
Clinical Features
Patients typically present with red eye, burning or gritty sensation, foreign body sensation, discharge, eyelid sticking on awakening, chemosis, eyelid edema, tearing, and itching. Bacterial conjunctivitis produces mucopurulent discharge. Gonococcal infection causes hyperacute, copious purulent discharge within 12 hours, severe chemosis, and eyelid swelling. Chlamydial conjunctivitis presents with lacrimation, mucopurulent discharge, photophobia, and frequent concomitant genital infection. Viral conjunctivitis often causes watery discharge, preauricular lymphadenopathy, and spreads to the other eye within 24–48 hours. Epidemic keratoconjunctivitis may reduce vision due to corneal infiltrates. Allergic conjunctivitis is marked by intense itching and watery discharge. Contact-related disease may present acutely with corneal ulceration but normal visual acuity and intraocular pressure.
Essential Evaluation
History should assess onset, exposures, sick contacts, sexual history, medication or cosmetic use, and systemic disease. A careful eye examination including slit-lamp evaluation and fluorescein staining is essential.
Diagnostic Tests And Interpretation
Routine cultures are not required in uncomplicated cases. Indications for bacteriologic studies include ophthalmia neonatorum, suspected gonococcal infection, immunocompromised patients, systemic illness, or lack of improvement within 48–72 hours. Identification of gram-negative intracellular diplococci on Gram stain is sufficient to initiate gonococcal therapy. Serologic testing such as rapid plasma reagin may be indicated when sexually transmitted infection is suspected.
Differential Diagnosis
Conditions to exclude include acute angle-closure glaucoma, anterior uveitis, keratitis, corneal abrasion, foreign body, dry eye, scleritis, episcleritis, nasolacrimal obstruction, and subconjunctival hemorrhage.
Initial Management
Empiric treatment with broad-spectrum topical antibiotics is appropriate for most suspected bacterial cases. Systemic therapy is mandatory for gonococcal, chlamydial, meningococcal infections, ophthalmia neonatorum, and severe disease. Herpetic infections require ophthalmology consultation.
Emergency Department Management
Discharge should be gently cleaned from the eye, and contact lens wearers must discontinue lens use and discard contaminated lenses. Emphasize hand hygiene and avoidance of shared towels or cosmetics. Warm soaks help remove debris. Bacterial conjunctivitis is treated with topical antibiotics continued for 48 hours after symptom resolution. Failure to improve within 48–72 hours warrants culture and reevaluation. Viral conjunctivitis requires supportive care only. Allergic conjunctivitis is treated with antihistamine or mast cell stabilizer drops, artificial tears, and avoidance of triggers. Noninfectious irritation is managed with lubricating drops or ointments.
Medications
All contact lens wearers require antipseudomonal coverage. Common topical agents include ciprofloxacin, gentamicin, tobramycin, erythromycin, and sulfacetamide. Chlamydial infection requires systemic therapy with doxycycline or erythromycin. Gonococcal conjunctivitis requires parenteral ceftriaxone plus topical antibiotics. Viral conjunctivitis is managed with artificial tears and topical antihistamines. Herpetic disease is treated with antiviral ophthalmic agents. Allergic conjunctivitis responds to antihistamine, mast cell stabilizer, or NSAID drops.
Pediatric Considerations
In neonates, conjunctivitis often reflects systemic infection acquired during birth. Chemical conjunctivitis occurs within the first 36 hours of life. Ophthalmia neonatorum occurs within the first four weeks and is commonly caused by gonococcal, chlamydial, or herpetic infection. Ointments are preferred over drops in infants.
Disposition And Follow-Up
Hospital admission is required for known or suspected gonococcal infection at any age. Most patients can be discharged with close follow-up.
Follow-Up Recommendations
Ophthalmology follow-up is recommended for all bacterial conjunctivitis cases and is mandatory for epidemic keratoconjunctivitis or severe disease.
Key Clinical Insights And Common Errors
Conjunctivitis is highly contagious, particularly viral forms and epidemic keratoconjunctivitis, which may remain transmissible for up to two weeks. Strict hand hygiene and meticulous disinfection of examination equipment are essential to prevent spread. Corticosteroids should be used with extreme caution, as they can exacerbate unrecognized herpes simplex infection and worsen outcomes.
- Published on
Emergency And Acute Medicine – Congenital Heart Disease, Cyanotic
Description
Cyanotic congenital heart disease results from abnormal embryologic cardiac development that allows mixing of deoxygenated and oxygenated blood into the systemic circulation. This occurs through right-to-left intracardiac shunting or anatomic defects involving the great vessels. Classic subtypes include the “five Ts,” the “two Es,” and single-ventricle physiology. These conditions include tetralogy of Fallot, transposition of the great arteries, tricuspid atresia, truncus arteriosus, total anomalous pulmonary venous return, Ebstein anomaly of the tricuspid valve, Eisenmenger syndrome, and single-ventricle physiology. All lead to varying degrees of systemic hypoxemia.
Etiology
For most cyanotic congenital heart defects, the precise cause is unknown. Genetic and environmental contributions may play a role, but no single unifying etiology is identified in the majority of cases.
Emergency Presentation
The most common initial emergency department presentations include central cyanosis, congestive heart failure, and circulatory collapse. In older children with known cyanotic heart disease, physiologic stress such as fever, dehydration, pulmonary disease, decreased systemic vascular resistance, or obstruction of a cardiac shunt can precipitate worsening cyanosis.
Clinical Features
Central cyanosis is typically visible in the lips, nail beds, and mucous membranes and worsens with crying or agitation, with minimal improvement on administration of 100% oxygen. Signs of congestive heart failure include rales, gallop rhythm, hepatomegaly, and scalp edema. Hypercyanotic spells, or “Tet spells,” present with restlessness, hyperpnea, progressive cyanosis, and possible syncope, often triggered by feeding, crying, or exertion. Older children may instinctively squat to improve symptoms.
History
A family history of congenital heart disease increases risk, especially if a parent or sibling is affected. Prenatal history may reveal teratogen exposure or abnormal fetal ultrasound findings. Tetralogy of Fallot is often asymptomatic at birth, with symptoms developing as right ventricular outflow obstruction worsens. Tricuspid atresia usually presents with cyanosis from birth. Ebstein anomaly may present later in adolescence with dysrhythmias. Transposition of the great arteries often presents within the first hours to days of life. Total anomalous pulmonary venous return may present with severe neonatal illness or later with heart failure if unobstructed. Truncus arteriosus causes mild neonatal cyanosis with progressive heart failure in infancy.
Physical Examination
Tetralogy of Fallot is characterized by a loud systolic murmur along the left sternal border, a single loud second heart sound, and right ventricular prominence. Chronic disease leads to clubbing and retinal engorgement. Tricuspid atresia presents with tachypnea, a regurgitant murmur from an associated ventricular septal defect, a single second heart sound, and a prominent left ventricular impulse. Ebstein anomaly produces holosystolic tricuspid regurgitation murmurs and may include gallop rhythms. Transposition of the great arteries is notable for severe hypoxemia with a single loud second heart sound. Total anomalous pulmonary venous return presents with tachypnea, murmurs, fixed split second heart sound, and hepatomegaly. Truncus arteriosus causes bounding pulses, wide pulse pressure, a loud single second heart sound, and systolic and diastolic murmurs.
Essential Diagnostic Evaluation
Initial evaluation includes pulse oximetry, arterial blood gas analysis, complete blood count, glucose testing, and a full sepsis evaluation. Chest radiography assesses pulmonary blood flow, while electrocardiography evaluates chamber hypertrophy and axis deviation. Early cardiology consultation is essential.
Diagnostic Tests And Interpretation
Arterial blood gases show reduced oxygen saturation on room air. The hyperoxia test helps differentiate pulmonary disease from cyanotic congenital heart disease, with a PaO₂ less than 100 mm Hg after 100% oxygen strongly suggesting intracardiac shunting. Chronic cyanosis leads to erythrocytosis on complete blood count. Chest radiography may show decreased pulmonary blood flow in tetralogy of Fallot or tricuspid atresia and increased flow in transposition, total anomalous pulmonary venous return, and truncus arteriosus. Classic radiographic signs include the boot-shaped heart of tetralogy of Fallot, the egg-on-a-string appearance of transposition of the great arteries, and the snowman sign in supracardiac total anomalous pulmonary venous return. Electrocardiography demonstrates characteristic patterns of axis deviation and ventricular hypertrophy depending on the lesion.
Differential Diagnosis
The differential includes pulmonary causes such as pneumothorax, pulmonary hypertension, pneumonia, bronchiolitis, and diaphragmatic hernia; cardiac causes such as congestive heart failure and cardiogenic shock; infectious causes including sepsis; neurologic causes such as seizures; and metabolic or hematologic conditions including hypoglycemia, dehydration, polycythemia, and methemoglobinemia.
Initial Stabilization And Therapy
Management focuses on maintaining warmth, correcting hypoglycemia and acidosis, ensuring adequate oxygenation, establishing intravenous access, and preparing for airway support. Excessive oxygen should be avoided because high oxygen tension promotes ductal closure. Air filters should be placed on intravenous lines to prevent paradoxical emboli.
Emergency Department Management
Prostaglandin E1 infusion should be initiated in duct-dependent lesions to maintain or reopen the ductus arteriosus, typically at 0.05–0.1 μg/kg/min. Complications include apnea, bradycardia, hypotension, and seizures, so airway readiness is essential. Prostaglandin is ineffective in obstructed total anomalous pulmonary venous return, which may require extracorporeal support. Fluid resuscitation should be performed cautiously in 10 mL/kg increments. Hypercyanotic spells are managed with a calm environment, knee-chest positioning, supplemental oxygen if tolerated, and morphine. Severe cases may require bicarbonate, phenylephrine to increase systemic vascular resistance, or propranolol for beta-blockade. Circulatory collapse requires aggressive resuscitation with fluids, inotropes, and correction of acidosis.
Medications
Commonly used medications include prostaglandin E1, morphine, phenylephrine, propranolol, dopamine, dobutamine, milrinone, antibiotics such as ampicillin and gentamicin, antipyretics, and sodium bicarbonate when indicated.
Disposition And Follow-Up
All newborns with suspected cyanotic congenital heart disease require admission to a pediatric intensive care unit. Admission is also indicated for acute worsening of cyanosis, heart failure, or respiratory infection. Discharge decisions should be made in consultation with pediatric cardiology and reserved for carefully selected, stable patients with ensured close follow-up.
Referral And Follow-Up Recommendations
Care should be coordinated among primary care providers, pediatric cardiologists, and cardiothoracic surgeons. Clear follow-up plans and return precautions are essential, as physiologic stress can rapidly worsen clinical status.
Clinical Pearls And Pitfalls
Visible cyanosis requires significant levels of deoxygenated hemoglobin. Duct-dependent lesions often present at two to three weeks of age with sudden cyanosis or cardiovascular collapse. Prostaglandin E1 can be lifesaving but requires close monitoring for apnea and hypotension.
Description
Cyanotic congenital heart disease results from abnormal embryologic cardiac development that allows mixing of deoxygenated and oxygenated blood into the systemic circulation. This occurs through right-to-left intracardiac shunting or anatomic defects involving the great vessels. Classic subtypes include the “five Ts,” the “two Es,” and single-ventricle physiology. These conditions include tetralogy of Fallot, transposition of the great arteries, tricuspid atresia, truncus arteriosus, total anomalous pulmonary venous return, Ebstein anomaly of the tricuspid valve, Eisenmenger syndrome, and single-ventricle physiology. All lead to varying degrees of systemic hypoxemia.
Etiology
For most cyanotic congenital heart defects, the precise cause is unknown. Genetic and environmental contributions may play a role, but no single unifying etiology is identified in the majority of cases.
Emergency Presentation
The most common initial emergency department presentations include central cyanosis, congestive heart failure, and circulatory collapse. In older children with known cyanotic heart disease, physiologic stress such as fever, dehydration, pulmonary disease, decreased systemic vascular resistance, or obstruction of a cardiac shunt can precipitate worsening cyanosis.
Clinical Features
Central cyanosis is typically visible in the lips, nail beds, and mucous membranes and worsens with crying or agitation, with minimal improvement on administration of 100% oxygen. Signs of congestive heart failure include rales, gallop rhythm, hepatomegaly, and scalp edema. Hypercyanotic spells, or “Tet spells,” present with restlessness, hyperpnea, progressive cyanosis, and possible syncope, often triggered by feeding, crying, or exertion. Older children may instinctively squat to improve symptoms.
History
A family history of congenital heart disease increases risk, especially if a parent or sibling is affected. Prenatal history may reveal teratogen exposure or abnormal fetal ultrasound findings. Tetralogy of Fallot is often asymptomatic at birth, with symptoms developing as right ventricular outflow obstruction worsens. Tricuspid atresia usually presents with cyanosis from birth. Ebstein anomaly may present later in adolescence with dysrhythmias. Transposition of the great arteries often presents within the first hours to days of life. Total anomalous pulmonary venous return may present with severe neonatal illness or later with heart failure if unobstructed. Truncus arteriosus causes mild neonatal cyanosis with progressive heart failure in infancy.
Physical Examination
Tetralogy of Fallot is characterized by a loud systolic murmur along the left sternal border, a single loud second heart sound, and right ventricular prominence. Chronic disease leads to clubbing and retinal engorgement. Tricuspid atresia presents with tachypnea, a regurgitant murmur from an associated ventricular septal defect, a single second heart sound, and a prominent left ventricular impulse. Ebstein anomaly produces holosystolic tricuspid regurgitation murmurs and may include gallop rhythms. Transposition of the great arteries is notable for severe hypoxemia with a single loud second heart sound. Total anomalous pulmonary venous return presents with tachypnea, murmurs, fixed split second heart sound, and hepatomegaly. Truncus arteriosus causes bounding pulses, wide pulse pressure, a loud single second heart sound, and systolic and diastolic murmurs.
Essential Diagnostic Evaluation
Initial evaluation includes pulse oximetry, arterial blood gas analysis, complete blood count, glucose testing, and a full sepsis evaluation. Chest radiography assesses pulmonary blood flow, while electrocardiography evaluates chamber hypertrophy and axis deviation. Early cardiology consultation is essential.
Diagnostic Tests And Interpretation
Arterial blood gases show reduced oxygen saturation on room air. The hyperoxia test helps differentiate pulmonary disease from cyanotic congenital heart disease, with a PaO₂ less than 100 mm Hg after 100% oxygen strongly suggesting intracardiac shunting. Chronic cyanosis leads to erythrocytosis on complete blood count. Chest radiography may show decreased pulmonary blood flow in tetralogy of Fallot or tricuspid atresia and increased flow in transposition, total anomalous pulmonary venous return, and truncus arteriosus. Classic radiographic signs include the boot-shaped heart of tetralogy of Fallot, the egg-on-a-string appearance of transposition of the great arteries, and the snowman sign in supracardiac total anomalous pulmonary venous return. Electrocardiography demonstrates characteristic patterns of axis deviation and ventricular hypertrophy depending on the lesion.
Differential Diagnosis
The differential includes pulmonary causes such as pneumothorax, pulmonary hypertension, pneumonia, bronchiolitis, and diaphragmatic hernia; cardiac causes such as congestive heart failure and cardiogenic shock; infectious causes including sepsis; neurologic causes such as seizures; and metabolic or hematologic conditions including hypoglycemia, dehydration, polycythemia, and methemoglobinemia.
Initial Stabilization And Therapy
Management focuses on maintaining warmth, correcting hypoglycemia and acidosis, ensuring adequate oxygenation, establishing intravenous access, and preparing for airway support. Excessive oxygen should be avoided because high oxygen tension promotes ductal closure. Air filters should be placed on intravenous lines to prevent paradoxical emboli.
Emergency Department Management
Prostaglandin E1 infusion should be initiated in duct-dependent lesions to maintain or reopen the ductus arteriosus, typically at 0.05–0.1 μg/kg/min. Complications include apnea, bradycardia, hypotension, and seizures, so airway readiness is essential. Prostaglandin is ineffective in obstructed total anomalous pulmonary venous return, which may require extracorporeal support. Fluid resuscitation should be performed cautiously in 10 mL/kg increments. Hypercyanotic spells are managed with a calm environment, knee-chest positioning, supplemental oxygen if tolerated, and morphine. Severe cases may require bicarbonate, phenylephrine to increase systemic vascular resistance, or propranolol for beta-blockade. Circulatory collapse requires aggressive resuscitation with fluids, inotropes, and correction of acidosis.
Medications
Commonly used medications include prostaglandin E1, morphine, phenylephrine, propranolol, dopamine, dobutamine, milrinone, antibiotics such as ampicillin and gentamicin, antipyretics, and sodium bicarbonate when indicated.
Disposition And Follow-Up
All newborns with suspected cyanotic congenital heart disease require admission to a pediatric intensive care unit. Admission is also indicated for acute worsening of cyanosis, heart failure, or respiratory infection. Discharge decisions should be made in consultation with pediatric cardiology and reserved for carefully selected, stable patients with ensured close follow-up.
Referral And Follow-Up Recommendations
Care should be coordinated among primary care providers, pediatric cardiologists, and cardiothoracic surgeons. Clear follow-up plans and return precautions are essential, as physiologic stress can rapidly worsen clinical status.
Clinical Pearls And Pitfalls
Visible cyanosis requires significant levels of deoxygenated hemoglobin. Duct-dependent lesions often present at two to three weeks of age with sudden cyanosis or cardiovascular collapse. Prostaglandin E1 can be lifesaving but requires close monitoring for apnea and hypotension.
- Published on
Emergency And Acute Medicine – Congenital Heart Disease, Acyanotic
Description
Acyanotic congenital heart disease refers to structural abnormalities of the cardiocirculatory system present at birth that do not result in mixing of deoxygenated and oxygenated blood. These defects commonly produce left-to-right shunting or obstruct ventricular outflow. Left-to-right shunt lesions include ventricular septal defect, atrial septal defect, patent ductus arteriosus, and endocardial cushion (atrioventricular canal) defects. Ventricular outflow obstruction lesions include coarctation of the aorta, aortic stenosis, pulmonic stenosis, and hypoplastic left heart syndrome. Several of these conditions are ductal dependent, with clinical deterioration occurring as the ductus arteriosus closes, particularly in coarctation of the aorta, critical aortic stenosis, critical pulmonic stenosis, and hypoplastic left heart syndrome.
Etiology
In most cases, the underlying cause is unknown. Genetic associations include trisomy 21 with atrioventricular canal defects and Turner syndrome with coarctation of the aorta. Environmental causes include congenital rubella infection, which is associated with patent ductus arteriosus and aortic stenosis.
Clinical Presentation
Many patients are asymptomatic early in life. Symptomatic infants may present with lethargy, poor feeding, failure to thrive, dyspnea with exertion or feeding, and recurrent respiratory infections.
Physical Examination
Ventricular septal defects and atrioventricular canal defects are associated with a dusky appearance, hepatomegaly, holosystolic or diastolic murmurs with thrills, a hyperdynamic precordium, and a displaced point of maximal impulse. Atrial septal defects typically produce a fixed split second heart sound with systolic ejection and diastolic murmurs. Patent ductus arteriosus presents with a continuous “machine-like” murmur and bounding peripheral pulses. Coarctation of the aorta is characterized by differential cyanosis, higher blood pressure in the upper extremities than the lower extremities, and diminished or absent femoral pulses. Aortic stenosis produces a harsh systolic murmur with a thrill and an aortic click. Pulmonic stenosis causes a systolic ejection murmur with a thrill, pulmonic click, widely split second heart sound, and jugular venous A waves. Hypoplastic left heart syndrome presents with a dusky, listless, tachypneic infant, diminished pulses, a single heart sound, and a systolic ejection murmur.
Essential Diagnostic Evaluation
Initial evaluation includes pre- and postductal oxygen saturation measurement, arterial blood gas analysis, complete blood count, basic metabolic panel, glucose testing, and a full sepsis evaluation. Chest radiography is used to assess pulmonary blood flow, while electrocardiography evaluates cardiac axis, chamber hypertrophy, and conduction abnormalities. Four-extremity blood pressure measurements are essential. Early cardiology consultation is required.
Diagnostic Tests And Interpretation
Chest radiography in left-to-right shunting lesions typically demonstrates cardiomegaly with increased pulmonary vascular markings. Chamber enlargement patterns vary by lesion, with atrial septal defects enlarging the right atrium and right ventricle, ventricular septal defects enlarging the right ventricle and left atrium, and patent ductus arteriosus enlarging the left atrium and left ventricle. Atrioventricular canal defects often produce a globular heart with enlargement of all chambers. Obstructive lesions may show a normal cardiac silhouette or cardiomegaly. Electrocardiographic findings vary by lesion and may include right or left axis deviation, ventricular hypertrophy, bundle branch block, prolonged PR interval, or peaked P waves, depending on the specific defect.
Differential Diagnosis
Conditions to consider include congestive heart failure, hypertrophic cardiomyopathy, cardiogenic shock, aortic dissection, myocarditis, bronchopulmonary dysplasia, pulmonary hypertension, pneumonia or bronchiolitis, hypoglycemia, adrenal insufficiency or congenital adrenal hyperplasia, glycogen storage diseases, sepsis, and other causes of shock.
Initial Stabilization And Therapy
Initial management focuses on maintaining warmth and adequate oxygenation, correcting hypoglycemia and metabolic acidosis, establishing intravenous access, and preparing for airway support if needed. Excessively high oxygen concentrations should be avoided, as they promote ductal closure.
Emergency Department Management
Prostaglandin E1 infusion should be initiated to maintain or reopen ductal patency in ductal-dependent lesions, typically at 0.05–0.1 μg/kg/min by continuous intravenous infusion. Potential complications include apnea, bradycardia, hypotension, and seizures. A full septic evaluation with empiric antibiotics should be performed while alternative causes are addressed. Circulatory collapse related to congenital heart disease is treated with cautious fluid resuscitation in 10 mL/kg increments, inotropic support, and aggressive correction of acidosis. Congestive heart failure is managed with diuretics and digoxin when appropriate.
Medications
Commonly used medications include ampicillin, gentamicin, prostaglandin E1, furosemide, digoxin, dopamine, dobutamine, epinephrine, milrinone, and sodium bicarbonate. Digoxin dosing requires extreme caution due to its narrow therapeutic window.
Disposition And Follow-Up
All newborns with suspected congenital heart disease require admission to a pediatric intensive care unit. Admission is also indicated for patients with acute worsening of heart failure, respiratory infection, or hemodynamic instability. Discharge decisions should only be made in conjunction with a pediatric cardiologist.
Referral And Follow-Up Recommendations
Ongoing care should be coordinated by the primary care physician in collaboration with pediatric cardiology and cardiothoracic surgery. Follow-up plans must be individualized based on the specific lesion and clinical course.
Clinical Pearls And Pitfalls
Acyanotic lesions often become symptomatic between 2 and 12 weeks of age as the ductus arteriosus closes or pulmonary vascular resistance decreases. Coarctation commonly presents as ductal closure occurs, while septal defects become apparent as pulmonary resistance falls. A superior QRS axis on ECG is characteristic of atrioventricular canal defects, and rib notching on chest radiography is a late finding in coarctation of the aorta.
Description
Acyanotic congenital heart disease refers to structural abnormalities of the cardiocirculatory system present at birth that do not result in mixing of deoxygenated and oxygenated blood. These defects commonly produce left-to-right shunting or obstruct ventricular outflow. Left-to-right shunt lesions include ventricular septal defect, atrial septal defect, patent ductus arteriosus, and endocardial cushion (atrioventricular canal) defects. Ventricular outflow obstruction lesions include coarctation of the aorta, aortic stenosis, pulmonic stenosis, and hypoplastic left heart syndrome. Several of these conditions are ductal dependent, with clinical deterioration occurring as the ductus arteriosus closes, particularly in coarctation of the aorta, critical aortic stenosis, critical pulmonic stenosis, and hypoplastic left heart syndrome.
Etiology
In most cases, the underlying cause is unknown. Genetic associations include trisomy 21 with atrioventricular canal defects and Turner syndrome with coarctation of the aorta. Environmental causes include congenital rubella infection, which is associated with patent ductus arteriosus and aortic stenosis.
Clinical Presentation
Many patients are asymptomatic early in life. Symptomatic infants may present with lethargy, poor feeding, failure to thrive, dyspnea with exertion or feeding, and recurrent respiratory infections.
Physical Examination
Ventricular septal defects and atrioventricular canal defects are associated with a dusky appearance, hepatomegaly, holosystolic or diastolic murmurs with thrills, a hyperdynamic precordium, and a displaced point of maximal impulse. Atrial septal defects typically produce a fixed split second heart sound with systolic ejection and diastolic murmurs. Patent ductus arteriosus presents with a continuous “machine-like” murmur and bounding peripheral pulses. Coarctation of the aorta is characterized by differential cyanosis, higher blood pressure in the upper extremities than the lower extremities, and diminished or absent femoral pulses. Aortic stenosis produces a harsh systolic murmur with a thrill and an aortic click. Pulmonic stenosis causes a systolic ejection murmur with a thrill, pulmonic click, widely split second heart sound, and jugular venous A waves. Hypoplastic left heart syndrome presents with a dusky, listless, tachypneic infant, diminished pulses, a single heart sound, and a systolic ejection murmur.
Essential Diagnostic Evaluation
Initial evaluation includes pre- and postductal oxygen saturation measurement, arterial blood gas analysis, complete blood count, basic metabolic panel, glucose testing, and a full sepsis evaluation. Chest radiography is used to assess pulmonary blood flow, while electrocardiography evaluates cardiac axis, chamber hypertrophy, and conduction abnormalities. Four-extremity blood pressure measurements are essential. Early cardiology consultation is required.
Diagnostic Tests And Interpretation
Chest radiography in left-to-right shunting lesions typically demonstrates cardiomegaly with increased pulmonary vascular markings. Chamber enlargement patterns vary by lesion, with atrial septal defects enlarging the right atrium and right ventricle, ventricular septal defects enlarging the right ventricle and left atrium, and patent ductus arteriosus enlarging the left atrium and left ventricle. Atrioventricular canal defects often produce a globular heart with enlargement of all chambers. Obstructive lesions may show a normal cardiac silhouette or cardiomegaly. Electrocardiographic findings vary by lesion and may include right or left axis deviation, ventricular hypertrophy, bundle branch block, prolonged PR interval, or peaked P waves, depending on the specific defect.
Differential Diagnosis
Conditions to consider include congestive heart failure, hypertrophic cardiomyopathy, cardiogenic shock, aortic dissection, myocarditis, bronchopulmonary dysplasia, pulmonary hypertension, pneumonia or bronchiolitis, hypoglycemia, adrenal insufficiency or congenital adrenal hyperplasia, glycogen storage diseases, sepsis, and other causes of shock.
Initial Stabilization And Therapy
Initial management focuses on maintaining warmth and adequate oxygenation, correcting hypoglycemia and metabolic acidosis, establishing intravenous access, and preparing for airway support if needed. Excessively high oxygen concentrations should be avoided, as they promote ductal closure.
Emergency Department Management
Prostaglandin E1 infusion should be initiated to maintain or reopen ductal patency in ductal-dependent lesions, typically at 0.05–0.1 μg/kg/min by continuous intravenous infusion. Potential complications include apnea, bradycardia, hypotension, and seizures. A full septic evaluation with empiric antibiotics should be performed while alternative causes are addressed. Circulatory collapse related to congenital heart disease is treated with cautious fluid resuscitation in 10 mL/kg increments, inotropic support, and aggressive correction of acidosis. Congestive heart failure is managed with diuretics and digoxin when appropriate.
Medications
Commonly used medications include ampicillin, gentamicin, prostaglandin E1, furosemide, digoxin, dopamine, dobutamine, epinephrine, milrinone, and sodium bicarbonate. Digoxin dosing requires extreme caution due to its narrow therapeutic window.
Disposition And Follow-Up
All newborns with suspected congenital heart disease require admission to a pediatric intensive care unit. Admission is also indicated for patients with acute worsening of heart failure, respiratory infection, or hemodynamic instability. Discharge decisions should only be made in conjunction with a pediatric cardiologist.
Referral And Follow-Up Recommendations
Ongoing care should be coordinated by the primary care physician in collaboration with pediatric cardiology and cardiothoracic surgery. Follow-up plans must be individualized based on the specific lesion and clinical course.
Clinical Pearls And Pitfalls
Acyanotic lesions often become symptomatic between 2 and 12 weeks of age as the ductus arteriosus closes or pulmonary vascular resistance decreases. Coarctation commonly presents as ductal closure occurs, while septal defects become apparent as pulmonary resistance falls. A superior QRS axis on ECG is characteristic of atrioventricular canal defects, and rib notching on chest radiography is a late finding in coarctation of the aorta.
- Published on
Emergency And Acute Medicine – Implantable Defibrillators
Basics And Description
An implantable cardioverter-defibrillator (ICD) is a small, battery-powered cardiac device implanted subcutaneously in patients at risk for sudden cardiac arrest due to malignant arrhythmias. One or more leads are positioned via venous access to the heart, typically endocardial in the right atrium and right ventricle, or epicardial via the coronary sinus to the left ventricle. The ICD detects atrial and ventricular arrhythmias and delivers electrical shocks between the generator (“can”) and coils in the right ventricle and superior vena cava/right atrial junction to restore sinus rhythm. Implantation technique is similar to pacemaker placement. Newer subcutaneous ICDs (S-ICD) avoid endocardial leads, reducing the risk of bloodstream infection. Approximately 450,000 sudden cardiac deaths occur annually in the United States, with over 100,000 ICDs implanted each year. ICDs reduce mortality more effectively than antiarrhythmic drugs in patients with left ventricular dysfunction, particularly when ejection fraction is below 35%, with an absolute mortality reduction of about 7% in the first two years. Benefit is demonstrated in ischemic and nonischemic dilated cardiomyopathy and hypertrophic cardiomyopathy.
Complications And Device Outcomes
Immediate postimplant complications include pneumothorax, vascular perforation, and acute lead dislodgement. Appropriate shocks occur in approximately 5% of patients annually for primary prevention and 20% annually for secondary prevention. Electrical storm is defined as two or more appropriate shocks within 24 hours. Inappropriate shocks occur in 10–20% of recipients and are commonly due to oversensing or misclassification of supraventricular tachycardia. Device infection occurs in 1–12% of patients, with acute infections (1–30 days) most often due to staphylococcal species and later infections commonly due to Staphylococcus epidermidis or gram-negative organisms. Mortality ranges from 31–66% if an infected device is not removed. Pocket hematomas should not be aspirated. Vascular occlusion related to leads may occur.
Etiology
Electrical storm may result from decompensated heart failure, acute ischemia, metabolic disturbances, drug-induced proarrhythmia, thyrotoxicosis, fever in dilated cardiomyopathy, genetic channelopathies (including Brugada syndrome, long QT syndrome, catecholaminergic polymorphic ventricular tachycardia, and arrhythmogenic right ventricular cardiomyopathy), postcardiac surgery states, or ICD-induced pacing phenomena. Inappropriate shocks may result from oversensing of cardiac or noncardiac signals, electromagnetic interference, lead fracture, loose set screws, or header circuitry problems, as well as misclassification of atrial fibrillation, atrial flutter, sinus tachycardia, or other supraventricular tachycardias. Device- and site-related issues include wound infection, pocket hematoma, and venous thrombosis from lead-related venous obstruction.
Clinical Presentation
Patients who feel unwell before a shock and improved afterward likely received appropriate therapy. Patients who feel well before and after a shock likely experienced inappropriate therapy. Persistent symptoms before and after a shock suggest ongoing arrhythmia or ischemia. Appropriate shocks may be associated with syncope, near syncope, dizziness, dyspnea, palpitations, chest discomfort, or diaphoresis. Inappropriate shocks may occur with palpitations from supraventricular tachycardia or may be asymptomatic in lead-related malfunction. Device infection presents with fever, chills, malaise, hypotension, new murmur, or local wound findings such as erythema, warmth, purulent drainage, skin erosion, or fluctuance. Vascular complications present with unilateral upper-extremity swelling or superficial venous distention.
Evaluation And Workup
Following ICD therapy, device interrogation is essential to determine whether shocks were appropriate and to identify lead malfunction. A 12-lead ECG may show transient ST changes or enzyme elevation after shock delivery that do not necessarily represent myocardial injury. Chest radiography can identify lead fracture or dislodgement. Upper-extremity swelling suggests venous thrombosis. Laboratory evaluation includes cardiac enzymes when ischemia is suspected, complete blood count and blood cultures for infection, and coagulation studies when thrombosis is suspected. MRI is absolutely contraindicated. Magnet application inhibits tachyarrhythmia therapies but does not affect bradycardia pacing.
Differential Diagnosis
Consider appropriate ICD therapy for ventricular tachycardia or fibrillation, inappropriate therapy due to supraventricular tachycardia or device malfunction, phantom shocks perceived during sleep, acute coronary syndrome, heart failure exacerbation, and systemic infection.
Management And Treatment
Initial management follows standard advanced cardiac life support protocols with continuous monitoring. Electrical storm may require intravenous antiarrhythmic therapy such as amiodarone. Inappropriate shocks are managed by treating the underlying supraventricular arrhythmia with beta blockers or calcium channel blockers and inhibiting ICD therapies with magnet placement if needed. Device infections require prompt blood cultures and broad-spectrum antibiotics, with early consultation for device removal. External defibrillation is safe but should not be delivered directly over the ICD generator.
Medications
Common agents include intravenous amiodarone for ventricular arrhythmias, beta blockers or diltiazem for rate control, and antibiotics such as cefazolin or vancomycin for suspected device infection. Anticoagulation with warfarin is indicated for documented venous thrombosis.
Disposition And Follow-Up
Admission is required for patients with ongoing ischemia, heart failure, multiple ICD shocks, suspected infection, expanding pocket hematoma, need for lead revision, or upper-extremity thrombosis. Stable patients with a single appropriate shock and no evidence of ischemia or heart failure may be discharged with electrophysiology follow-up. Device-related complications require surgical or electrophysiology consultation prior to discharge.
Key Clinical Lessons And Common Errors
Aspiration of an ICD pocket should be avoided. External defibrillation pads should not be placed directly over the device, as this may shunt energy away from the myocardium. Prompt differentiation between appropriate and inappropriate shocks guides management and disposition.
Basics And Description
An implantable cardioverter-defibrillator (ICD) is a small, battery-powered cardiac device implanted subcutaneously in patients at risk for sudden cardiac arrest due to malignant arrhythmias. One or more leads are positioned via venous access to the heart, typically endocardial in the right atrium and right ventricle, or epicardial via the coronary sinus to the left ventricle. The ICD detects atrial and ventricular arrhythmias and delivers electrical shocks between the generator (“can”) and coils in the right ventricle and superior vena cava/right atrial junction to restore sinus rhythm. Implantation technique is similar to pacemaker placement. Newer subcutaneous ICDs (S-ICD) avoid endocardial leads, reducing the risk of bloodstream infection. Approximately 450,000 sudden cardiac deaths occur annually in the United States, with over 100,000 ICDs implanted each year. ICDs reduce mortality more effectively than antiarrhythmic drugs in patients with left ventricular dysfunction, particularly when ejection fraction is below 35%, with an absolute mortality reduction of about 7% in the first two years. Benefit is demonstrated in ischemic and nonischemic dilated cardiomyopathy and hypertrophic cardiomyopathy.
Complications And Device Outcomes
Immediate postimplant complications include pneumothorax, vascular perforation, and acute lead dislodgement. Appropriate shocks occur in approximately 5% of patients annually for primary prevention and 20% annually for secondary prevention. Electrical storm is defined as two or more appropriate shocks within 24 hours. Inappropriate shocks occur in 10–20% of recipients and are commonly due to oversensing or misclassification of supraventricular tachycardia. Device infection occurs in 1–12% of patients, with acute infections (1–30 days) most often due to staphylococcal species and later infections commonly due to Staphylococcus epidermidis or gram-negative organisms. Mortality ranges from 31–66% if an infected device is not removed. Pocket hematomas should not be aspirated. Vascular occlusion related to leads may occur.
Etiology
Electrical storm may result from decompensated heart failure, acute ischemia, metabolic disturbances, drug-induced proarrhythmia, thyrotoxicosis, fever in dilated cardiomyopathy, genetic channelopathies (including Brugada syndrome, long QT syndrome, catecholaminergic polymorphic ventricular tachycardia, and arrhythmogenic right ventricular cardiomyopathy), postcardiac surgery states, or ICD-induced pacing phenomena. Inappropriate shocks may result from oversensing of cardiac or noncardiac signals, electromagnetic interference, lead fracture, loose set screws, or header circuitry problems, as well as misclassification of atrial fibrillation, atrial flutter, sinus tachycardia, or other supraventricular tachycardias. Device- and site-related issues include wound infection, pocket hematoma, and venous thrombosis from lead-related venous obstruction.
Clinical Presentation
Patients who feel unwell before a shock and improved afterward likely received appropriate therapy. Patients who feel well before and after a shock likely experienced inappropriate therapy. Persistent symptoms before and after a shock suggest ongoing arrhythmia or ischemia. Appropriate shocks may be associated with syncope, near syncope, dizziness, dyspnea, palpitations, chest discomfort, or diaphoresis. Inappropriate shocks may occur with palpitations from supraventricular tachycardia or may be asymptomatic in lead-related malfunction. Device infection presents with fever, chills, malaise, hypotension, new murmur, or local wound findings such as erythema, warmth, purulent drainage, skin erosion, or fluctuance. Vascular complications present with unilateral upper-extremity swelling or superficial venous distention.
Evaluation And Workup
Following ICD therapy, device interrogation is essential to determine whether shocks were appropriate and to identify lead malfunction. A 12-lead ECG may show transient ST changes or enzyme elevation after shock delivery that do not necessarily represent myocardial injury. Chest radiography can identify lead fracture or dislodgement. Upper-extremity swelling suggests venous thrombosis. Laboratory evaluation includes cardiac enzymes when ischemia is suspected, complete blood count and blood cultures for infection, and coagulation studies when thrombosis is suspected. MRI is absolutely contraindicated. Magnet application inhibits tachyarrhythmia therapies but does not affect bradycardia pacing.
Differential Diagnosis
Consider appropriate ICD therapy for ventricular tachycardia or fibrillation, inappropriate therapy due to supraventricular tachycardia or device malfunction, phantom shocks perceived during sleep, acute coronary syndrome, heart failure exacerbation, and systemic infection.
Management And Treatment
Initial management follows standard advanced cardiac life support protocols with continuous monitoring. Electrical storm may require intravenous antiarrhythmic therapy such as amiodarone. Inappropriate shocks are managed by treating the underlying supraventricular arrhythmia with beta blockers or calcium channel blockers and inhibiting ICD therapies with magnet placement if needed. Device infections require prompt blood cultures and broad-spectrum antibiotics, with early consultation for device removal. External defibrillation is safe but should not be delivered directly over the ICD generator.
Medications
Common agents include intravenous amiodarone for ventricular arrhythmias, beta blockers or diltiazem for rate control, and antibiotics such as cefazolin or vancomycin for suspected device infection. Anticoagulation with warfarin is indicated for documented venous thrombosis.
Disposition And Follow-Up
Admission is required for patients with ongoing ischemia, heart failure, multiple ICD shocks, suspected infection, expanding pocket hematoma, need for lead revision, or upper-extremity thrombosis. Stable patients with a single appropriate shock and no evidence of ischemia or heart failure may be discharged with electrophysiology follow-up. Device-related complications require surgical or electrophysiology consultation prior to discharge.
Key Clinical Lessons And Common Errors
Aspiration of an ICD pocket should be avoided. External defibrillation pads should not be placed directly over the device, as this may shunt energy away from the myocardium. Prompt differentiation between appropriate and inappropriate shocks guides management and disposition.
- Published on
Emergency And Acute Medicine – Deep Vein Thrombosis
Core Description
A constant balance exists between intravascular clot formation and clot dissolution. Thrombosis develops when clot formation overwhelms fibrinolysis. Venous clots may be superficial (above the fascia) or deep; the latter constitutes deep vein thrombosis (DVT). Pulmonary embolism (PE) and DVT represent two ends of the same disease spectrum known as venous thromboembolism (VTE). DVT may involve upper or lower extremities and may be distal or proximal relative to the popliteal vein. The incidence is approximately 2 first-time VTE events per 1,000 person-years, increases with age, and is common among hospitalized medical and surgical patients. Diagnosis is more accurate with active surveillance rather than clinical suspicion alone.
Pediatric Considerations
DVT is uncommon in children. When present, evaluation for underlying hypercoagulable conditions is essential. Upper-extremity DVT in children is frequently associated with central venous catheters.
Etiology And Risk Factors
Thrombus formation is influenced by multiple interacting factors. Hypercoagulable states include malignancy, myeloproliferative disorders, nephrotic syndrome, sepsis, inflammatory conditions such as ulcerative colitis, increased estrogen states including pregnancy and exogenous hormones, antiphospholipid syndrome, inherited thrombophilias (protein C, protein S, antithrombin III deficiencies, factor V Leiden, prothrombin gene mutation), and autoimmune conditions.
Venous stasis occurs with prolonged bed rest, immobilization (casts), long-distance travel, paralysis from neurologic disease, congestive heart failure, and obesity.
Vascular injury or anatomic abnormalities include trauma, surgery, central venous lines (particularly for upper-extremity DVT), and May–Thurner syndrome.
Additional contributors include advanced age, certain medications (hydralazine, procainamide, phenothiazines), tobacco use, prior DVT or PE, and genetic predisposition. There is no universal consensus on which VTE patients require testing for inherited thrombophilias.
Pregnancy And Geriatric Considerations
Pregnancy increases DVT risk, particularly during the third trimester and up to two weeks postpartum. Advanced age independently increases DVT and PE risk, and presentations may be atypical in older adults.
Clinical Features
Typical findings include unilateral leg swelling, with a circumference difference greater than 1 cm considered significant, warmth, erythema, pain, tenderness, and sometimes a palpable cord. Superficial thrombophlebitis may present as a visible, tender, cord-like structure. Upper-extremity DVT causes arm swelling, warmth, and tenderness.
Severe presentations include phlegmasia cerulea dolens, characterized by a cold, tender, swollen, cyanotic limb with secondary arterial insufficiency and venous gangrene, and phlegmasia alba dolens, presenting with a cold, tender, pale limb due to arterial compromise.
Essential Evaluation
Assessment of pretest probability is central to DVT evaluation. Careful history and physical examination interpreted within the patient’s risk-factor profile guide diagnostic decisions, as individual signs and symptoms lack sufficient predictive value. Consider evaluation for occult malignancy when clinically appropriate, as VTE may be its initial manifestation.
Diagnostic Testing And Interpretation
D-dimer testing detects fibrin degradation products and is useful only when negative, allowing exclusion of DVT in low-risk patients. A positive result is nonspecific and mandates further imaging. ELISA-based D-dimer assays are the most validated, particularly when combined with pretest probability assessment.
Compression ultrasonography is the first-line diagnostic modality. Normal veins compress fully, whereas thrombosed veins do not. Duplex ultrasonography, combining B-mode imaging with Doppler, has sensitivity in the high 90% range. In high-risk patients with an initial negative ultrasound, repeat imaging or contrast venography is recommended.
Contrast venography, once the gold standard, is now rarely used because of invasiveness and associated complications. Other modalities such as radionuclide venography and impedance plethysmography are infrequently used.
Differential Diagnosis
Consider superficial thrombophlebitis, cellulitis, muscle or ligament tears, ruptured Baker cyst, bilateral edema from cardiac, hepatic, or renal disease, venous insufficiency, drug-induced edema, unilateral edema from abdominal masses or lymphedema, and postphlebitic syndrome.
Initial Stabilization
In cases of phlegmasia alba or cerulea dolens, establish IV access, administer supplemental oxygen, and obtain urgent vascular or surgical consultation.
Emergency Department Management
Systemic anticoagulation is the cornerstone of therapy in patients without contraindications, as PE develops in approximately 50% of untreated DVT. Options include unfractionated heparin, low-molecular-weight heparin (LMWH), fondaparinux, or adjusted-dose subcutaneous heparin. Carefully selected patients may be managed as outpatients.
Warfarin should be initiated only after heparin therapy to avoid transient hypercoagulability. Current evidence is insufficient to universally recommend newer oral anticoagulants in this setting.
Inferior vena cava filters are indicated when anticoagulation is contraindicated or when thromboembolism occurs despite adequate anticoagulation. Filters may also be considered in select high-risk scenarios, though randomized trials show no superiority over anticoagulation alone. Filters can also be placed in the superior vena cava for upper-extremity DVT.
Thrombolysis is rarely indicated because of increased bleeding risk but may be considered in select cases, particularly catheter-directed therapy for upper-extremity DVT. Thrombectomy may be appropriate for extensive disease after vascular consultation. Septic thrombophlebitis requires antibiotics and may necessitate surgical intervention.
Medication Management
Anticoagulation is continued until the INR is therapeutic for two consecutive days. Typical regimens include unfractionated heparin with a bolus followed by infusion titrated to aPTT, LMWH such as enoxaparin or tinzaparin, and warfarin initiated at standard dosing with INR monitoring. Treatment duration is generally at least three months and individualized thereafter.
Disposition And Follow-Up
Admission is indicated for patients unable to receive outpatient anticoagulation, those with concomitant PE, high bleeding risk, phlegmasia, or serious comorbidities.
Outpatient management is appropriate for reliable patients without serious comorbid disease who can administer LMWH and adhere to follow-up.
Vascular surgery consultation is warranted if arterial insufficiency is suspected or when considering vena cava filter placement.
Follow-Up Recommendations
Patients managed as outpatients require close monitoring of hematocrit, platelet count, and INR within several days. Repeat imaging is recommended when clinical suspicion remains high despite an initial negative ultrasound.
Key Clinical Lessons And Common Errors
A negative Homans sign does not exclude DVT. Always assess pretest probability using clinical judgment or validated tools such as the Wells score. In high-risk patients, proceed directly to imaging rather than relying on D-dimer testing. In moderate-risk patients with negative initial studies, arrange repeat evaluation within one week.
Core Description
A constant balance exists between intravascular clot formation and clot dissolution. Thrombosis develops when clot formation overwhelms fibrinolysis. Venous clots may be superficial (above the fascia) or deep; the latter constitutes deep vein thrombosis (DVT). Pulmonary embolism (PE) and DVT represent two ends of the same disease spectrum known as venous thromboembolism (VTE). DVT may involve upper or lower extremities and may be distal or proximal relative to the popliteal vein. The incidence is approximately 2 first-time VTE events per 1,000 person-years, increases with age, and is common among hospitalized medical and surgical patients. Diagnosis is more accurate with active surveillance rather than clinical suspicion alone.
Pediatric Considerations
DVT is uncommon in children. When present, evaluation for underlying hypercoagulable conditions is essential. Upper-extremity DVT in children is frequently associated with central venous catheters.
Etiology And Risk Factors
Thrombus formation is influenced by multiple interacting factors. Hypercoagulable states include malignancy, myeloproliferative disorders, nephrotic syndrome, sepsis, inflammatory conditions such as ulcerative colitis, increased estrogen states including pregnancy and exogenous hormones, antiphospholipid syndrome, inherited thrombophilias (protein C, protein S, antithrombin III deficiencies, factor V Leiden, prothrombin gene mutation), and autoimmune conditions.
Venous stasis occurs with prolonged bed rest, immobilization (casts), long-distance travel, paralysis from neurologic disease, congestive heart failure, and obesity.
Vascular injury or anatomic abnormalities include trauma, surgery, central venous lines (particularly for upper-extremity DVT), and May–Thurner syndrome.
Additional contributors include advanced age, certain medications (hydralazine, procainamide, phenothiazines), tobacco use, prior DVT or PE, and genetic predisposition. There is no universal consensus on which VTE patients require testing for inherited thrombophilias.
Pregnancy And Geriatric Considerations
Pregnancy increases DVT risk, particularly during the third trimester and up to two weeks postpartum. Advanced age independently increases DVT and PE risk, and presentations may be atypical in older adults.
Clinical Features
Typical findings include unilateral leg swelling, with a circumference difference greater than 1 cm considered significant, warmth, erythema, pain, tenderness, and sometimes a palpable cord. Superficial thrombophlebitis may present as a visible, tender, cord-like structure. Upper-extremity DVT causes arm swelling, warmth, and tenderness.
Severe presentations include phlegmasia cerulea dolens, characterized by a cold, tender, swollen, cyanotic limb with secondary arterial insufficiency and venous gangrene, and phlegmasia alba dolens, presenting with a cold, tender, pale limb due to arterial compromise.
Essential Evaluation
Assessment of pretest probability is central to DVT evaluation. Careful history and physical examination interpreted within the patient’s risk-factor profile guide diagnostic decisions, as individual signs and symptoms lack sufficient predictive value. Consider evaluation for occult malignancy when clinically appropriate, as VTE may be its initial manifestation.
Diagnostic Testing And Interpretation
D-dimer testing detects fibrin degradation products and is useful only when negative, allowing exclusion of DVT in low-risk patients. A positive result is nonspecific and mandates further imaging. ELISA-based D-dimer assays are the most validated, particularly when combined with pretest probability assessment.
Compression ultrasonography is the first-line diagnostic modality. Normal veins compress fully, whereas thrombosed veins do not. Duplex ultrasonography, combining B-mode imaging with Doppler, has sensitivity in the high 90% range. In high-risk patients with an initial negative ultrasound, repeat imaging or contrast venography is recommended.
Contrast venography, once the gold standard, is now rarely used because of invasiveness and associated complications. Other modalities such as radionuclide venography and impedance plethysmography are infrequently used.
Differential Diagnosis
Consider superficial thrombophlebitis, cellulitis, muscle or ligament tears, ruptured Baker cyst, bilateral edema from cardiac, hepatic, or renal disease, venous insufficiency, drug-induced edema, unilateral edema from abdominal masses or lymphedema, and postphlebitic syndrome.
Initial Stabilization
In cases of phlegmasia alba or cerulea dolens, establish IV access, administer supplemental oxygen, and obtain urgent vascular or surgical consultation.
Emergency Department Management
Systemic anticoagulation is the cornerstone of therapy in patients without contraindications, as PE develops in approximately 50% of untreated DVT. Options include unfractionated heparin, low-molecular-weight heparin (LMWH), fondaparinux, or adjusted-dose subcutaneous heparin. Carefully selected patients may be managed as outpatients.
Warfarin should be initiated only after heparin therapy to avoid transient hypercoagulability. Current evidence is insufficient to universally recommend newer oral anticoagulants in this setting.
Inferior vena cava filters are indicated when anticoagulation is contraindicated or when thromboembolism occurs despite adequate anticoagulation. Filters may also be considered in select high-risk scenarios, though randomized trials show no superiority over anticoagulation alone. Filters can also be placed in the superior vena cava for upper-extremity DVT.
Thrombolysis is rarely indicated because of increased bleeding risk but may be considered in select cases, particularly catheter-directed therapy for upper-extremity DVT. Thrombectomy may be appropriate for extensive disease after vascular consultation. Septic thrombophlebitis requires antibiotics and may necessitate surgical intervention.
Medication Management
Anticoagulation is continued until the INR is therapeutic for two consecutive days. Typical regimens include unfractionated heparin with a bolus followed by infusion titrated to aPTT, LMWH such as enoxaparin or tinzaparin, and warfarin initiated at standard dosing with INR monitoring. Treatment duration is generally at least three months and individualized thereafter.
Disposition And Follow-Up
Admission is indicated for patients unable to receive outpatient anticoagulation, those with concomitant PE, high bleeding risk, phlegmasia, or serious comorbidities.
Outpatient management is appropriate for reliable patients without serious comorbid disease who can administer LMWH and adhere to follow-up.
Vascular surgery consultation is warranted if arterial insufficiency is suspected or when considering vena cava filter placement.
Follow-Up Recommendations
Patients managed as outpatients require close monitoring of hematocrit, platelet count, and INR within several days. Repeat imaging is recommended when clinical suspicion remains high despite an initial negative ultrasound.
Key Clinical Lessons And Common Errors
A negative Homans sign does not exclude DVT. Always assess pretest probability using clinical judgment or validated tools such as the Wells score. In high-risk patients, proceed directly to imaging rather than relying on D-dimer testing. In moderate-risk patients with negative initial studies, arrange repeat evaluation within one week.
- Published on
Emergency And Acute Medicine – Decompression Sickness
Core Description
Decompression sickness is a multisystem disease caused by the formation of inert gas bubbles, primarily nitrogen, that escape from solution into body tissues and fluids during or after a reduction in ambient pressure.
Etiology And Pathophysiology
Decompression sickness occurs when nitrogen that has dissolved in body tissues under increased ambient pressure comes out of solution too rapidly during ascent. As ambient pressure increases, the partial pressure of inspired nitrogen rises, leading to progressive nitrogen absorption into tissues, particularly with longer exposure times. When ascent occurs too quickly, the pressure gradient overwhelms the body’s ability to eliminate nitrogen gradually. Tissues become supersaturated, and gas bubbles form.
According to Henry’s law, the amount of gas dissolved in a liquid is directly proportional to the partial pressure of that gas. Increased partial pressure results in greater gas dissolution, while decreased partial pressure causes gas to come out of solution. Nitrogen bubbles act as foreign bodies, triggering inflammatory and coagulation pathways, increasing vascular permeability, reducing intravascular volume, and causing hemoconcentration.
Clinical manifestations depend on bubble location. Bubbles may obstruct blood flow or lymphatics, leading to ischemia, infarction, or lymphedema, or they may cause mechanical tissue distention resulting in pain.
Risk Factors
Dive-related factors include greater depth, longer bottom time, multiple dives within a day, rapid ascent, and cold water exposure. Human factors include obesity, dehydration, pulmonary disease, and intercurrent illness. Proper use of dive tables or computers reduces but does not eliminate risk. Predive vigorous exercise may reduce risk. Approximately 50% of patients develop symptoms within 1 hour and 90% within 6 hours. Air travel after diving can precipitate decompression sickness because of reduced cabin pressure.
Clinical Presentation
Cutaneous Manifestations
Skin findings include scarlatiniform, erysipeloid, or mottled rashes. Cutis marmorata, a mottled appearance, often indicates more severe disease. A peau d’orange appearance may occur due to lymphatic obstruction.
Musculoskeletal Manifestations (The Bends)
Patients experience dull, deep muscular or joint pain, most commonly affecting the elbows and shoulders. Pain is typically not worsened by movement and is not reproducible with palpation.
Gastrointestinal Manifestations
Symptoms include nausea, vomiting, and abdominal pain.
Pulmonary Manifestations (The Chokes)
Pulmonary symptoms result from obstruction of pulmonary vasculature by gas bubbles and include acute respiratory distress, substernal chest pain or pressure, cough, dyspnea, and hypoxia.
Central Nervous System Manifestations
Neurologic symptoms include weakness, fatigue, numbness, paresthesias, agitation, headache, dizziness, vertigo, seizures, bladder or bowel incontinence, lethargy, and visual disturbances. The spinal cord, particularly the lower thoracic and lumbar regions, is most commonly affected.
Inner Ear Manifestations (The Staggers)
Vestibular involvement causes dizziness, vertigo, tinnitus, and nausea. These symptoms resemble inner ear barotrauma but carry a worse prognosis.
History And Physical Examination
A detailed dive history is essential, including depth, duration, ascent profile, surface intervals, and timing of symptom onset. Physical examination should be comprehensive, with particular attention to a detailed neurologic assessment to identify subtle or evolving deficits.
Essential Evaluation
Diagnosis is primarily clinical and based on recognition of risk factors and characteristic presentations. Neurologic findings should be carefully documented, including improvement or progression. Definitive diagnosis may be supported by a trial of pressure, as rapid symptom relief during recompression in a hyperbaric chamber is often diagnostic.
Diagnostic Testing And Interpretation
Laboratory studies may show elevated hematocrit due to hemoconcentration. Electrolytes, renal function, glucose, and urinalysis should be obtained, with increased urine specific gravity suggesting volume depletion. Arterial blood gas analysis and pulse oximetry are used to monitor oxygenation.
Imaging may include chest radiography to assess for pulmonary barotrauma or noncardiogenic pulmonary edema. Extremity radiographs may help exclude traumatic causes of pain. Head CT is indicated for altered mental status or focal neurologic deficits.
Differential Diagnosis
Consider musculoskeletal injury unrelated to bubble formation, inner or middle ear barotrauma, arterial gas embolism, cerebrovascular accident, and trauma.
Prehospital Management
Early recognition is critical, as postdive extremity pain may be misattributed to muscle strain and neurologic symptoms may be minimized by patients. If air evacuation is required, altitude should be limited to less than 1,000 feet or a pressurized aircraft should be used. In-water recompression is controversial, technically difficult, and requires extensive support.
Initial Stabilization
Airway, breathing, and circulation should be managed promptly. Administer 100% normobaric oxygen via mask or endotracheal tube to enhance nitrogen elimination, reduce bubble size, and improve tissue oxygenation. Maintain the patient in a supine position to minimize cerebral involvement. Early recompression in a hyperbaric chamber is essential.
Emergency Department Management
Administer intravenous 0.9% normal saline to correct dehydration and maintain urine output of 1–2 mL/kg/hour. Dehydration is common due to pressure-induced diuresis, exertion, dry compressed air breathing, and capillary leak. Adequate hydration promotes nitrogen elimination.
Arrange urgent hyperbaric oxygen recompression therapy and transfer to the nearest facility. Insert a prophylactic chest tube for known pneumothorax to prevent tension pneumothorax during recompression. Inflate endotracheal and Foley catheter balloons with saline or water to prevent compression-related damage.
Provide analgesics and antiemetics as needed. Diazepam may be used for severe vertigo. Adjunctive NSAIDs or heliox may reduce the number of recompression treatments required. Consultation with Divers Alert Network is recommended for expert guidance and referral.
Disposition And Follow-Up
All patients with suspected or confirmed decompression sickness should be referred for hyperbaric therapy. Stable patients with mild symptoms may be discharged after treatment. Patients should avoid air travel after treatment, as reduced ambient pressure may worsen symptoms.
Follow-Up Recommendations
Ensure hyperbaric medicine follow-up and reinforce diving safety counseling.
Key Clinical Lessons And Common Errors
Musculoskeletal decompression sickness can be difficult to distinguish from benign musculoskeletal pain. Significant fatigue alone may represent decompression sickness. Even mild or resolving symptoms warrant hyperbaric recompression therapy. Do not delay recompression for laboratory testing or imaging when decompression sickness is the likely diagnosis. In-water recompression should be avoided.
Core Description
Decompression sickness is a multisystem disease caused by the formation of inert gas bubbles, primarily nitrogen, that escape from solution into body tissues and fluids during or after a reduction in ambient pressure.
Etiology And Pathophysiology
Decompression sickness occurs when nitrogen that has dissolved in body tissues under increased ambient pressure comes out of solution too rapidly during ascent. As ambient pressure increases, the partial pressure of inspired nitrogen rises, leading to progressive nitrogen absorption into tissues, particularly with longer exposure times. When ascent occurs too quickly, the pressure gradient overwhelms the body’s ability to eliminate nitrogen gradually. Tissues become supersaturated, and gas bubbles form.
According to Henry’s law, the amount of gas dissolved in a liquid is directly proportional to the partial pressure of that gas. Increased partial pressure results in greater gas dissolution, while decreased partial pressure causes gas to come out of solution. Nitrogen bubbles act as foreign bodies, triggering inflammatory and coagulation pathways, increasing vascular permeability, reducing intravascular volume, and causing hemoconcentration.
Clinical manifestations depend on bubble location. Bubbles may obstruct blood flow or lymphatics, leading to ischemia, infarction, or lymphedema, or they may cause mechanical tissue distention resulting in pain.
Risk Factors
Dive-related factors include greater depth, longer bottom time, multiple dives within a day, rapid ascent, and cold water exposure. Human factors include obesity, dehydration, pulmonary disease, and intercurrent illness. Proper use of dive tables or computers reduces but does not eliminate risk. Predive vigorous exercise may reduce risk. Approximately 50% of patients develop symptoms within 1 hour and 90% within 6 hours. Air travel after diving can precipitate decompression sickness because of reduced cabin pressure.
Clinical Presentation
Cutaneous Manifestations
Skin findings include scarlatiniform, erysipeloid, or mottled rashes. Cutis marmorata, a mottled appearance, often indicates more severe disease. A peau d’orange appearance may occur due to lymphatic obstruction.
Musculoskeletal Manifestations (The Bends)
Patients experience dull, deep muscular or joint pain, most commonly affecting the elbows and shoulders. Pain is typically not worsened by movement and is not reproducible with palpation.
Gastrointestinal Manifestations
Symptoms include nausea, vomiting, and abdominal pain.
Pulmonary Manifestations (The Chokes)
Pulmonary symptoms result from obstruction of pulmonary vasculature by gas bubbles and include acute respiratory distress, substernal chest pain or pressure, cough, dyspnea, and hypoxia.
Central Nervous System Manifestations
Neurologic symptoms include weakness, fatigue, numbness, paresthesias, agitation, headache, dizziness, vertigo, seizures, bladder or bowel incontinence, lethargy, and visual disturbances. The spinal cord, particularly the lower thoracic and lumbar regions, is most commonly affected.
Inner Ear Manifestations (The Staggers)
Vestibular involvement causes dizziness, vertigo, tinnitus, and nausea. These symptoms resemble inner ear barotrauma but carry a worse prognosis.
History And Physical Examination
A detailed dive history is essential, including depth, duration, ascent profile, surface intervals, and timing of symptom onset. Physical examination should be comprehensive, with particular attention to a detailed neurologic assessment to identify subtle or evolving deficits.
Essential Evaluation
Diagnosis is primarily clinical and based on recognition of risk factors and characteristic presentations. Neurologic findings should be carefully documented, including improvement or progression. Definitive diagnosis may be supported by a trial of pressure, as rapid symptom relief during recompression in a hyperbaric chamber is often diagnostic.
Diagnostic Testing And Interpretation
Laboratory studies may show elevated hematocrit due to hemoconcentration. Electrolytes, renal function, glucose, and urinalysis should be obtained, with increased urine specific gravity suggesting volume depletion. Arterial blood gas analysis and pulse oximetry are used to monitor oxygenation.
Imaging may include chest radiography to assess for pulmonary barotrauma or noncardiogenic pulmonary edema. Extremity radiographs may help exclude traumatic causes of pain. Head CT is indicated for altered mental status or focal neurologic deficits.
Differential Diagnosis
Consider musculoskeletal injury unrelated to bubble formation, inner or middle ear barotrauma, arterial gas embolism, cerebrovascular accident, and trauma.
Prehospital Management
Early recognition is critical, as postdive extremity pain may be misattributed to muscle strain and neurologic symptoms may be minimized by patients. If air evacuation is required, altitude should be limited to less than 1,000 feet or a pressurized aircraft should be used. In-water recompression is controversial, technically difficult, and requires extensive support.
Initial Stabilization
Airway, breathing, and circulation should be managed promptly. Administer 100% normobaric oxygen via mask or endotracheal tube to enhance nitrogen elimination, reduce bubble size, and improve tissue oxygenation. Maintain the patient in a supine position to minimize cerebral involvement. Early recompression in a hyperbaric chamber is essential.
Emergency Department Management
Administer intravenous 0.9% normal saline to correct dehydration and maintain urine output of 1–2 mL/kg/hour. Dehydration is common due to pressure-induced diuresis, exertion, dry compressed air breathing, and capillary leak. Adequate hydration promotes nitrogen elimination.
Arrange urgent hyperbaric oxygen recompression therapy and transfer to the nearest facility. Insert a prophylactic chest tube for known pneumothorax to prevent tension pneumothorax during recompression. Inflate endotracheal and Foley catheter balloons with saline or water to prevent compression-related damage.
Provide analgesics and antiemetics as needed. Diazepam may be used for severe vertigo. Adjunctive NSAIDs or heliox may reduce the number of recompression treatments required. Consultation with Divers Alert Network is recommended for expert guidance and referral.
Disposition And Follow-Up
All patients with suspected or confirmed decompression sickness should be referred for hyperbaric therapy. Stable patients with mild symptoms may be discharged after treatment. Patients should avoid air travel after treatment, as reduced ambient pressure may worsen symptoms.
Follow-Up Recommendations
Ensure hyperbaric medicine follow-up and reinforce diving safety counseling.
Key Clinical Lessons And Common Errors
Musculoskeletal decompression sickness can be difficult to distinguish from benign musculoskeletal pain. Significant fatigue alone may represent decompression sickness. Even mild or resolving symptoms warrant hyperbaric recompression therapy. Do not delay recompression for laboratory testing or imaging when decompression sickness is the likely diagnosis. In-water recompression should be avoided.
- Published on
Emergency And Acute Medicine – Dacryocystitis And Dacryoadenitis
Core Description
Dacryoadenitis and dacryocystitis are inflammatory disorders of the lacrimal system. Dacryoadenitis refers to inflammation or infection of the lacrimal gland, which produces tears. Dacryocystitis is a suppurative infection of the lacrimal drainage system, specifically the lacrimal sac, usually occurring in the setting of ductal obstruction. Dacryoadenitis may be inflammatory or infectious and can result from contiguous spread or systemic disease, whereas dacryocystitis is almost always infectious due to tear stasis within an obstructed duct.
Epidemiology
Dacryoadenitis is uncommon and is more frequently seen on the left side. Acquired cases are rare. Dacryocystitis is more common, most often affecting adult females older than 30 years, though it may also present in infants.
Etiology Of Dacryoadenitis
Dacryoadenitis is most commonly associated with systemic inflammatory and autoimmune conditions, including Sjögren syndrome, sarcoidosis, Crohn disease, and lacrimal gland tumors. Infectious causes may be primary or secondary to contiguous spread from bacterial conjunctivitis or periorbital cellulitis. Acute suppurative dacryoadenitis in adults is most often caused by Staphylococcus aureus, streptococci, Chlamydia trachomatis, and Neisseria gonorrhoeae. Chronic dacryoadenitis is more commonly related to nasal flora rather than ocular organisms.
Pediatric Considerations In Dacryoadenitis
In children, viral causes predominate, including mumps, measles, Epstein–Barr virus, cytomegalovirus, coxsackievirus, and varicella-zoster virus. A slowly enlarging lacrimal gland mass in children may represent a dermoid cyst rather than infection.
Etiology Of Dacryocystitis
Under normal conditions, tears drain through the lacrimal duct into the lacrimal sac and then into the middle turbinate and sinuses via a pumping mechanism. Dacryocystitis develops when the duct becomes partially or completely obstructed. In adults, chronic inflammation related to ethmoid sinusitis is a common underlying cause, though trauma, dacryoliths, nasal or sinus surgery, or any local obstructive process may contribute. Obstruction leads to tear stasis, bacterial overgrowth, and infection. The infection may be recurrent or chronic. Sinus flora predominate over ocular flora, with Staphylococcus aureus being the most common organism. Complications include draining fistulae, recurrent conjunctivitis, abscess formation, and orbital cellulitis.
Pediatric Considerations In Dacryocystitis
Congenital dacryocystitis typically presents in infancy due to dacryocystoceles and carries high morbidity and mortality, often from systemic spread of infection. The most common pathogen in this population is Streptococcus pneumoniae.
Clinical Presentation
Both dacryoadenitis and dacryocystitis usually present with unilateral eye pain, redness, and swelling.
Dacryoadenitis Symptoms And Signs
Patients may develop acute or indolent swelling and erythema of the upper eyelid, with maximal tenderness in the temporal portion beneath the orbital rim, producing an S-shaped eyelid. A palpable mass may be present. Associated findings include conjunctival injection, discharge, chemosis, variable tear production, ipsilateral preauricular lymphadenopathy, and surrounding cellulitis. Systemic toxicity may occur. Visual acuity, slit-lamp examination, and funduscopic findings are typically normal, though globe displacement may cause visual distortion. Chronic dacryoadenitis presents as a slowly progressive, painless swelling.
Alert: Rapidly assess for possible spread from gonococcal conjunctivitis, as morbidity is high, visual loss is likely, systemic illness is common, and treatment differs significantly.
Dacryocystitis Symptoms And Signs
Dacryocystitis presents as an acutely inflamed, localized mass inferior and medial to the inner canthus. Epiphora is the hallmark symptom due to tear outflow obstruction. Applying pressure to the mass may express purulent material from the punctum, which is diagnostically helpful. Lower eyelid cellulitis may occur. Fever is usually low grade, and patients rarely appear toxic.
Essential Evaluation
A complete ocular examination is required, including visual acuity, extraocular movements, slit-lamp examination, funduscopic examination, eyelid eversion, and nasal inspection.
Pediatric Alert: Carefully assess for extension to orbital cellulitis or meningitis.
Diagnostic Testing And Interpretation
Purulent material should be sent for Gram stain, culture, and sensitivity testing. Chocolate agar should be used if gonococcal infection is suspected. CBC and blood cultures may be obtained when systemic infection is suspected. CT imaging of the orbit and sinuses is indicated to assess for deep tissue involvement, recurrent dacryoadenitis, or suspected orbital extension, particularly in children or high-risk patients.
Differential Diagnosis
For dacryoadenitis, consider autoimmune disease, lacrimal gland tumors, hordeolum, periorbital or orbital cellulitis, severe blepharitis, insect bites, and traumatic injury.
For dacryocystitis, consider insect bites, trauma, acute ethmoid sinusitis, periorbital cellulitis, and acute conjunctivitis.
Emergency Department Management
Early recognition and treatment are essential to prevent local extension and systemic infection. Topical antibiotics may be used to prevent secondary conjunctivitis.
Management Of Dacryoadenitis
Supportive care includes cool compresses and nonsteroidal analgesics. Viral causes are typically self-limited. Bacterial infections require antibiotics, with oral agents such as cephalexin or amoxicillin/clavulanate for mild cases and intravenous therapy such as cefazolin or ticarcillin/clavulanate for severe infections. Administer tetanus toxoid when indicated. Incision and drainage are rarely required and should be performed only in severe cases with ophthalmology or facial surgery consultation.
In children, use cool compresses and analgesics; if the cause is unclear, treat empirically with antibiotics as in adults.
Management Of Dacryocystitis
Drainage of the infected lacrimal sac is essential. Warm compresses and gentle massage may relieve obstruction. Intranasal vasoconstrictors can facilitate drainage. Incision and drainage should be avoided in the ED when possible, as it increases the risk of fistula formation. Duct instrumentation is contraindicated in the acute setting due to risk of permanent scarring and stenosis. Use topical ophthalmic antibiotics to prevent conjunctivitis and systemic antibiotics to treat infection and prevent spread. Administer intravenous antibiotics for febrile or severe infections. Provide adequate analgesia.
Pediatric Management Considerations
Newborns typically respond to massage and topical antibiotics in approximately 95% of cases. Failure to resolve within the first year may require ophthalmologic probing. Children younger than 4 years with dacryocystitis are at increased risk for Haemophilus influenzae infection if not fully immunized. Afebrile, well-appearing children with reliable caregivers may be treated with oral cefaclor or amoxicillin/clavulanate, while acutely ill children require intravenous cefuroxime due to the high risk of bacteremia, septicemia, and meningitis.
Pharmacologic Therapy
Recommended agents include amoxicillin/clavulanate, cefaclor, cefazolin, cefuroxime, cephalexin, erythromycin ophthalmic ointment, trimethoprim–polymyxin ophthalmic ointment, and ticarcillin/clavulanate, dosed appropriately for adults and children. Intranasal tetracaine and phenylephrine may be used to facilitate drainage.
Disposition And Follow-Up
Hospital admission is indicated for febrile or toxic adults, immunocompromised patients, extensive cellulitis, suspected deep tissue or meningeal spread, and high-risk pediatric cases, including unimmunized children or those without reliable follow-up. Prompt ophthalmology referral is required for all cases. Patients with dacryocystitis require confirmation of complete drainage and assessment for definitive intervention to prevent recurrence before discharge.
Key Clinical Lessons And Common Errors
In any patient with a red eye and eyelid swelling, the lacrimal system must be carefully examined. Skin incision and drainage of dacryocystitis should be avoided whenever possible to prevent fistula formation; intranasal vasoconstrictors are preferred to facilitate drainage.
Core Description
Dacryoadenitis and dacryocystitis are inflammatory disorders of the lacrimal system. Dacryoadenitis refers to inflammation or infection of the lacrimal gland, which produces tears. Dacryocystitis is a suppurative infection of the lacrimal drainage system, specifically the lacrimal sac, usually occurring in the setting of ductal obstruction. Dacryoadenitis may be inflammatory or infectious and can result from contiguous spread or systemic disease, whereas dacryocystitis is almost always infectious due to tear stasis within an obstructed duct.
Epidemiology
Dacryoadenitis is uncommon and is more frequently seen on the left side. Acquired cases are rare. Dacryocystitis is more common, most often affecting adult females older than 30 years, though it may also present in infants.
Etiology Of Dacryoadenitis
Dacryoadenitis is most commonly associated with systemic inflammatory and autoimmune conditions, including Sjögren syndrome, sarcoidosis, Crohn disease, and lacrimal gland tumors. Infectious causes may be primary or secondary to contiguous spread from bacterial conjunctivitis or periorbital cellulitis. Acute suppurative dacryoadenitis in adults is most often caused by Staphylococcus aureus, streptococci, Chlamydia trachomatis, and Neisseria gonorrhoeae. Chronic dacryoadenitis is more commonly related to nasal flora rather than ocular organisms.
Pediatric Considerations In Dacryoadenitis
In children, viral causes predominate, including mumps, measles, Epstein–Barr virus, cytomegalovirus, coxsackievirus, and varicella-zoster virus. A slowly enlarging lacrimal gland mass in children may represent a dermoid cyst rather than infection.
Etiology Of Dacryocystitis
Under normal conditions, tears drain through the lacrimal duct into the lacrimal sac and then into the middle turbinate and sinuses via a pumping mechanism. Dacryocystitis develops when the duct becomes partially or completely obstructed. In adults, chronic inflammation related to ethmoid sinusitis is a common underlying cause, though trauma, dacryoliths, nasal or sinus surgery, or any local obstructive process may contribute. Obstruction leads to tear stasis, bacterial overgrowth, and infection. The infection may be recurrent or chronic. Sinus flora predominate over ocular flora, with Staphylococcus aureus being the most common organism. Complications include draining fistulae, recurrent conjunctivitis, abscess formation, and orbital cellulitis.
Pediatric Considerations In Dacryocystitis
Congenital dacryocystitis typically presents in infancy due to dacryocystoceles and carries high morbidity and mortality, often from systemic spread of infection. The most common pathogen in this population is Streptococcus pneumoniae.
Clinical Presentation
Both dacryoadenitis and dacryocystitis usually present with unilateral eye pain, redness, and swelling.
Dacryoadenitis Symptoms And Signs
Patients may develop acute or indolent swelling and erythema of the upper eyelid, with maximal tenderness in the temporal portion beneath the orbital rim, producing an S-shaped eyelid. A palpable mass may be present. Associated findings include conjunctival injection, discharge, chemosis, variable tear production, ipsilateral preauricular lymphadenopathy, and surrounding cellulitis. Systemic toxicity may occur. Visual acuity, slit-lamp examination, and funduscopic findings are typically normal, though globe displacement may cause visual distortion. Chronic dacryoadenitis presents as a slowly progressive, painless swelling.
Alert: Rapidly assess for possible spread from gonococcal conjunctivitis, as morbidity is high, visual loss is likely, systemic illness is common, and treatment differs significantly.
Dacryocystitis Symptoms And Signs
Dacryocystitis presents as an acutely inflamed, localized mass inferior and medial to the inner canthus. Epiphora is the hallmark symptom due to tear outflow obstruction. Applying pressure to the mass may express purulent material from the punctum, which is diagnostically helpful. Lower eyelid cellulitis may occur. Fever is usually low grade, and patients rarely appear toxic.
Essential Evaluation
A complete ocular examination is required, including visual acuity, extraocular movements, slit-lamp examination, funduscopic examination, eyelid eversion, and nasal inspection.
Pediatric Alert: Carefully assess for extension to orbital cellulitis or meningitis.
Diagnostic Testing And Interpretation
Purulent material should be sent for Gram stain, culture, and sensitivity testing. Chocolate agar should be used if gonococcal infection is suspected. CBC and blood cultures may be obtained when systemic infection is suspected. CT imaging of the orbit and sinuses is indicated to assess for deep tissue involvement, recurrent dacryoadenitis, or suspected orbital extension, particularly in children or high-risk patients.
Differential Diagnosis
For dacryoadenitis, consider autoimmune disease, lacrimal gland tumors, hordeolum, periorbital or orbital cellulitis, severe blepharitis, insect bites, and traumatic injury.
For dacryocystitis, consider insect bites, trauma, acute ethmoid sinusitis, periorbital cellulitis, and acute conjunctivitis.
Emergency Department Management
Early recognition and treatment are essential to prevent local extension and systemic infection. Topical antibiotics may be used to prevent secondary conjunctivitis.
Management Of Dacryoadenitis
Supportive care includes cool compresses and nonsteroidal analgesics. Viral causes are typically self-limited. Bacterial infections require antibiotics, with oral agents such as cephalexin or amoxicillin/clavulanate for mild cases and intravenous therapy such as cefazolin or ticarcillin/clavulanate for severe infections. Administer tetanus toxoid when indicated. Incision and drainage are rarely required and should be performed only in severe cases with ophthalmology or facial surgery consultation.
In children, use cool compresses and analgesics; if the cause is unclear, treat empirically with antibiotics as in adults.
Management Of Dacryocystitis
Drainage of the infected lacrimal sac is essential. Warm compresses and gentle massage may relieve obstruction. Intranasal vasoconstrictors can facilitate drainage. Incision and drainage should be avoided in the ED when possible, as it increases the risk of fistula formation. Duct instrumentation is contraindicated in the acute setting due to risk of permanent scarring and stenosis. Use topical ophthalmic antibiotics to prevent conjunctivitis and systemic antibiotics to treat infection and prevent spread. Administer intravenous antibiotics for febrile or severe infections. Provide adequate analgesia.
Pediatric Management Considerations
Newborns typically respond to massage and topical antibiotics in approximately 95% of cases. Failure to resolve within the first year may require ophthalmologic probing. Children younger than 4 years with dacryocystitis are at increased risk for Haemophilus influenzae infection if not fully immunized. Afebrile, well-appearing children with reliable caregivers may be treated with oral cefaclor or amoxicillin/clavulanate, while acutely ill children require intravenous cefuroxime due to the high risk of bacteremia, septicemia, and meningitis.
Pharmacologic Therapy
Recommended agents include amoxicillin/clavulanate, cefaclor, cefazolin, cefuroxime, cephalexin, erythromycin ophthalmic ointment, trimethoprim–polymyxin ophthalmic ointment, and ticarcillin/clavulanate, dosed appropriately for adults and children. Intranasal tetracaine and phenylephrine may be used to facilitate drainage.
Disposition And Follow-Up
Hospital admission is indicated for febrile or toxic adults, immunocompromised patients, extensive cellulitis, suspected deep tissue or meningeal spread, and high-risk pediatric cases, including unimmunized children or those without reliable follow-up. Prompt ophthalmology referral is required for all cases. Patients with dacryocystitis require confirmation of complete drainage and assessment for definitive intervention to prevent recurrence before discharge.
Key Clinical Lessons And Common Errors
In any patient with a red eye and eyelid swelling, the lacrimal system must be carefully examined. Skin incision and drainage of dacryocystitis should be avoided whenever possible to prevent fistula formation; intranasal vasoconstrictors are preferred to facilitate drainage.
- Published on
Emergency and Acute Medicine – Cardiac Arrest
Critical Update Notice
This summary reflects principles derived from the 2010 ACLS guidelines. Key updates emphasized early chest compressions with a C–A–B sequence, greater focus on post–cardiac arrest care including targeted temperature management, and removal of atropine from PEA/asystole algorithms.
Clinical Overview
Sudden cardiac arrest is defined by unresponsiveness, absence of a palpable pulse, and minimal or absent respirations. Survival is influenced by the presenting rhythm, total downtime, speed of defibrillation when indicated, and early initiation of high-quality basic life support.
Underlying Causes
Reversible contributors are commonly recalled as the “Hs and Ts”: hypovolemia, hypoxia, hydrogen ion excess (acidosis), hypo- or hyperkalemia, hypothermia, toxins, cardiac tamponade, tension pneumothorax, thrombosis (coronary or pulmonary), and trauma.
Special Populations
In children, arrest is more often secondary to respiratory failure rather than primary cardiac causes. Pediatric resuscitation requires shallower compressions (approximately one-third to one-half of chest depth), a 15:2 compression-to-ventilation ratio for two rescuers, and weight-based medication dosing.
In pregnancy, airway management may be difficult, compressions should be performed slightly higher on the sternum, and manual left uterine displacement should be used. Maternal survival remains the priority; emergent cesarean delivery may be considered if maternal resuscitation fails.
Clinical Recognition
Patients present with sudden loss of responsiveness, pulselessness, and agonal or absent respirations. Arrest may be preceded by chest pain, dyspnea, palpitations, seizure-like activity, hypotension, or altered mental status.
Immediate Assessment
Rapidly assess airway, breathing, and circulation, determine whether the rhythm is shockable or nonshockable, and initiate treatment according to ACLS algorithms without delay.
Diagnostic Evaluation After ROSC
Laboratory testing is indicated only after return of spontaneous circulation and may include electrolytes, renal function, cardiac biomarkers, arterial blood gas, CBC, lactate, therapeutic drug levels, and toxicology screening. ECG should assess for STEMI or acute coronary syndrome. Chest radiography confirms airway placement and evaluates for pulmonary causes. Echocardiography may identify tamponade or wall-motion abnormalities. Head CT may be required postresuscitation to evaluate neurologic causes.
Conditions To Exclude
Alternative causes of sudden collapse with a pulse include syncope, seizure, stroke, hypoglycemia, airway obstruction, head trauma, and toxic exposures.
Prehospital Management
Begin immediate high-quality CPR, confirm rhythm, and defibrillate pulseless VT or VF as early as possible. Secure the airway only if it does not interrupt compressions. After ROSC, stabilize blood pressure, obtain a 12-lead ECG, and transport to a facility capable of advanced postarrest and interventional cardiac care.
Early In-Hospital Resuscitation
Initiate ACLS with uninterrupted CPR, brief rhythm and pulse checks, early defibrillation when indicated, IV or IO access, continuous cardiac monitoring, and rhythm-directed therapy.
Definitive Emergency Treatment
For pulseless VT/VF, perform immediate defibrillation followed by CPR, epinephrine, and antiarrhythmics such as amiodarone or lidocaine; magnesium is used for torsades de pointes.
For asystole and pulseless electrical activity, confirm rhythm, administer epinephrine, and aggressively search for and correct reversible causes.
After ROSC, address the underlying etiology, provide ventilatory and hemodynamic support, correct metabolic abnormalities, evaluate for coronary ischemia with early catheterization when appropriate, initiate targeted temperature management in eligible patients, and monitor for seizures with continuous EEG when indicated.
Pharmacologic Support
Medications commonly used include epinephrine, amiodarone, lidocaine, magnesium sulfate, vasopressin (as an epinephrine substitute in adults), and sodium bicarbonate in select circumstances. Drug delivery should never interrupt CPR.
Disposition Planning
All patients with ROSC require ICU admission for comprehensive postarrest care and management of the precipitating cause. There are no discharge criteria directly from the arrest setting.
Follow-Up And Systems Care
Postarrest patients benefit from admission to intensive care units experienced in targeted temperature management and advanced cardiac support. Referral to regional cardiac arrest centers may improve outcomes.
Clinical Pearls And Pitfalls
Targeted temperature management improves neurologic outcomes in comatose postarrest patients. Recurrent arrest is common, requiring vigilant monitoring and rapid intervention. Early cardiology consultation is essential to determine candidacy for urgent cardiac catheterization.
Critical Update Notice
This summary reflects principles derived from the 2010 ACLS guidelines. Key updates emphasized early chest compressions with a C–A–B sequence, greater focus on post–cardiac arrest care including targeted temperature management, and removal of atropine from PEA/asystole algorithms.
Clinical Overview
Sudden cardiac arrest is defined by unresponsiveness, absence of a palpable pulse, and minimal or absent respirations. Survival is influenced by the presenting rhythm, total downtime, speed of defibrillation when indicated, and early initiation of high-quality basic life support.
Underlying Causes
Reversible contributors are commonly recalled as the “Hs and Ts”: hypovolemia, hypoxia, hydrogen ion excess (acidosis), hypo- or hyperkalemia, hypothermia, toxins, cardiac tamponade, tension pneumothorax, thrombosis (coronary or pulmonary), and trauma.
Special Populations
In children, arrest is more often secondary to respiratory failure rather than primary cardiac causes. Pediatric resuscitation requires shallower compressions (approximately one-third to one-half of chest depth), a 15:2 compression-to-ventilation ratio for two rescuers, and weight-based medication dosing.
In pregnancy, airway management may be difficult, compressions should be performed slightly higher on the sternum, and manual left uterine displacement should be used. Maternal survival remains the priority; emergent cesarean delivery may be considered if maternal resuscitation fails.
Clinical Recognition
Patients present with sudden loss of responsiveness, pulselessness, and agonal or absent respirations. Arrest may be preceded by chest pain, dyspnea, palpitations, seizure-like activity, hypotension, or altered mental status.
Immediate Assessment
Rapidly assess airway, breathing, and circulation, determine whether the rhythm is shockable or nonshockable, and initiate treatment according to ACLS algorithms without delay.
Diagnostic Evaluation After ROSC
Laboratory testing is indicated only after return of spontaneous circulation and may include electrolytes, renal function, cardiac biomarkers, arterial blood gas, CBC, lactate, therapeutic drug levels, and toxicology screening. ECG should assess for STEMI or acute coronary syndrome. Chest radiography confirms airway placement and evaluates for pulmonary causes. Echocardiography may identify tamponade or wall-motion abnormalities. Head CT may be required postresuscitation to evaluate neurologic causes.
Conditions To Exclude
Alternative causes of sudden collapse with a pulse include syncope, seizure, stroke, hypoglycemia, airway obstruction, head trauma, and toxic exposures.
Prehospital Management
Begin immediate high-quality CPR, confirm rhythm, and defibrillate pulseless VT or VF as early as possible. Secure the airway only if it does not interrupt compressions. After ROSC, stabilize blood pressure, obtain a 12-lead ECG, and transport to a facility capable of advanced postarrest and interventional cardiac care.
Early In-Hospital Resuscitation
Initiate ACLS with uninterrupted CPR, brief rhythm and pulse checks, early defibrillation when indicated, IV or IO access, continuous cardiac monitoring, and rhythm-directed therapy.
Definitive Emergency Treatment
For pulseless VT/VF, perform immediate defibrillation followed by CPR, epinephrine, and antiarrhythmics such as amiodarone or lidocaine; magnesium is used for torsades de pointes.
For asystole and pulseless electrical activity, confirm rhythm, administer epinephrine, and aggressively search for and correct reversible causes.
After ROSC, address the underlying etiology, provide ventilatory and hemodynamic support, correct metabolic abnormalities, evaluate for coronary ischemia with early catheterization when appropriate, initiate targeted temperature management in eligible patients, and monitor for seizures with continuous EEG when indicated.
Pharmacologic Support
Medications commonly used include epinephrine, amiodarone, lidocaine, magnesium sulfate, vasopressin (as an epinephrine substitute in adults), and sodium bicarbonate in select circumstances. Drug delivery should never interrupt CPR.
Disposition Planning
All patients with ROSC require ICU admission for comprehensive postarrest care and management of the precipitating cause. There are no discharge criteria directly from the arrest setting.
Follow-Up And Systems Care
Postarrest patients benefit from admission to intensive care units experienced in targeted temperature management and advanced cardiac support. Referral to regional cardiac arrest centers may improve outcomes.
Clinical Pearls And Pitfalls
Targeted temperature management improves neurologic outcomes in comatose postarrest patients. Recurrent arrest is common, requiring vigilant monitoring and rapid intervention. Early cardiology consultation is essential to determine candidacy for urgent cardiac catheterization.
