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Emergency And Acute Medicine - GHB Poisoning
Basics Description
γ-Hydroxybutyrate (GHB) is a naturally occurring analog of γ-aminobutyric acid (GABA). It has limited medical use, most notably in narcolepsy. Nonmedical use includes bodybuilding, recreational euphoria, and use as a predatory or date-rape drug. Precursors such as γ-butyrolactone (GBL), 1,4-butanediol (1,4-BD), γ-hydroxyvalerate (GHV), and γ-valerolactone (GVL) produce similar clinical effects. Onset typically occurs 15–30 minutes after ingestion, with duration of effects lasting approximately 2–6 hours.
Etiology
GHB toxicity results from deliberate or accidental ingestion of GHB or its precursors.
Diagnosis Signs And Symptoms
Central nervous system findings include CNS depression, dizziness, ataxia, impaired judgment, aggressive behavior, clonic extremity movements, coma, and seizures. Pulmonary manifestations include respiratory depression, apnea, and rarely laryngospasm. Gastrointestinal symptoms include nausea and vomiting. Cardiovascular effects include bradycardia, atrioventricular block, and hypotension. Other findings include nystagmus and hypothermia.
Withdrawal may present with hypertension, tachycardia, hyperthermia, agitation, diaphoresis, tremors, nausea, vomiting, abdominal cramping, hallucinations, delusions, and psychosis.
Essential Workup
Diagnosis is primarily clinical and based on history and presentation. Coingestants should be excluded if the clinical picture is atypical for GHB intoxication.
Diagnosis Tests And Interpretation
Confirmatory GHB testing is usually a send-out laboratory test and does not affect emergency department management. Urine toxicology screening may help identify coingestants. Serum ethanol level should be obtained. Urinalysis and creatine kinase are indicated if rhabdomyolysis is suspected. ECG may demonstrate sinus bradycardia or atrioventricular block. Chest radiography is indicated if aspiration pneumonia is suspected. Head CT should be considered if occult head trauma is possible.
Differential Diagnosis
Alcohol intoxication, barbiturate overdose, benzodiazepine overdose, neuroleptic overdose, opiate overdose, alcohol withdrawal, and sedative–hypnotic withdrawal.
Treatment Prehospital
All pills, containers, and drug paraphernalia involved in the overdose should be transported with the patient for identification.
Initial Stabilization Therapy
Airway management is the priority. Supplemental oxygen should be administered, and intubation performed if indicated. In patients with depressed mental status, administer thiamine, check glucose with bedside testing, provide dextrose if needed, and administer naloxone.
Ed Treatment Procedures
Management is primarily supportive. Bradycardia may be treated with atropine or temporary pacing. Hypotension is managed with intravenous 0.9% normal saline boluses, Trendelenburg positioning, and dopamine infusion if needed. Seizures should be treated initially with benzodiazepines; refractory seizures may require phenobarbital. Withdrawal should be treated aggressively with benzodiazepines, with phenobarbital or propofol used if benzodiazepines are insufficient.
Medication
Dextrose 50–100 mL of D50 IV (pediatrics: D25 2 mL/kg). Diazepam 5–10 mg IV. Lorazepam 2–4 mg IV. Dopamine infusion 2–20 μg/kg/min. Naloxone 0.4–2 mg IV or IM. Phenobarbital loading dose 10–20 mg/kg IV. Propofol loading dose 0.5–1 mg/kg IV followed by infusion. Thiamine 100 mg IV or IM.
Follow-Up Disposition
Admission is required for intubated patients, those with hypothermia or hemodynamic instability, or suspected coingestions that prolong intoxication. Discharge may be considered after at least 6 hours of observation if the patient is asymptomatic and shows no signs of withdrawal.
Alert: GHB withdrawal is life-threatening and closely resembles alcohol withdrawal; prolonged inpatient treatment may be necessary.
Follow-Up Recommendations
Patients with recreational drug use should receive substance abuse referral. Accidental poisonings require poison prevention counseling. Intentional ingestions require psychiatric evaluation.
Key Clinical Insights And Common Errors
Persistent altered mental status should prompt evaluation for non-toxicologic causes. Routine hospital toxicology screens do not reliably detect GHB or many recreational drugs of abuse.
Basics Description
γ-Hydroxybutyrate (GHB) is a naturally occurring analog of γ-aminobutyric acid (GABA). It has limited medical use, most notably in narcolepsy. Nonmedical use includes bodybuilding, recreational euphoria, and use as a predatory or date-rape drug. Precursors such as γ-butyrolactone (GBL), 1,4-butanediol (1,4-BD), γ-hydroxyvalerate (GHV), and γ-valerolactone (GVL) produce similar clinical effects. Onset typically occurs 15–30 minutes after ingestion, with duration of effects lasting approximately 2–6 hours.
Etiology
GHB toxicity results from deliberate or accidental ingestion of GHB or its precursors.
Diagnosis Signs And Symptoms
Central nervous system findings include CNS depression, dizziness, ataxia, impaired judgment, aggressive behavior, clonic extremity movements, coma, and seizures. Pulmonary manifestations include respiratory depression, apnea, and rarely laryngospasm. Gastrointestinal symptoms include nausea and vomiting. Cardiovascular effects include bradycardia, atrioventricular block, and hypotension. Other findings include nystagmus and hypothermia.
Withdrawal may present with hypertension, tachycardia, hyperthermia, agitation, diaphoresis, tremors, nausea, vomiting, abdominal cramping, hallucinations, delusions, and psychosis.
Essential Workup
Diagnosis is primarily clinical and based on history and presentation. Coingestants should be excluded if the clinical picture is atypical for GHB intoxication.
Diagnosis Tests And Interpretation
Confirmatory GHB testing is usually a send-out laboratory test and does not affect emergency department management. Urine toxicology screening may help identify coingestants. Serum ethanol level should be obtained. Urinalysis and creatine kinase are indicated if rhabdomyolysis is suspected. ECG may demonstrate sinus bradycardia or atrioventricular block. Chest radiography is indicated if aspiration pneumonia is suspected. Head CT should be considered if occult head trauma is possible.
Differential Diagnosis
Alcohol intoxication, barbiturate overdose, benzodiazepine overdose, neuroleptic overdose, opiate overdose, alcohol withdrawal, and sedative–hypnotic withdrawal.
Treatment Prehospital
All pills, containers, and drug paraphernalia involved in the overdose should be transported with the patient for identification.
Initial Stabilization Therapy
Airway management is the priority. Supplemental oxygen should be administered, and intubation performed if indicated. In patients with depressed mental status, administer thiamine, check glucose with bedside testing, provide dextrose if needed, and administer naloxone.
Ed Treatment Procedures
Management is primarily supportive. Bradycardia may be treated with atropine or temporary pacing. Hypotension is managed with intravenous 0.9% normal saline boluses, Trendelenburg positioning, and dopamine infusion if needed. Seizures should be treated initially with benzodiazepines; refractory seizures may require phenobarbital. Withdrawal should be treated aggressively with benzodiazepines, with phenobarbital or propofol used if benzodiazepines are insufficient.
Medication
Dextrose 50–100 mL of D50 IV (pediatrics: D25 2 mL/kg). Diazepam 5–10 mg IV. Lorazepam 2–4 mg IV. Dopamine infusion 2–20 μg/kg/min. Naloxone 0.4–2 mg IV or IM. Phenobarbital loading dose 10–20 mg/kg IV. Propofol loading dose 0.5–1 mg/kg IV followed by infusion. Thiamine 100 mg IV or IM.
Follow-Up Disposition
Admission is required for intubated patients, those with hypothermia or hemodynamic instability, or suspected coingestions that prolong intoxication. Discharge may be considered after at least 6 hours of observation if the patient is asymptomatic and shows no signs of withdrawal.
Alert: GHB withdrawal is life-threatening and closely resembles alcohol withdrawal; prolonged inpatient treatment may be necessary.
Follow-Up Recommendations
Patients with recreational drug use should receive substance abuse referral. Accidental poisonings require poison prevention counseling. Intentional ingestions require psychiatric evaluation.
Key Clinical Insights And Common Errors
Persistent altered mental status should prompt evaluation for non-toxicologic causes. Routine hospital toxicology screens do not reliably detect GHB or many recreational drugs of abuse.
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Emergency And Acute Medicine - Giant Cell Arteritis (Temporal Arteritis)
Basics Description
Giant cell arteritis is a chronic vasculitis of large- and medium-sized arteries occurring almost exclusively in individuals older than 50 years. It is commonly referred to as temporal arteritis. The median age at onset is approximately 72 years. The disease most often involves arteries arising from the aortic arch. Although frequently clinically silent, thoracic aortic involvement is common and may lead to aneurysm or dissection. Thoracic aortic aneurysm occurs at a rate nearly 17 times higher than in those without giant cell arteritis, while abdominal aortic aneurysm is about twice as common.
Pathologic specimens demonstrate patchy mononuclear granulomatous inflammation with marked intimal thickening and luminal occlusion. Occlusive arteritis may involve the ophthalmic artery, resulting in anterior ischemic optic neuropathy and acute visual loss, which constitutes an ophthalmic emergency. Inflammation of arteries supplying the muscles of mastication causes jaw claudication and tongue discomfort.
Age is the greatest risk factor; the disease is rare in patients younger than 50 years and more than 90% of cases occur in those older than 60 years. Prevalence in individuals over 50 is approximately 1:500, with higher rates in northern latitudes. It is two to four times more common in women, rare in African American patients, and more common in White populations. There is a strong association with polymyalgia rheumatica, present in approximately 50% of patients. A genetic predisposition is linked to HLA-DR4.
Etiology
The exact cause is unknown. Genetic, environmental, and autoimmune factors are believed to contribute.
Diagnosis
The diagnosis is supported by the presence of three or more of the following in a patient with vasculitis: age greater than 50 years, erythrocyte sedimentation rate greater than 50 mm/hr, new-onset localized headache, temporal artery tenderness or decreased pulsation, new visual symptoms, and biopsy demonstrating necrotizing arteritis.
Signs And Symptoms
Symptoms may be acute, subacute, or chronic. Headache is the most common symptom, occurring in approximately 70% of patients, and is often unilateral, localized to the temple, and described as boring or lancinating. Jaw or tongue claudication with chewing occurs in about 50%. Constitutional symptoms include fatigue, malaise, anorexia, weight loss, weakness, arthralgias, and low-grade fever.
Visual manifestations usually involve one eye and may develop weeks to months after other symptoms. These include amaurosis fugax, blindness, diplopia, ptosis, extraocular muscle weakness, scotomata, and blurred vision. Visual impairment typically does not improve, even with treatment.
Other findings include scalp tenderness, especially over the temporal artery; early increased pulsations followed by decreased pulsations later in disease; erythema, warmth, swelling, or nodules over scalp arteries; bruits or diminished pulses over large arteries; sore throat, cough, and dysphagia. Neurologic manifestations such as neuropathies, transient ischemic attacks, and strokes may occur in up to one-third of patients. Occult manifestations include glossitis, lingual infarction, tongue infarction, and Raynaud phenomenon. Up to 30% of patients may lack classic symptoms.
Polymyalgia rheumatica is frequently associated, characterized by morning stiffness and aching pain of proximal muscles that improves with activity and may be accompanied by synovitis, particularly in the knees.
Essential Workup
A focused physical examination should emphasize the temporal arteries and scalp, a complete neurologic examination, and a detailed ophthalmic examination including visual acuity and visual fields. Fundoscopy may be normal early but can show optic nerve edema, pallor, hemorrhages, cotton-wool spots, and exudates later. Pulse asymmetry or bruits over large arteries should be documented.
Diagnosis Tests And Interpretation
Laboratory findings typically include a markedly elevated ESR, often greater than 100 mm/hr, and elevated C-reactive protein. Mild normochromic anemia and mild thrombocytosis are common. White blood cell count is usually normal or mildly elevated. Liver enzymes and prothrombin time may be elevated, while renal function and urinalysis are usually normal. Interleukin-6 levels are elevated during disease flares.
Imaging may include Doppler ultrasound showing decreased flow and a characteristic halo sign in temporal arteries. MRI can assess large-vessel involvement. Angiography may reveal smooth, tapered stenoses or occlusions.
Temporal artery biopsy is the diagnostic gold standard and should include multiple sections. It should be performed as soon as feasible after starting steroids. If the initial biopsy is negative and suspicion remains high, contralateral biopsy is recommended.
Differential Diagnosis
Other vasculitides including polyarteritis nodosa, hypersensitivity vasculitis, systemic lupus erythematosus, Takayasu arteritis, and granulomatosis with polyangiitis; retinal, ophthalmic, or temporal artery thrombosis; Lyme disease; and nonarteritic anterior ischemic optic neuropathy.
Treatment Prehospital
Symptoms may be mistaken for stroke. Provide monitoring and supplemental oxygen. Hypotension may occur from rare complications such as aortic dissection, abdominal aortic aneurysm, or myocardial infarction.
Initial Stabilization Therapy
Although uncommon, patients may present with vascular catastrophes requiring aggressive early management consistent with standard emergency protocols.
Ed Treatment Procedures
High-dose corticosteroids are the cornerstone of therapy. When clinical suspicion is strong, steroid treatment should not be delayed for biopsy, as vascular pathologic changes persist for weeks. Early aggressive treatment significantly reduces the risk of blindness. Systemic and local symptoms typically improve within days to weeks, but treatment may be required for several years, with an average disease course of three to four years. Analgesia with NSAIDs, salicylates, or narcotics may be provided as needed.
Medication
Prednisone 60–100 mg orally daily for at least two weeks before tapering. For acute visual symptoms, intravenous methylprednisolone 1,000 mg daily for one to three days may be used. Low-dose aspirin is recommended to reduce thrombotic risk. NSAIDs or narcotics may be used for pain control.
Follow-Up Disposition
Admission is indicated for patients with acute visual loss, impending vascular complications, or acute focal neurologic deficits. Less symptomatic patients without evidence of end-organ damage may be discharged with close follow-up arranged within one to two days.
Issues For Referral
Rheumatology for disease management, ophthalmology for visual symptoms, and neurology for focal neurologic findings.
Follow-Up Recommendations
Ongoing care with rheumatology for steroid management and evaluation for associated connective tissue disease. Ophthalmology and neurology follow-up are required for visual or neurologic involvement.
Key Clinical Insights And Common Errors
Permanent visual loss is the most feared complication. Steroid therapy must not be delayed when clinical suspicion is high or visual symptoms are present. Jaw claudication and amaurosis fugax are often underreported and should be specifically queried. Between 25% and 50% of patients with untreated unilateral visual loss will progress to bilateral blindness.
Basics Description
Giant cell arteritis is a chronic vasculitis of large- and medium-sized arteries occurring almost exclusively in individuals older than 50 years. It is commonly referred to as temporal arteritis. The median age at onset is approximately 72 years. The disease most often involves arteries arising from the aortic arch. Although frequently clinically silent, thoracic aortic involvement is common and may lead to aneurysm or dissection. Thoracic aortic aneurysm occurs at a rate nearly 17 times higher than in those without giant cell arteritis, while abdominal aortic aneurysm is about twice as common.
Pathologic specimens demonstrate patchy mononuclear granulomatous inflammation with marked intimal thickening and luminal occlusion. Occlusive arteritis may involve the ophthalmic artery, resulting in anterior ischemic optic neuropathy and acute visual loss, which constitutes an ophthalmic emergency. Inflammation of arteries supplying the muscles of mastication causes jaw claudication and tongue discomfort.
Age is the greatest risk factor; the disease is rare in patients younger than 50 years and more than 90% of cases occur in those older than 60 years. Prevalence in individuals over 50 is approximately 1:500, with higher rates in northern latitudes. It is two to four times more common in women, rare in African American patients, and more common in White populations. There is a strong association with polymyalgia rheumatica, present in approximately 50% of patients. A genetic predisposition is linked to HLA-DR4.
Etiology
The exact cause is unknown. Genetic, environmental, and autoimmune factors are believed to contribute.
Diagnosis
The diagnosis is supported by the presence of three or more of the following in a patient with vasculitis: age greater than 50 years, erythrocyte sedimentation rate greater than 50 mm/hr, new-onset localized headache, temporal artery tenderness or decreased pulsation, new visual symptoms, and biopsy demonstrating necrotizing arteritis.
Signs And Symptoms
Symptoms may be acute, subacute, or chronic. Headache is the most common symptom, occurring in approximately 70% of patients, and is often unilateral, localized to the temple, and described as boring or lancinating. Jaw or tongue claudication with chewing occurs in about 50%. Constitutional symptoms include fatigue, malaise, anorexia, weight loss, weakness, arthralgias, and low-grade fever.
Visual manifestations usually involve one eye and may develop weeks to months after other symptoms. These include amaurosis fugax, blindness, diplopia, ptosis, extraocular muscle weakness, scotomata, and blurred vision. Visual impairment typically does not improve, even with treatment.
Other findings include scalp tenderness, especially over the temporal artery; early increased pulsations followed by decreased pulsations later in disease; erythema, warmth, swelling, or nodules over scalp arteries; bruits or diminished pulses over large arteries; sore throat, cough, and dysphagia. Neurologic manifestations such as neuropathies, transient ischemic attacks, and strokes may occur in up to one-third of patients. Occult manifestations include glossitis, lingual infarction, tongue infarction, and Raynaud phenomenon. Up to 30% of patients may lack classic symptoms.
Polymyalgia rheumatica is frequently associated, characterized by morning stiffness and aching pain of proximal muscles that improves with activity and may be accompanied by synovitis, particularly in the knees.
Essential Workup
A focused physical examination should emphasize the temporal arteries and scalp, a complete neurologic examination, and a detailed ophthalmic examination including visual acuity and visual fields. Fundoscopy may be normal early but can show optic nerve edema, pallor, hemorrhages, cotton-wool spots, and exudates later. Pulse asymmetry or bruits over large arteries should be documented.
Diagnosis Tests And Interpretation
Laboratory findings typically include a markedly elevated ESR, often greater than 100 mm/hr, and elevated C-reactive protein. Mild normochromic anemia and mild thrombocytosis are common. White blood cell count is usually normal or mildly elevated. Liver enzymes and prothrombin time may be elevated, while renal function and urinalysis are usually normal. Interleukin-6 levels are elevated during disease flares.
Imaging may include Doppler ultrasound showing decreased flow and a characteristic halo sign in temporal arteries. MRI can assess large-vessel involvement. Angiography may reveal smooth, tapered stenoses or occlusions.
Temporal artery biopsy is the diagnostic gold standard and should include multiple sections. It should be performed as soon as feasible after starting steroids. If the initial biopsy is negative and suspicion remains high, contralateral biopsy is recommended.
Differential Diagnosis
Other vasculitides including polyarteritis nodosa, hypersensitivity vasculitis, systemic lupus erythematosus, Takayasu arteritis, and granulomatosis with polyangiitis; retinal, ophthalmic, or temporal artery thrombosis; Lyme disease; and nonarteritic anterior ischemic optic neuropathy.
Treatment Prehospital
Symptoms may be mistaken for stroke. Provide monitoring and supplemental oxygen. Hypotension may occur from rare complications such as aortic dissection, abdominal aortic aneurysm, or myocardial infarction.
Initial Stabilization Therapy
Although uncommon, patients may present with vascular catastrophes requiring aggressive early management consistent with standard emergency protocols.
Ed Treatment Procedures
High-dose corticosteroids are the cornerstone of therapy. When clinical suspicion is strong, steroid treatment should not be delayed for biopsy, as vascular pathologic changes persist for weeks. Early aggressive treatment significantly reduces the risk of blindness. Systemic and local symptoms typically improve within days to weeks, but treatment may be required for several years, with an average disease course of three to four years. Analgesia with NSAIDs, salicylates, or narcotics may be provided as needed.
Medication
Prednisone 60–100 mg orally daily for at least two weeks before tapering. For acute visual symptoms, intravenous methylprednisolone 1,000 mg daily for one to three days may be used. Low-dose aspirin is recommended to reduce thrombotic risk. NSAIDs or narcotics may be used for pain control.
Follow-Up Disposition
Admission is indicated for patients with acute visual loss, impending vascular complications, or acute focal neurologic deficits. Less symptomatic patients without evidence of end-organ damage may be discharged with close follow-up arranged within one to two days.
Issues For Referral
Rheumatology for disease management, ophthalmology for visual symptoms, and neurology for focal neurologic findings.
Follow-Up Recommendations
Ongoing care with rheumatology for steroid management and evaluation for associated connective tissue disease. Ophthalmology and neurology follow-up are required for visual or neurologic involvement.
Key Clinical Insights And Common Errors
Permanent visual loss is the most feared complication. Steroid therapy must not be delayed when clinical suspicion is high or visual symptoms are present. Jaw claudication and amaurosis fugax are often underreported and should be specifically queried. Between 25% and 50% of patients with untreated unilateral visual loss will progress to bilateral blindness.
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Emergency And Acute Medicine - Giardiasis
Basics Description
Giardiasis is a noninvasive diarrheal illness caused by a protozoan parasite and is found worldwide. Prevalence ranges from 2–15% in developed countries and 20–40% in developing nations. It accounts for approximately 5% of travelers’ diarrhea and is the most common intestinal parasitic infection in the United States. Incidence peaks in early summer through fall, with highest rates in children aged 1–9 years and adults aged 30–39 years. Transmission occurs via the fecal–oral route. Humans are the primary reservoir, but domestic and wild mammals and contaminated surface water also serve as reservoirs. Populations at increased risk include travelers to endemic or wilderness areas, children in day care centers and their contacts, institutionalized individuals, and those engaging in anal sexual practices.
Etiology
Giardia lamblia is a flagellated protozoan, also known as Giardia intestinalis or Giardia duodenalis. After ingestion, organisms attach to intestinal villi and disrupt brush-border enzymes, leading to impaired digestion of lactose and other carbohydrates. No toxin is produced.
Diagnosis Signs And Symptoms
Symptoms typically begin 1–2 weeks after exposure. Infection is often asymptomatic. Symptomatic disease usually presents with acute-onset diarrhea that is foul-smelling, nonbloody, and frequently associated with steatorrhea. Illness is usually self-limited within 2–4 weeks but may be more severe in immunocompromised patients or those with underlying bowel disease. Common associated symptoms include flatulence, bloating, abdominal cramping, nausea, vomiting, malaise, anorexia, and weight loss. Fever is uncommon.
Thirty to fifty percent of patients develop chronic infection lasting longer than four weeks, characterized by fat malabsorption, secondary lactase deficiency, and macrocytic anemia due to folate deficiency. Pediatric patients may develop severe dehydration in acute disease and failure to thrive, growth retardation, or cognitive impairment in chronic infection. Physical examination is often benign. Extraintestinal manifestations include polyarthritis, urticaria, aphthous ulcers, maculopapular rash, and biliary tract disease.
Essential Workup
Evaluation should focus on exposure history, travel, high-risk group membership, and hydration status. The presence of gross or occult blood on rectal examination makes giardiasis unlikely.
Diagnosis Tests And Interpretation
Stool microscopy for ova and parasites has a sensitivity of 50–70% with one sample and up to 85–90% with three samples collected over several days. Specificity approaches 100%. Stool antigen detection by ELISA or immunofluorescent assay is highly sensitive and specific but does not detect other parasites. Stool PCR offers near-perfect sensitivity and specificity. Fecal leukocytes and stool cultures are unnecessary unless invasive bacterial infection is suspected. CBC may show macrocytic anemia in chronic disease. Electrolytes and renal function should be assessed if dehydration is present. Imaging studies are nonspecific and rarely required.
Differential Diagnosis
Viral gastroenteritis, bacterial enteritis, other protozoal infections, inflammatory bowel disease, irritable bowel syndrome, lactase deficiency, tropical sprue, medication or toxin-induced diarrhea, endocrine disorders, and gastrointestinal malignancy.
Treatment Initial Stabilization Therapy
Assess airway, breathing, and circulation. Administer intravenous isotonic fluids for significant dehydration. Children with severe dehydration require rapid fluid boluses and glucose monitoring.
Ed Treatment Procedures
Oral rehydration is sufficient for mild dehydration. Correct electrolyte abnormalities. Obtain stool studies when possible. If stool testing is negative but suspicion remains high, empiric treatment with metronidazole may be considered, and gastroenterology referral arranged for persistent symptoms.
Medication
First-line therapy includes metronidazole or tinidazole, each achieving cure rates near 90%. Metronidazole is given for 5–10 days, while tinidazole is administered as a single dose. Second-line agents include albendazole, nitazoxanide, quinacrine, paromomycin, or furazolidone when first-line therapy fails. Treatment choice should consider age, pregnancy status, renal function, and G6PD deficiency. Immunocompromised patients may require combination or prolonged therapy.
Follow-Up Disposition
Admission is indicated for patients with hemodynamic instability, severe electrolyte imbalance, inability to tolerate oral intake, or significant comorbid illness. Most patients can be discharged once hydration is adequate and symptoms are controlled.
Follow-Up Recommendations
Gastroenterology referral is recommended for persistent symptoms beyond four weeks despite therapy. Patients should be counseled regarding possible prolonged lactose intolerance and postinfectious fatigue.
Clinical Insights And Common Errors
Diagnosis is the primary challenge. Giardiasis should be considered in all patients with diarrhea, even without classic risk factors. A single stool specimen is often insufficient to exclude infection. Failure to recognize chronic disease and malabsorption can delay appropriate treatment.
Basics Description
Giardiasis is a noninvasive diarrheal illness caused by a protozoan parasite and is found worldwide. Prevalence ranges from 2–15% in developed countries and 20–40% in developing nations. It accounts for approximately 5% of travelers’ diarrhea and is the most common intestinal parasitic infection in the United States. Incidence peaks in early summer through fall, with highest rates in children aged 1–9 years and adults aged 30–39 years. Transmission occurs via the fecal–oral route. Humans are the primary reservoir, but domestic and wild mammals and contaminated surface water also serve as reservoirs. Populations at increased risk include travelers to endemic or wilderness areas, children in day care centers and their contacts, institutionalized individuals, and those engaging in anal sexual practices.
Etiology
Giardia lamblia is a flagellated protozoan, also known as Giardia intestinalis or Giardia duodenalis. After ingestion, organisms attach to intestinal villi and disrupt brush-border enzymes, leading to impaired digestion of lactose and other carbohydrates. No toxin is produced.
Diagnosis Signs And Symptoms
Symptoms typically begin 1–2 weeks after exposure. Infection is often asymptomatic. Symptomatic disease usually presents with acute-onset diarrhea that is foul-smelling, nonbloody, and frequently associated with steatorrhea. Illness is usually self-limited within 2–4 weeks but may be more severe in immunocompromised patients or those with underlying bowel disease. Common associated symptoms include flatulence, bloating, abdominal cramping, nausea, vomiting, malaise, anorexia, and weight loss. Fever is uncommon.
Thirty to fifty percent of patients develop chronic infection lasting longer than four weeks, characterized by fat malabsorption, secondary lactase deficiency, and macrocytic anemia due to folate deficiency. Pediatric patients may develop severe dehydration in acute disease and failure to thrive, growth retardation, or cognitive impairment in chronic infection. Physical examination is often benign. Extraintestinal manifestations include polyarthritis, urticaria, aphthous ulcers, maculopapular rash, and biliary tract disease.
Essential Workup
Evaluation should focus on exposure history, travel, high-risk group membership, and hydration status. The presence of gross or occult blood on rectal examination makes giardiasis unlikely.
Diagnosis Tests And Interpretation
Stool microscopy for ova and parasites has a sensitivity of 50–70% with one sample and up to 85–90% with three samples collected over several days. Specificity approaches 100%. Stool antigen detection by ELISA or immunofluorescent assay is highly sensitive and specific but does not detect other parasites. Stool PCR offers near-perfect sensitivity and specificity. Fecal leukocytes and stool cultures are unnecessary unless invasive bacterial infection is suspected. CBC may show macrocytic anemia in chronic disease. Electrolytes and renal function should be assessed if dehydration is present. Imaging studies are nonspecific and rarely required.
Differential Diagnosis
Viral gastroenteritis, bacterial enteritis, other protozoal infections, inflammatory bowel disease, irritable bowel syndrome, lactase deficiency, tropical sprue, medication or toxin-induced diarrhea, endocrine disorders, and gastrointestinal malignancy.
Treatment Initial Stabilization Therapy
Assess airway, breathing, and circulation. Administer intravenous isotonic fluids for significant dehydration. Children with severe dehydration require rapid fluid boluses and glucose monitoring.
Ed Treatment Procedures
Oral rehydration is sufficient for mild dehydration. Correct electrolyte abnormalities. Obtain stool studies when possible. If stool testing is negative but suspicion remains high, empiric treatment with metronidazole may be considered, and gastroenterology referral arranged for persistent symptoms.
Medication
First-line therapy includes metronidazole or tinidazole, each achieving cure rates near 90%. Metronidazole is given for 5–10 days, while tinidazole is administered as a single dose. Second-line agents include albendazole, nitazoxanide, quinacrine, paromomycin, or furazolidone when first-line therapy fails. Treatment choice should consider age, pregnancy status, renal function, and G6PD deficiency. Immunocompromised patients may require combination or prolonged therapy.
Follow-Up Disposition
Admission is indicated for patients with hemodynamic instability, severe electrolyte imbalance, inability to tolerate oral intake, or significant comorbid illness. Most patients can be discharged once hydration is adequate and symptoms are controlled.
Follow-Up Recommendations
Gastroenterology referral is recommended for persistent symptoms beyond four weeks despite therapy. Patients should be counseled regarding possible prolonged lactose intolerance and postinfectious fatigue.
Clinical Insights And Common Errors
Diagnosis is the primary challenge. Giardiasis should be considered in all patients with diarrhea, even without classic risk factors. A single stool specimen is often insufficient to exclude infection. Failure to recognize chronic disease and malabsorption can delay appropriate treatment.
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Emergency And Acute Medicine - Glaucoma
Basics Description
Glaucoma is a group of disorders characterized by elevated intraocular pressure, progressive optic neuropathy, and irreversible vision loss if untreated.
Etiology
Primary glaucoma includes open-angle and angle-closure forms. Primary open-angle glaucoma has a normal anterior chamber angle, insidious onset, and chronic elevation of intraocular pressure. It accounts for approximately 90% of glaucoma cases in the United States and is a leading cause of blindness in African Americans. Risk factors include African American race, age over 40 years, family history, myopia, diabetes, and hypertension.
Primary angle-closure glaucoma results from narrowing or closure of the anterior chamber angle, preventing normal aqueous humor outflow through the trabecular meshwork. It presents abruptly with a sudden rise in intraocular pressure. Risk factors include Asian and Eskimo ethnicity, hyperopia, increasing age, female sex, and family history.
Secondary glaucoma may be open or closed angle and occurs due to other conditions such as ocular disease, trauma, systemic illness, or medications. Common drug causes include steroids, sertraline, bronchodilators, and topiramate. Associated diseases include uveitis, neovascularization, neurofibromatosis, intraocular tumors, trauma, and rapid correction of hyperglycemia.
Diagnosis Signs And Symptoms
Open-angle glaucoma typically causes painless, gradual loss of peripheral vision and may present late. Angle-closure glaucoma classically presents with painful loss of vision and a fixed, mid-dilated pupil.
History in open-angle disease includes slow bilateral visual decline or night blindness without pain. Angle-closure disease presents with severe eye pain, ipsilateral headache, nausea, vomiting, decreased visual acuity, halos around lights, and visual clouding. Symptoms may be triggered by dim lighting or medications such as anticholinergics, sympathomimetics, antihistamines, antipsychotics, tricyclic antidepressants, and sulfonamides like topiramate.
Physical examination in angle-closure glaucoma reveals decreased visual acuity, a mid-dilated nonreactive pupil, corneal edema with hazy appearance, conjunctival injection with ciliary flush, and a firm globe on palpation.
Essential Workup
A complete ocular examination is required, including visual acuity testing, tonometry, and slit-lamp examination.
Diagnosis Tests And Interpretation
Normal intraocular pressure ranges from 10–21 mm Hg. In open-angle glaucoma, pressure elevation is variable and may be normal in up to 30% of patients. In angle-closure glaucoma, any elevation is abnormal and values are often greater than 40 mm Hg. Slit-lamp examination evaluates the anterior chamber and excludes other ocular pathology. Gonioscopy provides direct assessment of the chamber angle and confirms angle closure.
Differential Diagnosis
Cavernous sinus thrombosis, acute iritis or uveitis, retinal artery or vein occlusion, temporal arteritis, retinal detachment, conjunctivitis, and corneal abrasion.
Treatment Pre Hospital
No specific prehospital ocular intervention is required. Provide analgesia as needed and stabilize other injuries if trauma is involved.
Initial Stabilization Therapy
In suspected acute angle-closure glaucoma, immediately initiate measures to reduce intraocular pressure and discontinue precipitating medications when applicable.
Ed Treatment Procedures
Open-angle glaucoma requires recognition and urgent ophthalmology referral. Long-term management typically involves topical beta-blockers or prostaglandin analogs.
Acute angle-closure glaucoma is an ophthalmologic emergency. Immediate treatment includes topical beta-blockers and alpha-2 agonists to reduce aqueous humor production, carbonic anhydrase inhibitors such as acetazolamide, and hyperosmotic agents like mannitol in severe cases. Once intraocular pressure is below 40 mm Hg, pilocarpine is used to constrict the pupil and open the trabecular meshwork. Topical corticosteroids reduce inflammation. Emergent ophthalmology consultation is required for definitive management, often with laser iridectomy. Adequate analgesia and antiemetics should be provided.
Medication
Common agents include acetazolamide, mannitol, pilocarpine, prednisolone acetate, topical beta-blockers (timolol, betaxolol), alpha-agonists (apraclonidine, brimonidine), carbonic anhydrase inhibitors (dorzolamide, brinzolamide), and prostaglandin analogs (latanoprost, bimatoprost, travoprost). Prostaglandin analogs are first-line for open-angle glaucoma due to favorable side-effect profiles, though cost may limit use.
Follow-Up Disposition
Admission is indicated for severe pain, nausea, vomiting, need for parenteral therapy, or lack of improvement in intraocular pressure. Patients with symptom resolution and improved pressures may be discharged after ophthalmology evaluation with close follow-up within 24 hours.
Issues For Referral
If ophthalmology is unavailable, initiate treatment and transfer the patient to a facility with ophthalmologic services.
Follow-Up Recommendations
Open-angle glaucoma requires urgent outpatient ophthalmology follow-up. Angle-closure glaucoma requires immediate specialist intervention.
Key Clinical Insights And Avoidable Errors
Delayed reduction of intraocular pressure can lead to permanent vision loss. Eye pain or headache associated with abdominal symptoms should prompt ocular evaluation to avoid missed diagnosis. Patients using topical beta-blockers may develop systemic adverse effects such as bradycardia, hypotension, or syncope, which can complicate presentation and management.
Basics Description
Glaucoma is a group of disorders characterized by elevated intraocular pressure, progressive optic neuropathy, and irreversible vision loss if untreated.
Etiology
Primary glaucoma includes open-angle and angle-closure forms. Primary open-angle glaucoma has a normal anterior chamber angle, insidious onset, and chronic elevation of intraocular pressure. It accounts for approximately 90% of glaucoma cases in the United States and is a leading cause of blindness in African Americans. Risk factors include African American race, age over 40 years, family history, myopia, diabetes, and hypertension.
Primary angle-closure glaucoma results from narrowing or closure of the anterior chamber angle, preventing normal aqueous humor outflow through the trabecular meshwork. It presents abruptly with a sudden rise in intraocular pressure. Risk factors include Asian and Eskimo ethnicity, hyperopia, increasing age, female sex, and family history.
Secondary glaucoma may be open or closed angle and occurs due to other conditions such as ocular disease, trauma, systemic illness, or medications. Common drug causes include steroids, sertraline, bronchodilators, and topiramate. Associated diseases include uveitis, neovascularization, neurofibromatosis, intraocular tumors, trauma, and rapid correction of hyperglycemia.
Diagnosis Signs And Symptoms
Open-angle glaucoma typically causes painless, gradual loss of peripheral vision and may present late. Angle-closure glaucoma classically presents with painful loss of vision and a fixed, mid-dilated pupil.
History in open-angle disease includes slow bilateral visual decline or night blindness without pain. Angle-closure disease presents with severe eye pain, ipsilateral headache, nausea, vomiting, decreased visual acuity, halos around lights, and visual clouding. Symptoms may be triggered by dim lighting or medications such as anticholinergics, sympathomimetics, antihistamines, antipsychotics, tricyclic antidepressants, and sulfonamides like topiramate.
Physical examination in angle-closure glaucoma reveals decreased visual acuity, a mid-dilated nonreactive pupil, corneal edema with hazy appearance, conjunctival injection with ciliary flush, and a firm globe on palpation.
Essential Workup
A complete ocular examination is required, including visual acuity testing, tonometry, and slit-lamp examination.
Diagnosis Tests And Interpretation
Normal intraocular pressure ranges from 10–21 mm Hg. In open-angle glaucoma, pressure elevation is variable and may be normal in up to 30% of patients. In angle-closure glaucoma, any elevation is abnormal and values are often greater than 40 mm Hg. Slit-lamp examination evaluates the anterior chamber and excludes other ocular pathology. Gonioscopy provides direct assessment of the chamber angle and confirms angle closure.
Differential Diagnosis
Cavernous sinus thrombosis, acute iritis or uveitis, retinal artery or vein occlusion, temporal arteritis, retinal detachment, conjunctivitis, and corneal abrasion.
Treatment Pre Hospital
No specific prehospital ocular intervention is required. Provide analgesia as needed and stabilize other injuries if trauma is involved.
Initial Stabilization Therapy
In suspected acute angle-closure glaucoma, immediately initiate measures to reduce intraocular pressure and discontinue precipitating medications when applicable.
Ed Treatment Procedures
Open-angle glaucoma requires recognition and urgent ophthalmology referral. Long-term management typically involves topical beta-blockers or prostaglandin analogs.
Acute angle-closure glaucoma is an ophthalmologic emergency. Immediate treatment includes topical beta-blockers and alpha-2 agonists to reduce aqueous humor production, carbonic anhydrase inhibitors such as acetazolamide, and hyperosmotic agents like mannitol in severe cases. Once intraocular pressure is below 40 mm Hg, pilocarpine is used to constrict the pupil and open the trabecular meshwork. Topical corticosteroids reduce inflammation. Emergent ophthalmology consultation is required for definitive management, often with laser iridectomy. Adequate analgesia and antiemetics should be provided.
Medication
Common agents include acetazolamide, mannitol, pilocarpine, prednisolone acetate, topical beta-blockers (timolol, betaxolol), alpha-agonists (apraclonidine, brimonidine), carbonic anhydrase inhibitors (dorzolamide, brinzolamide), and prostaglandin analogs (latanoprost, bimatoprost, travoprost). Prostaglandin analogs are first-line for open-angle glaucoma due to favorable side-effect profiles, though cost may limit use.
Follow-Up Disposition
Admission is indicated for severe pain, nausea, vomiting, need for parenteral therapy, or lack of improvement in intraocular pressure. Patients with symptom resolution and improved pressures may be discharged after ophthalmology evaluation with close follow-up within 24 hours.
Issues For Referral
If ophthalmology is unavailable, initiate treatment and transfer the patient to a facility with ophthalmologic services.
Follow-Up Recommendations
Open-angle glaucoma requires urgent outpatient ophthalmology follow-up. Angle-closure glaucoma requires immediate specialist intervention.
Key Clinical Insights And Avoidable Errors
Delayed reduction of intraocular pressure can lead to permanent vision loss. Eye pain or headache associated with abdominal symptoms should prompt ocular evaluation to avoid missed diagnosis. Patients using topical beta-blockers may develop systemic adverse effects such as bradycardia, hypotension, or syncope, which can complicate presentation and management.
- Published on
Emergency And Acute Medicine - Globe Rupture
Basics Description
A globe rupture is a full-thickness injury of the cornea or sclera caused by trauma. Blunt trauma results in a sudden diffuse rise in intraocular pressure, leading to rupture at the weakest points of the eye such as the extraocular muscle insertions, corneoscleral junction, or limbus where the sclera is thinnest. Penetrating injuries occur when sharp objects or projectiles directly lacerate the sclera or anterior eye and are most commonly anterior due to protection from the bony orbit. Posterior injuries may occur with orbital fractures or penetrating trauma through the eyelid or eyebrow. Prognosis is worse with large lacerations, injuries posterior to rectus muscle insertions, blunt mechanisms, intraocular foreign bodies (especially organic), vitreous extrusion, lens damage, hyphema, retinal detachment, poor initial visual acuity, afferent pupillary defect, and delays to operative repair.
Etiology
Common causes include falls, blunt impact injuries, sports-related trauma, indirect concussive injuries such as explosions, sharp or stabbing injuries (accidental or intentional), and projectile injuries from industrial accidents, firearms, BB pellets, or blast-related shrapnel such as glass.
Diagnosis Signs And Symptoms
Patients may present with eye pain, localized swelling and ecchymosis, scleral or corneal laceration, extrusion of intraocular contents, markedly decreased visual acuity, restricted extraocular movements, hyphema, severe circumferential subconjunctival hemorrhage with bloody chemosis, abnormally deep or shallow anterior chamber, irregular pupil pointing toward the lesion, lens subluxation, commotio retinae, and low intraocular pressure. Tonometry should not be performed if globe rupture is suspected.
History
Assessment should include the mechanism of injury, concern for retained intraocular foreign body, prior eye surgery, preinjury visual acuity, tetanus status, and time of last oral intake.
Physical Exam
A careful penlight or slit-lamp examination should be performed to look for signs of rupture. Once a globe rupture is suspected or identified, further ocular examination should be deferred until surgical repair to avoid pressure on the eye and extrusion of contents. If rupture is excluded, a full ophthalmologic exam including visual acuity, slit-lamp evaluation, fundus exam, Seidel test, and intraocular pressure measurement may be performed. Ultrasound should only be used if rupture is not suspected.
Essential Workup
If globe rupture is suspected or confirmed, minimize examination and manipulation of the eye until operative repair.
Diagnosis Tests And Interpretation
Preoperative laboratory studies include CBC, electrolytes, and coagulation tests. Imaging may include orbital radiographs to identify metallic foreign bodies and CT of the orbits with axial and coronal views. MRI is contraindicated until metallic foreign bodies are excluded. B-scan ultrasound may be used only when rupture is not suspected.
Differential Diagnosis
Intraocular foreign body, hyphema, severe subconjunctival hemorrhage with chemosis, partial corneal laceration, and partial scleral laceration.
Treatment Pre Hospital
Place a rigid eye shield without applying pressure to the globe. If no shield is available, a protective cup may be used.
Initial Stabilization Therapy
Avoid manipulation of the eye and prevent activities that increase intraocular pressure such as coughing, vomiting, or straining.
Ed Treatment Procedures
Immediate ophthalmologic consultation is required for surgical management. Maintain NPO status, elevate the head of the bed, provide antiemetics, and apply a protective eye shield without pressure. Update tetanus immunization. Administer broad-spectrum IV antibiotics targeting skin flora and injury-specific contaminants, commonly vancomycin with ceftazidime or ciprofloxacin. Identify and manage associated injuries. Succinylcholine is relatively contraindicated but may be used with appropriate precautions if necessary for airway control.
In pediatric patients, consider nonaccidental trauma and minimize crying or agitation to prevent extrusion of ocular contents.
Medication
Commonly used agents include vancomycin, ceftazidime, ciprofloxacin, clindamycin, tobramycin, and antiemetics such as ondansetron or prochlorperazine.
Follow-Up Disposition
All patients with globe rupture or penetrating eye injury require admission. Discharge is appropriate only if globe penetration has been definitively excluded.
Issues For Referral
Emergent ophthalmologic consultation is essential, as delays increase the risk of infection and poor visual outcomes. Patients should be counseled on protective eyewear to prevent recurrence when appropriate.
Follow-Up Recommendations
Postoperative follow-up with ophthalmology is mandatory.
Key Clinical Insights And Avoidable Errors
Do not manipulate the eye when globe rupture is suspected or confirmed. Always place a protective eye shield without pressure. Treat nausea and vomiting aggressively to prevent increases in intraocular pressure. Ensure tetanus prophylaxis and initiate empiric antibiotics tailored to the injury mechanism promptly.
Basics Description
A globe rupture is a full-thickness injury of the cornea or sclera caused by trauma. Blunt trauma results in a sudden diffuse rise in intraocular pressure, leading to rupture at the weakest points of the eye such as the extraocular muscle insertions, corneoscleral junction, or limbus where the sclera is thinnest. Penetrating injuries occur when sharp objects or projectiles directly lacerate the sclera or anterior eye and are most commonly anterior due to protection from the bony orbit. Posterior injuries may occur with orbital fractures or penetrating trauma through the eyelid or eyebrow. Prognosis is worse with large lacerations, injuries posterior to rectus muscle insertions, blunt mechanisms, intraocular foreign bodies (especially organic), vitreous extrusion, lens damage, hyphema, retinal detachment, poor initial visual acuity, afferent pupillary defect, and delays to operative repair.
Etiology
Common causes include falls, blunt impact injuries, sports-related trauma, indirect concussive injuries such as explosions, sharp or stabbing injuries (accidental or intentional), and projectile injuries from industrial accidents, firearms, BB pellets, or blast-related shrapnel such as glass.
Diagnosis Signs And Symptoms
Patients may present with eye pain, localized swelling and ecchymosis, scleral or corneal laceration, extrusion of intraocular contents, markedly decreased visual acuity, restricted extraocular movements, hyphema, severe circumferential subconjunctival hemorrhage with bloody chemosis, abnormally deep or shallow anterior chamber, irregular pupil pointing toward the lesion, lens subluxation, commotio retinae, and low intraocular pressure. Tonometry should not be performed if globe rupture is suspected.
History
Assessment should include the mechanism of injury, concern for retained intraocular foreign body, prior eye surgery, preinjury visual acuity, tetanus status, and time of last oral intake.
Physical Exam
A careful penlight or slit-lamp examination should be performed to look for signs of rupture. Once a globe rupture is suspected or identified, further ocular examination should be deferred until surgical repair to avoid pressure on the eye and extrusion of contents. If rupture is excluded, a full ophthalmologic exam including visual acuity, slit-lamp evaluation, fundus exam, Seidel test, and intraocular pressure measurement may be performed. Ultrasound should only be used if rupture is not suspected.
Essential Workup
If globe rupture is suspected or confirmed, minimize examination and manipulation of the eye until operative repair.
Diagnosis Tests And Interpretation
Preoperative laboratory studies include CBC, electrolytes, and coagulation tests. Imaging may include orbital radiographs to identify metallic foreign bodies and CT of the orbits with axial and coronal views. MRI is contraindicated until metallic foreign bodies are excluded. B-scan ultrasound may be used only when rupture is not suspected.
Differential Diagnosis
Intraocular foreign body, hyphema, severe subconjunctival hemorrhage with chemosis, partial corneal laceration, and partial scleral laceration.
Treatment Pre Hospital
Place a rigid eye shield without applying pressure to the globe. If no shield is available, a protective cup may be used.
Initial Stabilization Therapy
Avoid manipulation of the eye and prevent activities that increase intraocular pressure such as coughing, vomiting, or straining.
Ed Treatment Procedures
Immediate ophthalmologic consultation is required for surgical management. Maintain NPO status, elevate the head of the bed, provide antiemetics, and apply a protective eye shield without pressure. Update tetanus immunization. Administer broad-spectrum IV antibiotics targeting skin flora and injury-specific contaminants, commonly vancomycin with ceftazidime or ciprofloxacin. Identify and manage associated injuries. Succinylcholine is relatively contraindicated but may be used with appropriate precautions if necessary for airway control.
In pediatric patients, consider nonaccidental trauma and minimize crying or agitation to prevent extrusion of ocular contents.
Medication
Commonly used agents include vancomycin, ceftazidime, ciprofloxacin, clindamycin, tobramycin, and antiemetics such as ondansetron or prochlorperazine.
Follow-Up Disposition
All patients with globe rupture or penetrating eye injury require admission. Discharge is appropriate only if globe penetration has been definitively excluded.
Issues For Referral
Emergent ophthalmologic consultation is essential, as delays increase the risk of infection and poor visual outcomes. Patients should be counseled on protective eyewear to prevent recurrence when appropriate.
Follow-Up Recommendations
Postoperative follow-up with ophthalmology is mandatory.
Key Clinical Insights And Avoidable Errors
Do not manipulate the eye when globe rupture is suspected or confirmed. Always place a protective eye shield without pressure. Treat nausea and vomiting aggressively to prevent increases in intraocular pressure. Ensure tetanus prophylaxis and initiate empiric antibiotics tailored to the injury mechanism promptly.
- Published on
Emergency And Acute Medicine - Glomerulonephritis
Basics Description
Glomerulonephritis is a clinical syndrome characterized by hematuria, proteinuria, red blood cell casts, hypertension, and varying degrees of renal insufficiency. It represents a common final pathway of multiple disease processes that lead to intraglomerular inflammation and cellular proliferation. Contributing factors include genetic predisposition, infectious triggers, and rheumatologic or autoimmune conditions. Pathogenesis involves antibody deposition either by direct binding to glomerular antigens or deposition of circulating immune complexes, leading to activation of inflammatory mediators such as leukocytes, complement, and cytokines. Cell-mediated immune mechanisms further contribute to glomerular injury. Persistent inflammation may result in glomerular scarring and permanent renal damage.
Etiology
Postinfectious causes include poststreptococcal glomerulonephritis, which typically occurs 7–21 days after streptococcal pharyngitis or skin infection and is most common in children aged 2–14 years and in the elderly, with a male predominance. IgA nephropathy is common in men in the third and fourth decades and is often associated with increased IgA production following upper respiratory infections; Henoch–Schönlein purpura represents a systemic IgA-mediated disease affecting younger patients. Rapidly progressive glomerulonephritis can destroy renal function within days and is characterized by crescent formation in glomeruli. Pauci-immune vasculitides, often ANCA-positive, include granulomatosis with polyangiitis, microscopic polyangiitis, and eosinophilic granulomatosis with polyangiitis and may involve lungs or skin. Immune complex–mediated causes include postinfectious GN, endocarditis-associated GN, systemic lupus erythematosus, and Henoch–Schönlein purpura. Anti–glomerular basement membrane disease, such as Goodpasture syndrome, typically affects older adults and may involve pulmonary hemorrhage. Membranoproliferative glomerulonephritis is associated with complement deposition and conditions such as hepatitis C, non-Hodgkin lymphoma, or occult infection.
Diagnosis Signs And Symptoms
Core clinical features include hematuria, proteinuria, edema due to salt and water retention (periorbital edema, ascites, pleural effusions), hypertension, oliguria, azotemia, congestive heart failure, and renal failure. Nonspecific symptoms include fatigue, weight loss, abdominal pain, nausea, and vomiting. Autoimmune-related findings may include arthralgias, arthritis, rash, fever, and systemic inflammation. Goodpasture syndrome may present with hemoptysis. Granulomatosis with polyangiitis can cause purulent rhinorrhea, sinus pain, arthritis, and hemoptysis. Henoch–Schönlein purpura may present with abdominal pain, purpura, and arthritis.
In older adults, pauci-immune rapidly progressive glomerulonephritis is common and requires urgent diagnosis and biopsy due to high risk of progression to end-stage renal disease.
Essential Workup
Urinalysis is essential to identify hematuria, proteinuria, and red blood cell casts.
Diagnosis Tests And Interpretation
Laboratory evaluation includes electrolytes, BUN, creatinine, and GFR to assess renal function, as well as evaluation for hyperkalemia. Albumin and total protein levels may demonstrate hypoalbuminemia. CBC may show anemia related to chronic kidney disease, systemic illness, or pulmonary hemorrhage. Coagulation studies may be abnormal in select forms of GN. Additional tests guided by consultants include cultures, 24-hour urine protein measurement, antistreptolysin O titers, complement levels, ANA, ANCA, anti-GBM antibodies, ESR, CRP, hepatitis B and C serologies, and HIV testing.
Imaging may include renal ultrasound to assess kidney size and reversibility of disease and chest radiography to evaluate for pulmonary edema or hemorrhage.
Renal biopsy is the definitive diagnostic test to distinguish primary glomerular disease from secondary causes. Cystoscopy may be considered if bladder malignancy is suspected.
Differential Diagnosis
Hematologic disorders such as sickle cell disease and coagulopathies; renal causes including infection, malformation, neoplasm, ischemia, trauma, and vasculitis; postrenal causes such as obstruction or reflux; inflammatory genitourinary conditions; pigmenturia; factitious hematuria; and vaginal bleeding.
Treatment Pre Hospital
Provide supportive care with attention to airway, breathing, and circulation. Restrict fluids in stable patients with significant edema.
Initial Stabilization Therapy
Stabilize airway, breathing, and circulation.
Ed Treatment Procedures
Management is largely supportive and includes strict blood pressure control with a target below 125/75 mm Hg, loop diuretics for volume overload, and ACE inhibitors for maintenance therapy. Dialysis is indicated for fluid overload, hyperkalemia, or uremia.
Poststreptococcal glomerulonephritis is treated with supportive care and typically resolves spontaneously; antibiotics do not alter renal outcomes.
IgA nephropathy is managed supportively, with immunosuppressive therapy considered when biopsy shows active inflammation.
Rapidly progressive glomerulonephritis requires emergent nephrology consultation and early initiation of immunosuppressive therapy due to the risk of irreversible renal failure.
Membranoproliferative glomerulonephritis management focuses on treating underlying disease and may include plasma exchange, immunosuppressants, and steroids.
Medication
Therapeutic agents may include ACE inhibitors such as benazepril, loop diuretics such as furosemide, corticosteroids including methylprednisolone and prednisone, immunosuppressants such as cyclophosphamide or rituximab, vasodilators for hypertensive emergencies, and renal replacement therapy when indicated.
Follow-Up Disposition
Admission is required for patients with unstable vital signs, oliguria or anuria, uremia, acute renal failure, significant electrolyte abnormalities, hypertensive emergencies, congestive heart failure, or infectious causes of glomerulonephritis.
Selected patients with mild hematuria and proteinuria, stable vitals, no infection, and otherwise normal laboratory findings may be discharged with close follow-up.
Follow-Up Recommendations
All patients with glomerulonephritis require nephrology follow-up for monitoring, definitive diagnosis, and long-term management.
Key Clinical Insights And Avoidable Errors
Early nephrology consultation is critical when immunosuppressive therapy is being considered. Any finding of hematuria or proteinuria warrants appropriate follow-up, as progression to clinically significant glomerulonephritis may occur if overlooked.
Basics Description
Glomerulonephritis is a clinical syndrome characterized by hematuria, proteinuria, red blood cell casts, hypertension, and varying degrees of renal insufficiency. It represents a common final pathway of multiple disease processes that lead to intraglomerular inflammation and cellular proliferation. Contributing factors include genetic predisposition, infectious triggers, and rheumatologic or autoimmune conditions. Pathogenesis involves antibody deposition either by direct binding to glomerular antigens or deposition of circulating immune complexes, leading to activation of inflammatory mediators such as leukocytes, complement, and cytokines. Cell-mediated immune mechanisms further contribute to glomerular injury. Persistent inflammation may result in glomerular scarring and permanent renal damage.
Etiology
Postinfectious causes include poststreptococcal glomerulonephritis, which typically occurs 7–21 days after streptococcal pharyngitis or skin infection and is most common in children aged 2–14 years and in the elderly, with a male predominance. IgA nephropathy is common in men in the third and fourth decades and is often associated with increased IgA production following upper respiratory infections; Henoch–Schönlein purpura represents a systemic IgA-mediated disease affecting younger patients. Rapidly progressive glomerulonephritis can destroy renal function within days and is characterized by crescent formation in glomeruli. Pauci-immune vasculitides, often ANCA-positive, include granulomatosis with polyangiitis, microscopic polyangiitis, and eosinophilic granulomatosis with polyangiitis and may involve lungs or skin. Immune complex–mediated causes include postinfectious GN, endocarditis-associated GN, systemic lupus erythematosus, and Henoch–Schönlein purpura. Anti–glomerular basement membrane disease, such as Goodpasture syndrome, typically affects older adults and may involve pulmonary hemorrhage. Membranoproliferative glomerulonephritis is associated with complement deposition and conditions such as hepatitis C, non-Hodgkin lymphoma, or occult infection.
Diagnosis Signs And Symptoms
Core clinical features include hematuria, proteinuria, edema due to salt and water retention (periorbital edema, ascites, pleural effusions), hypertension, oliguria, azotemia, congestive heart failure, and renal failure. Nonspecific symptoms include fatigue, weight loss, abdominal pain, nausea, and vomiting. Autoimmune-related findings may include arthralgias, arthritis, rash, fever, and systemic inflammation. Goodpasture syndrome may present with hemoptysis. Granulomatosis with polyangiitis can cause purulent rhinorrhea, sinus pain, arthritis, and hemoptysis. Henoch–Schönlein purpura may present with abdominal pain, purpura, and arthritis.
In older adults, pauci-immune rapidly progressive glomerulonephritis is common and requires urgent diagnosis and biopsy due to high risk of progression to end-stage renal disease.
Essential Workup
Urinalysis is essential to identify hematuria, proteinuria, and red blood cell casts.
Diagnosis Tests And Interpretation
Laboratory evaluation includes electrolytes, BUN, creatinine, and GFR to assess renal function, as well as evaluation for hyperkalemia. Albumin and total protein levels may demonstrate hypoalbuminemia. CBC may show anemia related to chronic kidney disease, systemic illness, or pulmonary hemorrhage. Coagulation studies may be abnormal in select forms of GN. Additional tests guided by consultants include cultures, 24-hour urine protein measurement, antistreptolysin O titers, complement levels, ANA, ANCA, anti-GBM antibodies, ESR, CRP, hepatitis B and C serologies, and HIV testing.
Imaging may include renal ultrasound to assess kidney size and reversibility of disease and chest radiography to evaluate for pulmonary edema or hemorrhage.
Renal biopsy is the definitive diagnostic test to distinguish primary glomerular disease from secondary causes. Cystoscopy may be considered if bladder malignancy is suspected.
Differential Diagnosis
Hematologic disorders such as sickle cell disease and coagulopathies; renal causes including infection, malformation, neoplasm, ischemia, trauma, and vasculitis; postrenal causes such as obstruction or reflux; inflammatory genitourinary conditions; pigmenturia; factitious hematuria; and vaginal bleeding.
Treatment Pre Hospital
Provide supportive care with attention to airway, breathing, and circulation. Restrict fluids in stable patients with significant edema.
Initial Stabilization Therapy
Stabilize airway, breathing, and circulation.
Ed Treatment Procedures
Management is largely supportive and includes strict blood pressure control with a target below 125/75 mm Hg, loop diuretics for volume overload, and ACE inhibitors for maintenance therapy. Dialysis is indicated for fluid overload, hyperkalemia, or uremia.
Poststreptococcal glomerulonephritis is treated with supportive care and typically resolves spontaneously; antibiotics do not alter renal outcomes.
IgA nephropathy is managed supportively, with immunosuppressive therapy considered when biopsy shows active inflammation.
Rapidly progressive glomerulonephritis requires emergent nephrology consultation and early initiation of immunosuppressive therapy due to the risk of irreversible renal failure.
Membranoproliferative glomerulonephritis management focuses on treating underlying disease and may include plasma exchange, immunosuppressants, and steroids.
Medication
Therapeutic agents may include ACE inhibitors such as benazepril, loop diuretics such as furosemide, corticosteroids including methylprednisolone and prednisone, immunosuppressants such as cyclophosphamide or rituximab, vasodilators for hypertensive emergencies, and renal replacement therapy when indicated.
Follow-Up Disposition
Admission is required for patients with unstable vital signs, oliguria or anuria, uremia, acute renal failure, significant electrolyte abnormalities, hypertensive emergencies, congestive heart failure, or infectious causes of glomerulonephritis.
Selected patients with mild hematuria and proteinuria, stable vitals, no infection, and otherwise normal laboratory findings may be discharged with close follow-up.
Follow-Up Recommendations
All patients with glomerulonephritis require nephrology follow-up for monitoring, definitive diagnosis, and long-term management.
Key Clinical Insights And Avoidable Errors
Early nephrology consultation is critical when immunosuppressive therapy is being considered. Any finding of hematuria or proteinuria warrants appropriate follow-up, as progression to clinically significant glomerulonephritis may occur if overlooked.
- Published on
Emergency And Acute Medicine – Penetrating Head Injury
Definition And Injury Characteristics
Penetrating head trauma involves direct violation of the skull with injury to intracranial contents. High-velocity injuries are most commonly caused by bullets and produce direct tissue destruction along with secondary cavitation or shock-wave injury to surrounding brain tissue. Low-velocity injuries are typically due to knives, picks, or other sharp objects and cause localized, direct damage to brain structures along the tract of penetration.
Mechanisms Of Injury
Penetration of the skull by a foreign object leads to direct brain tissue injury and is frequently complicated by intracranial hemorrhage, including epidural, subdural, and intraparenchymal bleeding. Even when a projectile strikes the skull and ricochets without fracturing bone, significant underlying brain injury may still occur due to transmitted force.
Clinical Presentation
The degree of altered consciousness and neurologic deficit varies widely depending on the object involved, its velocity, and the anatomic location of injury. Signs of rising intracranial pressure include declining level of consciousness, decreasing Glasgow Coma Scale score, Cushing response with bradycardia, hypertension, and abnormal respirations, as well as a dilated or “blown” pupil accompanied by decorticate or decerebrate posturing.
External indicators of penetrating injury or basilar skull fracture may include raccoon eyes, Battle sign over the mastoid, hemotympanum, and cerebrospinal fluid rhinorrhea or otorrhea. Retained foreign objects may still be present at the injury site.
History Assessment
Key historical elements include identification of the weapon or object involved, weapon caliber when applicable, loss of consciousness or amnesia, anticoagulant use, headache, visual or auditory disturbances, and focal neurologic complaints.
Physical Examination
Examination should focus on identifying entry and exit wounds, evaluating for multiple projectile sites, and performing a complete neurologic assessment. Mental status and focal findings correlate closely with injury location and severity.
Essential Evaluation
A thorough history and physical examination are required to assess the extent of injury, followed by urgent imaging to define intracranial damage and guide management.
Diagnostic Testing
Laboratory studies include complete blood count, platelet count, coagulation profile, type and crossmatch, and baseline electrolytes, blood urea nitrogen, and creatinine.
Imaging is centered on noncontrast CT of the head to identify hemorrhage, foreign bodies, bone fragments, and injury trajectory. Skull radiographs may assist in determining depth of penetration and retained fragments. Cervical spine imaging with helical CT or standard radiographs is required when indicated.
Alternative Diagnoses
Conditions to consider include blunt head trauma, isolated basilar skull fracture, or medical causes of altered mental status that may have resulted in secondary penetrating injury after a fall.
Prehospital Management Principles
Stabilization is prioritized while avoiding removal of any retained foreign object. Airway protection is essential to prevent hypoxemia, while routine hyperventilation should be avoided. Cervical spine precautions must be maintained. Patients should be transported to a trauma center. Hypoxia is prevented with supplemental oxygen, and hypotension is avoided using intravenous crystalloid fluids to maintain systolic blood pressure above 90 mm Hg.
Initial Emergency Department Stabilization
Management focuses on airway, breathing, and circulation. Rapid sequence intubation is indicated for Glasgow Coma Scale score below 8, inability to protect the airway, hypoxia, or signs of cerebral herniation. Induction agents may include etomidate or fentanyl with caution in hemodynamically unstable patients, followed by neuromuscular blockade. Carbon dioxide levels should be normalized, avoiding both hyperventilation and hypoventilation. Adequate intravenous access and fluid resuscitation are required, and associated traumatic injuries must be addressed. Cervical spine precautions continue throughout resuscitation.
Emergency Department Management
Immediate neurosurgical consultation is mandatory. In patients with signs of cerebral herniation, intracranial pressure reduction measures include mild hyperventilation targeting end-tidal CO₂ of 30–35 mm Hg, head elevation to 20–30 degrees, and cautious use of mannitol only if systolic blood pressure exceeds 100 mm Hg and volume status is adequate. Phenytoin is administered to prevent early post-traumatic seizures. Coagulopathies must be rapidly reversed. Glucocorticoids and barbiturates are not recommended for intracranial pressure control in penetrating head injury.
Blood transfusion may be required to maintain hematocrit above 30 percent. Hypothermia should be avoided due to increased risk of coagulopathy. Patients remain NPO. Definitive surgical management is based on clinical findings, imaging, and neurosurgical judgment. In rare cases without immediate neurosurgical access, a life-saving burr hole may be considered in comatose patients with known mass lesions and refractory herniation signs.
Medications Commonly Used
Medications include etomidate for induction, fentanyl for analgesia when hemodynamically stable, mannitol for intracranial pressure reduction, morphine for pain control, phenytoin for seizure prophylaxis, neuromuscular blockers such as succinylcholine, rocuronium, or vecuronium, vitamin K for warfarin reversal, and protamine sulfate for low–molecular-weight heparin–associated bleeding.
Disposition And Follow-Up
All patients with penetrating head trauma require ICU admission or immediate operative intervention. Discharge from the emergency department is not appropriate.
Key Clinical Lessons And Errors To Avoid
Common errors include failure to identify anticoagulant use, delayed or inadequate imaging, and insufficient reversal of hypocoagulable states. Prompt recognition and aggressive management are essential to reduce morbidity and mortality.
Definition And Injury Characteristics
Penetrating head trauma involves direct violation of the skull with injury to intracranial contents. High-velocity injuries are most commonly caused by bullets and produce direct tissue destruction along with secondary cavitation or shock-wave injury to surrounding brain tissue. Low-velocity injuries are typically due to knives, picks, or other sharp objects and cause localized, direct damage to brain structures along the tract of penetration.
Mechanisms Of Injury
Penetration of the skull by a foreign object leads to direct brain tissue injury and is frequently complicated by intracranial hemorrhage, including epidural, subdural, and intraparenchymal bleeding. Even when a projectile strikes the skull and ricochets without fracturing bone, significant underlying brain injury may still occur due to transmitted force.
Clinical Presentation
The degree of altered consciousness and neurologic deficit varies widely depending on the object involved, its velocity, and the anatomic location of injury. Signs of rising intracranial pressure include declining level of consciousness, decreasing Glasgow Coma Scale score, Cushing response with bradycardia, hypertension, and abnormal respirations, as well as a dilated or “blown” pupil accompanied by decorticate or decerebrate posturing.
External indicators of penetrating injury or basilar skull fracture may include raccoon eyes, Battle sign over the mastoid, hemotympanum, and cerebrospinal fluid rhinorrhea or otorrhea. Retained foreign objects may still be present at the injury site.
History Assessment
Key historical elements include identification of the weapon or object involved, weapon caliber when applicable, loss of consciousness or amnesia, anticoagulant use, headache, visual or auditory disturbances, and focal neurologic complaints.
Physical Examination
Examination should focus on identifying entry and exit wounds, evaluating for multiple projectile sites, and performing a complete neurologic assessment. Mental status and focal findings correlate closely with injury location and severity.
Essential Evaluation
A thorough history and physical examination are required to assess the extent of injury, followed by urgent imaging to define intracranial damage and guide management.
Diagnostic Testing
Laboratory studies include complete blood count, platelet count, coagulation profile, type and crossmatch, and baseline electrolytes, blood urea nitrogen, and creatinine.
Imaging is centered on noncontrast CT of the head to identify hemorrhage, foreign bodies, bone fragments, and injury trajectory. Skull radiographs may assist in determining depth of penetration and retained fragments. Cervical spine imaging with helical CT or standard radiographs is required when indicated.
Alternative Diagnoses
Conditions to consider include blunt head trauma, isolated basilar skull fracture, or medical causes of altered mental status that may have resulted in secondary penetrating injury after a fall.
Prehospital Management Principles
Stabilization is prioritized while avoiding removal of any retained foreign object. Airway protection is essential to prevent hypoxemia, while routine hyperventilation should be avoided. Cervical spine precautions must be maintained. Patients should be transported to a trauma center. Hypoxia is prevented with supplemental oxygen, and hypotension is avoided using intravenous crystalloid fluids to maintain systolic blood pressure above 90 mm Hg.
Initial Emergency Department Stabilization
Management focuses on airway, breathing, and circulation. Rapid sequence intubation is indicated for Glasgow Coma Scale score below 8, inability to protect the airway, hypoxia, or signs of cerebral herniation. Induction agents may include etomidate or fentanyl with caution in hemodynamically unstable patients, followed by neuromuscular blockade. Carbon dioxide levels should be normalized, avoiding both hyperventilation and hypoventilation. Adequate intravenous access and fluid resuscitation are required, and associated traumatic injuries must be addressed. Cervical spine precautions continue throughout resuscitation.
Emergency Department Management
Immediate neurosurgical consultation is mandatory. In patients with signs of cerebral herniation, intracranial pressure reduction measures include mild hyperventilation targeting end-tidal CO₂ of 30–35 mm Hg, head elevation to 20–30 degrees, and cautious use of mannitol only if systolic blood pressure exceeds 100 mm Hg and volume status is adequate. Phenytoin is administered to prevent early post-traumatic seizures. Coagulopathies must be rapidly reversed. Glucocorticoids and barbiturates are not recommended for intracranial pressure control in penetrating head injury.
Blood transfusion may be required to maintain hematocrit above 30 percent. Hypothermia should be avoided due to increased risk of coagulopathy. Patients remain NPO. Definitive surgical management is based on clinical findings, imaging, and neurosurgical judgment. In rare cases without immediate neurosurgical access, a life-saving burr hole may be considered in comatose patients with known mass lesions and refractory herniation signs.
Medications Commonly Used
Medications include etomidate for induction, fentanyl for analgesia when hemodynamically stable, mannitol for intracranial pressure reduction, morphine for pain control, phenytoin for seizure prophylaxis, neuromuscular blockers such as succinylcholine, rocuronium, or vecuronium, vitamin K for warfarin reversal, and protamine sulfate for low–molecular-weight heparin–associated bleeding.
Disposition And Follow-Up
All patients with penetrating head trauma require ICU admission or immediate operative intervention. Discharge from the emergency department is not appropriate.
Key Clinical Lessons And Errors To Avoid
Common errors include failure to identify anticoagulant use, delayed or inadequate imaging, and insufficient reversal of hypocoagulable states. Prompt recognition and aggressive management are essential to reduce morbidity and mortality.
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Emergency And Acute Medicine – Hallucinogen Poisoning
Core Concept
Hallucinogen poisoning refers to toxic exposure to substances that predominantly alter perception, cognition, and mood. These agents act by potentiating neurotransmitter release or binding directly to central nervous system receptors. The serotonergic system (5-hydroxytryptamine, 5-HT) is most commonly involved, with many hallucinogens acting as agonists or antagonists at 5-HT receptor subtypes. Additional pathways affected include norepinephrine, N-methyl-D-aspartate (NMDA), and dopamine systems.
Cause And Exposure Patterns
Most hallucinogen exposures are intentional. Common agents include indoleamines such as lysergic acid diethylamide (LSD), with effects lasting 6–12 hours, and morning glory (Ipomoea species). Tryptamines include psilocybin from Psilocybe mushrooms, which are frequently adulterated with LSD, as well as N,N-dimethyltryptamine (DMT), 5-MeO-DMT (“foxy-methoxy”), and related compounds. Phenylethylamines (hallucinogenic amphetamines) include methylenedioxyamphetamine (MDA), methylenedioxymethamphetamine (MDMA, “ecstasy,” duration 8–12 hours), methylenedioxyethylamphetamine (MDEA), paramethoxyamphetamine, dimethoxyamphetamine, and mescaline from the peyote cactus, which is often adulterated with LSD and lasts 6–12 hours. Arylcycloalkylamines include phencyclidine (PCP), with highly variable duration reported from 11–96 hours, and ketamine, with effects lasting 30–120 minutes depending on route. Anticholinergic plant sources include deadly nightshade (Atropa belladonna) and jimsonweed (Datura stramonium). Other agents include piperazines such as benzylpiperazine (BZP) and trifluoromethylphenylpiperazine (TFMPP), dextromethorphan (DXM) with duration 3–6 hours, and marijuana.
Clinical Findings And Presentation
Clinical effects vary considerably by agent, dose, and individual susceptibility. Symptoms may last 4–12 hours and up to 96 hours in some cases. Hallucinogen intoxication is typically characterized by sympathetic arousal. Patients are often oriented and able to provide a history of exposure even while experiencing delusions. Early symptoms include nausea, flushing, chills, and tremor. Neurologic effects often begin with restlessness and dizziness, and a desire to laugh is common with Psilocybe mushroom ingestion. Psychiatric manifestations include anxiety, despair, helplessness, and dread. Perceptual disturbances include visual distortion or intensification, tactile distortions (especially with mescaline), and synesthesia such as “seeing sounds.” Religious or mystical experiences and sleep disruption may occur.
Neurologic signs include bizarre behavior, speech disruption, mydriasis, piloerection, and hyperreflexia. Massive exposures may result in coma. Convulsions are most often associated with hallucinogenic amphetamines, and children may develop hyperpyrexia after Psilocybe ingestion. Pulmonary findings include mild tachypnea, with respiratory arrest possible in severe intoxication. Cardiovascular effects include tachycardia, hypertension, dysrhythmias, and intracerebral hemorrhage, particularly with hallucinogenic amphetamines. Gastrointestinal symptoms include nausea and vomiting, especially with mescaline. Metabolic complications include hyperpyrexia, particularly with MDMA use in crowded environments such as rave clubs, which may progress to hepatic failure, renal failure, and disseminated intravascular coagulation and can be fatal. Hyponatremia has been reported with MDMA. High doses may disrupt platelet serotonin function, leading to coagulopathies and hemorrhage.
History And Physical Examination
History should focus on identifying the substance or substances used, route of exposure, quantity, time of ingestion, and setting of exposure. Physical examination requires accurate vital signs, with particular attention to body temperature, and a detailed neurologic and psychiatric assessment.
Key Emergency Workup
Initial evaluation should include continuous monitoring of vital signs and core temperature measurement. Cardiac monitoring is recommended. Assess for rhabdomyolysis by measuring creatine kinase and evaluating urine for myoglobin.
Laboratory And Imaging Evaluation
Laboratory testing may include electrolytes, blood urea nitrogen, creatinine, glucose, coagulation studies, and arterial or venous blood gas analysis as clinically indicated. Urine toxicology screening is rarely helpful because most hallucinogens are not detected on routine screens, amphetamine assays may be negative for hallucinogenic amphetamines such as MDMA, and distinguishing specific agents rarely changes management. Imaging should be guided by clinical suspicion and may include chest radiography for suspected aspiration, aortic pathology, or trauma, head CT for intracranial hemorrhage or lesions, and abdominal radiography if ingested drug packets are suspected.
Differential Considerations
The differential diagnosis includes hypoglycemia, meningitis, encephalitis, sepsis, intracranial hemorrhage or mass lesions, withdrawal syndromes (ethanol, sedative–hypnotics, baclofen), serotonin syndrome (particularly with co-ingestion of serotonergic agents), primary psychiatric illness including prolonged psychosis associated with LSD, chronic amphetamine or cocaine use, steroid-induced psychosis, and infectious or febrile seizures in hyperpyrexic children.
Prehospital Management
Management controversies include the choice between benzodiazepines, neuroleptics, or physical restraints for agitation. Benzodiazepines are generally preferred. Sedation may obscure symptoms and limit history but is often necessary for safe transport. Hyperthermic patients should be sedated rather than physically restrained, and cooling measures should be initiated early.
Initial Stabilization Approach
Management begins with airway, breathing, and circulation assessment. Aggressive cooling is required for hyperthermia. Establish IV access and provide isotonic fluids for dehydration or suspected rhabdomyolysis. In patients with altered mental status, check blood glucose and consider naloxone, dextrose, and thiamine as indicated.
Emergency Department Treatment
Supportive care is the mainstay. Cooling measures include cool mist and fans. Benzodiazepines are first-line therapy for agitation, anxiety, or autonomic instability. Paralysis with intubation may be required in severe cases, generally avoiding succinylcholine. Neuroleptics are rarely used because they may intensify hallucinogenic effects and lower the seizure threshold. Activated charcoal is generally not helpful due to rapid absorption and delayed presentation, but may be considered within 2–3 hours of ingestion in patients with a protected airway, especially for anticholinergic agents or ingested seeds. Patients should be placed in a quiet, calm environment. Maintain urine output at 2–3 mL/kg/hr and consider urine alkalinization when treating rhabdomyolysis.
Medication Options
Benzodiazepines such as diazepam 5–10 mg IV (pediatric dose 0.2–0.5 mg/kg) or lorazepam 1–4 mg IV/IM (pediatric dose 0.02–0.05 mg/kg) may be repeated as needed. Dextrose should be administered for hypoglycemia. Haloperidol 2.5–5 mg IV/IM may be used cautiously in adults for refractory agitation, but is generally avoided in children. Naloxone may be administered when opioid co-ingestion is suspected. Sodium bicarbonate infusion may be used for rhabdomyolysis to maintain urine alkalinity. Thiamine 100 mg IV or IM is recommended in at-risk patients.
Disposition And Follow-Up
Admission is indicated for severe intoxication, atypical or prolonged presentations, symptoms persisting longer than 12 hours, or prolonged agitation and hyperthermia with risk of rhabdomyolysis or organ damage. Most patients may be discharged after observation once asymptomatic and clinically stable. Suspected pediatric abuse or neglect requires referral to child protective services. Discharged patients should be advised to follow up with a primary care provider, psychiatrist, or substance use counseling service.
Clinical Pearls And Pitfalls
Hyperthermia must be recognized and treated immediately with aggressive temperature reduction. Violent or agitated patients require appropriate physical and chemical restraints to ensure safety. Serial examinations and vital sign monitoring, especially temperature, are essential. Do not assume clinical improvement once agitation subsides, as deterioration to severe toxicity may still occur.
Core Concept
Hallucinogen poisoning refers to toxic exposure to substances that predominantly alter perception, cognition, and mood. These agents act by potentiating neurotransmitter release or binding directly to central nervous system receptors. The serotonergic system (5-hydroxytryptamine, 5-HT) is most commonly involved, with many hallucinogens acting as agonists or antagonists at 5-HT receptor subtypes. Additional pathways affected include norepinephrine, N-methyl-D-aspartate (NMDA), and dopamine systems.
Cause And Exposure Patterns
Most hallucinogen exposures are intentional. Common agents include indoleamines such as lysergic acid diethylamide (LSD), with effects lasting 6–12 hours, and morning glory (Ipomoea species). Tryptamines include psilocybin from Psilocybe mushrooms, which are frequently adulterated with LSD, as well as N,N-dimethyltryptamine (DMT), 5-MeO-DMT (“foxy-methoxy”), and related compounds. Phenylethylamines (hallucinogenic amphetamines) include methylenedioxyamphetamine (MDA), methylenedioxymethamphetamine (MDMA, “ecstasy,” duration 8–12 hours), methylenedioxyethylamphetamine (MDEA), paramethoxyamphetamine, dimethoxyamphetamine, and mescaline from the peyote cactus, which is often adulterated with LSD and lasts 6–12 hours. Arylcycloalkylamines include phencyclidine (PCP), with highly variable duration reported from 11–96 hours, and ketamine, with effects lasting 30–120 minutes depending on route. Anticholinergic plant sources include deadly nightshade (Atropa belladonna) and jimsonweed (Datura stramonium). Other agents include piperazines such as benzylpiperazine (BZP) and trifluoromethylphenylpiperazine (TFMPP), dextromethorphan (DXM) with duration 3–6 hours, and marijuana.
Clinical Findings And Presentation
Clinical effects vary considerably by agent, dose, and individual susceptibility. Symptoms may last 4–12 hours and up to 96 hours in some cases. Hallucinogen intoxication is typically characterized by sympathetic arousal. Patients are often oriented and able to provide a history of exposure even while experiencing delusions. Early symptoms include nausea, flushing, chills, and tremor. Neurologic effects often begin with restlessness and dizziness, and a desire to laugh is common with Psilocybe mushroom ingestion. Psychiatric manifestations include anxiety, despair, helplessness, and dread. Perceptual disturbances include visual distortion or intensification, tactile distortions (especially with mescaline), and synesthesia such as “seeing sounds.” Religious or mystical experiences and sleep disruption may occur.
Neurologic signs include bizarre behavior, speech disruption, mydriasis, piloerection, and hyperreflexia. Massive exposures may result in coma. Convulsions are most often associated with hallucinogenic amphetamines, and children may develop hyperpyrexia after Psilocybe ingestion. Pulmonary findings include mild tachypnea, with respiratory arrest possible in severe intoxication. Cardiovascular effects include tachycardia, hypertension, dysrhythmias, and intracerebral hemorrhage, particularly with hallucinogenic amphetamines. Gastrointestinal symptoms include nausea and vomiting, especially with mescaline. Metabolic complications include hyperpyrexia, particularly with MDMA use in crowded environments such as rave clubs, which may progress to hepatic failure, renal failure, and disseminated intravascular coagulation and can be fatal. Hyponatremia has been reported with MDMA. High doses may disrupt platelet serotonin function, leading to coagulopathies and hemorrhage.
History And Physical Examination
History should focus on identifying the substance or substances used, route of exposure, quantity, time of ingestion, and setting of exposure. Physical examination requires accurate vital signs, with particular attention to body temperature, and a detailed neurologic and psychiatric assessment.
Key Emergency Workup
Initial evaluation should include continuous monitoring of vital signs and core temperature measurement. Cardiac monitoring is recommended. Assess for rhabdomyolysis by measuring creatine kinase and evaluating urine for myoglobin.
Laboratory And Imaging Evaluation
Laboratory testing may include electrolytes, blood urea nitrogen, creatinine, glucose, coagulation studies, and arterial or venous blood gas analysis as clinically indicated. Urine toxicology screening is rarely helpful because most hallucinogens are not detected on routine screens, amphetamine assays may be negative for hallucinogenic amphetamines such as MDMA, and distinguishing specific agents rarely changes management. Imaging should be guided by clinical suspicion and may include chest radiography for suspected aspiration, aortic pathology, or trauma, head CT for intracranial hemorrhage or lesions, and abdominal radiography if ingested drug packets are suspected.
Differential Considerations
The differential diagnosis includes hypoglycemia, meningitis, encephalitis, sepsis, intracranial hemorrhage or mass lesions, withdrawal syndromes (ethanol, sedative–hypnotics, baclofen), serotonin syndrome (particularly with co-ingestion of serotonergic agents), primary psychiatric illness including prolonged psychosis associated with LSD, chronic amphetamine or cocaine use, steroid-induced psychosis, and infectious or febrile seizures in hyperpyrexic children.
Prehospital Management
Management controversies include the choice between benzodiazepines, neuroleptics, or physical restraints for agitation. Benzodiazepines are generally preferred. Sedation may obscure symptoms and limit history but is often necessary for safe transport. Hyperthermic patients should be sedated rather than physically restrained, and cooling measures should be initiated early.
Initial Stabilization Approach
Management begins with airway, breathing, and circulation assessment. Aggressive cooling is required for hyperthermia. Establish IV access and provide isotonic fluids for dehydration or suspected rhabdomyolysis. In patients with altered mental status, check blood glucose and consider naloxone, dextrose, and thiamine as indicated.
Emergency Department Treatment
Supportive care is the mainstay. Cooling measures include cool mist and fans. Benzodiazepines are first-line therapy for agitation, anxiety, or autonomic instability. Paralysis with intubation may be required in severe cases, generally avoiding succinylcholine. Neuroleptics are rarely used because they may intensify hallucinogenic effects and lower the seizure threshold. Activated charcoal is generally not helpful due to rapid absorption and delayed presentation, but may be considered within 2–3 hours of ingestion in patients with a protected airway, especially for anticholinergic agents or ingested seeds. Patients should be placed in a quiet, calm environment. Maintain urine output at 2–3 mL/kg/hr and consider urine alkalinization when treating rhabdomyolysis.
Medication Options
Benzodiazepines such as diazepam 5–10 mg IV (pediatric dose 0.2–0.5 mg/kg) or lorazepam 1–4 mg IV/IM (pediatric dose 0.02–0.05 mg/kg) may be repeated as needed. Dextrose should be administered for hypoglycemia. Haloperidol 2.5–5 mg IV/IM may be used cautiously in adults for refractory agitation, but is generally avoided in children. Naloxone may be administered when opioid co-ingestion is suspected. Sodium bicarbonate infusion may be used for rhabdomyolysis to maintain urine alkalinity. Thiamine 100 mg IV or IM is recommended in at-risk patients.
Disposition And Follow-Up
Admission is indicated for severe intoxication, atypical or prolonged presentations, symptoms persisting longer than 12 hours, or prolonged agitation and hyperthermia with risk of rhabdomyolysis or organ damage. Most patients may be discharged after observation once asymptomatic and clinically stable. Suspected pediatric abuse or neglect requires referral to child protective services. Discharged patients should be advised to follow up with a primary care provider, psychiatrist, or substance use counseling service.
Clinical Pearls And Pitfalls
Hyperthermia must be recognized and treated immediately with aggressive temperature reduction. Violent or agitated patients require appropriate physical and chemical restraints to ensure safety. Serial examinations and vital sign monitoring, especially temperature, are essential. Do not assume clinical improvement once agitation subsides, as deterioration to severe toxicity may still occur.
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Emergency And Acute Medicine - Gout/Pseudogout
Basics Description
Gout is a crystalline arthropathy caused by deposition of monosodium urate in tissues, most commonly affecting middle-aged men and postmenopausal women. It is the most common crystal-induced arthritis and classically progresses through four phases: asymptomatic hyperuricemia (serum urate >7 mg/dL), acute gout, intercritical gout with symptom-free intervals, and chronic tophaceous gout, which occurs in up to 45% of cases.
Risk factors include age >40 years, male sex (male-to-female ratio 2:1–6:1 before age 65, approaching 1:1 thereafter), hypertension, use of loop or thiazide diuretics, high intake of alcohol, meat, seafood, and fructose-sweetened beverages, and obesity. Uric acid nephrolithiasis may lead to renal dysfunction. Chronic disease can result in avascular necrosis and deforming arthritis.
Gout preferentially involves previously damaged tissues such as synovium, subchondral bone, bursae (olecranon, infrapatellar, prepatellar), Achilles tendon, and extensor surfaces of the forearms, toes, fingers, and ear. Rare involvement of the CNS or cardiac valves has been described.
Pseudogout is caused by calcium pyrophosphate crystal deposition and is the most common cause of acute monoarthritis in patients older than 60 years. Risk factors include hypercalcemia, hemochromatosis, hypothyroidism or hyperthyroidism, hypophosphatemia, hypomagnesemia, amyloidosis, and underlying gout.
Etiology
Gout results from deposition of monosodium urate crystals due to underexcretion (most common) or overproduction of uric acid. Acute attacks are often triggered by rapid changes in uric acid levels such as initiation or withdrawal of diuretics, alcohol intake, salicylates, niacin, cyclosporine, lead exposure, or starting uricosurics or allopurinol.
Pseudogout occurs due to excess accumulation of calcium pyrophosphate crystals within the synovium. Minor trauma and acute systemic illness, including surgery or ischemic heart disease, may precipitate attacks of either condition.
Diagnosis Signs And Symptoms
Both gout and pseudogout typically present as acute monoarticular or polyarticular arthritis with warmth, erythema, swelling, and pain. Early attacks often resolve spontaneously within 3–21 days, while later attacks may be longer, more severe, clustered, and polyarticular.
Gout symptoms usually peak within 12–24 hours. Tophi and skin desquamation may be present in advanced disease. Women often present after menopause and more commonly have polyarticular involvement. Presentations may be less dramatic in elderly or immunosuppressed patients. The first metatarsophalangeal joint is most commonly affected, followed by the ankle, knee, hand, and wrist.
Pseudogout more often involves large joints, particularly the knee, followed by the wrist, metacarpals, shoulder, elbow, ankle, hip, and tarsal joints. It may be monoarticular, asymptomatic, mimic osteoarthritis with symmetric degeneration, or present as a pseudorheumatoid arthritis variant with fever and confusion in elderly patients.
Essential Workup
Arthrocentesis with synovial fluid analysis is essential to confirm diagnosis and exclude infection. Aspirate should be examined for crystals, Gram stain, culture, leukocyte count, and differential. Gout fluid typically contains 20,000–100,000 WBC/mm³ without bacteria. Pseudogout fluid usually has fewer than 50,000 WBC/mm³.
Polarized light microscopy shows needle-shaped, strongly negatively birefringent crystals in gout and rhomboid-shaped, weakly positively birefringent crystals in pseudogout.
Diagnosis Tests And Interpretation
CBC often reveals leukocytosis. Chemistry panels assess renal function. Magnesium, calcium, TSH, and iron studies may identify associated conditions. Serum uric acid has limited diagnostic value during acute attacks. Blood and urine cultures are indicated if infection is suspected.
Plain radiographs may show soft tissue swelling in acute gout, while chronic gout demonstrates calcified tophi and characteristic erosions. Pseudogout may show chondrocalcinosis and calcification of cartilage or ligaments. Dual-energy CT can identify urate deposits or nephrolithiasis.
Differential Diagnosis
Septic arthritis, trauma, osteoarthritis, reactive arthritis, rheumatoid arthritis, systemic lupus erythematosus, avascular necrosis, osteomyelitis, sickle cell disease, and other crystal arthropathies.
Treatment Initial Stabilization Therapy
Primary goals are pain control and exclusion of infectious arthritis.
Ed Treatment Procedures
NSAIDs are first-line therapy if tolerated. If contraindicated or ineffective, corticosteroids (oral, IM, IV, or intra-articular) or colchicine may be used. Joint aspiration can provide symptomatic relief. Aspirin should be avoided.
Long-term urate-lowering therapy and prevention strategies are generally not initiated in the ED and include withdrawal of precipitating agents, uricosurics, allopurinol, hydration, urine alkalinization, and prophylactic colchicine or NSAIDs.
Medication
Therapeutic options include NSAIDs, colchicine, corticosteroids, allopurinol, febuxostat, probenecid, and biologic agents for refractory disease. Dosing should be adjusted for renal or hepatic impairment and patient age.
Follow-Up Disposition
Admission is indicated for suspected septic arthritis, acute renal failure, or intractable pain.
Patients without evidence of infection and with adequate pain control may be discharged.
Issues For Referral
Referral is indicated for septic arthritis, renal failure, or refractory disease.
Follow-Up Recommendations
Rheumatology follow-up is recommended for severe or difficult-to-control cases. Nephrology or urology referral is indicated for renal insufficiency or uric acid nephrolithiasis. Orthopedic follow-up is required for septic arthritis or significant joint damage. Patients should be counseled on a low-purine diet.
Key Clinical Insights And Frequent Errors
Septic arthritis may coexist with acute gout and must always be excluded. NSAIDs remain first-line therapy when tolerated. Acute attacks are often self-limited, but recurrent gout and pseudogout can result in progressive bony and cartilaginous damage if not appropriately managed.
Basics Description
Gout is a crystalline arthropathy caused by deposition of monosodium urate in tissues, most commonly affecting middle-aged men and postmenopausal women. It is the most common crystal-induced arthritis and classically progresses through four phases: asymptomatic hyperuricemia (serum urate >7 mg/dL), acute gout, intercritical gout with symptom-free intervals, and chronic tophaceous gout, which occurs in up to 45% of cases.
Risk factors include age >40 years, male sex (male-to-female ratio 2:1–6:1 before age 65, approaching 1:1 thereafter), hypertension, use of loop or thiazide diuretics, high intake of alcohol, meat, seafood, and fructose-sweetened beverages, and obesity. Uric acid nephrolithiasis may lead to renal dysfunction. Chronic disease can result in avascular necrosis and deforming arthritis.
Gout preferentially involves previously damaged tissues such as synovium, subchondral bone, bursae (olecranon, infrapatellar, prepatellar), Achilles tendon, and extensor surfaces of the forearms, toes, fingers, and ear. Rare involvement of the CNS or cardiac valves has been described.
Pseudogout is caused by calcium pyrophosphate crystal deposition and is the most common cause of acute monoarthritis in patients older than 60 years. Risk factors include hypercalcemia, hemochromatosis, hypothyroidism or hyperthyroidism, hypophosphatemia, hypomagnesemia, amyloidosis, and underlying gout.
Etiology
Gout results from deposition of monosodium urate crystals due to underexcretion (most common) or overproduction of uric acid. Acute attacks are often triggered by rapid changes in uric acid levels such as initiation or withdrawal of diuretics, alcohol intake, salicylates, niacin, cyclosporine, lead exposure, or starting uricosurics or allopurinol.
Pseudogout occurs due to excess accumulation of calcium pyrophosphate crystals within the synovium. Minor trauma and acute systemic illness, including surgery or ischemic heart disease, may precipitate attacks of either condition.
Diagnosis Signs And Symptoms
Both gout and pseudogout typically present as acute monoarticular or polyarticular arthritis with warmth, erythema, swelling, and pain. Early attacks often resolve spontaneously within 3–21 days, while later attacks may be longer, more severe, clustered, and polyarticular.
Gout symptoms usually peak within 12–24 hours. Tophi and skin desquamation may be present in advanced disease. Women often present after menopause and more commonly have polyarticular involvement. Presentations may be less dramatic in elderly or immunosuppressed patients. The first metatarsophalangeal joint is most commonly affected, followed by the ankle, knee, hand, and wrist.
Pseudogout more often involves large joints, particularly the knee, followed by the wrist, metacarpals, shoulder, elbow, ankle, hip, and tarsal joints. It may be monoarticular, asymptomatic, mimic osteoarthritis with symmetric degeneration, or present as a pseudorheumatoid arthritis variant with fever and confusion in elderly patients.
Essential Workup
Arthrocentesis with synovial fluid analysis is essential to confirm diagnosis and exclude infection. Aspirate should be examined for crystals, Gram stain, culture, leukocyte count, and differential. Gout fluid typically contains 20,000–100,000 WBC/mm³ without bacteria. Pseudogout fluid usually has fewer than 50,000 WBC/mm³.
Polarized light microscopy shows needle-shaped, strongly negatively birefringent crystals in gout and rhomboid-shaped, weakly positively birefringent crystals in pseudogout.
Diagnosis Tests And Interpretation
CBC often reveals leukocytosis. Chemistry panels assess renal function. Magnesium, calcium, TSH, and iron studies may identify associated conditions. Serum uric acid has limited diagnostic value during acute attacks. Blood and urine cultures are indicated if infection is suspected.
Plain radiographs may show soft tissue swelling in acute gout, while chronic gout demonstrates calcified tophi and characteristic erosions. Pseudogout may show chondrocalcinosis and calcification of cartilage or ligaments. Dual-energy CT can identify urate deposits or nephrolithiasis.
Differential Diagnosis
Septic arthritis, trauma, osteoarthritis, reactive arthritis, rheumatoid arthritis, systemic lupus erythematosus, avascular necrosis, osteomyelitis, sickle cell disease, and other crystal arthropathies.
Treatment Initial Stabilization Therapy
Primary goals are pain control and exclusion of infectious arthritis.
Ed Treatment Procedures
NSAIDs are first-line therapy if tolerated. If contraindicated or ineffective, corticosteroids (oral, IM, IV, or intra-articular) or colchicine may be used. Joint aspiration can provide symptomatic relief. Aspirin should be avoided.
Long-term urate-lowering therapy and prevention strategies are generally not initiated in the ED and include withdrawal of precipitating agents, uricosurics, allopurinol, hydration, urine alkalinization, and prophylactic colchicine or NSAIDs.
Medication
Therapeutic options include NSAIDs, colchicine, corticosteroids, allopurinol, febuxostat, probenecid, and biologic agents for refractory disease. Dosing should be adjusted for renal or hepatic impairment and patient age.
Follow-Up Disposition
Admission is indicated for suspected septic arthritis, acute renal failure, or intractable pain.
Patients without evidence of infection and with adequate pain control may be discharged.
Issues For Referral
Referral is indicated for septic arthritis, renal failure, or refractory disease.
Follow-Up Recommendations
Rheumatology follow-up is recommended for severe or difficult-to-control cases. Nephrology or urology referral is indicated for renal insufficiency or uric acid nephrolithiasis. Orthopedic follow-up is required for septic arthritis or significant joint damage. Patients should be counseled on a low-purine diet.
Key Clinical Insights And Frequent Errors
Septic arthritis may coexist with acute gout and must always be excluded. NSAIDs remain first-line therapy when tolerated. Acute attacks are often self-limited, but recurrent gout and pseudogout can result in progressive bony and cartilaginous damage if not appropriately managed.
- Published on
Emergency And Acute Medicine - Gonococcal Disease
Basics Description
Gonococcal disease is the second most frequently reported sexually transmitted infection in the United States, with an estimated 820,000 new cases annually and fewer than half reported. The highest incidence occurs in males and females aged 15–24 years, particularly among African Americans. Rates are increasing among men who have sex with men, especially those who are HIV-positive. Humans are the only known host. Coinfection with Chlamydia trachomatis is common. Infection may involve the urethra, rectum, cervical canal, pharynx, upper female genital tract, and conjunctiva. Urethritis is the most common presentation in men, while infection is often asymptomatic in women.
Etiology
The causative organism is Neisseria gonorrhoeae, a gram-negative aerobic diplococcus.
Diagnosis Signs And Symptoms
Cervicitis is defined by mucopurulent endocervical discharge or easily induced endocervical bleeding and is the most common site of infection. Up to 80% of women are asymptomatic, with nonspecific symptoms such as vaginal discharge, menorrhagia, pelvic pain, dyspareunia, urinary frequency, and dysuria.
Pelvic inflammatory disease develops in up to 20% of untreated cases, most commonly presenting with lower abdominal pain. Other symptoms include dyspareunia, abnormal bleeding or discharge, fever, and onset around menses. Fitz-Hugh–Curtis syndrome occurs in about 10% and presents with right upper quadrant pain. Bartholin abscess may also occur.
Urethritis typically has a 2–5 day incubation period and presents with penile discharge and dysuria; untreated cases may progress to prostatitis or epididymitis, which presents with acute unilateral testicular pain and swelling.
Proctitis is often asymptomatic and may be the only site of infection in many men who have sex with men. Rectal infection occurs in 35–50% of women with endocervical infection and significantly increases HIV acquisition risk. Symptoms include perianal pruritus, mucopurulent discharge, rectal bleeding, pain, tenesmus, and constipation.
Pharyngitis may present with sore throat or exudative tonsillitis.
Disseminated gonococcal infection occurs in 0.5–3% of untreated mucosal infections and presents with the triad of tenosynovitis, dermatitis, and polyarthralgia, often accompanied by fever, chills, and malaise. Dermatitis consists of tender necrotic pustules on an erythematous base. Septic arthritis typically affects the knee. Females are affected more commonly than males, with recent menstruation or pregnancy as risk factors. Rare complications include hepatitis, myocarditis, endocarditis, and meningitis.
Physical examination may reveal cervical friability and edema, uterine or adnexal tenderness in PID, and thick yellow-white urethral discharge with meatal erythema in urethritis.
Essential Workup
In symptomatic men, diagnosis is often clinical with Gram stain, which has high sensitivity. In women, cervical culture is recommended. Testing for chlamydia and syphilis should always be performed.
Diagnosis Tests And Interpretation
Cultures on Thayer-Martin medium remain the gold standard, particularly for blood and synovial fluid. Gram stain demonstrating intracellular gram-negative diplococci is highly sensitive in symptomatic men. Nucleic acid amplification tests using PCR are widely used for urethral, cervical, and urine specimens and frequently test for chlamydia concurrently. Pharyngeal and rectal cultures are indicated in symptomatic or high-risk patients.
In disseminated infection, synovial fluid typically shows neutrophilic leukocytosis, and multiple blood cultures should be obtained. Women with PID require CBC, urinalysis, pregnancy testing, and consideration of pelvic ultrasound to evaluate for tubo-ovarian abscess. Rapid plasma reagin testing is indicated to assess for syphilis.
Differential Diagnosis
Urethritis due to chlamydia, trichomonas, urinary tract infection, or syphilis; septic arthritis from other organisms; connective tissue diseases; poststreptococcal arthritis; viral infections; gout; HIV; secondary syphilis; and Lyme disease.
Treatment Ed Treatment Procedures
Provide IV fluids for dehydration or vomiting. Sexual partners should be treated, including expedited partner therapy where legally permitted. Patients are often treated empirically for chlamydial infection.
Uncomplicated cervical, urethral, or anorectal infection is treated with ceftriaxone 250 mg IM once plus azithromycin 1 g PO once or doxycycline 100 mg PO BID for 7 days.
Pelvic inflammatory disease may be treated as an outpatient with ceftriaxone or another third-generation cephalosporin plus doxycycline with or without metronidazole, or as an inpatient with IV cephalosporin-based or clindamycin-gentamicin regimens.
Pharyngitis is treated with ceftriaxone plus chlamydia coverage.
Epididymitis requires ceftriaxone plus doxycycline for 10 days.
Disseminated gonococcal infection is treated with ceftriaxone 1 g IV or IM daily, followed by oral therapy after clinical improvement.
Neonatal infections, conjunctivitis, meningitis, and endocarditis require weight-based or prolonged IV cephalosporin therapy. Severe cephalosporin allergy warrants infectious disease consultation.
Follow-Up Disposition
Admission is indicated for severe PID, pregnancy, inability to tolerate oral therapy, lack of response to outpatient treatment, tubo-ovarian abscess, or diagnostic uncertainty requiring surgical evaluation.
Patients with uncomplicated genital, pharyngeal, or conjunctival infection may be discharged after treatment.
Issues For Referral
Referral is indicated for infertility evaluation or recurrent infection despite appropriate therapy.
Key Clinical Insights And Common Errors
Always exclude testicular torsion in patients presenting with epididymitis. Disseminated gonococcal infection should be strongly considered in young, sexually active patients with acute, nontraumatic oligoarthritis or tenosynovitis, as delayed recognition can lead to significant morbidity.
Basics Description
Gonococcal disease is the second most frequently reported sexually transmitted infection in the United States, with an estimated 820,000 new cases annually and fewer than half reported. The highest incidence occurs in males and females aged 15–24 years, particularly among African Americans. Rates are increasing among men who have sex with men, especially those who are HIV-positive. Humans are the only known host. Coinfection with Chlamydia trachomatis is common. Infection may involve the urethra, rectum, cervical canal, pharynx, upper female genital tract, and conjunctiva. Urethritis is the most common presentation in men, while infection is often asymptomatic in women.
Etiology
The causative organism is Neisseria gonorrhoeae, a gram-negative aerobic diplococcus.
Diagnosis Signs And Symptoms
Cervicitis is defined by mucopurulent endocervical discharge or easily induced endocervical bleeding and is the most common site of infection. Up to 80% of women are asymptomatic, with nonspecific symptoms such as vaginal discharge, menorrhagia, pelvic pain, dyspareunia, urinary frequency, and dysuria.
Pelvic inflammatory disease develops in up to 20% of untreated cases, most commonly presenting with lower abdominal pain. Other symptoms include dyspareunia, abnormal bleeding or discharge, fever, and onset around menses. Fitz-Hugh–Curtis syndrome occurs in about 10% and presents with right upper quadrant pain. Bartholin abscess may also occur.
Urethritis typically has a 2–5 day incubation period and presents with penile discharge and dysuria; untreated cases may progress to prostatitis or epididymitis, which presents with acute unilateral testicular pain and swelling.
Proctitis is often asymptomatic and may be the only site of infection in many men who have sex with men. Rectal infection occurs in 35–50% of women with endocervical infection and significantly increases HIV acquisition risk. Symptoms include perianal pruritus, mucopurulent discharge, rectal bleeding, pain, tenesmus, and constipation.
Pharyngitis may present with sore throat or exudative tonsillitis.
Disseminated gonococcal infection occurs in 0.5–3% of untreated mucosal infections and presents with the triad of tenosynovitis, dermatitis, and polyarthralgia, often accompanied by fever, chills, and malaise. Dermatitis consists of tender necrotic pustules on an erythematous base. Septic arthritis typically affects the knee. Females are affected more commonly than males, with recent menstruation or pregnancy as risk factors. Rare complications include hepatitis, myocarditis, endocarditis, and meningitis.
Physical examination may reveal cervical friability and edema, uterine or adnexal tenderness in PID, and thick yellow-white urethral discharge with meatal erythema in urethritis.
Essential Workup
In symptomatic men, diagnosis is often clinical with Gram stain, which has high sensitivity. In women, cervical culture is recommended. Testing for chlamydia and syphilis should always be performed.
Diagnosis Tests And Interpretation
Cultures on Thayer-Martin medium remain the gold standard, particularly for blood and synovial fluid. Gram stain demonstrating intracellular gram-negative diplococci is highly sensitive in symptomatic men. Nucleic acid amplification tests using PCR are widely used for urethral, cervical, and urine specimens and frequently test for chlamydia concurrently. Pharyngeal and rectal cultures are indicated in symptomatic or high-risk patients.
In disseminated infection, synovial fluid typically shows neutrophilic leukocytosis, and multiple blood cultures should be obtained. Women with PID require CBC, urinalysis, pregnancy testing, and consideration of pelvic ultrasound to evaluate for tubo-ovarian abscess. Rapid plasma reagin testing is indicated to assess for syphilis.
Differential Diagnosis
Urethritis due to chlamydia, trichomonas, urinary tract infection, or syphilis; septic arthritis from other organisms; connective tissue diseases; poststreptococcal arthritis; viral infections; gout; HIV; secondary syphilis; and Lyme disease.
Treatment Ed Treatment Procedures
Provide IV fluids for dehydration or vomiting. Sexual partners should be treated, including expedited partner therapy where legally permitted. Patients are often treated empirically for chlamydial infection.
Uncomplicated cervical, urethral, or anorectal infection is treated with ceftriaxone 250 mg IM once plus azithromycin 1 g PO once or doxycycline 100 mg PO BID for 7 days.
Pelvic inflammatory disease may be treated as an outpatient with ceftriaxone or another third-generation cephalosporin plus doxycycline with or without metronidazole, or as an inpatient with IV cephalosporin-based or clindamycin-gentamicin regimens.
Pharyngitis is treated with ceftriaxone plus chlamydia coverage.
Epididymitis requires ceftriaxone plus doxycycline for 10 days.
Disseminated gonococcal infection is treated with ceftriaxone 1 g IV or IM daily, followed by oral therapy after clinical improvement.
Neonatal infections, conjunctivitis, meningitis, and endocarditis require weight-based or prolonged IV cephalosporin therapy. Severe cephalosporin allergy warrants infectious disease consultation.
Follow-Up Disposition
Admission is indicated for severe PID, pregnancy, inability to tolerate oral therapy, lack of response to outpatient treatment, tubo-ovarian abscess, or diagnostic uncertainty requiring surgical evaluation.
Patients with uncomplicated genital, pharyngeal, or conjunctival infection may be discharged after treatment.
Issues For Referral
Referral is indicated for infertility evaluation or recurrent infection despite appropriate therapy.
Key Clinical Insights And Common Errors
Always exclude testicular torsion in patients presenting with epididymitis. Disseminated gonococcal infection should be strongly considered in young, sexually active patients with acute, nontraumatic oligoarthritis or tenosynovitis, as delayed recognition can lead to significant morbidity.
