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Infectious disease and microbiology – Mucormycosis
Mucormycosis is a life-threatening opportunistic fungal infection characterized by vascular invasion, thrombosis, and extensive tissue necrosis. It primarily affects immunocompromised individuals, particularly those with uncontrolled diabetes or hematologic malignancies.
The disease is relatively rare, with an estimated incidence of 1.7 cases per million people annually in the United States, but it carries a very high mortality rate. It occurs worldwide and is increasingly recognized in patients receiving antifungal prophylaxis that does not cover Mucorales (e.g., voriconazole).
Major risk factors include uncontrolled diabetes mellitus (especially with ketoacidosis), hematologic malignancies, organ transplantation, prolonged neutropenia, chronic steroid use, deferoxamine therapy, burns, trauma, and intravenous drug use. HIV infection and malnutrition also predispose to disease. Nosocomial outbreaks have been reported, particularly due to contaminated dressings.
Infection occurs through inhalation, ingestion, or direct inoculation of fungal spores. Once inside the host, Mucorales organisms invade blood vessels, leading to thrombosis, infarction, and necrosis, with rapid spread to adjacent tissues and possible hematogenous dissemination.
The most common causative organisms are molds from the order Mucorales, including Rhizopus, Mucor, Rhizomucor, Absidia, Cunninghamella, and Saksenaea. These fungi are ubiquitous in the environment, especially in soil and decaying organic matter.
Clinical presentation varies depending on the site of infection but is typically rapidly progressive and severe.
Rhinocerebral (craniofacial) mucormycosis, most common in diabetics, begins in the sinuses and spreads to the orbit and brain. Patients may present with facial pain, nasal congestion, black necrotic lesions on the palate or nasal mucosa, orbital swelling, vision loss, and altered mental status.
Pulmonary mucormycosis occurs mainly in neutropenic patients and presents with fever, progressive lung infiltrates, and poor response to antibiotics.
Gastrointestinal mucormycosis is more common in malnourished children and presents with abdominal pain, bleeding, or perforation.
Cutaneous mucormycosis occurs after trauma or burns and presents with necrotic ulcers, eschars, and tissue destruction.
Disseminated disease may involve the brain, liver, spleen, or heart and carries a very poor prognosis.
Diagnosis relies on early clinical suspicion and histopathological confirmation. Microscopy shows broad, nonseptate, irregularly branching hyphae. Culture may be performed from tissue samples, and imaging (CT or MRI) helps assess the extent of disease. Unlike other fungal infections, β-D-glucan tests are not useful.
Treatment requires urgent, aggressive management.
First-line therapy includes intravenous amphotericin B (liposomal formulation preferred due to lower toxicity).
Second-line or salvage therapy includes posaconazole, sometimes used in combination regimens.
Equally important are reversal of underlying risk factors (e.g., control of diabetes, reduction of immunosuppression) and prompt surgical debridement of necrotic tissue, which is often lifesaving.
Additional supportive therapies may include granulocyte transfusions, growth factors, hyperbaric oxygen therapy, and iron chelation strategies in selected cases.
The prognosis remains poor, especially if diagnosis is delayed. Untreated rhinocerebral disease is almost universally fatal within days, while even with treatment, survival in diabetic patients is approximately 50%. Outcomes are worse in immunocompromised individuals and in disseminated disease.
Complications include vascular thrombosis, brain abscesses, pulmonary dissemination, bowel infarction, hemorrhage, and widespread tissue destruction, often leading to death if not rapidly treated.
Mucormycosis is a life-threatening opportunistic fungal infection characterized by vascular invasion, thrombosis, and extensive tissue necrosis. It primarily affects immunocompromised individuals, particularly those with uncontrolled diabetes or hematologic malignancies.
The disease is relatively rare, with an estimated incidence of 1.7 cases per million people annually in the United States, but it carries a very high mortality rate. It occurs worldwide and is increasingly recognized in patients receiving antifungal prophylaxis that does not cover Mucorales (e.g., voriconazole).
Major risk factors include uncontrolled diabetes mellitus (especially with ketoacidosis), hematologic malignancies, organ transplantation, prolonged neutropenia, chronic steroid use, deferoxamine therapy, burns, trauma, and intravenous drug use. HIV infection and malnutrition also predispose to disease. Nosocomial outbreaks have been reported, particularly due to contaminated dressings.
Infection occurs through inhalation, ingestion, or direct inoculation of fungal spores. Once inside the host, Mucorales organisms invade blood vessels, leading to thrombosis, infarction, and necrosis, with rapid spread to adjacent tissues and possible hematogenous dissemination.
The most common causative organisms are molds from the order Mucorales, including Rhizopus, Mucor, Rhizomucor, Absidia, Cunninghamella, and Saksenaea. These fungi are ubiquitous in the environment, especially in soil and decaying organic matter.
Clinical presentation varies depending on the site of infection but is typically rapidly progressive and severe.
Rhinocerebral (craniofacial) mucormycosis, most common in diabetics, begins in the sinuses and spreads to the orbit and brain. Patients may present with facial pain, nasal congestion, black necrotic lesions on the palate or nasal mucosa, orbital swelling, vision loss, and altered mental status.
Pulmonary mucormycosis occurs mainly in neutropenic patients and presents with fever, progressive lung infiltrates, and poor response to antibiotics.
Gastrointestinal mucormycosis is more common in malnourished children and presents with abdominal pain, bleeding, or perforation.
Cutaneous mucormycosis occurs after trauma or burns and presents with necrotic ulcers, eschars, and tissue destruction.
Disseminated disease may involve the brain, liver, spleen, or heart and carries a very poor prognosis.
Diagnosis relies on early clinical suspicion and histopathological confirmation. Microscopy shows broad, nonseptate, irregularly branching hyphae. Culture may be performed from tissue samples, and imaging (CT or MRI) helps assess the extent of disease. Unlike other fungal infections, β-D-glucan tests are not useful.
Treatment requires urgent, aggressive management.
First-line therapy includes intravenous amphotericin B (liposomal formulation preferred due to lower toxicity).
Second-line or salvage therapy includes posaconazole, sometimes used in combination regimens.
Equally important are reversal of underlying risk factors (e.g., control of diabetes, reduction of immunosuppression) and prompt surgical debridement of necrotic tissue, which is often lifesaving.
Additional supportive therapies may include granulocyte transfusions, growth factors, hyperbaric oxygen therapy, and iron chelation strategies in selected cases.
The prognosis remains poor, especially if diagnosis is delayed. Untreated rhinocerebral disease is almost universally fatal within days, while even with treatment, survival in diabetic patients is approximately 50%. Outcomes are worse in immunocompromised individuals and in disseminated disease.
Complications include vascular thrombosis, brain abscesses, pulmonary dissemination, bowel infarction, hemorrhage, and widespread tissue destruction, often leading to death if not rapidly treated.
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Infectious disease and microbiology – Mites (including chiggers)
Mites and chiggers are arthropods with four pairs of legs that infest humans, causing primarily cutaneous disease, but in some cases transmitting systemic infections such as scrub typhus.
The most important human mite is Sarcoptes scabiei, which causes scabies, while chiggers (larval forms of trombiculid mites) are responsible for intensely pruritic skin lesions and can transmit Orientia tsutsugamushi, the causative agent of scrub typhus.
Scabies has a worldwide distribution, with an estimated 300 million cases annually, and is more prevalent in tropical and resource-limited settings. Transmission occurs through close personal contact, including sexual contact, and less commonly via fomites. Household transmission rates can be high, especially in severe forms such as Norwegian (crusted) scabies, where mite burden is extensive.
Scrub typhus is endemic within the “tsutsugamushi triangle” (northern Japan to northern Australia and Afghanistan) and is commonly seen in rural areas, particularly among farmers and individuals exposed to vegetation.
The pathophysiology of scabies involves burrowing of mites into the skin, where they lay eggs. The resulting hypersensitivity reaction to the mites, eggs, and feces causes intense itching and inflammation.
In scrub typhus, the organism causes perivasculitis of small blood vessels, leading to systemic illness and potential multiorgan involvement.
Clinically, scabies presents with intensely pruritic papules and characteristic linear burrows, often found in the web spaces of fingers, wrists, and genital areas. Norwegian scabies, seen in immunocompromised individuals, presents with widespread crusted, hyperkeratotic lesions, which may resemble psoriasis and may not be itchy, leading to delayed diagnosis.
Chigger bites cause erythematous papules or pustules, commonly located around the ankles or waistline, appearing within hours of exposure.
Scrub typhus typically presents with fever, headache, and systemic symptoms, and is characterized by the presence of an eschar—a black necrotic scab—usually found in areas where clothing is tight, such as the groin or waist. Severe cases may progress to ARDS, renal failure, or hepatic dysfunction.
Diagnosis of scabies is primarily clinical, based on characteristic lesions and distribution.
Scrub typhus is diagnosed using serologic testing (IgM ELISA), with laboratory findings that may include thrombocytopenia, lymphocyte changes, and elevated liver enzymes. Chest imaging may be required if respiratory complications are suspected.
Treatment depends on the specific condition.
Scabies is treated with permethrin 5% cream, applied over the entire body and repeated after one week. Oral ivermectin is an alternative. Antihistamines may help relieve itching.
Norwegian scabies requires more aggressive and repeated therapy, often combining topical agents and systemic treatment.
Chigger bites are managed symptomatically with antihistamines or topical steroids.
Scrub typhus is treated with doxycycline, which is highly effective, while azithromycin is preferred in children and pregnant patients.
Preventive measures include good hygiene, contact precautions, and treatment of close contacts in scabies cases. For scrub typhus, protective clothing and insect repellents are essential in endemic areas.
The prognosis is generally excellent with treatment. However, untreated scrub typhus can have a mortality rate of 3–30%, especially when diagnosis is delayed.
Complications may include secondary bacterial skin infections in scabies.
In scrub typhus, severe complications include acute respiratory distress syndrome, renal failure, hepatitis, myocarditis, disseminated intravascular coagulation, meningoencephalitis, and hearing loss.
Mites and chiggers are arthropods with four pairs of legs that infest humans, causing primarily cutaneous disease, but in some cases transmitting systemic infections such as scrub typhus.
The most important human mite is Sarcoptes scabiei, which causes scabies, while chiggers (larval forms of trombiculid mites) are responsible for intensely pruritic skin lesions and can transmit Orientia tsutsugamushi, the causative agent of scrub typhus.
Scabies has a worldwide distribution, with an estimated 300 million cases annually, and is more prevalent in tropical and resource-limited settings. Transmission occurs through close personal contact, including sexual contact, and less commonly via fomites. Household transmission rates can be high, especially in severe forms such as Norwegian (crusted) scabies, where mite burden is extensive.
Scrub typhus is endemic within the “tsutsugamushi triangle” (northern Japan to northern Australia and Afghanistan) and is commonly seen in rural areas, particularly among farmers and individuals exposed to vegetation.
The pathophysiology of scabies involves burrowing of mites into the skin, where they lay eggs. The resulting hypersensitivity reaction to the mites, eggs, and feces causes intense itching and inflammation.
In scrub typhus, the organism causes perivasculitis of small blood vessels, leading to systemic illness and potential multiorgan involvement.
Clinically, scabies presents with intensely pruritic papules and characteristic linear burrows, often found in the web spaces of fingers, wrists, and genital areas. Norwegian scabies, seen in immunocompromised individuals, presents with widespread crusted, hyperkeratotic lesions, which may resemble psoriasis and may not be itchy, leading to delayed diagnosis.
Chigger bites cause erythematous papules or pustules, commonly located around the ankles or waistline, appearing within hours of exposure.
Scrub typhus typically presents with fever, headache, and systemic symptoms, and is characterized by the presence of an eschar—a black necrotic scab—usually found in areas where clothing is tight, such as the groin or waist. Severe cases may progress to ARDS, renal failure, or hepatic dysfunction.
Diagnosis of scabies is primarily clinical, based on characteristic lesions and distribution.
Scrub typhus is diagnosed using serologic testing (IgM ELISA), with laboratory findings that may include thrombocytopenia, lymphocyte changes, and elevated liver enzymes. Chest imaging may be required if respiratory complications are suspected.
Treatment depends on the specific condition.
Scabies is treated with permethrin 5% cream, applied over the entire body and repeated after one week. Oral ivermectin is an alternative. Antihistamines may help relieve itching.
Norwegian scabies requires more aggressive and repeated therapy, often combining topical agents and systemic treatment.
Chigger bites are managed symptomatically with antihistamines or topical steroids.
Scrub typhus is treated with doxycycline, which is highly effective, while azithromycin is preferred in children and pregnant patients.
Preventive measures include good hygiene, contact precautions, and treatment of close contacts in scabies cases. For scrub typhus, protective clothing and insect repellents are essential in endemic areas.
The prognosis is generally excellent with treatment. However, untreated scrub typhus can have a mortality rate of 3–30%, especially when diagnosis is delayed.
Complications may include secondary bacterial skin infections in scabies.
In scrub typhus, severe complications include acute respiratory distress syndrome, renal failure, hepatitis, myocarditis, disseminated intravascular coagulation, meningoencephalitis, and hearing loss.
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Infectious Disease and Microbiology – Mesenteric Adenitis
Mesenteric adenitis is an acute inflammation of the mesenteric lymph nodes, most commonly presenting with symptoms that closely mimic acute appendicitis. It may occur as a primary condition or secondary to other diseases such as Crohn’s disease, infectious colitis, appendicitis, diverticulitis, or systemic lupus erythematosus. In many cases, it is preceded or accompanied by enterocolitis.
It is most commonly seen in children aged 5–14 years and may account for up to 8% of hospital admissions initially suspected to be appendicitis. Although many infections are subclinical or mild, outbreaks have been associated with specific food exposures, particularly undercooked pork, unpasteurized milk, and contaminated food products. Intrafamilial transmission and rare cases linked to blood transfusion have also been reported.
The condition typically results from a gastrointestinal infection, most often involving Yersinia enterocolitica. The pathogen invades Peyer’s patches in the ileum and spreads to mesenteric lymph nodes, causing inflammation. Other infectious causes include Yersinia pseudotuberculosis, Salmonella, and Mycobacterium tuberculosis. Less commonly, viral agents such as Epstein–Barr virus or adenovirus may be involved.
Patients usually present with right lower quadrant abdominal pain and fever, making differentiation from appendicitis challenging. Associated symptoms often include diarrhea and nausea, while vomiting is less common. A history of recent ingestion of high-risk foods within 1–2 weeks prior to symptom onset may provide a clue. On examination, patients may appear acutely ill with localized tenderness in the right lower abdomen. Rebound tenderness can occur but is generally less pronounced than in appendicitis. Occasionally, immune-mediated complications such as erythema nodosum or reactive arthritis may develop, especially in individuals with HLA-B27.
Laboratory findings are nonspecific and may show elevated white blood cell counts, and stool studies may reveal leukocytes in cases with diarrhea. Diagnosis is primarily supported by imaging. Abdominal ultrasound is especially useful in children, demonstrating a normal appendix along with enlarged mesenteric lymph nodes. In adults, CT scanning can confirm the presence of clustered lymph nodes near the ileocecal region while excluding appendicitis. Stool cultures for Yersinia may require special techniques such as cold enrichment, and serologic tests can assist during outbreaks.
Mesenteric adenitis is usually a self-limited condition, and treatment is primarily supportive, including hydration and symptomatic care. Antibiotics are generally not required unless there is confirmed bacterial infection with significant symptoms. In such cases, trimethoprim-sulfamethoxazole is commonly used in children, while adults may receive trimethoprim-sulfamethoxazole or ciprofloxacin. Other antibiotic options include doxycycline, ampicillin, or aminoglycosides in selected cases.
Surgical consultation may be necessary when appendicitis cannot be excluded, and laparoscopy may be performed in uncertain cases. Hospital admission is indicated for patients with severe abdominal pain, fever, rebound tenderness, hypotension, or inability to tolerate oral intake.
The prognosis is excellent, as most cases resolve without complications. However, rare complications can occur, particularly in immunocompromised individuals. These include bacteremia, septic shock, intestinal necrosis, perforation, intussusception, and metastatic infections. Post-infectious immune conditions such as reactive arthritis, uveitis, nephritis, and erythema nodosum may also develop.
Mesenteric adenitis is an acute inflammation of the mesenteric lymph nodes, most commonly presenting with symptoms that closely mimic acute appendicitis. It may occur as a primary condition or secondary to other diseases such as Crohn’s disease, infectious colitis, appendicitis, diverticulitis, or systemic lupus erythematosus. In many cases, it is preceded or accompanied by enterocolitis.
It is most commonly seen in children aged 5–14 years and may account for up to 8% of hospital admissions initially suspected to be appendicitis. Although many infections are subclinical or mild, outbreaks have been associated with specific food exposures, particularly undercooked pork, unpasteurized milk, and contaminated food products. Intrafamilial transmission and rare cases linked to blood transfusion have also been reported.
The condition typically results from a gastrointestinal infection, most often involving Yersinia enterocolitica. The pathogen invades Peyer’s patches in the ileum and spreads to mesenteric lymph nodes, causing inflammation. Other infectious causes include Yersinia pseudotuberculosis, Salmonella, and Mycobacterium tuberculosis. Less commonly, viral agents such as Epstein–Barr virus or adenovirus may be involved.
Patients usually present with right lower quadrant abdominal pain and fever, making differentiation from appendicitis challenging. Associated symptoms often include diarrhea and nausea, while vomiting is less common. A history of recent ingestion of high-risk foods within 1–2 weeks prior to symptom onset may provide a clue. On examination, patients may appear acutely ill with localized tenderness in the right lower abdomen. Rebound tenderness can occur but is generally less pronounced than in appendicitis. Occasionally, immune-mediated complications such as erythema nodosum or reactive arthritis may develop, especially in individuals with HLA-B27.
Laboratory findings are nonspecific and may show elevated white blood cell counts, and stool studies may reveal leukocytes in cases with diarrhea. Diagnosis is primarily supported by imaging. Abdominal ultrasound is especially useful in children, demonstrating a normal appendix along with enlarged mesenteric lymph nodes. In adults, CT scanning can confirm the presence of clustered lymph nodes near the ileocecal region while excluding appendicitis. Stool cultures for Yersinia may require special techniques such as cold enrichment, and serologic tests can assist during outbreaks.
Mesenteric adenitis is usually a self-limited condition, and treatment is primarily supportive, including hydration and symptomatic care. Antibiotics are generally not required unless there is confirmed bacterial infection with significant symptoms. In such cases, trimethoprim-sulfamethoxazole is commonly used in children, while adults may receive trimethoprim-sulfamethoxazole or ciprofloxacin. Other antibiotic options include doxycycline, ampicillin, or aminoglycosides in selected cases.
Surgical consultation may be necessary when appendicitis cannot be excluded, and laparoscopy may be performed in uncertain cases. Hospital admission is indicated for patients with severe abdominal pain, fever, rebound tenderness, hypotension, or inability to tolerate oral intake.
The prognosis is excellent, as most cases resolve without complications. However, rare complications can occur, particularly in immunocompromised individuals. These include bacteremia, septic shock, intestinal necrosis, perforation, intussusception, and metastatic infections. Post-infectious immune conditions such as reactive arthritis, uveitis, nephritis, and erythema nodosum may also develop.
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Infectious Disease and Microbiology - Acute Meningitis
Acute meningitis is a rapidly developing inflammation of the meninges that typically evolves over hours to days. It may resolve spontaneously in viral cases or require urgent treatment when bacterial in origin. Despite advances in therapy, it remains a medical emergency due to its potential for rapid deterioration and severe complications.
Meningitis occurs worldwide and can affect individuals of all ages, including previously healthy people. The overall incidence in the United States is approximately 2–10 cases per 100,000 population annually, with significantly higher rates in neonates and young children. Among bacterial causes, Neisseria meningitidis is unique in its ability to cause epidemics. Vaccination programs have significantly reduced cases of Haemophilus influenzae type B meningitis.
Risk factors include extremes of age, crowded living conditions, close contact with infected individuals, head trauma, neurosurgical devices (e.g., shunts), immunosuppression, and chronic illnesses. Specific conditions predispose to certain pathogens—for example, asplenia increases risk for pneumococcal and meningococcal infections, while complement deficiencies increase susceptibility to meningococcal disease. Tick exposure may lead to Lyme meningitis.
The pathogenesis begins with colonization of the nasopharynx, followed by invasion into the bloodstream and crossing of the blood–brain barrier into the cerebrospinal fluid (CSF), where pathogens multiply. Inflammation in the subarachnoid space leads to increased intracranial pressure and neurologic dysfunction.
Etiologically, most cases are viral, particularly due to enteroviruses. However, bacterial meningitis is more severe and commonly caused by Streptococcus pneumoniae, Neisseria meningitidis, Group B Streptococcus, Listeria monocytogenes, and Haemophilus influenzae. Other pathogens include viruses (e.g., herpesviruses, HIV), spirochetes such as Treponema pallidum, and Borrelia burgdorferi.
Clinically, patients often present with fever, headache, vomiting, and altered mental status. Classical meningeal signs include nuchal rigidity, Kernig’s sign, and Brudzinski’s sign, although these may not always be present. A petechial or purpuric rash suggests meningococcal infection. Severe cases may progress to seizures, coma, or focal neurologic deficits.
Presentation may be atypical in elderly patients and neonates.
Diagnosis requires urgent evaluation. Initial laboratory tests include blood work and cultures, followed by lumbar puncture to analyze CSF. In bacterial meningitis, CSF typically shows high white blood cell count with neutrophil predominance, low glucose, and elevated protein. In viral meningitis, lymphocytes predominate, and glucose is usually normal. PCR testing improves detection of both bacterial and viral pathogens. A CT scan of the head is indicated before lumbar puncture in patients with risk factors for increased intracranial pressure or focal neurologic signs.
Treatment must be initiated immediately, often before confirmation of the causative organism. Empiric therapy typically includes a third- or fourth-generation cephalosporin combined with vancomycin, with the addition of ampicillin when Listeria is suspected. Therapy is later tailored based on culture results. Adjunctive corticosteroids may be beneficial in certain cases, particularly pneumococcal meningitis, to reduce inflammation and neurologic complications.
All patients require hospitalization for close monitoring and supportive care. Prognosis depends on factors such as age, underlying health, pathogen, and timeliness of treatment. Mortality and morbidity increase with delayed therapy, altered consciousness, or severe disease at presentation.
Complications can be severe and include seizures, hydrocephalus, brain abscess, hearing loss, cognitive impairment, paralysis, and even death. Survivors often require long-term neurologic follow-up and rehabilitation.
Acute meningitis is a rapidly developing inflammation of the meninges that typically evolves over hours to days. It may resolve spontaneously in viral cases or require urgent treatment when bacterial in origin. Despite advances in therapy, it remains a medical emergency due to its potential for rapid deterioration and severe complications.
Meningitis occurs worldwide and can affect individuals of all ages, including previously healthy people. The overall incidence in the United States is approximately 2–10 cases per 100,000 population annually, with significantly higher rates in neonates and young children. Among bacterial causes, Neisseria meningitidis is unique in its ability to cause epidemics. Vaccination programs have significantly reduced cases of Haemophilus influenzae type B meningitis.
Risk factors include extremes of age, crowded living conditions, close contact with infected individuals, head trauma, neurosurgical devices (e.g., shunts), immunosuppression, and chronic illnesses. Specific conditions predispose to certain pathogens—for example, asplenia increases risk for pneumococcal and meningococcal infections, while complement deficiencies increase susceptibility to meningococcal disease. Tick exposure may lead to Lyme meningitis.
The pathogenesis begins with colonization of the nasopharynx, followed by invasion into the bloodstream and crossing of the blood–brain barrier into the cerebrospinal fluid (CSF), where pathogens multiply. Inflammation in the subarachnoid space leads to increased intracranial pressure and neurologic dysfunction.
Etiologically, most cases are viral, particularly due to enteroviruses. However, bacterial meningitis is more severe and commonly caused by Streptococcus pneumoniae, Neisseria meningitidis, Group B Streptococcus, Listeria monocytogenes, and Haemophilus influenzae. Other pathogens include viruses (e.g., herpesviruses, HIV), spirochetes such as Treponema pallidum, and Borrelia burgdorferi.
Clinically, patients often present with fever, headache, vomiting, and altered mental status. Classical meningeal signs include nuchal rigidity, Kernig’s sign, and Brudzinski’s sign, although these may not always be present. A petechial or purpuric rash suggests meningococcal infection. Severe cases may progress to seizures, coma, or focal neurologic deficits.
Presentation may be atypical in elderly patients and neonates.
Diagnosis requires urgent evaluation. Initial laboratory tests include blood work and cultures, followed by lumbar puncture to analyze CSF. In bacterial meningitis, CSF typically shows high white blood cell count with neutrophil predominance, low glucose, and elevated protein. In viral meningitis, lymphocytes predominate, and glucose is usually normal. PCR testing improves detection of both bacterial and viral pathogens. A CT scan of the head is indicated before lumbar puncture in patients with risk factors for increased intracranial pressure or focal neurologic signs.
Treatment must be initiated immediately, often before confirmation of the causative organism. Empiric therapy typically includes a third- or fourth-generation cephalosporin combined with vancomycin, with the addition of ampicillin when Listeria is suspected. Therapy is later tailored based on culture results. Adjunctive corticosteroids may be beneficial in certain cases, particularly pneumococcal meningitis, to reduce inflammation and neurologic complications.
All patients require hospitalization for close monitoring and supportive care. Prognosis depends on factors such as age, underlying health, pathogen, and timeliness of treatment. Mortality and morbidity increase with delayed therapy, altered consciousness, or severe disease at presentation.
Complications can be severe and include seizures, hydrocephalus, brain abscess, hearing loss, cognitive impairment, paralysis, and even death. Survivors often require long-term neurologic follow-up and rehabilitation.
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Infectious Disease and Microbiology - Mediastinitis
Mediastinitis is a serious infection involving the mediastinum, the central compartment of the thoracic cavity. It may present as acute or chronic disease. Acute mediastinitis is a life-threatening condition often resulting from esophageal perforation, cardiothoracic surgery, trauma, or spread from nearby infections such as those of the head and neck. A particularly severe form is descending necrotizing mediastinitis, where infection spreads rapidly from the oropharynx into the chest. Chronic mediastinitis is less common and is typically associated with granulomatous diseases such as tuberculosis or histoplasmosis, or with retained foreign bodies.
Currently, most cases of mediastinitis occur as complications following cardiac surgery, especially after sternotomy. The incidence of post-surgical mediastinitis ranges from approximately 0.4% to 5%. Despite advances in surgical techniques and infection control, the incidence has remained stable due to increasing numbers of elderly and immunocompromised patients undergoing complex procedures. Risk factors include diabetes mellitus, obesity, chronic lung disease, prolonged surgical time, reoperation, and vascular comorbidities.
The pathophysiology involves invasion of the mediastinum by pathogens, leading to intense inflammation, fibrin deposition, and formation of abscesses. Infection can spread rapidly through fascial planes, creating extensive tissue damage and dead space beneath the sternum. Acute infections are usually polymicrobial. Common organisms include gram-positive bacteria such as Staphylococcus aureus and Staphylococcus epidermidis in post-surgical cases, while infections related to esophageal or oropharyngeal sources often involve gram-negative and anaerobic organisms. In severely ill patients, fungal pathogens like Candida and Aspergillus may also be involved.
Clinically, acute mediastinitis presents with fever, severe chest pain, dysphagia, and respiratory distress. Patients with esophageal perforation may also have epigastric pain. Physical findings can include a sternal click (indicating instability), crepitus due to subcutaneous air, and Hamman’s sign, a crunching sound heard over the chest. In contrast, chronic mediastinitis may initially be asymptomatic but later presents with symptoms due to compression of mediastinal structures, such as cough, dyspnea, or signs of superior vena cava syndrome.
Laboratory findings typically show leukocytosis and elevated inflammatory markers such as C-reactive protein. Blood cultures may be positive, especially in cases associated with head and neck infections. Imaging is essential for diagnosis. Chest radiographs may reveal mediastinal widening or air-fluid levels, while CT scans provide detailed visualization of fluid collections, gas, and the extent of infection. Diagnostic procedures such as CT-guided aspiration, mediastinoscopy, or thoracoscopy may be required to obtain microbiological samples.
Management of mediastinitis requires urgent and aggressive treatment. Broad-spectrum intravenous antibiotics should be initiated promptly and later tailored based on culture results. Common regimens include combinations of cephalosporins with anaerobic coverage or agents such as piperacillin-tazobactam. Coverage for MRSA may require vancomycin or linezolid. Therapy is typically prolonged, lasting several weeks.
Surgical intervention is critical and remains the cornerstone of treatment. Procedures include drainage of infected material, debridement of necrotic tissue, and sometimes more extensive approaches such as thoracotomy or video-assisted thoracic surgery. Negative pressure wound therapy may be used in postoperative cases. Supportive care, including airway management, oxygen therapy, and adequate nutrition, is essential.
The prognosis of mediastinitis is guarded, with mortality rates reaching up to 50%, especially in delayed or inadequately treated cases. Early diagnosis and prompt surgical drainage significantly improve outcomes. Complications can be severe and include sepsis, pleural empyema, sternal osteomyelitis, acute respiratory distress syndrome, thrombosis, and superior vena cava syndrome.
Mediastinitis is a serious infection involving the mediastinum, the central compartment of the thoracic cavity. It may present as acute or chronic disease. Acute mediastinitis is a life-threatening condition often resulting from esophageal perforation, cardiothoracic surgery, trauma, or spread from nearby infections such as those of the head and neck. A particularly severe form is descending necrotizing mediastinitis, where infection spreads rapidly from the oropharynx into the chest. Chronic mediastinitis is less common and is typically associated with granulomatous diseases such as tuberculosis or histoplasmosis, or with retained foreign bodies.
Currently, most cases of mediastinitis occur as complications following cardiac surgery, especially after sternotomy. The incidence of post-surgical mediastinitis ranges from approximately 0.4% to 5%. Despite advances in surgical techniques and infection control, the incidence has remained stable due to increasing numbers of elderly and immunocompromised patients undergoing complex procedures. Risk factors include diabetes mellitus, obesity, chronic lung disease, prolonged surgical time, reoperation, and vascular comorbidities.
The pathophysiology involves invasion of the mediastinum by pathogens, leading to intense inflammation, fibrin deposition, and formation of abscesses. Infection can spread rapidly through fascial planes, creating extensive tissue damage and dead space beneath the sternum. Acute infections are usually polymicrobial. Common organisms include gram-positive bacteria such as Staphylococcus aureus and Staphylococcus epidermidis in post-surgical cases, while infections related to esophageal or oropharyngeal sources often involve gram-negative and anaerobic organisms. In severely ill patients, fungal pathogens like Candida and Aspergillus may also be involved.
Clinically, acute mediastinitis presents with fever, severe chest pain, dysphagia, and respiratory distress. Patients with esophageal perforation may also have epigastric pain. Physical findings can include a sternal click (indicating instability), crepitus due to subcutaneous air, and Hamman’s sign, a crunching sound heard over the chest. In contrast, chronic mediastinitis may initially be asymptomatic but later presents with symptoms due to compression of mediastinal structures, such as cough, dyspnea, or signs of superior vena cava syndrome.
Laboratory findings typically show leukocytosis and elevated inflammatory markers such as C-reactive protein. Blood cultures may be positive, especially in cases associated with head and neck infections. Imaging is essential for diagnosis. Chest radiographs may reveal mediastinal widening or air-fluid levels, while CT scans provide detailed visualization of fluid collections, gas, and the extent of infection. Diagnostic procedures such as CT-guided aspiration, mediastinoscopy, or thoracoscopy may be required to obtain microbiological samples.
Management of mediastinitis requires urgent and aggressive treatment. Broad-spectrum intravenous antibiotics should be initiated promptly and later tailored based on culture results. Common regimens include combinations of cephalosporins with anaerobic coverage or agents such as piperacillin-tazobactam. Coverage for MRSA may require vancomycin or linezolid. Therapy is typically prolonged, lasting several weeks.
Surgical intervention is critical and remains the cornerstone of treatment. Procedures include drainage of infected material, debridement of necrotic tissue, and sometimes more extensive approaches such as thoracotomy or video-assisted thoracic surgery. Negative pressure wound therapy may be used in postoperative cases. Supportive care, including airway management, oxygen therapy, and adequate nutrition, is essential.
The prognosis of mediastinitis is guarded, with mortality rates reaching up to 50%, especially in delayed or inadequately treated cases. Early diagnosis and prompt surgical drainage significantly improve outcomes. Complications can be severe and include sepsis, pleural empyema, sternal osteomyelitis, acute respiratory distress syndrome, thrombosis, and superior vena cava syndrome.
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Ophthalmology – Dry Eye Syndrome (Keratoconjunctivitis Sicca)
Dry eye syndrome is a multifactorial disease of the ocular surface characterized by an unstable or insufficient tear film, leading to discomfort, visual disturbance, and potential damage to the cornea and conjunctiva. It is broadly classified into three main types: aqueous tear-deficient, evaporative, and exposure-related dry eye. The condition may occur as an isolated ocular disorder or as part of systemic diseases such as autoimmune conditions.
This is a very common condition, particularly in older adults and females. Prevalence increases with age, affecting up to 19% of individuals over 80 years. Risk factors include aging, female sex, ocular surgeries (such as LASIK or cataract surgery), diabetes, and contact lens use. Environmental factors like low humidity and prolonged screen use also contribute significantly.
The pathophysiology involves tear film instability and ocular surface desiccation, which leads to inflammation, loss of goblet cells, and epithelial damage. Over time, this can result in keratinization and chronic surface changes. In aqueous deficiency, there is reduced tear production, whereas evaporative dry eye is usually due to meibomian gland dysfunction, causing rapid tear evaporation. Exposure-related dry eye results from incomplete eyelid closure or reduced blinking.
Patients commonly report burning, itching, gritty sensation, foreign body sensation, and intermittent blurred vision, especially with prolonged visual tasks like reading or computer use. Symptoms often worsen in dry, windy, or air-conditioned environments and improve in humid conditions. Some patients paradoxically experience excess tearing, which is a reflex response to irritation.
On examination, findings may include conjunctival redness, reduced tear meniscus, and superficial punctate keratitis in exposed areas of the cornea. In evaporative dry eye, signs of meibomian gland dysfunction such as thickened secretions, lid margin inflammation, and foamy tear film may be present. Severe cases may show filamentary keratitis or epithelial defects.
Diagnosis is supported by clinical tests. The Schirmer test measures tear production, with low values indicating aqueous deficiency. The tear breakup time (TBUT) assesses tear film stability, with values less than 10 seconds suggesting evaporative dry eye. Rose Bengal staining highlights damaged or devitalized epithelial cells and helps assess severity.
Management is stepwise and depends on severity and type. First-line treatment includes artificial tears, gels, and ointments to supplement and preserve moisture. Environmental modifications such as using humidifiers and avoiding irritants are also important. For evaporative causes, warm compresses and lid hygiene are essential, and oral doxycycline or omega-3 supplements may be beneficial.
Second-line therapies include topical cyclosporine, autologous serum eye drops, and systemic secretagogues such as pilocarpine or cevimeline in selected cases. In more severe disease, procedures such as punctal plugs or punctal occlusion help retain tears. For exposure-related cases, interventions like lid taping, moisture chambers, or surgical options (e.g., tarsorrhaphy) may be required.
Patients should be advised to stay hydrated, blink frequently during screen use, and avoid dry environments. Referral to a specialist is indicated if systemic conditions like Sjögren’s syndrome are suspected.
The prognosis is generally excellent, with most patients achieving good symptom control with appropriate therapy. However, untreated or severe cases can lead to complications such as filamentary keratitis, corneal ulceration, or rarely corneal perforation, highlighting the importance of early recognition and management.
Dry eye syndrome is a multifactorial disease of the ocular surface characterized by an unstable or insufficient tear film, leading to discomfort, visual disturbance, and potential damage to the cornea and conjunctiva. It is broadly classified into three main types: aqueous tear-deficient, evaporative, and exposure-related dry eye. The condition may occur as an isolated ocular disorder or as part of systemic diseases such as autoimmune conditions.
This is a very common condition, particularly in older adults and females. Prevalence increases with age, affecting up to 19% of individuals over 80 years. Risk factors include aging, female sex, ocular surgeries (such as LASIK or cataract surgery), diabetes, and contact lens use. Environmental factors like low humidity and prolonged screen use also contribute significantly.
The pathophysiology involves tear film instability and ocular surface desiccation, which leads to inflammation, loss of goblet cells, and epithelial damage. Over time, this can result in keratinization and chronic surface changes. In aqueous deficiency, there is reduced tear production, whereas evaporative dry eye is usually due to meibomian gland dysfunction, causing rapid tear evaporation. Exposure-related dry eye results from incomplete eyelid closure or reduced blinking.
Patients commonly report burning, itching, gritty sensation, foreign body sensation, and intermittent blurred vision, especially with prolonged visual tasks like reading or computer use. Symptoms often worsen in dry, windy, or air-conditioned environments and improve in humid conditions. Some patients paradoxically experience excess tearing, which is a reflex response to irritation.
On examination, findings may include conjunctival redness, reduced tear meniscus, and superficial punctate keratitis in exposed areas of the cornea. In evaporative dry eye, signs of meibomian gland dysfunction such as thickened secretions, lid margin inflammation, and foamy tear film may be present. Severe cases may show filamentary keratitis or epithelial defects.
Diagnosis is supported by clinical tests. The Schirmer test measures tear production, with low values indicating aqueous deficiency. The tear breakup time (TBUT) assesses tear film stability, with values less than 10 seconds suggesting evaporative dry eye. Rose Bengal staining highlights damaged or devitalized epithelial cells and helps assess severity.
Management is stepwise and depends on severity and type. First-line treatment includes artificial tears, gels, and ointments to supplement and preserve moisture. Environmental modifications such as using humidifiers and avoiding irritants are also important. For evaporative causes, warm compresses and lid hygiene are essential, and oral doxycycline or omega-3 supplements may be beneficial.
Second-line therapies include topical cyclosporine, autologous serum eye drops, and systemic secretagogues such as pilocarpine or cevimeline in selected cases. In more severe disease, procedures such as punctal plugs or punctal occlusion help retain tears. For exposure-related cases, interventions like lid taping, moisture chambers, or surgical options (e.g., tarsorrhaphy) may be required.
Patients should be advised to stay hydrated, blink frequently during screen use, and avoid dry environments. Referral to a specialist is indicated if systemic conditions like Sjögren’s syndrome are suspected.
The prognosis is generally excellent, with most patients achieving good symptom control with appropriate therapy. However, untreated or severe cases can lead to complications such as filamentary keratitis, corneal ulceration, or rarely corneal perforation, highlighting the importance of early recognition and management.
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Ophthalmology – Down Syndrome (Trisomy 21)
Down syndrome, also known as Trisomy 21, is a chromosomal disorder caused by the presence of an extra copy of chromosome 21. It was first described by John Langdon Down in 1866. The condition affects individuals worldwide across all ethnic and socioeconomic groups and is one of the most common genetic causes of intellectual disability.
The incidence is approximately 1 in 733 live births in the United States, with risk strongly associated with advanced maternal age. For example, the risk increases significantly from about 1 in 1,562 in women aged 20–24 to about 1 in 19 in women over 45. Increased paternal age has also been identified as a contributing risk factor. Most cases result from meiotic nondisjunction, leading to a full extra chromosome, although partial or mosaic forms may also occur.
Clinically, Down syndrome presents with a characteristic set of physical features. These include a round face, small chin (microgenia), macroglossia (large tongue), and short neck. Ocular findings are particularly relevant in ophthalmology and include epicanthal folds, upward slanting palpebral fissures, and Brushfield spots—small whitish or grayish speckles seen at the periphery of the iris. Patients often also have strabismus, cataracts, and other visual abnormalities. General features include hypotonia, short stature, single palmar crease, and varying degrees of intellectual disability and speech delay.
Down syndrome is associated with multiple systemic conditions. These include thyroid disorders, gastrointestinal anomalies, hematologic malignancies, and an increased risk of early-onset Alzheimer’s disease, often developing before age 50. Fertility is typically reduced, especially in males.
Diagnosis can be made prenatally through screening and diagnostic techniques such as amniocentesis, chorionic villus sampling, or umbilical cord blood sampling. Postnatally, diagnosis is confirmed by karyotype analysis. Ophthalmic evaluation may include imaging such as optical coherence tomography (OCT), which can demonstrate macular hypoplasia, and visual electrophysiologic testing.
There is no cure for Down syndrome, so management focuses on supportive care and treatment of associated conditions. Early intervention programs, including speech therapy, occupational therapy, and educational support, significantly improve developmental outcomes. Ophthalmic issues such as strabismus or cataracts should be managed appropriately to optimize visual function.
Follow-up care is lifelong and multidisciplinary. With advances in medical care and supportive services, life expectancy has improved significantly, increasing from approximately 25 years in 1980 to nearly 50 years or more today. Many individuals now live into adulthood with improved quality of life, although neurodegenerative complications remain a concern later in life.
Down syndrome, also known as Trisomy 21, is a chromosomal disorder caused by the presence of an extra copy of chromosome 21. It was first described by John Langdon Down in 1866. The condition affects individuals worldwide across all ethnic and socioeconomic groups and is one of the most common genetic causes of intellectual disability.
The incidence is approximately 1 in 733 live births in the United States, with risk strongly associated with advanced maternal age. For example, the risk increases significantly from about 1 in 1,562 in women aged 20–24 to about 1 in 19 in women over 45. Increased paternal age has also been identified as a contributing risk factor. Most cases result from meiotic nondisjunction, leading to a full extra chromosome, although partial or mosaic forms may also occur.
Clinically, Down syndrome presents with a characteristic set of physical features. These include a round face, small chin (microgenia), macroglossia (large tongue), and short neck. Ocular findings are particularly relevant in ophthalmology and include epicanthal folds, upward slanting palpebral fissures, and Brushfield spots—small whitish or grayish speckles seen at the periphery of the iris. Patients often also have strabismus, cataracts, and other visual abnormalities. General features include hypotonia, short stature, single palmar crease, and varying degrees of intellectual disability and speech delay.
Down syndrome is associated with multiple systemic conditions. These include thyroid disorders, gastrointestinal anomalies, hematologic malignancies, and an increased risk of early-onset Alzheimer’s disease, often developing before age 50. Fertility is typically reduced, especially in males.
Diagnosis can be made prenatally through screening and diagnostic techniques such as amniocentesis, chorionic villus sampling, or umbilical cord blood sampling. Postnatally, diagnosis is confirmed by karyotype analysis. Ophthalmic evaluation may include imaging such as optical coherence tomography (OCT), which can demonstrate macular hypoplasia, and visual electrophysiologic testing.
There is no cure for Down syndrome, so management focuses on supportive care and treatment of associated conditions. Early intervention programs, including speech therapy, occupational therapy, and educational support, significantly improve developmental outcomes. Ophthalmic issues such as strabismus or cataracts should be managed appropriately to optimize visual function.
Follow-up care is lifelong and multidisciplinary. With advances in medical care and supportive services, life expectancy has improved significantly, increasing from approximately 25 years in 1980 to nearly 50 years or more today. Many individuals now live into adulthood with improved quality of life, although neurodegenerative complications remain a concern later in life.
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Toxicology – Drugs Causing Hypertension
Amphetamines
Amphetamines enhance the release of catecholamines, producing significant increases in blood pressure and heart rate.
Caffeine
Caffeine stimulates adrenergic activity, causing hypertension and tachycardia. In large overdoses, it may paradoxically result in hypotension and cardiovascular collapse.
Cocaine
Cocaine increases synaptic concentrations of serotonin, dopamine, and norepinephrine by blocking their reuptake, resulting in elevated blood pressure and heart rate.
Anticholinergics
Anticholinergic drugs suppress parasympathetic activity, leading to increased heart rate and elevated blood pressure.
Nicotine
Nicotine toxicity initially presents with hypertension and tachycardia, which may later progress to bradycardia and hypotension.
Sympathomimetics
These agents increase blood pressure and heart rate by promoting catecholamine release, decreasing their reuptake, or inhibiting their breakdown.
Thyroid Hormone
Excess thyroid hormone elevates basal metabolic rate and enhances responsiveness to catecholamines. In severe overdose, this may lead to cardiac dysrhythmias followed by hypotension and cardiovascular collapse.
Treatment
Benzodiazepines are the first-line treatment for hypertension due to sympathomimetic toxicity. Pure β-blockers should be avoided because they can cause unopposed α-adrenergic stimulation and worsen hypertension. Agents such as labetalol are preferred due to their combined α- and β-blocking effects.
Amphetamines
Amphetamines enhance the release of catecholamines, producing significant increases in blood pressure and heart rate.
Caffeine
Caffeine stimulates adrenergic activity, causing hypertension and tachycardia. In large overdoses, it may paradoxically result in hypotension and cardiovascular collapse.
Cocaine
Cocaine increases synaptic concentrations of serotonin, dopamine, and norepinephrine by blocking their reuptake, resulting in elevated blood pressure and heart rate.
Anticholinergics
Anticholinergic drugs suppress parasympathetic activity, leading to increased heart rate and elevated blood pressure.
Nicotine
Nicotine toxicity initially presents with hypertension and tachycardia, which may later progress to bradycardia and hypotension.
Sympathomimetics
These agents increase blood pressure and heart rate by promoting catecholamine release, decreasing their reuptake, or inhibiting their breakdown.
Thyroid Hormone
Excess thyroid hormone elevates basal metabolic rate and enhances responsiveness to catecholamines. In severe overdose, this may lead to cardiac dysrhythmias followed by hypotension and cardiovascular collapse.
Treatment
Benzodiazepines are the first-line treatment for hypertension due to sympathomimetic toxicity. Pure β-blockers should be avoided because they can cause unopposed α-adrenergic stimulation and worsen hypertension. Agents such as labetalol are preferred due to their combined α- and β-blocking effects.
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Toxicology – Drugs causing Hypotenssion
C – Clonidine:
A central-acting α₂ receptor agonist that can initially cause hypertension followed by hypotension.
C – Calcium Channel Blockers:
A class of antihypertensive and antianginal medications that decrease heart rate and dilate peripheral vasculature.
R – Reserpine:
A sympatholytic antihypertensive medication that blocks the reuptake of norepinephrine, dopamine, and serotonin, leading to enhanced degradation by MAO in the synaptic space.
A – Antidepressants:
Tricyclic antidepressants (TCAs) can induce hypotension through α₁ receptor blockade and by causing cardiac dysrhythmias and subsequent cardiac collapse.
A – Aminophylline:
A methylxanthine that acts as an adenosine receptor antagonist, β-blocker, and phosphodiesterase inhibitor that can cause hypotension and cardiac collapse in overdose settings.
S – Sedative–Hypnotics:
Hypotension can occur secondary to myocardial depression.
H – Heroin:
Opiates can induce hypotension secondary to histamine release, direct vasodilation, or through a centrally mediated decrease of vagal tone.
Treatment:
Hypotension is best treated with large fluid boluses followed by the administration of antidotes and/or treatment of the respective toxin. Pressors may be indicated if the patient remains hypotensive after fluid resuscitation.
C – Clonidine:
A central-acting α₂ receptor agonist that can initially cause hypertension followed by hypotension.
C – Calcium Channel Blockers:
A class of antihypertensive and antianginal medications that decrease heart rate and dilate peripheral vasculature.
R – Reserpine:
A sympatholytic antihypertensive medication that blocks the reuptake of norepinephrine, dopamine, and serotonin, leading to enhanced degradation by MAO in the synaptic space.
A – Antidepressants:
Tricyclic antidepressants (TCAs) can induce hypotension through α₁ receptor blockade and by causing cardiac dysrhythmias and subsequent cardiac collapse.
A – Aminophylline:
A methylxanthine that acts as an adenosine receptor antagonist, β-blocker, and phosphodiesterase inhibitor that can cause hypotension and cardiac collapse in overdose settings.
S – Sedative–Hypnotics:
Hypotension can occur secondary to myocardial depression.
H – Heroin:
Opiates can induce hypotension secondary to histamine release, direct vasodilation, or through a centrally mediated decrease of vagal tone.
Treatment:
Hypotension is best treated with large fluid boluses followed by the administration of antidotes and/or treatment of the respective toxin. Pressors may be indicated if the patient remains hypotensive after fluid resuscitation.
- Published on
Toxicology – APPROACH TO THE POISONED PATIENT
ABC’s:
As with all emergency department patients, first ensure the patient has a patent airway, is breathing, and has a pulse. Immediate intervention is required if any or all of these are absent.
Vital Signs:
Temperature, heart rate, blood pressure, respiratory rate, and O₂ saturation will help guide the diagnosis and help categorize the intoxication or overdose into one of the more common toxidromes.
History:
Attempt to get a good history using collateral sources if possible, as the poisoned patient is often unreliable or containers altered. EMS, family members, occupation, past medical records, and empty pill bottles can provide insight into the potential toxin or overdose.
Physical:
In addition to vital signs, physical examination will help tease out the clinical toxidrome.
PEARLS
ABC’s:
As with all emergency department patients, first ensure the patient has a patent airway, is breathing, and has a pulse. Immediate intervention is required if any or all of these are absent.
Vital Signs:
Temperature, heart rate, blood pressure, respiratory rate, and O₂ saturation will help guide the diagnosis and help categorize the intoxication or overdose into one of the more common toxidromes.
History:
Attempt to get a good history using collateral sources if possible, as the poisoned patient is often unreliable or containers altered. EMS, family members, occupation, past medical records, and empty pill bottles can provide insight into the potential toxin or overdose.
- What: Consider what medications the patient has access to including his or her own, as well as those of parents, friends, significant others, children and visiting relatives. Ask if the drug is an immediate-release or sustained-release product.
- When: A time frame of suspected ingestion can influence treatment options and patient disposition. For example, some toxins have a delayed onset and some antidotes must be given within a specific time frame.
- Dose: Assume that any unreliable patient took the highest possible dose. Count the number of pills remaining in their prescription bottles and subtract that amount from the initial number prescribed. Assume all missing pills were taken as a single overdose.
- Why: Was this an accidental ingestion, a therapeutic misadventure in pursuit of a “high” or in pursuit of better treatment outcomes, or was it a suicide attempt? The answer will help determine the patient’s disposition.
- Coingestions: Multiple drug ingestions are common; alcohol is the most common coingestion.
Physical:
In addition to vital signs, physical examination will help tease out the clinical toxidrome.
- Mental Status: Agitation / somnolence / paranoid / obtunded / comatose
- Skin: Wet / dry / cyanotic / erythematous / pale / hot / cold
- Eyes: Miosis / mydriasis / nystagmus / conjunctival injection / jaundice
- Mucous Membranes: Wet and salivating / dry and chapped
- Heart/EKG: Tachycardia / bradycardia / QRS widened / QT prolongation
- Lungs: Tachypnea / bradypnea / rales / wheezing / crackles
- Bowel Sounds: Hyperactive / normal / absent
- Neurological: Hyperreflexia / hyporeflexia
PEARLS
- US Poison Control Center: 1-800-222-1222
