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A 51-year-old female with poorly controlled type 1 diabetes, hyperthyroidism, and long-term smoking history.
He was admitted to the hospital with persistent nausea, vomiting, abdominal discomfort, dry cough, runny nose, and sore throat.
On physical examination, his body temperature was 36.
8°C at the time of admission, and then rose to 38.
4.
P 140 beats/min, R 28 beats/min, BP 171/79mmHg, indoor air oxygen 100%.
The patient's mental appearance is not good, the abdomen is soft, tender, and no rebound.
Auscultation of the lungs and heart was normal, and the skin was dry and spotty.
The rest of the physical examination showed no obvious abnormalities.
Laboratory examination found positive for influenza B virus at the time of admission to the emergency department, and no obvious abnormality was found on the chest radiograph (Figure 1A).
Blood gas analysis showed that the pH was 6.
96, PCO2 was 8.
8mmHg, and PO2 was 124.
4mmHg.
The blood CO2 concentration is less than 10mEq/L, and the anion gap is 20.
The blood sugar level is 586mg/dL, and the glycosylated hemoglobin (HbA1c) is 13%.
The white blood cell count was 16060/mL, and the original procalcitonin was 0.
65ng/ml, but the peak value could reach 8.
16 ng/ml.
Reexamination of chest radiograph 36 hours after admission showed consolidation of the left hilar, suggesting the rapid development of lung infiltration (Figure 1B, C).
Abdominal CT showed no obvious abnormalities.
CT angiography of the chest showed embolism in the lower lobe of the right lung, and mass consolidation in the left lung near the hilum.
(Figure 2A,B) Figure 1A The chest radiograph was normal on admission.
B chest radiograph shows new left hilar consolidation (rapid development of lung infiltration).
C Chest radiograph shows rapid development of lung infiltration.
Figure 2 A.
Chest CTA shows a large lump-like shadow in the upper left lobe.
B Chest CTA showed a large mass-like shadow in the upper left lobe, without blood vessels.
Sputum cultures were positive for Acinetobacter baumannii and Stenotrophomonas maltophilia.
Fungal examinations included serum cryptococcal antigen, histoplasmosis urine antigen, coccidioidomycosis urine antigen, serum galactomannan detection, 1, The 3-β-D glucan test was negative.
Fiberoptic bronchoscopy showed that there was obvious gray mucus extending from the left main bronchus to the left lower lobe bronchus, and bifurcated to the left upper lobe.
The tissue was fragile and necrotic.
(Figure 3A,B) Figure 3A Bronchoscopy shows healthy bronchus and necrotic bronchus in the upper left lobe.
B Bronchoscopy showed that there was obvious gray mucus extending from the left main bronchus to the left lower lobe bronchus, and bifurcated to the left upper lobe bronchoalveolar lavage fluid.
The examination of malignant cells was negative and the tissue culture was negative, but the lung tissue pathology showed wide and no septal bacteria wire.
(Fig.
4A, B) Fig.
4A.
HE staining of bronchial biopsy shows wide hyphae without separation.
B Bronchial biopsy Grocott's urotropine silver staining showed no division, irregularly branched hyphae.
Diagnosis of vascular invasive pulmonary mucormycosis.
Discussion The most common pathogens of mucormycosis are Rhizopus and Mucor.
The diagnosis is made by finding pathogenic fungi in the tissues of symptomatic patients.
Under the microscope, the hyphae are wide and not separated, with irregular right-angle branches and thin walls.
Mucor grows best in acidic high-sugar medium, which explains the susceptibility to diabetic ketoacidosis.
Men are more susceptible.
Bacterial pneumonia may initially appear in patients.
About 39% of patients are accompanied by bacteria or infected viruses, of which 74% are bacterial lung pathogens.
Despite antibiotic treatment, the disease still progresses rapidly and is life-threatening.
Pulmonary mucormycosis is characterized by infringement of blood vessels and secondary infarction, necrosis of the affected tissues, and prone to severe or even fatal hemoptysis.
Granulocytopenia, immunosuppression, diabetes, malignant tumors, bone marrow transplantation, solid organ transplantation, deferoxamine therapy, renal failure, penetrating trauma are the susceptibility factors of mucor, and there are also patients with obvious immune impairment.
Report.
Although chest radiography is abnormal in most patients with pulmonary mucormycosis, infiltrates and masses are common, and consolidation, cavitation, and effusion are relatively rare, but it usually does not indicate the source of the fungus.
Pulmonary mucormycosis should be highly suspected for patients with underlying diseases and rapid development of pulmonary infiltration, especially patients whose disease still worsens after using broad-spectrum antibiotics.
CT showing halo sign, anti-halo sign, and air crescent sign may indicate invasive fungal infection.
CT found multiple pulmonary nodules (>10) and pleural effusion are independent predictors of pulmonary mucormycosis.
Most diagnoses are made after bronchoscopy or bronchoscopy biopsy.
Others such as bronchoalveolar lavage, lung biopsy, surgery, etc.
can also be confirmed.
The mortality rate of this disease is extremely high, with a systemic disseminated mortality rate of about 96%, a gastrointestinal infection rate of 85%, and a pulmonary mucormycosis rate of 76%.
Antifungal therapy can improve survival, and surgical treatment can also provide additional benefits.
According to a study, the overall survival rate of patients receiving amphotericin B deoxycholate treatment was 61%, the survival rate of patients receiving surgery was 57%, and the survival rate of patients receiving both was 70%.
Pulmonary mucormycosis is an acute and fatal disease.
Early identification and combination of antifungal therapy and surgical treatment is the key to patient survival.
The clinical course was based on his positive test for influenza B, and he was treated with oseltamivir; he was intubated after admission to the hospital due to respiratory failure caused by severe metabolic acidosis.
After being diagnosed with diabetic ketoacidosis, he received a diabetic ketoacidosis treatment program and broad-spectrum antibiotics, and was transferred to the ICU, where heparin was injected intravenously for anticoagulation.
Despite antibiotic treatment, the fever persisted, and consolidation around the left hilar appeared.
Empiric treatment with amphotericin B was started immediately after bronchoscopy and lung histopathological examination. After pathologically confirmed as mucormycosis, he underwent left pneumonectomy and 6 weeks of amphotericin injection treatment, and then switched to 3 months of isaconazole sulfate treatment.
One year later, the patient performed well, with little impact on daily life.
Summary ➤Mormycosis is a rare vascular invasive and fatal disease caused by filamentous fungi that are ubiquitous.
➤The risk factors for mucormycosis include neutropenia, immunosuppression, diabetes, malignant tumors, bone marrow transplantation, solid organ transplantation, deferoxamine therapy, renal failure, penetrating trauma ➤for immunosuppression or risk factors In patients with rapid development of lung infiltration, mucormycosis needs to be suspected and further evaluated.
➤The drug of choice for mucormycosis is amphotericin B.
Other drugs such as pasaconazole and isaconazole sulfate can also be considered.
➤Early diagnosis combined with surgical treatment and antifungal therapy can improve patient survival.
Yimaitong compiled from: Coomes DS, et al.
Chest.
2021 Mar;159(3):e141-e145.
He was admitted to the hospital with persistent nausea, vomiting, abdominal discomfort, dry cough, runny nose, and sore throat.
On physical examination, his body temperature was 36.
8°C at the time of admission, and then rose to 38.
4.
P 140 beats/min, R 28 beats/min, BP 171/79mmHg, indoor air oxygen 100%.
The patient's mental appearance is not good, the abdomen is soft, tender, and no rebound.
Auscultation of the lungs and heart was normal, and the skin was dry and spotty.
The rest of the physical examination showed no obvious abnormalities.
Laboratory examination found positive for influenza B virus at the time of admission to the emergency department, and no obvious abnormality was found on the chest radiograph (Figure 1A).
Blood gas analysis showed that the pH was 6.
96, PCO2 was 8.
8mmHg, and PO2 was 124.
4mmHg.
The blood CO2 concentration is less than 10mEq/L, and the anion gap is 20.
The blood sugar level is 586mg/dL, and the glycosylated hemoglobin (HbA1c) is 13%.
The white blood cell count was 16060/mL, and the original procalcitonin was 0.
65ng/ml, but the peak value could reach 8.
16 ng/ml.
Reexamination of chest radiograph 36 hours after admission showed consolidation of the left hilar, suggesting the rapid development of lung infiltration (Figure 1B, C).
Abdominal CT showed no obvious abnormalities.
CT angiography of the chest showed embolism in the lower lobe of the right lung, and mass consolidation in the left lung near the hilum.
(Figure 2A,B) Figure 1A The chest radiograph was normal on admission.
B chest radiograph shows new left hilar consolidation (rapid development of lung infiltration).
C Chest radiograph shows rapid development of lung infiltration.
Figure 2 A.
Chest CTA shows a large lump-like shadow in the upper left lobe.
B Chest CTA showed a large mass-like shadow in the upper left lobe, without blood vessels.
Sputum cultures were positive for Acinetobacter baumannii and Stenotrophomonas maltophilia.
Fungal examinations included serum cryptococcal antigen, histoplasmosis urine antigen, coccidioidomycosis urine antigen, serum galactomannan detection, 1, The 3-β-D glucan test was negative.
Fiberoptic bronchoscopy showed that there was obvious gray mucus extending from the left main bronchus to the left lower lobe bronchus, and bifurcated to the left upper lobe.
The tissue was fragile and necrotic.
(Figure 3A,B) Figure 3A Bronchoscopy shows healthy bronchus and necrotic bronchus in the upper left lobe.
B Bronchoscopy showed that there was obvious gray mucus extending from the left main bronchus to the left lower lobe bronchus, and bifurcated to the left upper lobe bronchoalveolar lavage fluid.
The examination of malignant cells was negative and the tissue culture was negative, but the lung tissue pathology showed wide and no septal bacteria wire.
(Fig.
4A, B) Fig.
4A.
HE staining of bronchial biopsy shows wide hyphae without separation.
B Bronchial biopsy Grocott's urotropine silver staining showed no division, irregularly branched hyphae.
Diagnosis of vascular invasive pulmonary mucormycosis.
Discussion The most common pathogens of mucormycosis are Rhizopus and Mucor.
The diagnosis is made by finding pathogenic fungi in the tissues of symptomatic patients.
Under the microscope, the hyphae are wide and not separated, with irregular right-angle branches and thin walls.
Mucor grows best in acidic high-sugar medium, which explains the susceptibility to diabetic ketoacidosis.
Men are more susceptible.
Bacterial pneumonia may initially appear in patients.
About 39% of patients are accompanied by bacteria or infected viruses, of which 74% are bacterial lung pathogens.
Despite antibiotic treatment, the disease still progresses rapidly and is life-threatening.
Pulmonary mucormycosis is characterized by infringement of blood vessels and secondary infarction, necrosis of the affected tissues, and prone to severe or even fatal hemoptysis.
Granulocytopenia, immunosuppression, diabetes, malignant tumors, bone marrow transplantation, solid organ transplantation, deferoxamine therapy, renal failure, penetrating trauma are the susceptibility factors of mucor, and there are also patients with obvious immune impairment.
Report.
Although chest radiography is abnormal in most patients with pulmonary mucormycosis, infiltrates and masses are common, and consolidation, cavitation, and effusion are relatively rare, but it usually does not indicate the source of the fungus.
Pulmonary mucormycosis should be highly suspected for patients with underlying diseases and rapid development of pulmonary infiltration, especially patients whose disease still worsens after using broad-spectrum antibiotics.
CT showing halo sign, anti-halo sign, and air crescent sign may indicate invasive fungal infection.
CT found multiple pulmonary nodules (>10) and pleural effusion are independent predictors of pulmonary mucormycosis.
Most diagnoses are made after bronchoscopy or bronchoscopy biopsy.
Others such as bronchoalveolar lavage, lung biopsy, surgery, etc.
can also be confirmed.
The mortality rate of this disease is extremely high, with a systemic disseminated mortality rate of about 96%, a gastrointestinal infection rate of 85%, and a pulmonary mucormycosis rate of 76%.
Antifungal therapy can improve survival, and surgical treatment can also provide additional benefits.
According to a study, the overall survival rate of patients receiving amphotericin B deoxycholate treatment was 61%, the survival rate of patients receiving surgery was 57%, and the survival rate of patients receiving both was 70%.
Pulmonary mucormycosis is an acute and fatal disease.
Early identification and combination of antifungal therapy and surgical treatment is the key to patient survival.
The clinical course was based on his positive test for influenza B, and he was treated with oseltamivir; he was intubated after admission to the hospital due to respiratory failure caused by severe metabolic acidosis.
After being diagnosed with diabetic ketoacidosis, he received a diabetic ketoacidosis treatment program and broad-spectrum antibiotics, and was transferred to the ICU, where heparin was injected intravenously for anticoagulation.
Despite antibiotic treatment, the fever persisted, and consolidation around the left hilar appeared.
Empiric treatment with amphotericin B was started immediately after bronchoscopy and lung histopathological examination. After pathologically confirmed as mucormycosis, he underwent left pneumonectomy and 6 weeks of amphotericin injection treatment, and then switched to 3 months of isaconazole sulfate treatment.
One year later, the patient performed well, with little impact on daily life.
Summary ➤Mormycosis is a rare vascular invasive and fatal disease caused by filamentous fungi that are ubiquitous.
➤The risk factors for mucormycosis include neutropenia, immunosuppression, diabetes, malignant tumors, bone marrow transplantation, solid organ transplantation, deferoxamine therapy, renal failure, penetrating trauma ➤for immunosuppression or risk factors In patients with rapid development of lung infiltration, mucormycosis needs to be suspected and further evaluated.
➤The drug of choice for mucormycosis is amphotericin B.
Other drugs such as pasaconazole and isaconazole sulfate can also be considered.
➤Early diagnosis combined with surgical treatment and antifungal therapy can improve patient survival.
Yimaitong compiled from: Coomes DS, et al.
Chest.
2021 Mar;159(3):e141-e145.
