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Author: Li Yunan, Tianjin Medical University General Hospital Airport Hospital -24 admissions
.
History of present illness: One month before admission, the patient developed subcostal pain during nighttime sleep without obvious incentive, first on the left side, then on the right side, persistent, aggravated by deep breathing, accompanied by wheezing and suffocation during activities; the pain did not affect sleep; none Fever, cough, expectoration, hemoptysis; no dizziness, syncope, edema of both lower extremities; no rash, joint pain; no fatigue, night sweats and other discomforts
.
He was then admitted to a tertiary hospital, and chest CT showed: nodular thickening of the right pleura, bilateral pleural effusion, right pulmonary lesions, nodules in the right lower lobe, right middle lobe, left lingual lobe and both lower lobes Inflation, pericardial effusion, anemia changes
.
After moxifloxacin anti-infection and other treatment, the symptoms of chest pain were slightly relieved, and there was no change in the chest CT scan
.
One week before admission, the symptoms of suffocation were worse than before, and suffocation occurred after climbing 2 stairs, and there was no other discomfort
.
Followed up to the outpatient department of our hospital, and the chest examination showed: patchy nodular subsolid lesions in the left lower lobe, the nature is to be determined, patch shadows, ground-glass density shadows and cord shadows at the bottom of both lungs, considering poor expansion of lung tissue and chronic inflammation , bilateral pleural thickening, right pleural effusion (see Figure 1)
.
Immune complete item + rheumatic antibody: ANA positive (cytoplasmic type 1:160 homogeneous type 1:160) IgG1700mg/dl, CRP1.
31mg/dl; ANCA negative
.
Treated with cefdinir and carbocisteine
.
She is now admitted to the hospital for further diagnosis and treatment
.
Since the onset of the disease, the patient's spirit, sleep, and appetite are normal
.
Past history: cesarean section performed 9 years ago
.
Personal history and family history are unremarkable
.
Physical examination: body temperature 36.
5°C, pulse 72 beats/min, respiration 20 beats/min, blood pressure 113/68mmHg
.
Sober and sane
.
The skin and mucous membranes of the whole body are not yellow or pale, the lips are not cyanotic, there is no superficial lymph node enlargement, the neck is soft, there is no sense of resistance, there is no jugular vein filling, the trachea is in the middle, the thoracic shape is normal, there is no widening of the intercostal space, and both lungs are breathing.
Coarse sound, palpable sputum sound in both lungs, no enlargement of cardiac borders on percussion, heart rate 72 beats/min, regular rhythm, no murmur, flat abdomen, no abdominal tenderness, no abdominal rebound tenderness, no liver, no spleen, Hepatic jugular venous reflux sign was negative, and there was no edema in both lower extremities
.
2021-11-16 Auxiliary examination of chest CT scan: blood gas analysis: FiO2 29%, pH 7.
45, pCO2 34.
9mmHg, PO2 91.
5mmHg, HCO3 23.
7mmol/L
.
Blood routine: WBC 6.
47*10^9/L, RBC3.
89*10^12/L, HB 99g/L, PLT 108*10^9/L, N56.
9%, L 28.
9%, E% 8.
5%
.
Coagulation function: APTT 50.
9s ↑ , FIB4.
43g/L ↑ , DD3972/ml ↑
.
Biochemical: liver, kidney function, electrolytes normal
.
Infection indicators: T-SPOT negative, Cryptococcus capsular polysaccharide antigen negative
.
Anti-cancer + lung standard: CA125 106.
3U/mL↑, SCC 1.
8ug/L↑, NSE 19.
64ug/L↑
.
Urine and stool routine were normal
.
B-ultrasound of lower extremity veins: thrombosis in the distal end of the right external iliac vein and common femoral vein; no thrombosis in the right great saphenous vein, superficial femoral vein, and popliteal vein; left great saphenous vein, common femoral vein, superficial femoral vein, and popliteal vein No abnormality was found in veins and intermuscular veins
.
2021-11-25 Electrocardiogram 2021-11-25 Multiple pulmonary embolism was found in chest CTPA.
The chest CTPA found multiple filling defects in both pulmonary arteries and diagnosed acute pulmonary embolism
.
Myocardial markers: CK, CK-MB, TNT were normal, bedside echocardiography: echocardiography: mild mitral valve, tricuspid valve regurgitation, pulmonary artery systolic blood pressure 37mmHg
.
Although according to the Chinese Medical Association's pulmonary thromboembolism guidelines, the patient has no hemodynamics and right ventricular dysfunction, the risk stratification is low risk, and anticoagulation therapy should be given; but according to the patient's lower extremity vein B-ultrasound results, the right external iliac vein is far away Thrombosis in the distal and common femoral veins, the D-dimer level was significantly increased, and CTPA indicated multiple filling defects of bilateral pulmonary arteries.
The embolization site was close to the main pulmonary artery, and the thrombus burden was high
.
Therefore, the inferior vena cava filter was implanted at the same time as anticoagulation
.
The course of treatment went well, and at the same time we wanted to further explore the cause behind the patient's pulmonary embolism
.
The etiology of pulmonary embolism is mainly divided into: 1.
Genetic risk factors such as antithrombin deficiency, protein C, protein S, plasminogen, factor VII deficiency, etc.
; 2.
Acquired risk factors such as paralysis, long-term bed rest, long-distance travel Venous blood flow stasis caused by etc.
, fractures, major surgery, use of intravenous chemotherapy drugs, central venous catheters, pacemakers, etc.
caused by vascular endothelial damage, tumors, nephrotic syndrome, inflammatory bowel disease, anticardiolipin antibodies, oral Contraceptives, obesity, etc.
cause blood hypercoagulability
.
First of all, we carefully asked the patient's medical history.
The cause of the patient's cesarean section 9 years ago was pregnancy-induced hypertension and premature birth
.
Further improve the immune system + rheumatic antibody + ANCA: ANA positive (homogeneity 1:160, cytoplasmic type 1:160), immunoglobulin G2070mg/dl, CRP2.
55mg/dl, light chain KAP 1530mg/dl ↑, Light chain LAM 1190 mg/dl ↑
.
RA5 item + SLE2 item: RA33 antibody 50.
8U/L, anti-double-stranded DNA antibody 37.
7IU/ml, anti-complement C1q antibody 7.
3U/ml
.
Anticardiolipin antibodies: positive
.
Lupus anticoagulant test: standardized dRWT ratio 3.
03 ↑, standardized SCT ratio 2.
52 ↑, detected lupus anticoagulant
.
Anti-β2 glycoprotein 1 antibody IgG301.
37RU/ml, anti-β2 glycoprotein 1 antibody IgM84.
64RU/ml
.
According to the 2006 sapporo classification of antiphospholipid syndrome, the patient had a history of pathological pregnancy, pulmonary embolism and positive antiphospholipid antibodies, and the diagnosis of antiphospholipid syndrome was clear
.
Discussion Chest pain is a very common complaint in clinical practice and may be the first manifestation of fatal diseases such as myocardial infarction, aortic dissection, and acute pulmonary embolism
.
Past medical history, nature of chest pain, monitoring of vital signs, careful physical examination, electrocardiogram, detection of serum myocardial markers and D-dimer can help us identify most acute diseases
.
The clinical presentation of pulmonary embolism is highly heterogeneous, ranging from asymptomatic to chest pain, severe dyspnea, syncope, and sudden death
.
Simplified Wells score and Genava score can help to quickly identify patients with high probability of acute pulmonary embolism, but for patients with atypical presentation, even low probability of D-dimer detection should be further refined
.
For young women with pulmonary embolism, focus on contraceptive use, pregnancy history, and family history (thrombosis, tumor, rheumatic immune disease)
.
Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by thrombosis and/or pathological pregnancy as the main clinical features, and a group of syndromes with persistent positive antiphospholipid antibodies in laboratory tests
.
APS can occur alone, called primary APS; it can also coexist with autoimmune diseases such as systemic lupus erythematosus or rheumatoid arthritis, called secondary APS
.
Rarely, multiple-site thrombosis occurs in a short period of time, resulting in multiple organ failure, known as catastrophic APS
.
For APS patients with first-episode venous thrombosis, warfarin therapy is recommended (INR2-3), and new oral anticoagulants are not recommended
.
References 1.
Wang Chen, et al.
Guidelines for the diagnosis, treatment and prevention of pulmonary thromboembolism Chinese Journal of Medicine.
2018.
98(14): p.
1060-102.
Chaturvedi, S.
and KR McCrae, Diagnosis and management of the antiphospholipid syndrome.
Blood Rev, 2017.
31(6): p.
406-417.
3.
Miyakis, S.
, et al.
, International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS).
J Thromb Haemost, 2006.
4( 2): p.
295-306.
.
History of present illness: One month before admission, the patient developed subcostal pain during nighttime sleep without obvious incentive, first on the left side, then on the right side, persistent, aggravated by deep breathing, accompanied by wheezing and suffocation during activities; the pain did not affect sleep; none Fever, cough, expectoration, hemoptysis; no dizziness, syncope, edema of both lower extremities; no rash, joint pain; no fatigue, night sweats and other discomforts
.
He was then admitted to a tertiary hospital, and chest CT showed: nodular thickening of the right pleura, bilateral pleural effusion, right pulmonary lesions, nodules in the right lower lobe, right middle lobe, left lingual lobe and both lower lobes Inflation, pericardial effusion, anemia changes
.
After moxifloxacin anti-infection and other treatment, the symptoms of chest pain were slightly relieved, and there was no change in the chest CT scan
.
One week before admission, the symptoms of suffocation were worse than before, and suffocation occurred after climbing 2 stairs, and there was no other discomfort
.
Followed up to the outpatient department of our hospital, and the chest examination showed: patchy nodular subsolid lesions in the left lower lobe, the nature is to be determined, patch shadows, ground-glass density shadows and cord shadows at the bottom of both lungs, considering poor expansion of lung tissue and chronic inflammation , bilateral pleural thickening, right pleural effusion (see Figure 1)
.
Immune complete item + rheumatic antibody: ANA positive (cytoplasmic type 1:160 homogeneous type 1:160) IgG1700mg/dl, CRP1.
31mg/dl; ANCA negative
.
Treated with cefdinir and carbocisteine
.
She is now admitted to the hospital for further diagnosis and treatment
.
Since the onset of the disease, the patient's spirit, sleep, and appetite are normal
.
Past history: cesarean section performed 9 years ago
.
Personal history and family history are unremarkable
.
Physical examination: body temperature 36.
5°C, pulse 72 beats/min, respiration 20 beats/min, blood pressure 113/68mmHg
.
Sober and sane
.
The skin and mucous membranes of the whole body are not yellow or pale, the lips are not cyanotic, there is no superficial lymph node enlargement, the neck is soft, there is no sense of resistance, there is no jugular vein filling, the trachea is in the middle, the thoracic shape is normal, there is no widening of the intercostal space, and both lungs are breathing.
Coarse sound, palpable sputum sound in both lungs, no enlargement of cardiac borders on percussion, heart rate 72 beats/min, regular rhythm, no murmur, flat abdomen, no abdominal tenderness, no abdominal rebound tenderness, no liver, no spleen, Hepatic jugular venous reflux sign was negative, and there was no edema in both lower extremities
.
2021-11-16 Auxiliary examination of chest CT scan: blood gas analysis: FiO2 29%, pH 7.
45, pCO2 34.
9mmHg, PO2 91.
5mmHg, HCO3 23.
7mmol/L
.
Blood routine: WBC 6.
47*10^9/L, RBC3.
89*10^12/L, HB 99g/L, PLT 108*10^9/L, N56.
9%, L 28.
9%, E% 8.
5%
.
Coagulation function: APTT 50.
9s ↑ , FIB4.
43g/L ↑ , DD3972/ml ↑
.
Biochemical: liver, kidney function, electrolytes normal
.
Infection indicators: T-SPOT negative, Cryptococcus capsular polysaccharide antigen negative
.
Anti-cancer + lung standard: CA125 106.
3U/mL↑, SCC 1.
8ug/L↑, NSE 19.
64ug/L↑
.
Urine and stool routine were normal
.
B-ultrasound of lower extremity veins: thrombosis in the distal end of the right external iliac vein and common femoral vein; no thrombosis in the right great saphenous vein, superficial femoral vein, and popliteal vein; left great saphenous vein, common femoral vein, superficial femoral vein, and popliteal vein No abnormality was found in veins and intermuscular veins
.
2021-11-25 Electrocardiogram 2021-11-25 Multiple pulmonary embolism was found in chest CTPA.
The chest CTPA found multiple filling defects in both pulmonary arteries and diagnosed acute pulmonary embolism
.
Myocardial markers: CK, CK-MB, TNT were normal, bedside echocardiography: echocardiography: mild mitral valve, tricuspid valve regurgitation, pulmonary artery systolic blood pressure 37mmHg
.
Although according to the Chinese Medical Association's pulmonary thromboembolism guidelines, the patient has no hemodynamics and right ventricular dysfunction, the risk stratification is low risk, and anticoagulation therapy should be given; but according to the patient's lower extremity vein B-ultrasound results, the right external iliac vein is far away Thrombosis in the distal and common femoral veins, the D-dimer level was significantly increased, and CTPA indicated multiple filling defects of bilateral pulmonary arteries.
The embolization site was close to the main pulmonary artery, and the thrombus burden was high
.
Therefore, the inferior vena cava filter was implanted at the same time as anticoagulation
.
The course of treatment went well, and at the same time we wanted to further explore the cause behind the patient's pulmonary embolism
.
The etiology of pulmonary embolism is mainly divided into: 1.
Genetic risk factors such as antithrombin deficiency, protein C, protein S, plasminogen, factor VII deficiency, etc.
; 2.
Acquired risk factors such as paralysis, long-term bed rest, long-distance travel Venous blood flow stasis caused by etc.
, fractures, major surgery, use of intravenous chemotherapy drugs, central venous catheters, pacemakers, etc.
caused by vascular endothelial damage, tumors, nephrotic syndrome, inflammatory bowel disease, anticardiolipin antibodies, oral Contraceptives, obesity, etc.
cause blood hypercoagulability
.
First of all, we carefully asked the patient's medical history.
The cause of the patient's cesarean section 9 years ago was pregnancy-induced hypertension and premature birth
.
Further improve the immune system + rheumatic antibody + ANCA: ANA positive (homogeneity 1:160, cytoplasmic type 1:160), immunoglobulin G2070mg/dl, CRP2.
55mg/dl, light chain KAP 1530mg/dl ↑, Light chain LAM 1190 mg/dl ↑
.
RA5 item + SLE2 item: RA33 antibody 50.
8U/L, anti-double-stranded DNA antibody 37.
7IU/ml, anti-complement C1q antibody 7.
3U/ml
.
Anticardiolipin antibodies: positive
.
Lupus anticoagulant test: standardized dRWT ratio 3.
03 ↑, standardized SCT ratio 2.
52 ↑, detected lupus anticoagulant
.
Anti-β2 glycoprotein 1 antibody IgG301.
37RU/ml, anti-β2 glycoprotein 1 antibody IgM84.
64RU/ml
.
According to the 2006 sapporo classification of antiphospholipid syndrome, the patient had a history of pathological pregnancy, pulmonary embolism and positive antiphospholipid antibodies, and the diagnosis of antiphospholipid syndrome was clear
.
Discussion Chest pain is a very common complaint in clinical practice and may be the first manifestation of fatal diseases such as myocardial infarction, aortic dissection, and acute pulmonary embolism
.
Past medical history, nature of chest pain, monitoring of vital signs, careful physical examination, electrocardiogram, detection of serum myocardial markers and D-dimer can help us identify most acute diseases
.
The clinical presentation of pulmonary embolism is highly heterogeneous, ranging from asymptomatic to chest pain, severe dyspnea, syncope, and sudden death
.
Simplified Wells score and Genava score can help to quickly identify patients with high probability of acute pulmonary embolism, but for patients with atypical presentation, even low probability of D-dimer detection should be further refined
.
For young women with pulmonary embolism, focus on contraceptive use, pregnancy history, and family history (thrombosis, tumor, rheumatic immune disease)
.
Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by thrombosis and/or pathological pregnancy as the main clinical features, and a group of syndromes with persistent positive antiphospholipid antibodies in laboratory tests
.
APS can occur alone, called primary APS; it can also coexist with autoimmune diseases such as systemic lupus erythematosus or rheumatoid arthritis, called secondary APS
.
Rarely, multiple-site thrombosis occurs in a short period of time, resulting in multiple organ failure, known as catastrophic APS
.
For APS patients with first-episode venous thrombosis, warfarin therapy is recommended (INR2-3), and new oral anticoagulants are not recommended
.
References 1.
Wang Chen, et al.
Guidelines for the diagnosis, treatment and prevention of pulmonary thromboembolism Chinese Journal of Medicine.
2018.
98(14): p.
1060-102.
Chaturvedi, S.
and KR McCrae, Diagnosis and management of the antiphospholipid syndrome.
Blood Rev, 2017.
31(6): p.
406-417.
3.
Miyakis, S.
, et al.
, International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS).
J Thromb Haemost, 2006.
4( 2): p.
295-306.
