Septic thrombosis

Introduction Sepsis is a general term for a surgical infection with a systemic inflammatory response. It refers to a systemic severe reaction caused by an infection, a general term for a surgical infection that has a marked change in body temperature, circulation, and breathing. Sepsis, sepsis. It is a clinical syndrome caused by infection. Suppurative pathogens invade the bloodstream and multiply in them, and spread to the whole body with blood flow, new multiple suppurative lesions caused by tissues and organs. For example, sepsis caused by Staphylococcus aureus, often caused by multiple liver abscess, kidney abscess and so on.

Cause

After the purulent bacteria invade the bloodstream, they multiply and spread through the bloodstream to other tissues or organs of the host to produce new purulent lesions.

an examination

Related inspection

White blood cell count (WBC) body temperature measurement

Sepsis

Evidence of pathogenic microbial infection with two or more of the following:

Body temperature > 38oC or, heart rate > 90 beats / min, respiration > 20 beats / min or CO2 partial pressure, white blood cell count > 12 × 109 / L or 10%.

Severe sepsis, with symptoms of sepsis, and has the following manifestations:

Organ dysfunction, hypotension (arterial systolic blood pressure drop > 40 mmHg), systemic low blood perfusion (lactic acidosis, oliguria, central nervous system symptoms, other organ symptoms.

Infectious (sepsis) shock, with sepsis, severe sepsis symptoms, and the following manifestations: hypotension, and infusion is ineffective; low blood perfusion (severe sepsis), hypoperfusion, The systolic blood pressure is 40 mm Hg relative to the basal pressure, and the low perfusion due to other factors is excluded.

Multiple organ dysfunction syndrome (MODS): A clinical syndrome in which an acutely ill patient cannot maintain homeostasis without intervention, or two or more acute organ dysfunctions.

Differential diagnosis

Internal carotid artery traumatic thrombosis: The common carotid artery is the main artery of the head and neck, and the upper thyroid cartilage branches into the internal carotid artery and the external carotid artery. The incidence of traumatic embolism is higher in the internal carotid artery. Because the internal carotid artery mainly supplies blood to the brain and the visual device, the embolization has serious consequences. Internal carotid artery embolization can occur in the cervical segment, the rock segment, the cavernous sinus segment or the upper segment of the bed. According to the analysis of 70 cases, 85% occurred in the cervical segment and 10% in the rock segment. Internal carotid artery embolism occurs in patients with cervical contusion after a transient ischemic attack, followed by neurological symptoms, which is characteristic of internal carotid artery embolism.

Venous thrombosis: In the case of venous blood flow, hypercoagulable state and endovascular damage, acute non-suppurative inflammation occurs in the vein, and thrombosis is secondary. The vast majority of venous thrombosis occurs in the deep veins of the pelvis and lower extremities. More common in postpartum, fractures and trauma, patients after surgery. In the event of limb pain, swelling, superficial venous engorgement and a cord that can be touched along the vein, the possibility of the disease should be considered. Ultrasound Doppler, radionuclide venography can help diagnose. It is easy to fall off in the early stage of thrombosis, which can cause large pulmonary infarction, which is often one of the causes of sudden death.

Thrombotic neoplasm: The neoplasm is a general term for various protrusions formed in the pathological process inside and outside the body or organ. Thrombotic neoplasms are more common in non-bacterial thrombotic endocarditis. Non-bacterial thrombotic endocarditis can involve any heart valve, primarily affecting the mitral and aortic valves.

Second, the mitral mites are mostly located in the atrial surface, and the aortic and pulmonary valves are mostly located on the ventricular surface. The main pathological change of non-bacterial thrombotic endocarditis is the formation of aseptic neoplasms on the valve. The early changes are the degeneration of valvular collagen under the influence of allergies, vitamin deficiency, hemodynamic damage and aging. The matrix edema, followed by partial exfoliation of the intima of the valve, exposes the collagen and the matrix to the bloodstream. When the antibody is in a hypercoagulable state, platelets and the like easily adhere to the surface to form non-bacterial thrombotic neoplasms. The lesions are more superficial, and there is often no inflammatory reaction in the local area. Once the neoplasms fall off, the signs of arterial embolism can be generated.

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