M31.19

Clinical Causes: Autoimmune responses where the body's immune system mistakenly attacks its own tissues, leading to clotting abnormalities. Genetic factors that may predispose individuals to develop TMA, often involving deficiencies in specific enzymes such as ADAMTS13. Certain medications that can trigger TMA as a side effect, including some chemotherapeutic agents and drug combinations. Infections caused by bacteria or viruses which can lead to blood vessel inflammation and clot formation. Other underlying health conditions, such as cancer or organ transplants, that can increase the risk of developing TMA. Pregnancy-related complications, including preeclampsia or eclampsia, which can sometimes precipitate TMA.

Key Symptoms: Pallor or unusual skin paleness due to anemia Bruising or bleeding tendencies caused by low platelet counts Neurological symptoms such as headaches, confusion, or seizures Fever and general malaise or weakness Abdominal pain, nausea, or vomiting Dark urine indicating possible kidney involvement Swelling or signs of kidney failure in severe cases

Diagnosis Path: Diagnosing TMA involves a combination of clinical assessment and laboratory tests. Healthcare providers may perform blood tests to check for low platelet counts, anemia, and signs of hemolysis (destruction of red blood cells). Additional tests might include blood clotting studies, kidney function tests, and specific antibody or enzyme level assessments. Sometimes, a blood film examination under a microscope can reveal abnormal blood cell shapes. In some cases, genetic testing helps identify hereditary forms of TMA.

Treatment Protocols: Treatment strategies depend on the specific type and severity of TMA. Common approaches include: