Hypercoagulable state (primary or secondary), when documented in the medical record is a CC and can, therefore, impact the length of stay, reimbursement, severity of illness and risk of mortality. Secondary hypercoagulable state is often under documented and underreported. Provider education is key in addressing this situation.
The diagnosis of hypercoagulable state is documented, is it coded? That all depends on if it meets one of the criteria for reporting a diagnosis in ICD-10-CM. Chances are, the patient is under medical treatment for the condition or monitoring and follow up is normally required.
Hypercoagulable state, secondary; Thrombophilia; ICD-10-CM D68.69 is grouped within Diagnostic Related Group(s) (MS-DRG v 38.0): 814 Reticuloendothelial and immunity disorders with mcc; 815 Reticuloendothelial and immunity disorders with cc; 816 Reticuloendothelial and immunity disorders without cc/mcc; Convert D68.69 to ICD-9-CM. Code History
The most common cause of inherited hypercoagulable state is activated protein C resistance (factor V Leiden) Malignancy/cancer is the second most common cause of hypercoagulable state and accounts for 10% to 20% of spontaneous venous thromboses
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Secondary hypercoagulable states are primarily acquired disorders that. predispose to thrombosis through complex and multifactorial mechanisms. These involve blood flow abnormalities or defects in blood composition and of. vessel walls.
Examples of conditions that can cause secondary hypercoagulable states are atrial fibrillation, malignancy, pregnancy, trauma, myeloproliferative disorders, and antiphospholipid antibody syndrome.
Primary hypercoagulable states are inherited clotting disorders in which there's a defect in a natural anticoagulant mechanism. Inherited disorders include factor V Leiden, prothrombin gene mutation, protein C and S deficiency, and antithrombin III deficiency.
Tests used to help diagnose inherited hypercoagulable states include: Genetic tests, including factor V Leiden (Activated protein C resistance) and prothrombin gene mutation (G20210A)* Antithrombin activity. Protein C activity.
eloproliferative neoplasms (MPNs), antiphospholipid syn- drome, hormone replacement therapy, use of oral contracep- tives, pregnancy, and puerperium. Most of these acquired factors cause stasis or hypercoagulability of blood, both known to predispose to venous thrombosis.
The pathophysiology of throm- boembolism is AF is multi-factorial but increasing evidence points to the fulfillment of Virchow's triad in this arrhyth- mia, leading to a prothrombotic or hypercoagulable state in AF. The loss of atrial systole in AF results in increased stasis of blood within the left atrium.
Abstract. Acquired hypercoagulable states comprise a diverse group of clinical conditions that are associated with an increased risk of thrombosis.
Patients initially become hypercoagulable because warfarin depresses levels of the anticoagulant proteins C and S more quickly than it does coagulant proteins II, VII, IX, and X. Extensive thrombosis of the venules and capillaries occurs within the subcutaneous fat.
A procoagulant state has been found to exist in diabetes mellitus. There may be activation of the intrinsic coagulation system, decreased fibrinolytic activity, or alterations in platelet function.
Heparin-induced thrombocytopenia is an example of an acquired hypercoagulable state that has been well studied and, when recognized, responds to appropriate therapy.
Hypercoagulation is a condition that causes your blood to clot more easily than normal. Hypercoagulation can be an acquired or inherited condition. Acquired hypercoagulation is caused by a disease or other condition. Examples include obesity, pregnancy, use of birth control pills, or cancer.
code to identify the carrier state ( Z22.-)
R45.7 State of emotional shock and stress, unspecif...
Hypercoagulable states are blood disorders that increase the risk of deep vein thrombosis or embolic disease. The state is either inherited or acquired. About 80% of patients with blood clots have been found to have either an inherited or acquired clotting disorder. These blood clots can be lethal and some require life-long therapy. Hypercoagulable state is also known as thrombophilia. The patients that fall into one of these disorders have an increased tendency to develop blood clots. This is due to the presence of either an inherited factor or an acquired factor.
Malignancy/cancer is the second most common cause of hypercoagulable state and accounts for 10% to 20% of spontaneous venous thromboses
These include the disorders such as protein C and S, heparin cofactor, antithrombin III, fibrinogen, factor XIII, prothrombin, and plasminogen
Factor V Leiden mutation—this is the most common inherited factor associated hypercoagulopathy
If only hypercoagulable state is diagnosed, can the coder look at the patient’s other diseases/diagnoses and determine by that if they have primary or secondary? NO! Only the physician can make the link between the cause/effect.
The diagnosis of hypercoagulable state is documented, is it coded? That all depends on if it meets one of the criteria for reporting a diagnosis in ICD-10-CM. Chances are, the patient is under medical treatment for the condition or monitoring and follow up is normally required. If documentation is unclear, a query would be needed to clarify if this was clinically significant on the current admission. Most often, primary hypercoagulable state will be reported as these don’t go away. For the secondary hypercoagulable state, if the acquired disorder resolves, so may the hypercoagulable state in most patients.
If labs show that a patient has a prolonged prothrombin time, is this the same as hypercoagulable state? No!
The hypercoagulable states are a group of acquired and inherited disorders that increase the risk of abnormal development of blood clots.
The mechanisms of activation of the coagulation system following surgery or trauma are incompletely understood as of this presentation, but may include decreased venous blood flow in the lower extremities, diminished fibrinolysis, immobilization, the release or exposure of tissue factor, and depletion of endogenous anticoagulants such as antithrombin.
The prophylactic intervention is regarding VTE. You will not code DVT for example since the patient has not developed it (yet.) You can, however, code the HCS if documented and supported by the provider since the patient has already developed it.