Lack of documentation
We have received a couple of denials for D68.69 Other Thrombophillia/Hypercoagulable State due to "lack of documentation". I discussed the rational the insurance company sent with our internal medicine doctors. However, our docs believe that due to the nature of procedure (joint replacements) that this is a condition being monitored and treated. Their rational is that a major surgery such as a joint replacement places the patient in a temporary hypercoagulable state that must be monitored. The insurance company state that "it is not unexpected to administer prophylactic anticoagulant therapy in the setting of orthopedic surgery to guard against the possible development of thrombi".
My question is, what documentation is needed? Has any one had this same problem, and what did you do? Sorry if this is unclear. I can try to explain more if needed.
Thanks,
Karen
Comments
yeah. I mean this is standard prophylaxis. I have never seen this dx documented in our joint program. to me its similar to 'empiric PNA coverage'. does not meet criteria as a reportable condition.
IMO there is no basis to code a disease in this situation...documentation w. actual existence of hypercoagulable status would be a different manner. Providing treatment to prevent something from happening, alone, does not result in a reportable disorder..again, my opinion.
P. Evans, RHIA
I agree paul. but then there is this....
ICD-9-CM Coding Clinic, First Quarter 2002 Page: 16 to 17 Effective with discharges: March 15, 2002
Related Information
Question:
What is the appropriate code assignment for hypercoagulable state?
Answer:
Note from 3M :
As of October 1, 2003, code 289.8 has been expanded to the fifth digit to further specify other specified diseases of blood and blood-forming organs.
Assign code 289.8, Other specified disease of blood and blood-forming organs, for the hypercoagulable state. A hypercoagulable state is a condition in which there is an increased tendency for blood clotting, which may be demonstrated by fibrin deposition in the small blood vessels, and caused by excess thrombin generation. The hypercoagulable state may be due to a number of conditions, including a genetic predisposition to clotting. Other causes include, but are not limited to the following: medications (estrogen), postsurgical period (particularly
after joint procedures), pregnancy, anticardiolipin antibodies, phospholipid antibodies in blood (i.e., lupus anticoagulant or anticardiolipin antibodies), malignancy, elevated blood homocysteine levels and inherited protein deficiencies (antithrombin lll, factor V Leiden, protein S, protein C, etc.).
to me that CC confuses things. But I have never personally seen our MD's document this and we don't query for it. I think we should also be considering what's inherent. Much like ABLA. We generally are looking for something outside the norm. Not typical surgical blood loss.
Perhaps construct a query using concepts from Virchow's Triangle?
Virchow's triad or the triad of Virchow (/ˈfɪrkoʊ/) describes the three broad categories of factors that are thought to contribute to thrombosis.[1]
The new guideline for 2017 states that you cant use clinical criteria to determine if coding is appropriate. As always, coding should be based off physician documentation alone. Though we still have to unsure that UHDDS criteria is met prior to coding.
Here is what I would do. You have already spoken to the physician. I am assuming you explained the denial issue. I would tell him that you understand that he feels this diagnosis and this is fine. But ask if he can help formulate an appeals letter that can be submitted (with his signature) when these cases are denied. I have found physician statements to be incredibly powerful in denial appeals and this is a great opportunity to engage the physician in this process.
We did get an appeals letter from the physician, and sent it in to help with a denial for D68.69. Unfortunately, the denial was upheld. My question now is should we have the coders not code D68.69? The physician insists on using it. Any ideas would be greatly appreciated.
I am going to side with the physician. The source below indicates the clinical truth is that this goes beyond preventative treatment and is a legitimate clinical diagnoses in this population.
Once again, the auditors are under-educated (as was I on this topic).
References:
"In patients undergoing total hip or total knee arthroplasty (THA or TKA, respectively), different patterns of altered venous hemodynamics and hypercoagulability have been found, thus the rate of distal DVT is higher than that of proximal DVT after TKA.
During major orthopedic surgery (such as THA and TKA), substantial trauma to the soft tissues and bone is inevitable. Injury to the vascular wall causes raised levels of tissue factor, one of the potent activators of coagulation. Activation of coagulation results in the generation of excessive amounts of thrombin, which then leads to thrombus formation and platelet activation.10 In addition, mechanical destruction of the bone marrow during these surgical procedures can also cause release of marrow cells and cell fragments into the circulation.11 The type and extent of surgery may also have different impacts on hemodynamics and thrombosis.12,13 After THA, the activation of coagulation was reported to continue for more than 5 weeks.1
Cessation or a decrease in blood flow may occur during manipulation of the limb during surgery. Distension of the vessel wall as a result of the pooled blood can also cause further endothelial damage and the subsequent activation of coagulation.15 There is evidence that blood flow is reduced in both legs after joint arthroplasty, mostly on the same side of the body as the operation.13 However, different patterns of altered venous hemodynamics have been observed in patients undergoing THA or TKA. After TKA, venous blood flow is temporarily reduced for up to 6 days, whereas it is reduced for more than 6 weeks after THA.12,13 Moreover, venous flow in the operated leg has been shown to be significantly lower in patients with DVT than in those without DVT.12 Manipulation of the limb and the use of a tourniquet in patients undergoing TKA also contribute to venous stasis. In addition, postoperative immobilization and swelling of the leg after surgery are among the other reasons contributing to the reduced venous return and thus increase the risk of DVT. Most clinically relevant DVTs occur in the lower extremities.16
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3195664/
My question would be if it is ALWAYS present wouldn't it be integral?
"https://www.cms.gov/Medicare/Coding/ICD10/Downloads/2017-ICD-10-CM-Guidelines.pdf... page 14
Conditions that are an integral part of a disease process
Signs and symptoms that are associated routinely with a disease process should not be assigned as additional codes, unless otherwise instructed by the classification.
Conditions that are not an integral part of a disease process Additional signs and symptoms that may not be associated routinely with a
disease process should be coded when present.
Fair point. Does it always result? Note the specific language above: 1: "Have been found" (ie, in SOME patients, not all). 2: "Can also cause" (some times happens, not always) 3: "May also have" (depends on the specific surgery and patient variables). 4) "May occur during" (depends on the position) 5) "Different patterns...have been observed".
It is common yes, but I don't think one could reasonably make the argument that every joint replacement surgery will automatically result in a DVT nor that everyone has the same occurrence rate and severity of coagulopathy post operative.
Since there is so much variability then I would assume it is not "routinely" associated. However we are on a slipper slope, because coding clinic does not define a specific occurrence rate to meet the threshold of "routine".
What is routinely associated for sure is the "increased risk". If the diagnosis was "risk of coagulopathy" then it absolutely would be integral and not reportable.
Increased risk however is not a part of the definition you cited from the guidelines. The definition you cited from the guidelines is actual occurrence of the disorder (which would be the manifestation of significantly reduced clotting times and the presence of DVT's).
I can't solve the issues, I just like dissecting them.