Thrombocytopenia, unspecified. D69.6 is a billable/specific ICD-10-CM code that can be used to indicate a diagnosis for reimbursement purposes. The 2020 edition of ICD-10-CM D69.6 became effective on October 1, 2019.
Thrombocytopenia is defined as a platelet count less than 150,000/μL [1]. Up to 76% of patients with chronic liver disease are thought to have some degree of thrombocytopenia which higher incidence observed in patients with cirrhosis [2].
Liver disease, unspecified. K76.9 is a billable/specific ICD-10-CM code that can be used to indicate a diagnosis for reimbursement purposes. The 2020 edition of ICD-10-CM K76.9 became effective on October 1, 2019.
When a type 2 excludes note appears under a code it is acceptable to use both the code ( D61.81) and the excluded code together. pancytopenia (due to) (with) myelodysplastic syndromes (. ICD-10-CM Diagnosis Code D46. D46 Myelodysplastic syndromes.
ICD-10-CM Code for Thrombocytopenia, unspecified D69. 6.
ICD-10 | Thrombocytopenia, unspecified (D69. 6)
D69. 5 - Secondary thrombocytopenia | ICD-10-CM.
Secondary ITP is known to be caused by systemic autoimmune disorders, primary or secondary immunodeficiency, infectious diseases, paraneoplastic syndromes (e.g., lymphomas and other malignancies), and drug-dependent antibodies (5).
ICD-10-CM Code for Liver disease, unspecified K76. 9.
Table 1ICD-10-AM coden with codeCirrhosisK70.3 Alcoholic cirrhosis of liver193K74.4 Secondary biliary cirrhosis*12K74.5 Biliary cirrhosis, unspecified617 more rows•Sep 17, 2020
Leucopenia is a condition with too few white blood cells. Low platelet count is called thrombocytopenia. Pancytopenia occurs when a person has a decrease in all three blood cell types. This happens when something is wrong with the bone marrow, where blood cells are formed.
Other secondary thrombocytopenia D69. 59 is a billable/specific ICD-10-CM code that can be used to indicate a diagnosis for reimbursement purposes. The 2022 edition of ICD-10-CM D69. 59 became effective on October 1, 2021.
9: Fever, unspecified.
Abstract. Secondary thrombocytopenia is similar to primary or idiopathic thrombocytopenia (ITP) in that it is characterized by reduced platelet production or increased platelet destruction resulting in platelet levels<60,000/microL.
What causes thrombocytopenia?Alcohol use disorder and alcoholism.Autoimmune disease which causes ITP. ... Bone marrow diseases, including aplastic anemia, leukemia, certain lymphomas and myelodysplastic syndromes.Cancer treatments like chemotherapy and radiation therapy.More items...•
Thrombocytopenia occurs occasionally after naturally occurring infection with cytomegalovirus, rubella, Epstein-Barr virus, VZV, the severe acute respiratory syndrome coronavirus, and many others.
Clinical Information. A condition in which there is a lower-than-normal number of platelets in the blood. It may result in easy bruising and excessive bleeding from wounds or bleeding in mucous membranes and other tissues.
The 2022 edition of ICD-10-CM D69.6 became effective on October 1, 2021.
A decrease in the number of platelets in the blood that may result in easy bruising and excessive bleeding from wound s or bleeding in mucous membranes and other tissues. A finding based on laboratory test results that indicate a decrease in number of platelets in a blood specimen. A subnormal level of blood platelets.
The 2022 edition of ICD-10-CM D69.5 became effective on October 1, 2021.
D50-D89 Diseases of the blood and blood-forming organs and certain disorders involving the immune mechanism
Liver disorder in pregnancy. Liver disorder in pregnancy - delivered. Liver disorder of pregnancy, after childbirth. Nonalcoholic liver disease, chronic. Clinical Information. A non-neoplastic or neoplastic disorder that affects the liver parenchyma and intrahepatic bile ducts.
The 2022 edition of ICD-10-CM K76.9 became effective on October 1, 2021.
Others can be the result of drugs, poisons or drinking too much alcohol. If the liver forms scar tissue because of an illness, it's called cirrhosis. jaundice, or yellowing of the skin, can be one sign of liver disease. cancer can affect the liver. You could also inherit a liver disease such as hemochromatosis.
441 Disorders of liver except malignancy, cirrhosis or alcoholic hepatitis with mcc. 442 Disorders of liver except malignancy, cirrhosis or alcoholic hepatitis with cc. 443 Disorders of liver except malignancy, cirrhosis or alcoholic hepatitis without cc/mcc. 791 Prematurity with major problems.
The 2022 edition of ICD-10-CM K71.11 became effective on October 1, 2021.
K71.6 Toxic liver disease with hepatitis, not elsewhere classified. K71.7 Toxic liver disease with fibrosis and cirrhosis of liver. K71.8 Toxic liver disease with other disorders of liver. K71.9 Toxic liver disease, unspecified.
Deficiency of all three cell elements of the blood, erythrocytes, leukocytes and platelets.
The 2022 edition of ICD-10-CM D61.81 became effective on October 1, 2021.
D50-D89 Diseases of the blood and blood-forming organs and certain disorders involving the immune mechanism
Thrombocytopenia is a common hematological abnormality in patients with chronic liver disease (CLD). Thrombocytopenia is defined as a platelet count less than 150,000/μL [1]. Up to 76% of patients with chronic liver disease are thought to have some degree of thrombocytopenia which higher incidence observed in patients with cirrhosis [2]. The clinical significance of mild thrombocytopenia (75,000/μL- 150,000/μL) is minimal and usually does not require treatment [2]. However, severe thrombocytopenia (<50,000/μL) can often complicate the management of patients with chronic liver disease due to increased risk of bleeding. This review focuses on the pathophysiology and the current treatment strategies for the treatment of thrombocytopenia in chronic liver disease.
This can be broken down into two broader causes: decreased production of platelets, and increased destruction. The decreased production of platelets can be attributed to both a reduction in thrombopoietin production in the liver and reduced bone marrow production of platelets secondary to several inhibiting causes [3]. Hepatic production of thrombopoietin plays a pivotal role in thrombopoiesis. Thrombopoietin (TPO), in turn, binds to the c-mpl receptor on megakaryocytes regulating their differentiation into platelets [3]. There is a recognized direct correlation between chronic liver disease and a decrease in circulating TPO and it has been suggested that monitoring circulating TPO levels can evaluate the degree of thrombocytopenia in chronic liver disease [4]. Additionally, reduced bone marrow production most commonly secondary to viruses, alcohol use, iron overload, or medications contributes to reduced platelet production [3]. Hepatitis C and B, most frequently associated with liver cirrhosis, inhibits growth and differentiation of human bone marrow progenitor cells resulting in direct bone marrow suppression [3]. Alcohol use, a major contributor to CLD, both reduces platelet life span and leads to ineffective megakaryopoiesis [3]. CLD also notably impairs the liver’s ability to esterify cholesterol resulting in spur cell hemolytic anemia which causes iron overload. Increased iron levels decrease prohepcidin expression and increase iron absorption, causing platelets to have a diminished response to EPO. Medications like interferon (used to treat Hepatitis B/C) are associated with impaired thrombopoiesis as well.
Thrombocytopenia is a common hematologic complication seen in patients with chronic liver disease (CLD). The pathophysiology of thrombocytopenia in CLD is multifactorial, primarily stemming from platelet sequestration and decreased platelet production. This review focuses on the pathophysiology and current treatment options in the treatment of thrombocytopenia in chronic liver disease. While platelet transfusions are the gold standard of treatment, considerations ought to be given to CLD patients who can benefit from transjugular intrahepatic portosystemic shunt and splenic artery embolization. Finally, the recent approval of thrombopoietin receptor agonists for use in CLD patients paves a way for a safe and effective alternative method of improving platelet levels and reducing the need for recurrent platelet transfusions.
Furthermore, increased destruction of platelets in CLD is ascribed to splenic sequestration and immune-mediated destruction [3,5]. In chronic liver disease, the spleen is enlarged because of portal hypertension, increasing pooling of platelets. Conversely an inverse relationship has been observed between spleen size and platelet count. Additionally, immune-mediated destruction plays a large role in platelet destruction in chronic liver disease. Most associated causes include autoimmune conditions such as immune-mediated thrombocytopenia, hepatitis C or sepsis [4]. In autoimmune or viral disease, antiplatelet antibodies are formed resulting in platelet destruction. Sepsis in cirrhotic patients is triggered by endotoxemia accelerating platelet consumption through the stimulation of B-cell activity and production of IgG [3,5]. Although thrombocytopenia in end-stage liver disease is the most commonly documented abnormality at this time, there is no direct evidence correlating platelet count and disease severity. While studies have shown that a progressive decline in liver function does directly correlate to a lower platelet count, there are no formal guidelines for indicators of disease severity [6]. However, since individuals with cirrhosis or chronic liver disease often require frequent interventions or medications, those with severe thrombocytopenia are often associated with poorer prognosis due to delay to treatment [4,7,8].
Following PSE, a substantial improvement is noted in thrombocytopenia. However, the duration of improvement and optimal volume of splenic infarction varies widely. Various studies have used 50-80% infarcted splenic volume as a target following PSE [14-16]. A study of 13 patients with cirrhotic hypersplenism who underwent 80% PSE had marked improvement in platelet counts with sustained effect up to 36 months following the procedure [15]. Another retrospective analysis of cancer patients with hypersplenism who underwent PSE showed that the percentage volume of infarcted splenic tissue linearly correlated with the magnitude of platelet increase (p= 0.001). Following PSE, 41% of patients did not have a recurrence of thrombocytopenia for the duration of their survival [17]. While encouraging, the data from this study may not indicate similar outcomes in cirrhosis patients potentially due to increased lifespan compared to a cohort of cancer patients. Indeed, studies have shown the occurrence of recurrent thrombocytopenia in cirrhotic patients either due to revascularization or reperfusion of the embolized splenic arteries [18].
Splenomegaly is a frequent sequela of cirrhosis and is associated with decreased hematologic indices including thrombocytopenia. As such, spleen interventions may effectively increase hematologic values in patients with cirrhosis and concurrent hypersplenism. Currently, two methods of interventions are considered: splenectomy and partial splenic embolization. Splenectomy remains a risky procedure with significant associated morbidity [13]. While many patients with advanced cirrhosis may not be candidates for the surgery, other major risks include the risk of portal vein thrombosis, bacterial infection, and rarely, liver failure [13]. Alternatively, partial splenic artery embolization (PSE) has been proposed as a safer alternative treatment to hypersplenism with significant improvement in leukopenia and thrombocytopenia in the immediate months following the procedure [14].
assessed the effect of TIPS on thrombocytopenia by monitoring 74 patients with liver cirrhosis who were referred for TIPS [9]. Platelet counts were measured three different times over a three-month period prior to and following the placement of TIPS. They set a significant increase in platelet count as 20% or higher from the pre-TIPS value. Results of the study showed that 46% of individuals who underwent TIPS showed a significant increase in platelet count, with an average increase of 22%. Most notably, patients with severe thrombocytopenia showed the greatest response to TIPS: 8 out of 11 patients had a significant increase of on average 55% in platelet count. The study found that TIPS may improve thrombocytopenia in liver cirrhosis with the most significant benefit shown in patients with severe thrombocytopenia (<50,000/µL) [9]. The results of this study corroborated evidence from five other past studies showing similar benefits of TIPS on thrombocytopenia in chronic liver disease. Alvarez et al was a case series performed in 1996 that followed 11 patients in the 12-month follow-up period after TIPS [10]. They concluded a statistically significant improvement in thrombocytopenia and hemodynamic improvement.
The liver will appear enlarged, firm, and yellowish as the organ’s cells become swollen with fat from the body’s fat cells and the person’s daily diet. Alcoholic fatty liver can be reversed if a person stops drinking. Alcoholic hepatitis (571.1) is liver inflammation due to alcohol.
To diagnose alcoholic liver disease, the physician may order liver function tests and blood tests. The physician will look for elevated creatine phosphokinase (CPK), serum glutamic-oxaloacetic transaminase (SGOT), lactate dehydrogenase (LDH), and alanine transaminase (ALT)/aspartate transaminase (AST) to prothrombin time (PT)/international normalized ratio (INR) to substantiate the diagnosis. In addition, the physician may order a liver biopsy for definitive diagnosis and also review ultrasound and CT scans to rule out other diseases.
Alcoholic hepatitis (571.1) is liver inflammation due to alcohol. The liver also appears enlarged, firm, and yellowish, and the damage may be reversible with alcohol cessation. With more severe cases of alcoholic hepatitis, liver cells may die. This is the middle step between fatty liver and alcoholic cirrhosis.
If there are complications such as malnutrition, gastrointestinal bleeding, or portal hypertension, these conditions will also have to be managed. If cirrhosis develops, then a liver transplant may be necessary.
The immediate goal is discontinuation of alcohol use, and the treatment objective is to provide a high-carbohydrate, high-calorie diet to reduce protein breakdown in the body.
It is a common, often “silent” liver disease. The major features are fatty deposits in the liver, inflammation, and damage. Most people with NAFLD are unaware that they have a liver problem. The prevalence of NAFLD and NASH are increasing and are presumably more likely to occur in people who are obese or have diabetes.
If cirrhosis develops, then a liver transplant may be necessary . Nonalcoholic fatty liver disease (NAFLD, 571.8) refers to a wide spectrum of liver disease ranging from simple fatty liver (steatosis) to nonalcoholic steatohepatitis (NASH, 571.8) and finally cirrhosis.