May 12, 2025
Definition: Tumor lysis syndrome (TLS) is an oncologic emergency caused by massive tumor cell lysis and the release of large amounts of potassium, phosphate, and uric acid into the systemic circulation. Deposition of uric acid and/or calcium phosphate crystals in the renal tubules can result in acute kidney injury.
Cairo-Bishop Definition and Grading System
- The Cairo-Bishop definition provides specific laboratory criteria for the diagnosis of TLS both at presentation and within seven days of treatment. There is also a grading system to define the degree of severity of TLS.
- Laboratory TLS: any two or more abnormal serum values for uric acid, potassium, calcium, or phosphorus
- Clinical TLS: grading system for severity of TLS in patients with laboratory TLS was based on the degree of elevation in serum creatinine, the presence and type of cardiac arrhythmia, and the presence and severity of seizures
ICD-10-CM Codes and Current Coding Advice
- E88.3, Tumor Lysis Syndrome
- Classifies as an MCC when reported as a secondary diagnosis
- When applicable, report an additional code to report adverse effect to identify the drug (T45.1X5)
- Prior advice suggests when TLS and CRS are present together that E88.3 and R65.10, SIRS of non-infectious origin, w/o acute organ dysfunction would be reported. However, there are now specific codes to report CRS (D89.831-D89.839)
CDI Clinical Scenario:
- HPI: A 25‐year‐old male with newly diagnosed high‐grade Burkitt lymphoma was admitted for induction chemotherapy. He had bulky disease with elevated lactate dehydrogenase (LDH) and an initial workup that documented dehydration. Baseline renal function was normal (serum creatinine 0.9 mg/dL)
- On admission, the patient’s workup noted high tumor burden and risk factors for tumor lysis syndrome (TLS), including elevated LDH (2.5× ULN) and a large mediastinal mass. Prophylactic measures were initiated with aggressive intravenous hydration and oral allopurinol.
- Chemotherapy Initiation & Onset of TLS: Approximately 18 hours after starting a multiagent chemotherapy regimen (cyclophosphamide, vincristine, and prednisone), the patient developed nausea, vomiting, and left flank pain. His urine output declined, and he reported a new-onset weakness.
- Laboratory Findings:
- Uric acid: 12 mg/dL (elevated)
- Potassium: 5.8 mmol/L
- Phosphorus: 8.0 mg/dL
- Calcium: 7.0 mg/dL (low)
- Creatinine: increased from 0.9 to 1.8 mg/d
- Provider documentation upon transfer to the ICU:
- “The patient was transferred to the intensive care unit for close monitoring and telemetry. Treatment was escalated to include aggressive IV hydration, a single dose of IV rasburicase (administered four hours before planned continuation of chemotherapy), and supportive electrolyte management. Documentation noted that allopurinol was held once rasburicase therapy was initiated”
CDI Query Example:
Dear Dr. _____,
Using your medical judgment, please clarify the condition that caused ICU admission for this patient.
- Tumor lysis syndrome
- Other etiology of clinical indicators (please specify)
Clinical Indicators:
- Newly diagnosed high‐grade Burkitt lymphoma admitted for induction chemotherapy with initial labs indicating dehydration.
- Approximately 18H after chemo, developed nausea, vomiting, and left flank pain. Urine output declined, and he reported new-onset weakness.
- Labs: Uric acid: 12 mg/dL (elevated); Potassium: 5.8 mmol/L; Phosphorus: 8.0 mg/dL; Calcium: 7.0 mg/dL (low); Creatinine: increased from 0.9 to 1.8 mg/d
- H&P states patient was transferred to the intensive care unit for close monitoring and telemetry. Treatment was escalated to include aggressive IV hydration, a single dose of IV rasburicase (administered four hours before planned continuation of chemotherapy), and supportive electrolyte management. Documentation noted that allopurinol was held once rasburicase therapy was initiated.
References:
- Centers for Medicare and Medicaid Services. ICD-10-CM Official Coding Guidelines for Coding and Reporting FY’ 2025. www.cms.gov.
- AHIMA, ACDIS (2022). Guidelines for Achieving a Compliant Query Practice (2022 Update).
- American Hospital Association. (2020). Coding Clinic ICD-10-CM/PCS, First Quarter 2020; Page 37
- Larson, R. (2024). Tumor Lysis Syndrome: Pathogenesis, clinical manifestations, definition, etiology and risk factors. UpToDate.
- Larson, R. (2022). Tumor Lysis Syndrome: Prevention and Treatment. UpToDate.
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Background: With the 2026 IPPS Proposed Final Rule comes a new diabetes code, E11.A, Type II diabetes mellitus without complications in remission. This is a non-CC/MCC and is assigned to MDC 10. ICD-10-CM Official Guidelines for Coding and Reporting 2026: Section I.C.4.a.1.(b) - “Code E11.A, Type 2 diabetes mellitus without complications in remission, is assigned based on provider documentation that the diabetes mellitus is in remission. If the documentation is unclear as to whether the Type 2 diabetes mellitus has achieved remission, the provider should be queried. For example, the term “resolved” is not synonymous with remission.” Clinical criteria for diabetes in remission: Note* - Remission does not mean cure. Ongoing monitoring is essential as relapse is possible. 1. Prior Diagnosis of Diabetes Mellitus Documented history of type 2 diabetes mellitus, diagnosed using standard criteria: HbA1c ≥ 6.5% Fasting plasma glucose ≥ 126 mg/dL 2-hour plasma glucose ≥ 200 mg/dL during an OGTT Random plasma glucose ≥ 200 mg/dL with classic symptoms 2. Normal or Controlled Glucose Levels Without Medications The patient is not taking any antidiabetic medications (oral agents, insulin, or non-insulin injectables). Glycemic control is sustained through lifestyle modifications, such as diet and exercise. HbA1c < 6.5%, and sometimes < 6.0%, on two occasions at least 6 months apart without pharmacologic therapy. 3. Duration of Remission Partial remission: HbA1c < 6.5% and fasting glucose 100–125 mg/dL for at least 1 year without medications. Complete remission: HbA1c in the normal range (<5.7%) and fasting glucose <100 mg/dL for at least 1 year. Prolonged remission: Complete remission lasting ≥5 years. 4. Documentation Must Include Clear statement that diabetes is in remission or resolution. No current use of diabetes medications. Current HbA1c values. Lifestyle interventions being used. Absence of ongoing diabetic complications (or if present, they are noted as sequelae) 5. What about Type I diabetes? Is remission associated? “Honeymoon Phase” vs. Remission Some individuals newly diagnosed with type 1 diabetes may experience a "honeymoon phase": This is a temporary period (weeks to months) where insulin needs to decrease and blood glucose levels may normalize. However, this is not true remission, as the autoimmune process continues and insulin dependence eventually returns. Clinical Scenario Dr. Doctor, Documentation in your visit note indicates the patient has a documented history of type 2 diabetes mellitus, but current labs show: HbA1c: 5.6% No diabetes medications (e.g., insulin, metformin) currently prescribed Patient reports lifestyle changes (e.g., diet and weight loss) No hyperglycemia documented during this admission or recent visits Query Based on the clinical picture, can you please clarify the patient’s current diabetic status? ☐ Type 2 diabetes mellitus – continue to document and treat as active ☐ History of type 2 diabetes mellitus, currently in remission (no medications, normal glucose values) ☐ Other: ________________
Definition: Neonatal encephalopathy (NE) is a clinically defined syndrome of disturbed neurologic function in the earliest days of life in a term or late preterm infant, manifested by difficulty with initiating and maintaining respiration, depression of tone and reflexes, subnormal level of consciousness, and often seizures. Clinical presentation: Low APGAR scores and/or weak/absent cry in the delivery room. Hyperalert, irritable, lethargic, obtunded. Decreased spontaneous movements, poor tone, blunted or absent primitive reflexes, seizure activity. Breathing and/or feeding difficulties. Documentation Tips: The CDS should review to identify the underlying etiology . (e.g., hypoxic-ischemic event, infection, metabolic disorder). Review clinical indicators that may indicate associated conditions , such as seizures, abnormal imaging, acidosis, or multi-organ dysfunction. Review the documentation for the timing of onset (e.g., at birth, delayed). Common clinical indicators include low APGAR scores, need for resuscitation, abnormal tone, or altered level of consciousness. ICD-10-CM Coding: P91.811, Neonatal encephalopathy in diseases classified elsewhere P91.819, Neonatal encephalopathy, unspecified Use when the type or etiology of NE is not documented Query Example: To the Attending Neonatologist: Documentation in the medical record indicates the newborn infant delivered from mother with placental abruption demonstrates seizures, abnormal muscle tone, low APGAR scores, and required resuscitation at birth. Imaging showed evidence of cerebral edema. The diagnosis of “neonatal encephalopathy” was documented in the assessment. Query: Based on the clinical indicators, can you clarify the type and cause of the encephalopathy in this newborn? Please select the most appropriate option below or specify another diagnosis: Neonatal encephalopathy due to Hypoxic-ischemic encephalopathy (HIE) Neonatal encephalopathy due to other etiology (please specify) Other (please specify): __________
Syndrome of Inappropriate Antidiuretic Hormone (SIADH) occurs when the pituitary gland releases excessive antidiuretic hormone (ADH) , leading the body to retain fluid and dilute sodium levels in the bloodstream. This condition causes hyponatremia and hypo-osmolality , often triggering a complex clinical picture. What Causes SIADH? SIADH can develop in response to several underlying conditions or external factors: CNS disturbances: Stroke, hemorrhage, infection, and trauma can trigger abnormal ADH release. Cancer: Especially small cell lung cancer, extrapulmonary small cell carcinomas, head and neck cancers, and olfactory neuroblastomas. Medications: SSRIs, NSAIDs, opiates, some antineoplastic drugs, ciprofloxacin, haloperidol, and high-dose imatinib. Surgery: Often linked to pain response. Hormonal deficiencies: Including hypothyroidism and hypopituitarism. Exogenous hormone use: Vasopressin, desmopressin, and oxytocin. HIV infection Hereditary SIADH Diagnostic Criteria: Schwartz and Bartter Clinical Framework A diagnosis of SIADH typically includes: Serum sodium < 135 mEq/L Serum osmolality < 275 mOsm/kg Urine sodium > 40 mEq/L Urine osmolality > 100 mOsm/kg Normal skin turgor and blood pressure (absence of clinical volume depletion) Exclusion of other hyponatremia causes Correction of sodium levels via fluid restriction Important Note: Code only the SIADH, not the hyponatremia, as hyponatremia is considered integral to the disease process . Clinical Scenario A 68-year-old male presents to the ED with confusion , nausea , and a 12-pound weight gain over the past week. He was diagnosed with small cell lung cancer two months ago. Vitals: BP: 160/90 mmHg HR: 110 bpm Labs: Serum sodium: 122 mEq/L Serum osmolality: Decreased Urine: Elevated osmolality and high sodium concentration Indicators Suggestive of SIADH Hyponatremia: Sodium level of 122 mEq/L Diluted Serum Osmolality: From water retention Concentrated Urine: High osmolality and sodium levels despite low serum sodium Recent Weight Gain: 12 lbs in one week, pointing to fluid overload Underlying Malignancy: Small cell lung cancer is a well-known cause of ectopic ADH production Documentation Tips 1. Accurate Diagnosis Clearly state “SIADH” and link it to the underlying cause , such as cancer. 2. Clinical Findings Review provider and nursing notes for symptoms like confusion, nausea, and fluid retention. Confirm vital signs and weight gain. Include lab values: sodium, serum/urine osmolality, and urine sodium. 3. Treatment Plan Document fluid restriction orders . Check MAR for medications such as vasopressin receptor antagonists . Note any improvements in symptoms and lab values after treatment. Tip: High blood glucose can artificially lower serum sodium levels. Use a sodium correction calculator to determine the true sodium level. References Centers for Medicare and Medicaid Services. (2024). ICD-10-CM Official Coding Guidelines. Available here: cms.gov Pinson, R., & Tang, C. (2024). The CDI Pocket Guide. Available here: cdiplus.com Prescott, L., & Manz, J. (2024). ACDIS CDI Pocket Guide. Available here: https://acdis.org/ Sterns, R. (2024). Pathophysiology and etiology of SIADH. UpToDate. Yasir, M., & Mechanic, O.J. (2023). Syndrome of Inappropriate Antidiuretic Hormone Secretion. StatPearls Publishing.
