Definition : Acute Kidney Injury (AKI) is an abrupt decline in kidney function, leading to retention of waste products, electrolyte imbalance, and fluid dysregulation. It is classified based on etiology and severity. 1. Types of AKI by Etiology Pre-Renal AKI Cause: Decreased renal perfusion without intrinsic kidney damage. Examples: Hypovolemia (dehydration, hemorrhage). Hypotension/shock (sepsis, cardiogenic shock) Heart failure, liver failure Documentation Tip: Specify underlying cause (e.g., “AKI due to hypovolemia from GI bleed”). Intrinsic (Intra-Renal) AKI Cause: Direct damage to kidney tissue. Examples: Acute Tubular Necrosis (ATN\) – ischemia or nephrotoxins Acute Interstitial Nephritis (AIN) – drug-induced, autoimmune Glomerulonephritis Documentation Tip: If ATN or AIN is suspected, document specifically (e.g., “AKI secondary to ATN from contrast exposure”). Post-Renal AKI Cause: Obstruction of urine flow. Examples: Ureteral obstruction (stones, tumors) Bladder outlet obstruction (BPH, neurogenic bladder) Documentation Tip: State the obstructive cause (e.g., “AKI due to bilateral ureteral obstruction from stones”). 2. Diagnostic Criteria (KDIGO) Increase in serum creatinine by ≥ 0.3 mg/dL within 48 hrs, OR Increase in serum creatinine to ≥ 1.5 times baseline within 7 days, OR Urine output < 0.5 mL/kg/hr for 6 hrs 3. Severity Staging Stage 1: 1.5–1.9 × baseline creatinine or ≥ 0.3 mg/dL rise Stage 2: 2.0–2.9 × baseline Stage 3: ≥ 3 × baseline or creatinine ≥ 4.0 mg/dL or dialysis required 4. CDI and Current Coding Guidance Avoid vague terms like “renal insufficiency”; use “acute kidney injury” or “acute renal failure” (interchangeable per coding). Always link AKI to the underlying cause (e.g., sepsis, dehydration, obstruction). If ATN or AIN are present, document explicitly (these are MCCs). Do not abbreviate AKI without context; clarify in the first mention. Trend labs and urine output to support diagnosis before querying. Assign code N17.0, Acute kidney failure with tubular necrosis, with a POA of N for documentation of a patient with AKI on admission who then develops ATN after admission. For a case of acute kidney injury (AKI) due to acute tubular necrosis (ATN) secondary to contrast-induced nephropathy, the correct coding assignment is N17.0 for acute kidney failure with tubular necrosis, N14.11 for contrast-induced nephropathy, and T50.8X5A for adverse effect of diagnostic agents, initial encounter. This combination accurately reflects the underlying cause, the specific kidney injury type, and the adverse effect of the contrast agent. Pro Tip: AKI impacts severity of illness and quality metrics (e.g., PSI-10 Post-Op AKI). Accurate documentation ensures correct DRG assignment and patient safety. References: AHA Coding Clinic, Third Quarter 2025, p. 22 AHA Coding Clinic, Fourth Quarter 2022, p. 33 Centers for Medicare and Medicaid Services. (2025). Official Guidelines for Coding and Reporting. www.cms.gov. Fatehi, P., & Hsu, C-Y. (2024). Evaluation of acute kidney injury among hospitalized adult patients. UpToDate. Palevsky, P. M. (2025). Definition and staging criteria of acute kidney injury in adults. UpToDate. Prescott, L., Manz, J. (2025). The ACDIS Inpatient CDI Pocket Guide. www.acdis.org

CDI Tip: Capturing Firearm Injury Intent from Other Clinicians’ Documentation What’s New in FY 2026? CMS and ICD-10-CM guidelines now allow documentation by clinicians other than the patient’s provider (e.g., nurses, social workers, trauma team) to be used for assigning external cause codes, including firearm injury intent. This change supports more accurate public health reporting and injury surveillance Key Actions for CDI Specialists Review All Clinical Notes Check ED notes, nursing assessments, social work documentation, and EMS reports for statements about firearm injury intent (e.g., accidental, assault, self-harm, undetermined). Apply the New Intent Hierarchy If intent is clearly documented by any clinician, code accordingly: Accidental: W34 series Assault: X93–X95 series Self-harm: X72–X74 series Undetermined: Y22–Y24 series If no intent is documented, follow the updated guideline: default to undetermined intent for firearm injuries (Y24.9), unless otherwise specified. Query When Needed If conflicting documentation exists (e.g., ED note states “possible assault,” nursing note says “accidental”), query the provider for clarification. Document Source When coding based on another clinician’s note, ensure the documentation is clearly attributed in the record. Pro Tip: Incorporate firearm injury intent review into your trauma and ED CDI workflows. Educate providers that intent matters for coding, quality metrics, and injury prevention programs. Example Clinical Scenario with Query: Setting: ED, trauma bay Patient: 28-year-old male with a through and through gunshot wound of the left thigh; hemodynamically stable. Documentation in record: ED triage RN note: “Pt states he was shot by someone outside a bar.” EMS run sheet: “Bystanders report drive by shooting; single GSW to L thigh.” ED SW note: “Patient reports unknown assailant; denies self-harm.” ED provider note: “GSW L thigh; hemorrhage controlled; analgesia given.” Intent not specified in provider note or discharge summary Query: Documentation in the medical record shows that the patient was injured by a firearm. Please clarify the intent of the firearm injury for this encounter, based on your clinical judgment and the medical record. Assault (injury inflicted by another person) Accidental/unintentional Intentional self-harm Undetermined (unable to determine intent from available information) Other (please specify): _______________________

What is ventricular standstill? SA node is functioning, and P waves are present on EKG. There is no ventricular response, no contractions of the muscle. The presence of complete heart block with no escape rhythm. No cardiac output with the patient in full arrest. May be paroxysmal or prolonged.

What does it mean when “neurostorming” is documented? “Neuro storm” and other similar terms such as autonomic storms, hypothalamic dysregulation syndrome and sympathetic storms all equate to the condition paroxysmal sympathetic hyperactivity (PSH). This syndrome was formally named in 2014 by an international panel looking at preferred nomenclature, definition and diagnostic criteria. PSH is defined as a disorder in the regulation of autonomic function most observed in patients with acute brain injury, most notably severe traumatic brain injury. What are the risk factors for PSH? Traumatic brain injury (TBI) Hypoxic ischemic injury What are the clinical indicators of PSH? Sinus tachycardia Elevated systolic blood pressure Tachypnea associated with respiratory alkalosis Diaphoresis that can progress to dehydration Hyperthermia in some cases Severe cases may have dystonic posturing How is PSH treated? Reducing stimulation Managing hyperthermia and hyperventilation Medications IV Morphine Gabapentin Beta blockers Baclofen Precedex infusion Dantrolene Coding and CDI considerations for the documentation of “neurostorming” The ICD-10-CM condition code most appropriate for reporting of PSH is G90.89, Other disorders of autonomic nervous system. There is no specific code to identify neurostorm or PSH. There are also no instructional notes for the code G90.89. Per the ICD10-CM Official Coding Guidelines, “ If a main term cannot be located, consider a synonym, an eponym, or another alternative term. Once the main term is located, search for subterms, notes, or cross-references. Subterms provide many types of more specific information and must be checked carefully, following all the rules of alphabetization. The main term code entry should not be assigned until all subterm possibilities have been exhausted. During this process, it may be necessary to refer again to the medical record to determine whether any additional information is available to permit assignment of a more specific code. If a subterm cannot be located, the nonessential modifiers following the main term should be reviewed to see whether the subterm may be included there. If not, alternative terms should be considered” Current coding advice notes that when the index is confusing, leading to an inappropriate code, further research is needed when the title of the code suggested by the index clearly does not identify the condition correctly. Regarding the CDI professional, it is allowable to report code G90.89, Other disorders of autonomic nervous system in the instance where “neurostorm” is documented by the provider. A query would not be needed for clarification. References: American Hospital Association (AHA). ICD-10-CM Coding Clinic, Second Quarter 2025, p. 4. Available from: AHA Coding Clinic Centers for Medicare & Medicaid Services (CMS). (2025). ICD-10-CM Official Guidelines for Coding and Reporting. Available from: CMS ICD-10-CM Guidelines Rabinstein, A. (2024). Paroxysmal sympathetic hyperactivity. UpToDate. Available from: UpToDate – Paroxysmal sympathetic hyperactivity

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: ________________ References: American Diabetes Association. Standards of Care in Diabetes—2024: Section 2 and Section 6. 2024. Section 2: https://pubmed.ncbi.nlm.nih.gov/38078586/ Full guidelines: https://professional.diabetes.org/standards-of-care Section 6: https://diabetesjournals.org/care/article/47/Supplement_1/S111/153951/6-Glycemic-Goals-and-Hypoglycemia-Standards-of PMC version: https://pmc.ncbi.nlm.nih.gov/articles/PMC10725808/ Buse, John B., et al. “How Do We Define Cure of Diabetes?” Diabetes Care, vol. 32, no. 11, 2009, pp. 2133–2135. DOI: 10.2337/dc09-9036. PubMed: https://pubmed.ncbi.nlm.nih.gov/19875608/ PMC: https://pmc.ncbi.nlm.nih.gov/articles/PMC2768219/ Centers for Medicare & Medicaid Services. ICD-10-CM Official Guidelines for Coding and Reporting 2026. 2025. https://www.cms.gov Centers for Medicare & Medicaid Services. IPPS 2026 Proposed Final Rule. 2025. https://www.cms.gov

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): __________

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.

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. cms.gov Pinson, R., & Tang, C. (2024). The CDI Pocket Guide. cdiplus.com Prescott, L., & Manz, J. (2024). ACDIS CDI Pocket Guide. acdispro.com Sterns, R. (2024). Pathophysiology and etiology of SIADH. UpToDate. Yasir, M., & Mechanic, O.J. (2023). Syndrome of Inappropriate Antidiuretic Hormone Secretion. StatPearls Publishing.

Understanding Stroke and Its Long-Term Impact Stroke is the third most common cause of disability and the second most common cause of mortality worldwide. The global 30-day fatality rate following an initial ischemic stroke is estimated at 16–23% . A U.S. study of 220 ischemic stroke survivors revealed a range of neurologic deficits at six months post-stroke, including: Hemiparesis (50%) Cognitive defects (46%) Hemianopia (20%) Aphasia (19%) Sensory deficits (15%) Additionally, survivors experienced long-term disabilities such as: Depression (35%) Inability to walk without assistance (31%) Institutionalization (26%) Bladder incontinence (22%) What is a Stroke? A stroke , also known as a cerebrovascular accident (CVA) , occurs when the blood supply to part of the brain is interrupted or reduced , preventing brain tissue from receiving oxygen and nutrients. As a result, brain cells begin to die within minutes . Types of Strokes Ischemic Stroke The most common type, accounting for approximately 87% of all strokes. It occurs when a blood clot blocks or narrows an artery leading to the brain. Hemorrhagic Stroke Occurs when a blood vessel in the brain bursts , leading to bleeding in or around the brain . Common Late Effects of CVA Physical: Hemiplegia, hemiparesis, dysphagia, ataxia Cognitive: Memory loss, attention deficits, executive function impairments Speech and Language: Aphasia, dysarthria Sensory: Visual field loss, neglect (lack of awareness of one side of the body) Emotional and Behavioral: Depression, anxiety, personality changes Other: Bladder and bowel control issues, fatigue Recrudescence of Stroke Symptoms Recrudescence refers to the reappearance of previously resolved neurological deficits from a prior stroke. These symptoms are typically mild , short-lived , and not due to a new stroke . Key considerations: Recrudescence is coded as a “late effect of stroke.” Follows the same coding and sequencing guidance as the principal diagnosis (PDX). Can be reported alongside a new acute infarction , if applicable. Clarity in documentation is essential to accurately capture the etiology of stroke-related symptoms— query the provider if necessary. Query Example for Clarification Dear Dr. Carlson , Patient with PMH of CVA. Per H&P, admitted with “dysphagia.” Other diagnoses include severe malnutrition, with plans for a PEG tube. Can this patient’s dysphagia be specified as the most likely cause? For example: Dysphagia is recrudescence of previous stroke Dysphagia related to other (please specify) ___ Unknown/undetermined Other clinical indicators/treatment from the patient’s record: H&P notes: “dysphagia, severe malnutrition, and failure to thrive. ST/PT/OT to see. Family thinks dysphagia has been going on for a while.” Treatment: RD consult, PEG tube placement, PT/OT/ST Why It Matters: A favorable query response could shift the DRG from DRG 392 (Esoph, gastro, and misc digestive disorders w/o MCC) with the PDX of dysphagia , to DRG 057 (Degenerative nervous system disorders w/o MCC) with the PDX of weakness/dysarthria as a late effect of CVA .