Understand Acute Metabolic Acidosis, including Lactic Acidosis and Elevated Anion Gap Acidosis. Find information on diagnosis, clinical documentation, and medical coding for healthcare professionals. Learn about causes, symptoms, and treatment of Acute Metabolic Acidosis for accurate medical record keeping and appropriate billing. This resource offers guidance on coding and documentation best practices related to metabolic acidosis conditions.
Also known as
Acidosis
Covers metabolic acidosis and lactic acidosis.
Other abnormal findings
May be used for unspecified elevated anion gap acidosis.
Aplastic and other anemias
Some anemias can cause lactic acidosis as a complication.
Follow this step-by-step guide to choose the correct ICD-10 code.
Is the acidosis due to a documented underlying condition?
Yes
Is it due to Diabetic Ketoacidosis?
No
Is it lactic acidosis?
When to use each related code
| Description |
|---|
| Body produces too much acid, or kidneys cannot remove it. |
| Build-up of lactic acid. Impaired tissue oxygenation. |
| Reduced bicarbonate due to renal loss or GI loss. |
Coding E87.2 (Acidosis NOS) instead of a specific type like lactic acidosis (E87.21) leads to lower reimbursement and data inaccuracy.
Lack of proper documentation to support acute metabolic acidosis diagnosis can lead to claim denials for medical necessity.
Incorrectly coding both acute metabolic acidosis and underlying causes like diabetic ketoacidosis (E10.10, E11.10, E13.10) results in overcoding.
Q: How to differentiate between the various causes of high anion gap metabolic acidosis in a critically ill patient?
A: Differentiating the causes of high anion gap metabolic acidosis (HAGMA) in critically ill patients requires a systematic approach integrating clinical presentation, laboratory findings, and patient history. While lactic acidosis is the most common etiology, particularly in septic or hypoperfused patients, other causes like diabetic ketoacidosis (DKA), renal failure, and certain intoxications (e.g., methanol, ethylene glycol) must be considered. Start by evaluating the patient's serum lactate levels. Elevated lactate suggests lactic acidosis, often related to tissue hypoxia or impaired lactate clearance. Assess for signs of infection, hypovolemia, or other conditions that may compromise tissue perfusion. If lactate is normal or only mildly elevated, investigate other possibilities. Check for ketones in urine and serum to rule out DKA, particularly in patients with diabetes. Assess renal function via serum creatinine and BUN; renal failure can contribute to HAGMA due to impaired acid excretion. A thorough medication and toxin exposure history can point towards specific intoxications. Osmolal gap can be helpful; an elevated osmolal gap may suggest toxic alcohol ingestion. Explore how arterial blood gas analysis can further clarify the acid-base disturbance and guide management. Consider implementing a point-of-care lactate measurement to rapidly assess for lactic acidosis in unstable patients. Remember, a mixed acid-base disorder may be present, complicating the clinical picture. Further investigations, including specialized metabolic testing, might be necessary in complex cases.
Q: What are the best practices for the initial management of severe acute lactic acidosis in the emergency department?
A: The initial management of severe acute lactic acidosis in the emergency department focuses on stabilizing the patient and identifying and treating the underlying cause. This requires a multi-pronged approach. First, ensure adequate oxygenation and ventilation to optimize tissue oxygen delivery. Administer supplemental oxygen and consider intubation if necessary. Second, address hemodynamic instability. Aggressive fluid resuscitation is often required to restore circulating volume and improve tissue perfusion. Vasopressors may be needed to maintain adequate blood pressure. Third, identify and treat the underlying etiology. This might involve administering antibiotics for sepsis, managing diabetic ketoacidosis with insulin and fluids, or reversing the effects of toxins. Closely monitor serum lactate, blood glucose, electrolytes, and arterial blood gases to assess the patient's response to therapy. Learn more about targeted therapies for specific etiologies of lactic acidosis to optimize patient outcomes. Consider implementing early goal-directed therapy protocols for sepsis-induced lactic acidosis. Early consultation with critical care specialists may be warranted in severe cases.
Patient presents with acute metabolic acidosis, evidenced by a low pH, low bicarbonate level, and potentially an elevated anion gap. Differential diagnosis includes lactic acidosis, diabetic ketoacidosis, renal tubular acidosis, and ingestion of toxins such as salicylates or methanol. Symptoms may include tachypnea, Kussmaul respirations, nausea, vomiting, confusion, and lethargy. Initial laboratory evaluation includes arterial blood gas analysis, serum electrolytes including potassium, chloride, and bicarbonate, anion gap calculation, lactate level, creatinine, and blood urea nitrogen. Further investigations may include serum ketone levels, toxicology screen, and urinalysis depending on suspected etiology. Treatment for acute metabolic acidosis focuses on addressing the underlying cause. Fluid resuscitation is often initiated with isotonic crystalloids. In cases of severe acidosis, bicarbonate therapy may be considered after careful evaluation of risks and benefits. Monitoring of vital signs, arterial blood gases, and electrolytes is essential for assessment of treatment response and prevention of complications. ICD-10-CM coding may include E87.2 (acidosis) or more specific codes depending on the underlying etiology, for example, E87.21 (lactic acidosis). Correct coding and documentation are essential for medical billing and reimbursement. This documentation should be updated as the patient's condition evolves and the underlying cause is further elucidated.