Acidosis is the overarching term for the pathological process that drives blood pH below normal — when fully realized as a drop in arterial pH below 7.35, the state is more precisely called acidemia (“acid blood”). The distinction matters clinically: a patient can have an active acidotic process yet maintain a compensated normal pH, and conversely, a patient inacidemia by pH may have concurrent alkalotic processes; coding should reflect the documented pathological process, not simply the pH number. The two primary physiological mechanisms produce the major divisions: metabolic acidosis results from either the accumulation of fixed/organic acids (lactic acid, ketoacids, toxic alcohols) or the primary loss of bicarbonate (HCO₃⁻), driving serum bicarbonate below 22 mEq/L and the pH downward; respiratory acidosis results from alveolar hypoventilation causing carbon dioxide (CO₂) retention — elevated PaCO₂ above 45 mmHg — driving the carbonic acid equilibrium toward lower pH. Mixed acid-base disorders occur when both processes are simultaneously present.
Clinical Indicators: In ICD-10-CM, E87.2 is the general acidosis category but specificity is required — coders must identify whether acidosis is metabolic (acute E87.21 or chronic E87.22 or unspecifiedE87.20), respiratory (E87.29), or mixed (E87.4). Critically, diabetic ketoacidosis (DKA) is NEVER coded with E87.2x — DKA is captured exclusively within the E10-E13 diabetes code families with ketoacidosis subcategories; attempting to also report E87.2x alongside a DKA code constitutes duplicate coding per ICD-10-CM Excludes1 notation.
”Sour, sharp, pungent” — describing the sensory quality of acid substances; derived from the Latin verb acere (“to be sour”); the root present in acid, acetic, acetylsalicylic
“Process, condition, abnormal state” — a highly productive Greek suffix indicating a pathological or physiological process; appears in acidosis, alkalosis, stenosis, fibrosis
Literally: “A process or condition of sourness/acidity” — a medically elegant descriptor of the physiological state. The compound was coined in New Latin circa 1895-1900, at the dawn of systematic biochemical understanding of acid-base balance in human physiology. The distinction between acidosis (the process generating acid) and acidemia (the measurable state of low blood pH) was formalized in the twentieth century as blood gas measurement technology advanced. The antonym alkalosis (excess base/elevated pH) follows the same Latin-Greek hybrid construction: alkali- (from Arabic al-qili, “plant ash”) + -osis, making the acid-base nomenclature pair one of the rare Arabic-Latin-Greek compound hybrids in medical terminology.
🔀 ALIASES / ALTERNATE TERMS
Term
Context
Acidemia
The technically precise term for the state of low blood pH (arterial pH < 7.35); acidosis is the process, acidemia is the result; ICD-10-CM uses “acidosis” as the coded entity but clinical documentation may use either — both map to the E87.2x family.
Metabolic acidosis
The subtype arising from bicarbonate deficit or organic/inorganic acid accumulation; maps to E87.20 (unspecified), E87.21 (acute), or E87.22 (chronic) per FY2023 expansion.
Respiratory acidosis
The subtype arising from CO₂ retention due to alveolar hypoventilation; indexes to E87.29 (other acidosis) in ICD-10-CM — there is no standalone respiratory acidosis code; the primary code is the underlying respiratory failure (J96.0x/J96.1x).
Lactic acidosis
A subtype of metabolic acidosis caused by excess lactic acid production (type A: hypoperfusion; type B: metabolic/drug causes); maps to E87.20 or E87.21 — ICD-10-CM does not have a standalone lactic acidosis code.
Diabetic ketoacidosis (DKA)
Acidosis from ketone body accumulation in uncontrolled diabetes; NEVER coded with E87.2x — use E10.10 / E10.11 (Type 1), E11.10 / E11.11 (Type 2) per ICD-10-CM Excludes1.
Renal tubular acidosis (RTA)
Acidosis from impaired renal H⁺ excretion or HCO₃⁻ reabsorption; specifically maps to N25.89 (other disorders of impaired renal tubular function) — NOT E87.2x.
🔗 RELATED TERMS
alkalosis — E87.3 (alkalosis); the opposing acid-base disorder of excess bicarbonate or CO₂ depletion raising pH above 7.45; metabolic alkalosis most commonly from vomiting or diuretic overuse; respiratory alkalosis from hyperventilation.
Mixed acid-base disorder — E87.4; coexisting acidotic and alkalotic processes simultaneously present (e.g., lactic acidosis + respiratory alkalosis in sepsis, or metabolic alkalosis superimposed on chronic respiratory acidosis in COPD); requires explicit physician documentation — do NOT infer mixed disorder from ABG values alone.
Acute respiratory failure with hypercapnia — J96.02; the correct primary code for respiratory acidosis driven by CO₂ retention; E87.29 should be listed as an additional code, not the primary diagnosis, when respiratory failure is the lead clinical condition.
Chronic respiratory failure with hypercapnia — J96.12; chronic CO₂ retention in COPD, obesity hypoventilation, or neuromuscular disease; the primary driver of chronic respiratory acidosis in outpatient and inpatient settings.
Sepsis — A41.9 (unspecified organism); the most common clinical trigger for lactic acidosis (Type A) — tissue hypoperfusion drives anaerobic metabolism and lactate overproduction; always query the physician for documentation of sepsis when lactic acidosis and infection are co-present.
Acute kidney injury (AKI) — N17.9; renal failure impairs the kidneys’ ability to excrete hydrogen ions and regenerate bicarbonate, directly causing uremic metabolic acidosis; code additionally when documented.
hypokalemia — E87.6; a common metabolic consequence and co-contributor in renal tubular acidosis (types 1 and 2 RTA cause potassium wasting); code separately when documented.
Diabetic ketoacidosis — E10.10 (Type 1 without coma) / E10.11 (Type 1 with coma); the most severe form of ketoacidotic acidosis; requires the diabetes code family only — see Excludes1 notation under E87.2.
CODING CORNER
🏥 ICD-10-CM CODES
Primary Diagnosis — Acidosis (Category E87.2)
⚠️ ICD-10-CM / Chapter Nuances: E87.2 is BILLABLE but represents the least specific option — always code to the maximum specificity supported by documentation. The FY2023 update expanded E87.2 into subcategories for metabolic acidosis (E87.20/21/22) and other acidosis (E87.29). Respiratory acidosis indexes to E87.29 but should be secondary to the underlying respiratory failure code (J96.x family) when respiratory failure is the primary condition. Per the Excludes1 note under E87.2, diabetic acidosis/ketoacidosis must use the E08-E13 diabetes families — E87.2x cannot be reported with DKA codes.
Code
Description
E87.2
Acidosis, unspecified (Use only when acidosis is documented but the type — metabolic vs. respiratory — and acuity cannot be further specified; last resort)
E87.20
Metabolic acidosis, unspecified (Use when metabolic acidosis is documented but not specified as acute or chronic; appropriate for lactic acidosis when acuity is unspecified)
E87.21
Acute metabolic acidosis (Use when the physician explicitly documents ACUTE metabolic acidosis, or when lactic acidosis or DKA-equivalent metabolic acidosis is documented as acute — note: do NOT report alongside DKA diabetes codes)
E87.22
Chronic metabolic acidosis (FY2023 addition; use for chronically reduced serum bicarbonate in the setting of CKD, renal tubular acidosis on ongoing treatment, or documented chronic metabolic acidosis)
E87.29
Other acidosis (The code for RESPIRATORY acidosis in ICD-10-CM; also captures mixed forms not elsewhere classified; typically reported as a secondary code to the J96.x respiratory failure primary code)
E87.4
Mixed disorder of acid-base balance (Billable; use only when the physician explicitly documents a mixed acid-base disorder — never infer from lab values alone without physician documentation)
Diabetic Ketoacidosis (DKA) — Separate Families (NOT E87.2x)
⚠️ Excludes1 Warning: These codes include the ketoacidotic acidosis component. Do NOT additionally report E87.20/E87.21 with these codes — it constitutes a coding violation per ICD-10-CM Excludes1 instruction.
Code
Description
E10.10
Type 1 diabetes mellitus with ketoacidosis without coma (DKA in T1DM without altered consciousness — the most common DKA inpatient presentation; ketoacidosis is fully captured in this code)
E10.11
Type 1 diabetes mellitus with ketoacidosis with coma
E11.10
Type 2 diabetes mellitus with ketoacidosis without coma (DKA in T2DM; less common but increasingly recognized, especially with SGLT-2 inhibitor use)
E11.11
Type 2 diabetes mellitus with ketoacidosis with coma
E13.10
Other specified diabetes mellitus with ketoacidosis without coma (Post-pancreatectomy, secondary, or genetic diabetes DKA)
E13.11
Other specified diabetes mellitus with ketoacidosis with coma
Respiratory Acidosis — Primary Code First
Code
Description
J96.02
Acute respiratory failure with hypercapnia(Primary code for acute respiratory acidosis — CO₂ retention driving pH below 7.35; append E87.29 as secondary when physician documents respiratory acidosis)
J96.12
Chronic respiratory failure with hypercapnia (Primary code for chronic respiratory acidosis — chronic CO₂ retention in COPD, OHS, NMD; append E87.29 secondarily when documented)
J96.22
Acute and chronic respiratory failure with hypercapnia (Use when an acute-on-chronic decompensation is explicitly documented by the physician)
Renal Tubular Acidosis
Code
Description
N25.89
Other disorders resulting from impaired renal tubular function (The ICD-10-CM home for Renal Tubular Acidosis [RTA] NOS, Lightwood-Albright syndrome, and hypokalemic nephropathy — the index entry “Renal tubular acidosis NOS” explicitly maps here)
🔧 COMMON CPT CODES (Evaluation & Laboratory Diagnostics)
Arterial Blood Gas (ABG) Analysis — The Cornerstone Diagnostic
⚠️ CPT Nuance: ABG components are reported as individual analyte codes, not as a panel. Each measured parameter has its own CPT code. 82803 covers pH + pCO₂ + pO₂ together (the core gas trio) — it is NOT reported three times for three values; it is reported ONCE per specimen. If O₂ saturation is measured separately by co-oximetry, add 82805. Additional metabolites (lactate, electrolytes) each have their own codes and may be reported separately.
CPT Code
Description
82803
Gases, blood, any combination of pH, pCO₂, pO₂, CO₂, HCO₃ (including calculated O₂ saturation) (The core ABG CPT code; report ONCE per arterial blood specimen regardless of how many gas parameters are measured — each additional listed parameter is included; critical for confirming and typing acidosis)
82805
Gases, blood, any combination of pH, pCO₂, pO₂, CO₂, HCO₃ (including calculated O₂ saturation); with O₂ saturation by co-oximetry, when performed (Report in place of 82803 — NOT in addition to it — when measured O₂ saturation by co-oximetry is included in the same specimen)
83605
Lactate (lactic acid) (Report separately when serum or whole blood lactate is ordered to work up suspected lactic acidosis; critical for Type A vs. Type B differentiation and sepsis-driven lactic acidosis evaluation)
82374
Carbon dioxide (bicarbonate) (Venous CO₂/bicarbonate level; report when serum bicarbonate is drawn separately from the ABG to monitor chronic metabolic acidosis, CKD acid-base status, or RTA management)
82435
Chloride; blood (Report separately for serum chloride when calculating anion gap — critical for metabolic acidosis typing: elevated anion gap vs. normal anion gap [hyperchloremic] acidosis)
84295
Sodium (Report separately for serum sodium when calculating anion gap: Anion Gap = Na⁺ − [Cl⁻ + HCO₃⁻]; required to characterize metabolic acidosis type)
84132
Potassium; serum, plasma or whole blood (Report separately; hypokalemia or hyperkalemia accompanies various acidosis subtypes — hypo K in RTA types 1/2; hyper K in RTA type 4/adrenal insufficiency acidosis)
82947
Glucose; quantitative, blood (except reagent strip) (Required in DKA workup and lactic acidosis differential — hyperglycemia in DKA; hypoglycemia as a cause of lactic acidosis)
80047
Basic metabolic panel (Calcium, ionized; when this panel is ordered, it includes HCO₃, glucose, BUN, creatinine, electrolytes — do NOT separately report individual components already included in the panel)
80048
Basic metabolic panel (Calcium, total) (The more common basic metabolic panel ordered on admission; includes CO₂/bicarbonate — do NOT additionally report 82374 if BMP is already billed)
Intravenous infusion, for therapy, prophylaxis, or diagnosis; initial, up to 1 hour (Report for IV sodium bicarbonate infusion when administered therapeutically for severe metabolic acidosis — pH < 7.10 or in select RTA management; requires documentation of medical necessity for alkalinizing agent use)
+Intravenous infusion, each additional hour (Add-on; report for each additional hour of IV bicarbonate infusion beyond the first; always listed in addition to 96365, never alone)
94002
Ventilation assist and management, initiation of pressure or volume preset ventilators for assisted or controlled breathing; hospital inpatient/observation, initial day (Report when mechanical ventilation is initiated for respiratory acidosis/hypercapnic respiratory failure requiring ventilatory CO₂ management)
94003
…each subsequent inpatient/observation day (Report for each subsequent day of active ventilator management for ongoing respiratory acidosis; requires daily documentation of ventilator settings and clinical assessment)
94660
Continuous positive airway pressure ventilation (CPAP), initiation and management (Report when CPAP is initiated for hypercapnic respiratory acidosis in a patient not requiring full mechanical ventilation — e.g., acute COPD exacerbation with moderate CO₂ retention)
90760
Intravenous infusion, hydration; initial, 31 minutes to 1 hour (Report for IV fluid resuscitation in lactic acidosis/sepsis-driven acidosis — note: hydration codes 90760/90761 are distinct from therapeutic infusion codes 96365/96366; select based on documentation of therapeutic vs. hydration intent)
Significant, separately identifiable E/M service — Append to 99213 / 99214 / 99223 when the physician performs a significant, separately documented E/M on the same day as a procedure (e.g., initiation of mechanical ventilation 94002 or IV infusion 96365)
Distinct procedural service — Append to a separately identifiable lab code (e.g., 83605 for lactate) when it might be bundled with a panel code by the payer, but clinical documentation supports its separate medical necessity
Repeat clinical diagnostic laboratory test — Append when the same laboratory test (e.g., 82803 ABG or 83605 lactate) is repeated on the same day for serial monitoring of acidosis treatment response — do NOT use -91 to rerun a test due to equipment malfunction (use QW or -QW for waived testing context)
⚠️ Coding Note: The two highest-risk compliance areas in acidosis coding are the DKA Excludes1 violation and the respiratory acidosis sequencing error. On the DKA front, many coders or automated tools erroneously append E87.21 alongside E10.10 — this is a direct ICD-10-CM Excludes1 violation since DKA codes fully capture the ketoacidotic acidosis component; submitting both will likely result in a claim edit and potential audit finding. On the respiratory front, respiratory acidosis should never be sequenced as the principal diagnosis when the underlying hypercapnic respiratory failure (J96.02 or J96.12) is the documented primary condition — respiratory acidosis is a manifestation/consequence of the respiratory failure, and sequencing guidelines require the etiology (respiratory failure) to be coded first. For lactic acidosis, the key profee query is identifying the cause: Type A (tissue hypoperfusion — sepsis, shock, cardiac arrest) vs. Type B (drugs — especially metformin, NRTIs; liver failure; malignancy) — both map to E87.20 or E87.21, but documenting the cause supports additional diagnoses (sepsis, medication adverse effect) that significantly impact DRG and risk-adjusted reimbursement. When coding the ABG, never report 82803 and 82805 for the same specimen — 82805 includes everything in 82803 plus co-oximetry and is reported instead of, not in addition to, 82803.
A Word from MedlinePlus:
Acidosis is a condition in which there is too much acid in the body fluids. It is the opposite of alkalosis (a condition in which there is too much base in the body fluids).
Causes
The kidneys and lungs maintain the balance (proper pH level) of chemicals called acids and bases in the body. Acidosis occurs when acid builds up or when bicarbonate (a base) is lost. Acidosis is classified as either respiratory or metabolic acidosis.
Respiratory acidosis means there is too much carbon dioxide (an acid) in the body. This type of acidosis occurs when the body is unable to remove enough carbon dioxide through breathing. Other names for respiratory acidosis are hypercapnic acidosis and carbon dioxide acidosis. Causes of respiratory acidosis include:
Metabolic acidosis develops when too much acid is produced in the body. It can also occur when the kidneys cannot remove enough acid from the body. There are several types of metabolic acidosis:
Diabetic acidosis (also called diabetic ketoacidosis or DKA) develops when substances called ketone bodies (which are acidic) build up during uncontrolled diabetes (usually type 1 diabetes).
Hyperchloremic acidosis is caused by the loss of too much sodium bicarbonate from the body, which can happen with severe diarrhea.
Lactic acidosis is a buildup of lactic acid. Lactic acid is mainly produced in muscle cells and red blood cells. It forms when the body breaks down carbohydrates to use for energy when oxygen levels are low. This can be caused by:
Sepsis — severe illness due to infection with bacteria or other germs
Severe asthma
Compensated acidosis occurs when the body returns the acid-base balance and blood pH to near normal in cases of acidosis, but bicarbonate and carbon dioxide levels remain abnormal.
Symptoms
Metabolic acidosis symptoms depend on the underlying disease or condition. Metabolic acidosis itself causes rapid and deep breathing as your body tries to compensate for it by breathing out carbon dioxide at a higher rate. Confusion or lethargy may also occur. Severe metabolic acidosis can lead to shock or death. In some situations, metabolic acidosis can be a mild, ongoing (chronic) condition.
Basic metabolic panel (group of blood tests that measure sodium and potassium levels, kidney function, and other chemicals and functions) to show whether the type of acidosis is metabolic or respiratory
The treatment is aimed at the health problem causing the acidosis. Rarely, sodium bicarbonate (the chemical in baking soda) may be given to reduce the acidity of the blood. Often, you will receive lots of fluids through your vein.
Outlook (Prognosis)
Acidosis can be dangerous if untreated. Many cases respond well to treatment. The outlook will depend on the underlying disease causing the condition.
Possible Complications
Complications depend on the specific type of acidosis.
When to Contact a Medical Professional
All the types of acidosis will cause symptoms that require treatment by your provider.
Prevention
Prevention depends on the cause of the acidosis. Many causes of metabolic acidosis can be prevented, including diabetic ketoacidosis and some causes of lactic acidosis. Normally, people with healthy kidneys and lungs do not have serious acidosis.
Kliegman RM, St. Geme JW, Blum NJ, et al. Electrolyte and acid-base disorders. In: Kliegman RM, St. Geme JW, Blum NJ, et al, eds. Nelson Textbook of Pediatrics. 22nd ed. Philadelphia, PA: Elsevier; 2025:chap 73.
Oh MS, Briefel G, Pincus MR. Evaluation of renal function, water, electrolytes, and acid-base balance. In: McPherson RA, Pincus MR, eds. *Henry’s Clinical Diagnosis and Management by Laboratory Methods.*24th ed. Philadelphia, PA: Elsevier; 2022:chap 15.
Sanghavi S, Albert TJ, Swenson ER. Acid-base balance. In: Broaddus VC, Ernst JD, King TE, et al. Murray and Nadel’s Textbook of Respiratory Medicine. 7th ed. Philadelphia, PA: Elsevier; 2022:chap 12.
Updated by: Jacob Berman, MD, MPH, Associate Professor of Medicine, Division of General Internal Medicine, University of Washington School of Medicine, Seattle, WA. Also reviewed by David C. Dugdale, MD, Medical Director, Brenda Conaway, Editorial Director, and the A.D.A.M. Editorial team.
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