Recognize Clinical Indicators to Improve Pulmonary Disease Coding
ICD-10 reporting of chronic obstructive pulmonary disease (COPD) services requires an understanding of common pathologies.
Categorize Pulmonary Disease
Pulmonary disease is divided into two basic categories: obstructive and restrictive.
Obstructive disease affects the patient’s ability to ventilate. Ventilation is the movement of air in (inspiration) and out (expiration) of the lungs:
- Inspiration is an active process that occurs when the diaphragm contracts, causing atmospheric air/oxygen to enter the lungs. Inspiration requires muscular contraction.
- Expiration occurs during the natural elastic recoil of the lungs. Elastic recoil does not require muscular contraction to occur, so it is considered passive. During acute respiratory distress caused by pulmonary disease or trauma, however, exhalation can become active. Active exhalation requires using the accessory muscles of ventilation, in addition to diaphragmatic function. This condition is described as dyspnea (difficulty breathing).
During the expiratory phase, we vent out (exhaust) carbon dioxide (CO2). Removing CO2 (which is acidic) is essential to maintain a normal blood pH of 7.40.
Restrictive disease affects the patient’s ability to oxygenate. The lungs have approximately 300 million alveoli, or microscopic air sacs, which account for a total surface area close to the size of a tennis court and allow for gas exchange. The alveolar surface area is significant because oxygenation is the most critical function of the lungs: ventilation is second, and protein synthesis is third (see accompanying sidebar “The Lungs’ Role in Protein Synthesis”).
Progression of either restrictive or obstructive disease may disrupt both the patient’s ventilatory and oxygenation processes. Cardiac and renal side effects also may occur.
Obstructive Disease Patterns
There are five primary obstructive disease patterns: increased airway resistance, decreased flow rate, increased lung volumes and capacities, increased compliance, and increased wasted ventilation.
1. Increased Airway Resistance
An increase in airway resistance occurs due to narrowing of the airway. An excellent way to understand increased airway resistance is to take a deep breath and exhale through a straw. Your chest will feel “fuller,” which is due to air that is trapped in your lungs because of the narrowed airway and the inability to completely exhale.
There are three fundamental causes of increased airway resistance:
I Bronchospasm is caused by the constriction of bronchial smooth muscle. Bronchial smooth muscle constriction is treated with medications known as bronchodilators. Asthma is an obstructive disease characterized by bronchospasm; ICD-10-CM category J45 Asthma is used to code the type of asthma, frequency, and severity.
II Airway Inflammation is caused by irritants, such as smoking, or environmental and industrial exposures. Inflammation of the airways occurs towards the middle of the airway, causing it to narrow. Chronic bronchitis, ICD-10-CM category J41, is an obstructive disease characterized by a chronic non-curable inflammation of the airways.
Inhaled corticosteroids are used to treat both types of chronic inflammation of the airways. Intravenous corticosteroids may be used in severe acute cases.
III Excessive production of mucus has some of the same causes as airway inflammation, described above. Patients with chronic bronchitis — category J41 Simple and mucopurulent chronic bronchitis (e.g., J41.1 Mucopurulent chronic bronchitis) and category J47 Bronchiectasis — have an overproduction of mucus.
There are two possible effects of increased airway resistance:
I The patient is unable to complete exhalation, resulting in “air trapping” (a sign/symptom of increased airway resistance and the presence of an obstructive disease). Incomplete exhalation causes a decrease in the excretion of CO2. When CO2 is not excreted through exhalation, it is retained in the blood. When the lungs are unable to excrete the necessary amount of CO2, the blood pH will decrease, causing acidosis in the blood. When blood acidosis occurs due to chronic retention of CO2, the kidneys must produce more bicarbonate to normalize the blood pH, referred to as a compensation. A compensation is not a cure.
II Air trapping impairs the patient’s ability to inhale, which decreases the volume of air that is inhaled. Less volume of inhaled air is equal to a decrease in oxygen volume. A patient suffering from air trapping will also develop hypoxemia.
In obstructive disease, the primary problem is the inability to exhale, and oxygenation is secondary. An increase in airway resistance is the first symptom of an obstructive disease, which is why obstructive diseases are airway diseases that affect ventilation. An increase in airway resistance may be audible: “wheezing” is an indication of increased airway resistance and obstructive disease pattern.
2. Decreased Flow Rates
Flow is defined as volume per unit of time. In pulmonary physiology, flow is measured in liters per second (LPS). Flow is the “speed” at which air is exhaled air out of the lungs. If exhalation could occur for one full minute without needing to take an inhalation, air trapping would not be an issue. The normal respiratory rate is 12 to 20 breaths per minute — this means we must inhale 12 to 20 times per minute to obtain the necessary oxygen to maintain cellular life. We can’t extend our exhalation time to improve the degree of air trapping. Instead, we must treat the cause of the decrease in flow, which are the factors causing the increased airway resistance. These patterns are characteristic of all diseases that classify as COPD.
3. Increased Lung Volumes and Capacities
Patients with increased airway resistance and decreased flow rates have lung volumes and capacities that are above normal. Patients who have increased lung volumes are often described as having a “barrel chest,” which is a clinically observed disease pattern common with obstructive diseases. The anomaly is visible on a chest X-ray: The spaces between the ribs are larger than normal (e.g., increased intercostal space).
4. Increased Compliance
Compliance describes the ability of the lungs to expand. The lungs have the physical property of elasticity, which is the ability to stretch. Elasticity is governed by the Frank-Starling Law, which says that elasticity is preserved to a certain point but if that point is exceeded then elasticity will decrease due to over-stretching. Lung volumes and capacities that are greater than normal will overstretch the lungs past the Frank-Starling point. The result is a loss of elasticity and impairment of the lung’s normal elastic recoil during exhalation.
5. Increased Wasted Ventilation/Pulmonary Dead Space
Increased physiologic dead space is defined as “wasted ventilation.” There are three types of dead space: anatomical, alveolar, and physiologic (which is the sum of anatomical and alveolar dead space). Anatomical dead space normally occurs in the areas of the lungs where there are no alveoli, which begins at the nose and ends where the alveoli begin. Alveolar dead space increases in emphysema (ICD-10-CM category J43 Emphysema), the only obstructive disease that causes a diffusion impairment.
Restrictive Disease Patterns
Restrictive disease patterns include decreased volumes and capacities, decreased lung compliance, and reduced oxygenation. Airway resistance, flow rates, and dead space do not play a role in the restrictive disease patterns.
Pneumonias and influenza, ICD-10-CM categories J09-J18, are restrictive diseases that commonly occur in patients with COPD. Most cases of pneumonia can be resolved.
Pneumonia may cause a patient with COPD to go into severe respiratory distress and cause acute exacerbation of COPD (ICD-10-CM code J44.1 Chronic obstructive pulmonary disease with (acute) exacerbation), a condition that typically requires the patient to be hospitalized.
Coding Combined Disorders
A patient with characteristics of both obstructive and restrictive patterns is diagnosed with a combined disorder. Obesity is restrictive and is the most common cause of a combined disorder. Industrial exposures to organic dusts, chemical exposure, inhalation of gases, fumes, and vapors are also restrictive diseases and complications. For pneumoconiosis, inhalation of organic, inorganic, silica, and mineral dusts, see ICD-10-CM categories J60-J66. For pneumonitis due to organic dust hypersensitivity, chemical inhalation, fumes, liquids, solids, gas, and vapor exposures, see ICD-10-CM categories J67-J70.
The Lungs’ Role in Protein Synthesis
The protein synthesis function of the lungs occurs through the alveolar type II cells, which produce an essential protein known as surfactant. The primary function of surfactant is to keep the alveoli from collapsing. Babies born prematurely (between weeks 24 and 28) do not produce enough surfactant and require respiratory support. The following disease processes are complications that involve the protein synthesis function of the lungs:
- Chemical inhalation ICD-10-CM categories J67 – J70
- Smoke inhalation ICD-10-CM code J70 Respiratory conditions due to other external agents
- Sepsis ICD-10-CM categories A40 Streptococcal sepsis and A41 Other sepsis. If the patient has severe sepsis, also report R65.20 Severe sepsis without septic shock.
These types of pulmonary impairments can be difficult to resolve, resulting in high morbidity.
Emphysema and Bronchitis ICD-10-CM Codes
Pulmonary Diseases Classified as COPD
- J43.1 Panlobular emphysema – Emphysema that affects the alveoli
- J43.2 Centrilobular emphysema – Emphysema that affects the respiratory bronchioles
- Alpha 1 antitrypsin emphysema (J43.1) – Hereditary panlobular emphysema
- Bullous emphysema (paraseptal emphysema) (J43.9 Emphysema, unspecified) – Advanced form of emphysema with severe loss of alveolar tissue
- Senile emphysema (J43.9) – Panlobular emphysema due to aging
Causes of Emphysema:
- Smoking – Current non-smoker with history Z87.891 Personal history of nicotine dependence and current smoker Z72.0 Tobacco use
- Secondhand smoke, Z77.22 Contact with and (suspected) exposure to environmental tobacco smoke (acute) (chronic) and occupational exposure to secondhand smoke, Z57.31 Occupational exposure to environmental tobacco smoke
- Harmful pollutants, not necessarily industrial exposures (J60 – J70)
- Industrial exposures (J60-J70)*
Chronic Bronchitis J41
Chronic bronchitis is an inflammation and swelling of the lining of the airways that leads to airway narrowing and obstruction and is characterized by excessive mucus production. Patients who suffer from chronic bronchitis have chronic productive coughing episodes. The daily production of mucus serves to increase the likelihood of bacterial infections and pneumonia.
- J41.1 Mucopurulent chronic bronchitis is a type of chronic bronchitis that produces pus in addition to mucus.
- J47 Bronchiectasis is an advanced form of chronic bronchitis where erosion and dilation of the bronchioles occurs together with chronic inflammation. Patients who suffer from bronchiectasis produce foul smelling sputum that may settle in three layers.
Causes of Chronic Bronchitis:
- Smoking – Current non-smoker with history (Z87.891) and current smoker (Z72.0)
- Secondhand smoke (Z77.22) and occupational exposure to secondhand smoke (Z57.31)
- Harmful pollutants, not necessarily industrial exposures (J60-J70)
- Industrial exposures* (J60-J70)
*Note: Industrial exposures are usually combined pulmonary disorders. Pneumoconiosis, pulmonary fibrosis, and pneumonitis are restrictive diseases and conditions caused by exposures to dusts and chemicals.
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