Infarction means 'tissue death' in medical terminology. It is caused by obstruction of blood supply to the tissue leading to lack of oxygen. Infarct, which refers to the resulting lesion is derived from Latin, 'infarctus' which means 'stuffed into'. Pulmonary infarction refers to the death of a small area of lung resulting from pulmonary embolism. It occurs in a small, dead end pulmonary artery.
How does pulmonary infarction occur ?
Pulmonary infarction results from free floating thrombus, when many material substances including fat, tumor, septic emboli, air, and amniotic fluid and injected foreign material may form an emboli and move to the pulmonary circulation. In other words, plugging of a branch of the pulmonary artery by a clot (thrombosis) or by a piece of clot carried by the blood stream to the lung from a thrombus located elsewhere can result in pulmonary infarction. The involved area of the lung ceases to function and complication of the thrombosed veins leads to heart disease.
Causes of pulmonary infarction
The most common cause of pulmonary infarction is pulmonary embolism, but there are other conditions which can cause pulmonary infarction including cancer, and autoimmune diseases such as lupus. Sometimes, this condition may occur following a surgery. Other underlying conditions especially in children with pulmonary emboli include sickle cell disease, nephrotic syndrome, chemotherapy and Inherited hyper coagulable state and Vasculitis.
Symptoms of pulmonary infarction
Symptoms associated with pulmonary infarction include shortness of breath, chest pain, and blood sputum or hemoptysis. Sudden piercing pain in the chest which often radiates to the shoulder is noticed. Difficulty in breathing, irritating cough and blood tinged sputum are other signs. Persistent hiccups are present. Most often the patient is anxious with a rapid pulse, sweats profusely and has an elevated body temperature. In some severe cases, the patient may be in a state of shock.
Diagnosis of pulmonary infarction
Reflex broncho constriction is often associated with pulmonary embolism. Increased breathing and decreased pulmonary compliance with diminished surfactant levels may occur due to pulmonary infarction. This contributes to increased work of breathing and diminished oxygen levels. In sickle cell disease, there is sickling of RBCs within the small blood vessels of the lungs due to dehydration as a result of fever, Tachypnea (rapid breathing) and decreased intake, which can precipitate in a cycle of relative de oxygenation that further exacerbates the sickling tendency. Many also suffer a component of reactive airway disease and oxygenation is further decreased due to this factor.
Morbidity may include pulmonary hypertension, right ventricular failure and Cor Pulmonale, paradoxical embolization in patients with intracardiac defects, and sometimes side effects of medications used to treat pulmonary embolism. If pulmonary embolism is large, there could develop right ventricular strain and right heart failure as there is sudden increase in pulmonary artery pressure leading to right heart failure. A sudden pressure in the right ventricle can cause a leftward shift of the intraventricular septum, which may result in a classic obstructive shock, thereby impairing left ventricular filling.
Treating pulmonary infarction
It is timely treatment that is vital. If symptoms of pulmonary infection develop while at home, consult a physician at once. In case, shock develops, it is essential to get first aid treatment. Many times, patients are already in the hospital when pulmonary infarction occurs. Administration of oxygen, use of anticoagulants and prevention of infection are some other suggested line of treatment. Surgery may also be indicated.
CK blood test
A Creatinine Kinase test is a blood test that measures the levels of Creatinine phosphokinase (CPK). It is an enzyme found predominantly in the heart tissue, brain and skeletal muscle. The CK blood test is commonly used to diagnose the existence of heart muscle damage. The CK blood test result shows an increase above normal in a person's blood test about six hours after the start of a heart attack.
It reaches its peak in about 18 hours and returns to normal in 24 to 36 hours. When the total CPK level is substantially elevated, then it is indicative of injury or stress to heart, brain or skeletal areas. The small amount of CPK that is normally in the blood comes from the muscles. The CPK blood test also helps in cost-effective management of people with suspected coronary atherosclerosis. It also evaluates the extent of muscle damage caused by drugs, trauma or immobility.
Abnormal CK-MB (one of three CK isoenzymes) or troponin levels are associated with Myocyte Necrosis and the diagnosis of Myocardial infarction. The Cardiac Markers of Cardiac Myocyte Necrosis (damage to the Cardiac muscle cells), myoglobin, CK, CK-MB and troponin I and T are primarily used to identify acute Myocardial Infarction.
It is used in early detection of dermatomyositis and polymyositis. It is also used to distinguish malignant hyperthermia from a post operative infection. It helps to discover carriers of muscular dystrophy.
The normal range for Creatinine Kinase (CK or CPK) blood test:
Male: 38 - 174 units/L
Female: 96 - 140 units/L
Increased levels of CK also can be found in viral myositis and hypothyroidism. Higher than normal CPK levels is indicative of the following conditions:
Serum CKMB levels are tested to check for myocardial injury. It is another important cardiac marker. The primary source of CKMB is myocardium although it is also found in skeletal muscle. Typically CKMB tests have now been replaced by Troponin test. But in cases of abnormal Troponin assay results or suspected re-infarction in the hospital, the CKMB serum test is still used.
High levels of CK MB are noticed in cases of polymyositis and rhabdomyolysis. Patients suffering pulmonary embolism, hypothyroidism, and muscular dystrophy or carbon monoxide poisoning can also show higher levels of serum CKMB. The reference range is about 56.2 pg/mL.
Bibliography / Reference
Collection of Pages - Last revised Date: December 10, 2017