Laboratory Interpretation Nursing CE Course for APRNs

Potassium is the primary intracellular ion and helps regulate the communication channels between nerve fibers and muscles, serving an essential role in heart contraction and muscle functioning. Hypokalemia results when the potassium level drops below the normal range. There are three primary etiologies of hypokalemia: urinary loss (usually drug-induced by diuretic medications), gastrointestinal loss (usually due to diarrhea, vomiting, or malabsorption), or the movement of potassium from extracellular to intracellular fluid (due to alkalosis or insulin or glucose administration). Symptoms of hypokalemia may include constipation, muscle weakness or spasms, numbness or tingling sensations, cardiac arrhythmia, flattened T waves, prominent U waves, and fatigue. Hyperkalemia occurs when the potassium level is higher than the upper limit of normal and can be due to increased dietary potassium intake or impaired renal clearance secondary to acute or chronic renal failure, the most common cause of hyperkalemia. Hyperkalemia can also be drug-induced by potassium-sparing diuretics such as aldosterone antagonists (i.e., spironolactone [Aldactone]). If a serum sample is hemolyzed (cells are ruptured) during sample collection or processing, hyperkalemia can be inaccurately reported on the lab results, reinforcing the need to associate all laboratory data with the patient's clinical presentation. Symptoms of hyperkalemia may include muscle fatigue, weakness, paralysis, cardiac arrhythmias, peaked T waves, widened QRS complex, and nausea. Because more than 90% of potassium is excreted in the urine, which is then filtered and reabsorbed proximally before being excreted by the distal tubules, it is not uncommon for patients with severe renal disease to exhibit abnormal potassium levels (Pagana et al., 2022; Shrimanker & Bhattarai, 2023).

Calcium 

Calcium is one of the body's essential minerals required for muscle contraction, nerve function, and healthy bones and teeth. Calcium also serves a vital role in blood clotting and cellular division. The CMP reports only the total calcium level in the bloodstream. Low calcium levels, or hypocalcemia, may be caused by hypoparathyroidism, renal failure, vitamin D deficiency or insufficiency, magnesium deficiency, acute pancreatitis, or other conditions. Symptoms of hypocalcemia most commonly include paresthesia, muscle spasms or cramps, tetany, numbness, and in severe cases, seizures. Higher than normal calcium levels, or hypercalcemia, may be due to hyperparathyroidism, tuberculosis, or drug-induced secondary to diuretics, calcium-containing antacids, or excess vitamin D intake. Hypercalcemia also raises suspicion of malignancy, especially metastatic breast or lung cancer or multiple myeloma. In its most severe form, hypercalcemia related to malignancy is considered a life-threatening medical emergency. Symptoms of hypercalcemia include excessive thirst, frequent urination, bone pain, muscle weakness, confusion, fatigue, or rarely, palpitations or cardiac arrhythmias. Since calcium in the blood is bound to albumin, the total calcium level reported may be an inaccurate representation of the free (ionized) calcium in patients with high or low albumin levels. Therefore, it is essential to determine the accurate (corrected) calcium level before treating abnormally high or low calcium. Several online calculators are available to assist clinicians (see Figure 1 for an example; (Goltzman, 2023).

Figure 1

Corrected Calcium Formula

(Goltzman, 2023)

Chloride and Bicarbonate

Chloride helps to regulate fluid balance within the body, and bicarbonate provides information regarding the acid-base status. Due to their direct inverse relationship, the clinical significance of chloride and bicarbonate should always be interpreted together and in conjunction with the anion gap. The anion gap is a calculated result that measures how much acid is in the blood, which provides valuable information for delineating the etiology of acid-base disturbances. These tests help to distinguish between respiratory alkalosis (acute versus chronic) and metabolic acidosis. They can also help to identify diabetes insipidus, renal tubular acidosis, Addison's disease, hyperparathyroidism, or Cushing syndrome (Pagana et al., 2022; Shrimanker & Bhattarai, 2023).

Renal Function

While the electrolyte panel provides valuable information regarding renal function, three tests within the CMP explicitly evaluate the health status and functioning of the renal system: blood urea nitrogen (BUN), creatinine, and estimated glomerular filtration rate (eGFR; Gounden et al., 2022).

Blood Urea Nitrogen

Urea is a nitrogen-containing waste product generated from the breakdown of dietary protein within the liver. It is released into the blood and circulates until it is excreted. Approximately 85% is filtered by the kidneys and excreted via the urine; the rest is excreted in the stool. The BUN measures the amount of waste products in the blood. The BUN increases when the kidneys are not functioning correctly. This can be due to easily correctable causes such as dehydration, diarrhea, a high-protein diet, or certain nephrotoxic medications, including chemotherapy or steroids. Alternatively, an elevated BUN may indicate a more complex condition such as congestive heart failure, renal disease (e.g., glomerulonephritis, pyelonephritis, or tubular necrosis), tissue necrosis, shock, or severe burns. A low BUN level is not as common and generally due to fluid overload, syndrome of inappropriate antidiuretic hormone (SIADH), pregnancy, malnutrition, or liver failure (Gounden et al., 2022; Pagana et al., 2022).

Creatinine

Creatinine is a chemical waste byproduct of creatine phosphate, essential in creating muscle energy and skeletal muscle contraction. Produced primarily in the liver, creatine is transported to the muscles and is phosphorylated into creatine phosphate. Creatinine is excreted solely by the kidneys and is a good indicator of kidney function, although levels can vary widely based on age, gender, and body size (muscle mass). High creatinine levels generally indicate kidney dysfunction, which may be secondary to dehydration, starvation, acute trauma, infection, urinary tract obstruction, burns, or acute or chronic kidney failure. Low creatinine levels indicate the presence of decreased muscle mass, which may result from an underlying condition such as muscular dystrophy or myasthenia gravis (Pagana et al., 2022).

Glomerular Filtration Rate 

The eGFR is the most sensitive and widely utilized test to measure how well the kidneys function and stage existing kidney disease. The eGFR reflects the creatinine level in the blood, using a specific formula to calculate a result based on the patient's age, gender, and body size. The normal eGFR in adults is greater than 90 ml/min/1.73 m², but as demonstrated in Table 3, a normal eGFR is commonly reported as greater than 60 ml/min/1.73 m². Chronic kidney disease (CKD) is staged based on the eGFR value and reflects the severity of impairment. An eGFR below 60 for at least three months or an eGFR above 60 with kidney damage (marked by high levels of albumin in the urine) indicates CKD (Kidney Disease Improving Global Outcomes (KDIGO), 2021). The KDIGO stages of chronic kidney disease are as follows:

Bilirubin

Bilirubin is the byproduct of the breakdown of RBCs, and it is reported in three values: total, direct, and indirect. Total bilirubin is a combination of both direct and indirect bilirubin values. Indirect (unconjugated) bilirubin is the amount of bilirubin bound to albumin and circulating through the bloodstream. Indirect bilirubin is insoluble in water and cannot be excreted in the urine. The liver absorbs indirect bilirubin, which is conjugated with glucuronic acid to a water-soluble form. Direct (conjugated) bilirubin is then secreted into bile and transported through the gallbladder and digestive tract before being excreted in the stool. Hyperbilirubinemia occurs when there is an increase in bilirubin production or a decrease in uptake or conjugation of indirect bilirubin or excretion. Since bilirubin is a yellowish substance, pathologic accumulation in the blood can lead to jaundice or yellowing of the skin (mucosal membranes) and eyes (scleral icterus). Hyperbilirubinemia can cause abdominal pain, fevers, chills, systemic pruritus, dark-colored urine, fatigue, weakness, nausea, or vomiting. The differential diagnosis of hyperbilirubinemia can vary widely, but the most common etiologies of hyperbilirubinemia include liver disease, bile duct inflammation or blockage, gallstones, cholelithiasis, or hemolytic anemia. When interpreting bilirubin values, it is essential to consider the patient's age and other health conditions (Lindenmeyer, 2022; Pagana et al., 2022).   

Indirect (unconjugated) Bilirubin. At least 70 to 85% of bilirubin should be unconjugated in healthy adults. Liver disease can be excluded as the culprit when the total bilirubin level is elevated, and the breakdown of the direct and indirect values reveals that at least 75% is unconjugated. Hemolysis or Gilbert's syndrome are more likely etiologies; both conditions usually demonstrate normal direct bilirubin levels. Gilbert's syndrome is a genetic liver condition seen in approximately 5% of the population that impairs the liver's ability to process bilirubin correctly. It generally causes mild hyperbilirubinemia without clinical symptoms (Lindenmeyer, 2022; Pagana et al., 2022).

             Direct (conjugated) bilirubin. Direct bilirubin is considered the most sensitive test in diagnosing liver disease. Therefore, elevated levels of direct bilirubin are often accompanied by elevated liver enzymes. When direct bilirubin is elevated, it will spill over into the urine, suggesting a problem with bilirubin metabolism or excretion. The most common etiologies include gallstones, extensive liver metastasis, alcohol abuse, hepatocellular disease, drug reactions, and biliary tract obstruction (extrahepatic or intrahepatic; Lindenmeyer, 2022; Pagana et al., 2022).

Liver Enzymes

Liver enzymes that are evaluated include alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). These tests further assess the liver’s function and detect liver injury or disease. ALT, AST, and ALP elevations are most commonly drug-induced due to lipid-lowering statin therapy (i.e., atorvastatin [Lipitor]), chemotherapy, or numerous other medications processed through the liver. Elevations may also be related to excess alcohol consumption, underlying cirrhosis, or fatty liver. An AST/ALT ratio greater than one may indicate liver cirrhosis or the presence of liver metastasis. An AST/AT ratio of less than one may indicate viral hepatitis, acute hepatitis, or infectious mononucleosis (Lindenmeyer, 2022; Pagana et al., 2022).

ALT. ALT is an enzyme primarily produced by the liver and found in high concentrations within the hepatocytes (liver cells). The ALT is considered the most specific test when evaluating liver injury, as it directly indicates hepatocellular injury (hepatic jaundice). Moderately or mildly increased levels may occur due to cirrhosis, obstructive jaundice, severe burns, pancreatitis, or infectious mononucleosis (Lindenmeyer, 2022; Pagana et al., 2022).

AST. AST is an enzyme in highly metabolic tissues such as heart or skeletal muscle tissue, liver cells, kidneys, pancreas, and RBCs. While elevations in AST can infer liver damage, they can also be seen in cases of acute cardiac muscle injury (i.e., myocardial infarction), skeletal muscle injury, heat stroke, and progressive muscular dystrophy (Lindenmeyer, 2022; Pagana et al., 2022).

ALP. ALP is an enzyme concentrated within the liver, biliary tract, epithelium, and bone cells. Most extrahepatic ALP comes from the bones. Due to this, elevations in ALP can indicate liver damage or bone problems such as rickets, Paget's disease, or bone cancer (primary bone tumors or metastatic bone lesions). Due to the different sources of elevated ALP, isoenzymes are measured to differentiate between hepatic or bone factors. ALP1 is expected to be elevated when liver disease is the elevation source. ALP2 is elevated when there is an underlying bone disease. When ALP is elevated due to liver pathology, it primarily responds to cholestasis (a decrease in bile flow due to post-hepatic or obstructive jaundice; Lindenmeyer, 2022; Pagana et al., 2022).

Lactate Dehydrogenase 

Lactate dehydrogenase (LDH), or lactic acid/lactate dehydrogenase, is an enzyme in the blood that generates energy within the body. LDH is widespread throughout nearly all body tissues. When tissues become damaged, they release LDH into the blood, making it a nonspecific marker of tissue damage and inflammation. Patients with metastatic cancer often have elevated LDH levels due to cancer spread or liver damage from cancer treatments. LDH can be elevated in conditions such as acute myocardial infarction, skeletal muscle disease, tissue necrosis, shock, congestive heart disease, systemic infections, liver disease, and beyond (Pagana et al., 2022).

Total Protein

Protein is necessary for cellular growth, development, and overall health. The total protein is the sum of two circulating proteins in the blood: albumin and globulin. Therefore, the total protein is easier to interpret with the albumin and globulin values, also reported within the CMP. Albumin is produced within the liver and is the predominant protein within the bloodstream, accounting for approximately 60% of the total protein. The albumin provides essential information about nutritional status; hypoalbuminemia (decreased albumin level) is commonly seen in malnutrition and malabsorptive disorders. The albumin also serves as a marker of liver and kidney damage, as albumin production within the liver is decreased in severe liver disease or inflammation. Typically, the only clinically significant cause of increased albumin levels is dehydration. Globulins comprise the remaining 40% of the protein in the bloodstream; they assist the immune system with fighting infection and transporting nutrients. Globulins may increase in the presence of infection, inflammation, and some types of cancers, particularly plasma cell tumors and lymphomas (Pagana et al., 2022).

The A-G ratio refers to the albumin ratio in relation to the amount of globulin present in the blood. It is calculated automatically by many labs and reported in CMP results. The A-G- ratio should be slightly higher than 1 in healthy adults. It can provide insight into the etiology of changes in the total serum protein value. Higher than normal A-G ratios are often due to the underproduction of globulins and can be caused by hypothyroidism, glucocorticoid excess, certain types of blood cancers such as leukemia, and some genetic disorders. Low A-G ratios may indicate an autoimmune disorder, cirrhosis, or kidney disease (Pagana et al., 2022).

Lipid Panel

A lipid panel (or lipid profile) measures the amount of cholesterol and triglycerides within the blood. Lipids are fats and fatty substances within the blood that serve as energy sources and are required by the body to maintain the health of cells and specific cellular functions. These are either synthesized by the liver or absorbed from the diet. When cholesterol is present in excess, it can lead to atherosclerosis or the buildup of fatty plaque within the arteries. Plaque growth within the arteries leads to damage, narrowing, or blockage of the arteries and blood vessels, which can develop into coronary artery disease (CAD) and lead to myocardial infarction and stroke. Hyperlipidemia, or high cholesterol levels, is considered a significant risk factor for cardiovascular and blood vessel disease, but this usually does not cause any warning signs or symptoms. Therefore, the lipid panel provides valuable information regarding a patient's risk for atherosclerosis and is also performed when monitoring response to lipid-lowering therapy. As demonstrated in Table 4, a standard lipid panel includes total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides. Since dietary intake can impact the lipid panel results, patients are advised to fast for at least eight hours before the test. Patients should also be advised to take their usual medications with water only (Bakerman et al., 2014; Pagana et al., 2022). The reference ranges listed in Table 4 are values based on fasting.

Table 4

Lipid Panel Components and Reference Ranges

(ABIM, 2023)

HDL-C is considered good cholesterol, as high levels are cardioprotective and associated with a reduced risk of cardiovascular and blood vessel disease. Since HDL-C takes up excess cholesterol and carries it to the liver for removal, the higher the HDL-C, the better. Alternatively, decreased levels of HDL-C are associated with an increased risk of cardiovascular disease, especially in males. LDL-C is considered bad cholesterol, as high levels are linked to increased cardiovascular damage, atherosclerosis, and associated morbidity and mortality. LDL-C deposits excess cholesterol in the walls of blood vessels. Generally, the higher the LDL-C, the greater the risk for fatty plaque buildup within the arteries. The basis for cholesterol management is centered on lipid-lowering agents and diets targeting a reduction in LDL-C. Like LDL-C, high triglyceride levels are associated with an increased risk of cardiovascular and blood vessel disease (Bakerman et al., 2014).

Elevated LDL-C and triglycerides levels are closely linked to unhealthy lifestyle choices such as a poor diet (excess intake of fatty foods and simple sugar), a sedentary lifestyle (lack of physical activity), obesity and excess weight, smoking or exposure to tobacco smoke, and excessive alcohol intake (Grundy et al., 2019). Hyperlipidemia and type 2 diabetes mellitus (T2DM) commonly occur together. Patients with T2DM have a higher prevalence of lipid abnormalities in the peripheral venous circulation, increased atherosclerotic plaque accumulation, and smaller coronary artery lumen diameter than those without T2DM. The American Diabetes Association (ADA) recommends that patients with T2DM strive for lower target cholesterol levels than those listed in Table 4 (Joseph et al., 2022). Optimal cholesterol values for patients with T2DM include:

Thyroid Function Tests 

Thyroid function tests (TFTs) are performed to determine if the appropriate amount of thyroid hormone is present within the bloodstream. TFTs may be ordered individually or collectively as a group (thyroid panel) to help diagnose or monitor thyroid disorders. The thyroid gland has several vital functions and is responsible for maintaining various aspects of homeostasis within the body, including regulating body temperature, metabolism, and calcitonin. It also impacts the way tissues outside the thyroid function. The thyroid gland generates two primary hormones: thyroxine (T4) and triiodothyronine (T3). T4 contains four iodine atoms and is converted to T3, which contains three iodine atoms and has a stronger and more rapid metabolic action than T4. The pituitary gland regulates the amounts of T4 and T3 secreted into the blood (Ross, 2022).

Interpreting TFTs can be daunting and requires a rudimentary understanding of how thyroid hormones are produced and released. As demonstrated in Figure 2, the release rate of T3 and T4 is controlled by the anterior pituitary gland and hypothalamus, which acts as a sensory controller. The hypothalamus initiates the process by secreting thyrotropin-releasing hormone (TRH). TRH is essentially the first thyroid messenger signal, as it stimulates the release of thyroid-stimulating hormone (TSH) from the anterior pituitary gland. TSH is critical in modulating the release of T4, which is then converted to T3. The amount of TSH that the pituitary releases into the bloodstream depends on the amount of T4 that the pituitary perceives, as it functions on a negative feedback system. The pituitary constantly measures the amount of T3 and T4 and responds to changes to maintain an appropriate balance. If the pituitary senses insufficient T4, it will ramp up the TSH production, signaling the thyroid gland to produce more T4. Once the level of T4 reaches a specific level within the blood, TSH production decreases (Ross, 2022).

Figure 2

Thyroid Hormones

Thyroid disease is most characterized as overactive (hyperthyroidism) or underactive (hypothyroidism). Hypothyroidism is classified as primary or secondary; primary is much more common. Hashimoto's thyroiditis, an autoimmune disease that causes the body to attack the thyroid gland, is the most common cause of primary hypothyroidism in the US. Secondary hypothyroidism is caused by the failure of the pituitary gland or hypothalamic disease, whereby the body does not make adequate amounts of TSH to stimulate the release of T3 and T4 (Braunstein, 2022b). The differential diagnosis for hyperthyroidism is more complex and includes thyrotoxicosis, Grave's disease, and subacute thyroiditis. The main distinction between hyperthyroidism and thyrotoxicosis is in the underlying pathophysiology of the hormones. Hyperthyroidism is characterized by the increased production and secretion of T3/4 from the thyroid gland and includes three primary subtypes: thyrotoxicosis, Grave's disease, and subacute thyroiditis. Thyrotoxicosis is a clinical disorder with excess circulating T3 and T4, irrespective of the source. Graves' disease is an autoimmune disorder that leads to hyperthyroidism, as the body attacks the thyroid gland, inducing overactivity. While it carries many of the same symptoms of hyperthyroidism, Grave's disease has characteristic physical signs, including exophthalmos (prominence of the eyes), goiter, and extraocular muscle weakness (Braunstein, 2022a). Table 5 outlines the most common clinical features of hypothyroidism and hyperthyroidism.

Table 5

Clinical Features of Hypothyroidism vs. Hyperthyroidism

(Braunstein, 2022a, 2022b)

A thyroid panel typically comprises three main tests: free T4 (FT4), free T3 or total T3, and TSH, described in Table 6. Patients are not advised to fast before the test, as some clinical studies have demonstrated that early morning fasting leads to higher TSH levels compared to tests performed in the afternoon on patients who did not fast. Before TFTs, patients should be screened for any iodine contrast administration within the previous ten days of the test, as the thyroid takes up iodine and can skew results. TFT results can be altered in pregnant patients or those who take estrogen medications such as oral contraceptives or hormone replacement therapy. Patients should also be counseled to stop biotin (an over-the-counter supplement rich in B vitamins) at least two days before having their TFTs performed, as this supplement is known to interfere with the accuracy of TFT results (Ross, 2022).

Table 6

Thyroid Panel 

(ABIM, 2023)

Thyroid Stimulating Hormone 

TSH is the first-line screening test for patients with suspected thyroid dysfunction. The level of circulating TSH in the blood is used to determine if the thyroid is functioning correctly or is overactive or underactive. If the TSH is high, the thyroid gland is not producing enough T3 or T4, which would raise clinical suspicion for primary hypothyroidism. Conversely, if the TSH is low, it usually suggests that the thyroid produces too much T3 and T4, raising clinical suspicion for hyperthyroidism. Less commonly, a low TSH level may be caused by an abnormality in the pituitary gland or hypothalamic disease, preventing the body from making adequate amounts of TSH to stimulate the release of T3 and T4. This condition is referred to as secondary hypothyroidism (Ross, 2022). The most recent guideline from the US Preventive Services Task Force (USPSTF) recommends that multiple tests over three to six months be performed to confirm abnormal TSH results (LeFevre & USPSTF, 2015).

T4 Tests

T4 can be measured as total T4 or FT4. Total T4 measures both the free and the bound hormone available, whereas FT4 measures the T4 hormone freely circulating in the blood and available for use. FT4 is more commonly performed as it provides the most insight into the severity of an abnormal TSH level. FT4 is most accurate when performed with the TSH level; therefore, these tests are usually ordered together (Ross, 2022). When interpreting the FT4, the APRN must exclude conditions that are commonly associated with transient elevations of the FT4, such as:

Figure 3

Interpreting Thyroid Function Testing 

(Flowchart based on BCGuidelines.ca, 2018)

Table 7

Thyroid Conditions

(Ross, 2022)

Thyroid Antibody Tests

Thyroid antibody tests are a separate subtype of TFTs that measure the level of the blood's thyroid antibodies. Thyroid peroxidase antibody, or antithyroid peroxidase antibodies (TPO), is one of the most common antibody tests currently used in clinical practice. It is performed to determine if hyperthyroidism is autoimmune, such as in Grave's or Hashimoto’s disease. In patients with suspected Hashimoto disease, antithyroglobulin antibody (Tg) testing may also be performed to confirm the diagnosis, as these patients typically have high levels of TPO and Tg. Although the presence of these antibodies can contribute to the initial diagnosis, there is no benefit to monitoring their levels over time. The levels of these antibodies do not indicate disease severity or response to treatment. The presence of thyroid-stimulating immunoglobulin (TSI) or TSH-receptor-thyrotropin receptor antibody (TRAb) strongly supports a diagnosis of Grave's disease. Clinicians should monitor TSI or TRAb levels over time to determine the effectiveness and duration of treatment (Ross, 2022).

Fasting Blood Glucose (FBG) and Glycated Hemoglobin (HbA1C)

FBG and HbA1C are used to diagnose and monitor diabetes. The FBG is one of the most common routine tests. The test can be performed by drawing a blood sample or as a simple fingerstick with a glucometer machine. Patients should be advised to fast for at least eight hours before having the FBG test performed to ensure the accuracy of the results. Patients may drink water and take prescription medications but should not take anything else by mouth. The normal FBG should range between 70–99 mg/dL. Diabetes occurs when the FBG is 126 mg/dL (7.0 mmol/L) or higher, whereas an FBG of 100 mg/dL (5.6 mmol/L) to 125 mg/dL (6.9 mmol/L) is categorized as prediabetes. Prediabetes is the precursor to diabetes, in which the blood glucose levels are higher than normal but not high enough to meet the diagnostic classification of diabetes. The HbA1C measures the average blood glucose levels over the past three months. The patient is not required to fast before the HbA1C test. The normal HbA1C for non-diabetic adults should be less than 5.7%. Diabetes is considered when the HbA1C is 6.5% or higher, whereas an HbA1C of 5.7% to 6.4% is considered prediabetes (ADA, 2023; National Institute of Diabetes and Digestive and Kidney Diseases, 2020).

Coagulation Profile

A coagulation profile measures the blood's clotting capacity and typically includes the prothrombin time (PT), international normalized ratio (INR), activated partial thromboplastin time (aPTT), platelets, and fibrinogen. These tests are performed routinely before surgery to ensure patient safety, to evaluate why a patient is experiencing abnormal bruising or bleeding, or as a screening test for an underlying blood or blood clotting disorder. The normal values for a coagulation profile are listed in Table 8. PT is measured in seconds and refers to the amount of time it takes for the plasma portion of the blood to clot. The INR is a standardized number calculated from the PT result. Usually, the INR is reported and monitored in patients treated with anticoagulant therapy such as warfarin (Coumadin). Patients prescribed warfarin (Coumadin) must undergo routine blood tests at least monthly, but sometimes testing may occur more frequently, such as twice weekly. The testing ensures that the patient’s blood clotting time is within a safe and effective range, as the warfarin (Coumadin) dose is adjusted according to the INR. Higher than normal INR levels indicate a higher risk for bleeding due to the blood's impaired ability to clot. While on warfarin (Coumadin), the INR must not exceed therapeutic thresholds; otherwise, the risk of bleeding heightens. Similarly, blood clots may not be prevented if the patient’s INR is too low. For most warfarin (Coumadin) therapy patients, an INR of 2.0 to 3.0 is generally considered an effective therapeutic range. The aPTT test is performed alongside the PT/INR in patients with suspected bleeding or blood clotting disorders. While the PT test assesses how well all of the coagulation factors in the extrinsic and common pathways of the coagulation cascade are functioning collectively, the aPTT evaluates the clotting factors within the intrinsic and common pathways (Pagana et al., 2022; Shikdar et al., 2023).

Fibrinogen is a plasma glycoprotein synthesized within the liver that helps control bleeding by assisting with blood clot formation. An abnormal fibrinogen level may be due to fibrinolysis (the breakdown of fibrin), congenital or acquired fibrinogen deficiency, or a condition in which the body uses too much fibrinogen (disseminated intravascular coagulation [DIC]). An imbalance of these components poses a risk of acute bleeding, hemorrhage, and death (Kaur & Jain, 2023)

Table 8

Coagulation Profile 

(ABIM, 2023; Pagana et al., 2022)