Background of the Case Study
M.M., a 76-year old retired schoolteacher, had a fall in her retirement home and underwent Open Reduction Internal Fixation of her left femur. Open reduction internal fixation is a method of surgically repairing a fractured bone. Her preoperative control prothrombin time (PT) was 11 seconds.
She was then on bed rest for the first 2 days after the operation. At six in the morning on the second post operative day, her vital signs were 132/84mm Hg blood pressure, regular pulse of 84 beats, 16 respirations which are unlaboured, and temperature of 37.2° C. She is awake, alert and oriented. There are no adventitious heart sounds and breath sounds are clear but diminished in the bases bilaterally. Bowel sounds are present, and she is taking sips of clear liquids. Her medication orders include O2 to maintain an oxygen saturation (SaO2) of greater than 90%.
Based on the patient’s vital signs, her vital signs are normal, as well as her heart and breath sounds, and bowel sounds. The oxygen saturation value is normally 95-100% of capacity. She is on an oxygen medication in order to maintain normal saturation since she was just operated and the tendency is for oxygen to lower. Right to left shunts in the heart are strongly suspected if the arterial oxygen saturation is less than normal in the absence of lung disease, pulmonary congestion, or alveolar hypoventilation. Tests have therefore to be done to rule out the possibility of a heart disease or infarction in the patient.
M.M.’s laboratory results show her hematocrit at 34%, Hemoglobin at 113 g/L, potassium at 4.1 mmol/L, and activated partial prothrombin time at 44 sec. Normal values for hematocrit in women are 37-47% (0.37-0.47) ( 2001). Laboratory results show that M.M.’s hematocrit is slightly lowered from the normal values. Normal values for hemoglobin in women are 12-16 g/dL (1.86-2.48 mmol/L). Normal potassium values range from 3.5-5 meq/L or 3.5-5 mmol/L (2000) which would reflect that the patient’s normal values are normal. Normal values for the activated partial thromboplastin time is between 25-37 seconds (2000), showing that the patient has a slightly elevated partial thromboplastin time.
Pain is controlled with morphine sulfate 4 mg IV and promethazine (Phenergan) 25 mg IV q3h. She is also taking clexane 20mg units sub cutaneous injection daily, docusate sodium, and wearing a glyceryl trinitrate patch.
At 2330 on the second postoperative day, the nurse answers M.M. call light and finds her lying in bed breathing rapidly and rubbing her right chest. She is complaining of right-sided chest pain and appears to be restless. She is slightly hypotensive, tachypnoeic, restless, and slightly confused. The pulse oximeter reads 86%, so the nurse started her on 3 to 6 L O2/NC. The nurse identified faint crackles in the posterior bases bilaterally; they were clear that morning. The monitor shows non-specific T wave changes and tachycardia.
The ventricular T wave represents the stage of repolarization of the ventricles, at which time the ventricular fibers begin to relax. It is normally positive in all the standard bipolar limb leads of an electrocardiogram. The T wave becomes abnormal or shows changes when the normal sequence of repolarization does not occur. Several factors can change this sequence of repolarization and cause non-specific T wave changes ( 2000).
Question 1: What will the nurse do?
The nurse notified the physician and gave a comprehensive handover describing the condition of the patient and what he/she had instigated. The physician ordered the patient to be transferred to intensive care unit (ICU), undergo blood coagulation studies, tests on arterial blood gases (ABGs) on room air, continued pulse oximetry, STAT chest x-ray (CXR), and STAT 12-lead electrocardiogram (ECG). These are tests that could check if the patient has pulmonary embolism.
Once pulmonary embolism is diagnosed, the nurse should provide Airway management and oxygen administration. It is safe and efficacious to start anticoagulation therapy as soon as an embolism is strongly suspected and while diagnostic testing is in progress. Anticoagulants prevent the development of clots but do not aid in the lysis of an already existing clot (2004).
Question 2: What information will the physician gain from each of the above orders?
The patient’s vital sign at this time are 150/92 mm Hg blood pressure, 110 beats per minute pulse rate, 28 respirations per minute, and a temperature of 37.2°C. Note that from the vital signs alone, the patient is already hypertensive and is breathing rapidly.
When pulmonary embolism is first suspected, patients should receive heparin at therapeutic doses until pulmonary embolism is excluded, provided that no contraindications to anticoagulation are present (2002). Such procedure is a blood coagulation study. Blood coagulation studies are used to rule out any diseases that have blood coagulation as a manifestation. Virchow’s triad on embolism are as follows: hypercoagulability; stasis; and injury to the vessel wall ( 2002). The case study did not mention what the results of the blood coagulation study were.
An arterial blood gas determination on room air is typically ordered during the evaluation of a patient with suspected pulmonary embolism ( 1996). Determination of oxygen content of blood at different levels within the heart and the great vessels aids in determining the presence, direction, and volume of central shunt which could also rule out the presence of a serious heart condition.
ABG analysis is the best way to evaluate acid-base balance. Measurement of ABGs involves analysis of six components. Deviation from a normal value will indicate that the patient is experiencing an acid-base imbalance (2004). These six components are pH, PaCO2, PaO2, oxygen saturation, base excess and bicarbonate (HCO3).
The ABGs return for M.M. are as follows: pH 7.55, arterial carbon dioxide pressure (PaCO2) 24 mm Hg, bicarbonate 24 mmol/L, and arterial oxygen pressure (PaO2) 56 mm Hg. Oxygen saturation is 86% on room air.
Question 3: What is your interpretation of the ABGs, and what do you think the physician will order next?
The pH or arterial plasma which measures hydrogen ion concentration in the body fluids (2004) is normally 7.35 to 7.45 in value. PaCO2 which is the arterial and alveolar carbon dioxide tension is normally 35 to 45 mm Hg ( 2000). M.M.’s pH values are above the normal values. Normal values for bicarbonate is 24-28 meq/L or 24-28 mmol/L (2000). Compared to the normal values, the ABG results of M.M. show normal bicarbonate values.
Her PaCO2 is less than the normal values. This is an indication that hyperventilation has occurred (2004). Her PaO2 is 56 mm Hg which is bad since values lesser than 60 mm Hg can lead to anaerobic metabolism, resulting in lactic acid production and metabolic acidosis ( 2004).
The oxygen saturation is 86% on room air. Since M.M.’s arterial PaO2, falls below 60 mm Hg, there is also a large drop in the oxygen saturation (2004). This is reflected also in the pulse oximeter that is why M.M. was started on 3 to 6 L O2/NC. There is no mention of base excess in the laboratory results.
Findings reveal that there is no acid base imbalance in the patient since these values are not manifestations of certain signs and symptoms that are characteristic of any of the acid base imbalances (2004). Yet, deviances from the normal values show that there is indeed something wrong which the ABG analysis alone cannot point out. Therefore there is a need to do more tests.
An electrocardiogram is used to rule out any heart problems which could be possibly given the presence of restlessness and severe pain on the chest of the patient. Since ECG changes are characteristically transient, serial tracings may be helpful in the diagnosis and exclusion of a myocardial infarction (Merck Manual, 2006). The standard 12-lead ECG is very useful in the detection of infarctions of the inferior, anterior, and lateral walls of the left ventricle. 12-lead ECG has been useful in the early detection and rapid reperfusion of patients with acute MI ( 2002). ECG tracings can be used to support and extend impressions gathered from the history, physical signs, blood gases, and x-rays. There is no mention of ECG tracings indicative of a heart failure, therefore that condition is ruled out as what the patient is experiencing. In pulmonary embolism, the electrocardiogram is usually abnormal, but nonspecific ST-segment or T-wave changes are the most common finding (1996), the last one being the case for M.M. prompting tests to identify the presence of pulmonary embolism.
The use of chest x-rays can rule out the presence of infarctions also ( 2006). Chest x-ray findings show a small right infiltrate on M.M. The chest x-ray findings of M.M. indicates some sort of characteristic of infarction, yet the case study did not mention also anything that would indicate an embolism. An infiltrative lesion is usually characteristic of a myocardial infarction (2000).
From the results of all the tests and medical screenings that were done, a pulmonary embolus is suspected. The physician could order a lung scan to further verify that it is indeed a pulmonary embolus. The physician should then order appropriate treatment for the patient.
Question 4: A pulmonary embolus is suspected. What are the most likely sources of the embolus?
This condition is known as pulmonary embolism or otherwise called thromboembolism. It is the lodgment of a blood clot in a pulmonary artery with subsequent obstruction of blood supply to the lung parenchyma. The most common type of pulmonary embolus is a thromboembolus which usually has formed in the deep leg veins or the pelvic veins. Most of the causing serious hemodynamic disturbances form in the ileofemoral veins.
When the emboli or the lodge blood clot block larger branches of the pulmonary artery, they provoke a rise in the pulmonary arterial pressure, which is reflected in the ABG tests, and a rapid, shallow respiration, a medical condition called as tachypnea (2001), which was already observed by the nurse. Tachypnea almost always occur following an embolic episode, therefore there is a need to do tests that will check if what the patient is experiencing is embolism or something else. This tachypnea experienced by M.M. is a reflex response to activation of vagally innervated receptors close to the vessel walls that appear to be activated by serotonin released from platelets at the site of embolization (2000).
The site of thrombus formation is usually clinically inapparent in more than 50% of cases since associated inflammatory changes are insufficient. It can be detected in cases without physical signs only by using angiographic or isotopic diagnostic technics.
The pathophysiologic changes that occur following pulmonary embolism are complex, involving alterations in pulmonary hemodynamics, gas exchange, and mechanics. All the results of the tests show pathophysiologic changes that are characteristic of pulmonary embolism. Cardiopulmonary function is affected in the event of embolism (2000), that is why M.M. is experiencing breathing problems.
Although at first the patient was hypotensive, later on her vital signs taken by the nurse show that her blood pressure increased indicative of hypertension which is a characteristic of pulmonary embolism. Hypertension is the most important physiologic alteration following embolization which results from the increased pulmonary vascular resistance.
Risk factors for pulmonary embolism include immobilization, trauma and surgery, particularly for hip fracture (1996). The last one could be the reason why M.M. developed pulmonary embolism. Surgery further increases the risk of having pulmonary embolism. The frequency of pulmonary embolism in patients after undergoing an operation varies with site of operation. A rate 40 % of pulmonary embolism after operation on back and extremities was reported ( 1995). Major orthopedic surgery such as hip or knee replacement or fractures is related to a higher prevalence of pulmonary embolism (1995), thus could be the major reason of M.M. developing the condition.
Summary, Conclusion and Recommendations
Based on the findings of the medical tests and procedures that were ordered by the physician to be performed on M.M., it was found out that the patient has pulmonary embolism. Her pulmonary embolism probably resulted from the open reduction internal fixation surgery of her left femur.
Yet although she has already been diagnosed as having pulmonary embolism in the case study, certain descriptions merit further investigation on her condition. Some of the symptoms exhibited by M.M., such as infiltrations in the chest x-ray findings, are actually characteristic of a heart failure or myocardial infarction. The presence also of faint crackles in the lungs could be indicative of a myocardial infarction since examination of the lungs in a condition of pulmonary embolism alone is usually normal ( 2006). Pulmonary infarction is defined as one with the presence of an infiltrate (2002).
It should also be taken into consideration that the manifestations of a pulmonary embolus usually develops abruptly over a period of minutes which is not the case for M.M. The manifestations of infarction, on the other hand, develops over a period of hours ( 2006). The physician should order more medical tests and procedures to be done since it is not unlikely that with pulmonary embolism the patient has also developed myocardial infarction which the first set of tests and procedures have not shown.
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