ACNP 1 Case Studies 3 and 4 - Weeblylauralangenhop.weebly.com/uploads/1/3/4/1/13414304/... · Web viewAnother important aspect in this case study is the inadequate ventilator settings

Running head: CASE STUDIES 3 AND 4 1

ACNP 1 Case Studies 3 and 4

Laura Langenhop

Wright State University

CASE STUDIES 3 AND 4 2

ACNP 1 Case Studies 3 and 4

1. What is the differential diagnosis of this patient’s clinical deteriorations and why?

The differential diagnoses of this patient are based upon clinical signs and symptoms.

The differential diagnoses include acute respiratory distress syndrome (ARDS), acute lung injury

(ALI), transfusion related acute lung injury (TRALI), pneumonia, pneumothorax, and pulmonary

embolism (Chesnutt, Prendergast, & Taven, 2014). The most likely diagnosis for this patient is

ARDS. ARDS is defined as acute respiratory failure without the presence of heart failure

(Chesnutt, Prendergast, & Taven, 2014). In a patient with ARDS, there are bilateral pulmonary

opacities on a chest radiograph and the partial pressure of oxygen in the arterial blood (PaO2) to

fractional concentration of oxygen (FIO2) ratio is less than 200 mmHg with a positive end

expiratory pressure (PEEP) of > 5 mmHg (Chesnutt et al., 2014).

Most recently, the Berlin definition of ARDS is recognized as a more specific indicator

of the severity of the patient’s pulmonary disease (American Medical Association [AMA],

2012). There are three distinct classes of ARDS. First, mild ARDS is defined as a PaO2/FiO2

ratio of 200 mmHg to 300 mmHg with a PEEP or CPAP > 5 cmH20 (AMA, 2012). Moderate

ARDS is defined as a PaO2/FiO2 ratio of 100 mmHg to 200 mmHg with a PEEP of > 5 cmH20.

Finally, severe ARDS is defined as a PaO2/FiO2 ratio of <100 mmHg with a PEEP of >5

cmH20 (AMA, 2012).

ARDS occurs within one week of insult to the pulmonary system (Chesnutt, Predergast,

& Tavern, 2014). Specifically, this patient, as a result of a motorcycle accident, acquired a

hemopneumothorax and required a chest tube insertion. The chest radiograph following surgery

revealed a pulmonary contusion to the right lower lobe. The patient also received multiple blood

products, another risk factor for ARDS (Chesnutt, Predergast, & Tavern, 2014). The patient’s


PaO2/FIO2 ratio is 97.5 mmHg where 12 hours prior the PaO2/FIO2 ratio was 147.5 mmHg.

Based on the Berlin definition, the patient has severe ARDS (AMA, 2012).

Acute lung injury (ALI) is another differential diagnosis. ALI is described as a less

severe hypoxemia with a PaO2/FiO2 ratio of < 300 mmHg when compared to ARDS (AMA,

2012). The different stages and designations of oxygenation in patients with ARDS replaced any

ALI terminology in the Berlin definition (AMA, 2012). With this change in definition, ALI

cannot be considered a possible diagnosis. However, the patient received multiple blood products

during resuscitation from his trauma. Transfusion related acute lung injury (TRALI) is the

leading cause of death in patients who have received blood products (Lerner, Rafaai, &

Blumberg, 2010). There are two hypotheses related to TRALI. The first hypothesis is the

antibodies in the blood being transfused attack the neutrophils in the lungs causing damage to the

endothelium (Lerner, Rafaai, & Blumberg, 2010). The end result is vasculature leakage and

consequently, pulmonary edema arises (Lerner, Rafaai, & Blumberg, 2010).

The second hypothesis is neutrophils accumulate in the lungs due to an underlying

inflammatory process. Activation of these neutrophils by mediators causes endothelium damage

and vascular leakage leading to TRALI (Lerner, Rafaai, & Blumberg, 2010). Chest radiographs

of patients with TRALI reveal bilateral diffuse patchy densities without cardiac enlargement

(Lerner, Rafaai, & Blumberg, 2010). Typically, a fever occurs within six hours of administration

of the blood products in patients with TRALI. However, it can be challenging to distinguish

TRALI from ARDS. In the case presented, TRALI may be a cause of the patient’s ARDS

(Lerner, Rafaai, & Blumberg, 2010).

Pneumothorax, or in this patient’s case, a tension pneumothorax is another possible

diagnosis. The patient already had a hemopneumothorax from the accident trauma. The patient


was placed on a ventilator posing a risk for a tension pneumothorax (Light, 2012). In a patient

with a tension pneumothorax there is an inability to ventilate the patient with elevated peak

inspiratory pressures (Light, 2012). On physical examination, the patient will have absent breath

sounds on the affected side, hyperresonance upon percussion, and a mediastinal shift (Light,

2012). Though this patient is experiencing increased airway pressures, the other physical

findings conclude a different acute event. The patient has no mediastinal shift, absent breath

sounds, and the chest radiograph reveals diffuse airspace disease without tracheal deviation and

no evidence of a pneumothorax. The diagnosis of a pneumothorax is an unlikely cause for this

patient’s worsening blood gas and chest radiograph report (Light, 2012).

Pneumonia is another differential diagnosis for this patient. Pneumonia is suspected

when patients experience a fever, dyspnea, cough, sputum production, and when rales or rhonchi

can be heard on auscultation (Smith, 2011). The patient may have acquired pneumonia from

aspiration of gastric secretions upon intubation. Ventilator associated pneumonia is unlikely

since the patient has not been intubated for more than one day. Pneumonia can be suspected

since the first chest radiograph revealed a right lower lobe infiltrate that was thought to be a

contusion sustained from injuries (Smith, 2011). The second chest radiograph reveals diffuse

airway pattern, which is more suspect of ARDS. Pneumonia could be a contributing factor to the

patient’s ARDS, but more information and testing is necessary (Marino, 2014).

The patient is at an increased risk for a pulmonary embolism (PE) due to multiple

fractures. In patients with a PE however, hypoxemia results due to the intrapulmonary right to

left shunting, an increase in alveolar dead space, and a ventilation perfusion mismatch is detected

(Fedullo, 2011). Typically, patients with a PE do not have increase peak inspiratory pressures

and patients with a PE do respond to increase in FIO2 (Fedullo, 2011). Since a PE is not a


ventilation problem, the patient would not have problems being ventilated (Chesnutt et al.,

2014). The chest radiograph also shows little findings suggestive of a PE. Because of lack of

evidence, a PE in this patient is unlikely. ARDS caused by trauma and multiple blood

transfusions is the more logical diagnosis for this patient (Fedullo, 2011).

2. What are the risk factors that put this patient at risk for ARDS? Provide rationale.

Acute respiratory distress syndrome (ARDS) is a result of infectious and non-infectious

disorders (Marino, 2014). This patient’s risk factors for ARDS include multisystem trauma,

possible gastric aspiration secondary to trauma and intubation, multiple blood transfusions, and

insufficient ventilator settings (Marino, 2014).

The patient may have aspirated during the intubation causing an aspiration pneumonia

followed by ARDS pathology. Another important aspect in this case study is the inadequate

ventilator settings (Chesnutt et al., 2014). The patient was placed on assist-control with a tidal

volume (TV) of 90 mL. Unless the patient was 15 kg, which is highly unlikely, the TV setting is

not acceptable. An unacceptable TV and low respiratory rate place the patient at high risk for

atelectasis and ARDS (Marino, 2014).

As a result of the accident, the patient sustained multiple fractures to the lower

extremities and pelvis and blunt trauma to the right lung. Abdominal lavage reveals bloody fluid

suspected to be internal bleeding. Patients with trauma, such as the patient in this case, are at a

severe risk for developing ARDS (Marino, 2014). The patient was most likely supine multiple

hours for stabilization of injuries and during surgery putting the patient at risk for atelectasis and

ARDS (Chesnett, et al. 2014). The blunt trauma to the chest also may have caused and increased

the inflammatory response by increasing neutrophils and inflammatory mediators resulting in a

capillary leak (Lerner et al., 2010).


As previously stated, patients who receive multiple blood products are at increased risk

for ARDS. TRALI, an inflammatory response as a result of receiving blood products, can cause

ARDS (Lerner et al., 2010). In this case scenario, the patient received 21 units of blood placing

him at an increased risk for ARDS. TRALI occurs from neutrophils in the lungs attacking

antibodies received from the blood transfusion (Lerner et al., 2010). The inflammatory response

from neutrophils and other mediators cause pulmonary vascular leakage. TRALI occurs up to

six hours after receiving blood products and can be resolved within 48 to 96 hours in cases where

it is suspected and treated early (Lerner et al., 2010).

3. What are specific considerations for managing an elderly trauma victim? Provide

rationale.

Special considerations should be made regarding elderly trauma patients. In comparison

to younger patients with chest wall injuries, elderly patients with the same injuries have twice the

mortality rate (Mitra & Cameron, 2012). With each rib fracture that an elderly individual

sustains, the mortality rate increases by 19% (Mitra & Cameron, 2012). Elderly patients

admitted for a trauma should be considered a medical patient as well because of other co-

morbidities that this specific population can present (Ma, Edwards, & Meldon, 2011). It is

important to note that many elderly traumas may be caused by patients’ inappropriate self

medicating at home for disease states such as coronary artery disease, heart failure, diabetes, and

atrial fibrillation (Ma, Edwards, & Meldon, 2011).

There is major importance to receiving an adequate medication history. Contact with

family members, nursing facilities, or the pharmacy where the patient fills prescriptions is

important in order to obtain an accurate report of present medications. The elderly population is

typically on medications for heart disease, anticoagulants for irregular heart rhythms,


psychotropic medications, and diuretics for heart failure (Ma, Edwards, & Meldon, 2011).

Anticoagulant therapy increases the risk of bleeding. The importance of recognizing this in

patients taking these medications is they require quick reversal with fresh frozen plasma if

needed and may indicate further testing by the ACNP (Mitra & Cameron, 2012). Many

medications the elderly population consumes may mask physiologic changes in the patient,

affect the patient’s ability to compensate stress, and can complicate the resuscitation of the

patient (Ma, Edwards, & Meldon, 2011). For example, beta-blockers or calcium channel

blockers in elderly patients can falsely skew vital signs while patients with chronic lung disease

may have limited the ability to compensate for pulmonary trauma (Ma, Edwards, & Meldon,

2011).

Vital signs have also been shown to be an inadequate representation of the elderly

patient’s status (Ma, Edwards, & Meldon, 2011). Studies have shown elderly patients with

normal blood pressures and who appear to be hemodynamically stable had cardiac outputs of less

than 3.5 L/min and suboptimal oxygen delivery (Ma, Edwards, & Meldon, 2011). Elderly

trauma patients with blood pressures of 90 mmHg systolic have shown to have mortality rates

between 80 and 100 % (Ma, Edwards, & Meldon, 2011). Insertion of a pulmonary artery

catheter is recommended in elderly trauma patients to monitor fluid status more closely with a

goal to achieve a cardiac index of at least 4 L/min (Victorino, Chong, & Pal, 2003). Trending

lactate levels and arterial blood gases help the ACNP in recognizing and correcting the patient’s

acidemia or decreased perfusion (Victorino, Chong & Pal, 2003). Early invasive monitoring can

increase survival up to 53% (Ma, Edwards, & Meldon, 2011).

The moment the elderly trauma patient is admitted to the emergency room, there must be

a thorough inspection of all wounds. Elderly patients’ thermoregulatory mechanisms decline


with age resulting in an inability to maintain their core body temperatures (Pudelek, 2002).

Hypothermia should be prevented since it can lead to cardiac instability (Pudelek, 2002). With

an elderly patient, it is important to use heated blankets, a heated trauma light if possible, and to

minimize exposure of the patient in order to maintain warmth (Pudelek, 2002).

In an elderly patient needing intubation, close attention should be applied if the patient

wears dentures or has cervical arthritis (Ma, Edwards, & Meldon, 2011). An elderly patient may

also have an inspiratory and expiratory force half of that of a young adult (Ma, Edwards, &

Meldon, 2011). When fluid resuscitating the elderly individual, it is important to note that a

patient can decompensate from over resuscitation just as easily as under resuscitation due to from

decreased cardiac non-compliance (Ma, Edwards, & Meldon, 2011).

The goal in management of the elderly patient with trauma is to return them back to the

functional state they were in prior to the trauma (Ma, Edwards, & Meldon, 2011). With early

detection, adequate fluid resuscitation, and stabilizing the patient hemodynamically, the hope is

the elderly patient’s survival rate will increase.

4. How would you manage this patient’s hypoxemia? Provide rationale.

The first consideration when managing a patient with ARDS is finding and treating the

underlying cause (Chesnutt et al., 2014). The patient is already mechanically ventilated, helping

the acute care nurse practitioner (ACNP) to optimize oxygenation and deliver PEEP (Chesnutt et

al., 2014). The goal in ARDS management is to optimize oxygenation and decrease further lung

and organ damage (Marino, 2014).

In the presence of ARDS, patients are at increase risk for alveolar collapse. Positive end

expiratory pressure (PEEP) is essential in these patients in preventing alveolar collapse and

increasing oxygen delivery (Levy & Choi, 2012). The ultimate management of PEEP is


maintaining the setting at 12 to 15 mmHg to optimize alveolar recruitment (Levy & Choi, 2012).

The use of PEEP helps increase PaO2 and minimize the use of FiO2 (Levy & Choi, 2012). The

goal for this patient is to mechanically ventilate the patient with PEEP and FiO2 to increase the

SaO2 to 55% or greater and achieve a PaO2 of greater than 88% (Chesnutt et al., 2014).

Decreased mortality rates have been associated with decreasing tidal volumes (TV) from

a conventional 12mL/kg to 6mL/kg of the predictive body weight (Levy & Choi, 2012). It is

important for this patient to have an adequate tidal volume of 6mL/kg of predictive body weight

in order to increase survival. Ventilator management is also based upon plateau inspiratory

pressure (Levy & Choi, 2012). The plateau inspiratory pressure is the pressure of the alveoli at

the end of inspiration (Marino, 2014). The goal plateau inspiratory pressure is 30 cm H20 or less

(Marino, 2014). The patient’s ventilator settings can be changed to pressure control ventilation

(PCV) for limitation on maximal peak airway pressures and alveolar pressures (Christie &

Lanken, 2005). In PCV, the sum of the inspiratory pressure and the PEEP is the pressure sign

the patient receives at the end of inspiration (Christie & Lanken, 2005).

Oxygenation can also be increased by an increase in the mean airway pressure through

the technique of inverse ratio ventilation (Levy & Choi, 2012). Inverse ratio ventilation

increases the inspiratory time greater than the expiratory time (Levy & Choi, 2012). Inverse

ratio ventilation creates hyperinflation resulting in increased end expiratory pressure. Inverse

ratio ventilation has shown to decrease peak pressures and reduce FiO2, avoiding oxygen

toxicity (Levy & Choi, 2012).

Another vital aspect in the management of patients with ARDS is the management of

fluids. In a patient with ARDS, there is increased vascular permeability in the lungs. The

increase in permeability leads to edema, specifically in the lungs, leading to an increase in left


atrial filling pressures (Levy & Choi, 2012). Using diuretics and restricting fluids may help to

decrease left atrial filling pressures and decrease pulmonary edema (Levy & Choi, 2012).

Contraindications to using diuretics would be hypotension and inadequate perfusion in a patient

with ARDS (Levy & Choi, 2012).

Pain management after chest wall trauma is important for ventilation and to minimize

splinting (Ma et al., 2011). Pain management also reduces atelectasis and the risk of infection,

further increasing oxygen delivery. Pain control is challenging due to risk for hypoventilation

and hypotension (Ma et al., 2011).

Finally, placing a patient in a prone position has shown to be of benefit to the patient by

increasing oxygenation. Prone positioning of the patient has shown to increase functional

residual capacity (FRC), increase perfusion, increase clearance of secretions, and also helps to

change regional diaphragm motion (Christie & Lanken, 2005). Typically prone positioning is

used as a salvage therapy for patients (Christie & Lanken, 2005). There is evidence that for

every one mmHg the PaCO2 decreases during prone positioning, the mortality rate decreases

around 20% (Christie & Lanken, 2005). Besides placing the patient in prone positioning, the

use of inhaled nitric oxide can be use as a last option for its dilatory effects on the lung fields

(Christie & Lanken, 2005).

5. What are the problems associated with PEEP?

PEEP has proven to be helpful in the treatment of patients with ARDS. However, there

are problems that may arise with the increasing need for PEEP. Problems associated with PEEP

include increased intra-thoracic pressure causing decreased preload reflective of decreased

cardiac output, decreased renal blood flow, and decreased cerebral blood flow (Butterworth,

Mackey, & Wasnick, 2013). Circulatory depression typically occurs when PEEP is greater than


15 cmH20 (Butterworth, Mackey, & Wasnick, 2013). When cardiac output is decreased,

antidiuretic hormone is increased resulting in decreased urinary output and decreased glomerular

filtration (Butterworth, Mackey, & Wasnick, 2013).

PEEP has also been associated with ventilator associated lung injury, barotrauma, and

spontaneous pneumothorax due to increased intra-thoracic pressure and hyperinflation (Levy &

Choi, 2012). It is important in the patient with ARDS to maximize PaO2 and minimize FiO2

while also protecting the patient’s pulmonary vasculature and hemodynamic stability without

causing trauma to the patient (Levy & Choi, 2012).

6. What is the mortality rate associated with ARDS?

The mortality rate of ARDS remains a major problem today. Much research has been

conducted to find ways to battle and prevent this growing dilemma. In the United States, the

incidence of ARDS is 200,000 cases per year (Levy & Choi, 2011). Even with continuing

research and growing knowledge on ARDS, the mortality rate for ARDS is between 26% and

44% (Levy & Choi, 2012). In the presence of sepsis, the mortality rate associated with ARDS

can reach up to 90% (Chesnutt et al., 2014). Patients who have received blood transfusions,

patients who have sepsis, patients with underlying co-morbid conditions, and patients who have

had surgery remain at increased risk for early death (Chesnutt et al., 2014).

Unfortunately, patients with ARDS die primarily due to sepsis or multi-organ system

failure rather than succumb to hypoxia (Kollef & Isakow, 2012). Survivors of ARDS remain

with pulmonary symptoms such as cough, dyspnea, and sputum production (Chesnutt et al.,

2014). It is important to note the need of early detection of ARDS for increased survival. The

American European Consensus Conference on ARDS continues to meet to form diagnostic

criteria and recommendations for treatment in order to increase survival of patients (Kollef &


Isakow, 2012). Though ARDS remains a many facetted problem, early detection of ARDS

continues to be the key in early treatment and recovery.

Case Study 4

A 56 year-old white male patient presents with chest pain in the emergency department.

The pain is constant and worse on inspiration that has lasted for a week. The patient describes

the pain as dull and uncomfortable. The patient has taken Tylenol to alleviate the pain, but says

the pain has not subsided. The patient states he feels short of breath at rest as well as during

exertion. The past medical history includes controlled type 2 diabetes, atrial fibrillation and

hyperlipidemia. On the monitor, the patient is in rate controlled atrial fibrillation at 87 bpm.

Blood pressure (BP) is 127/80, respirations (RR) are 24, SpO2 is 89% on RA and 93% on 4L

nasal cannula. On physical examination, the patient has diminished breath sounds, dullness to

percussion, and egophony over the right lower lobe. The abdomen is soft and non-distended.

The patient’s skin is warm, dry and intact. Peripheral pulses are 2+. There is no JVD noted on

examination. There are no bruits noted on the carotids or abdominal area. A portable chest

radiograph reveals a large fluid filled covering the right lower lobe of the lung without evidence

of cardiomegaly. The patient’s lab work includes the following: WBC 5.2, RBC 5 cells/mcL,

H/H 9.3/27.8, platelets 156 platelets/mcL, Na 134, K 4.0, and BUN/Cr 28/1.56. The patient’s

proBNP is 175, Troponin 1 is 0.02 ng/dL, CKMB 36 mU/mL. The EKG reveals atrial

fibrillation with a heart rate at 88 bpm. No ST-depression or elevation is seen. The patient is a

one pack per day smoker over a 20-year span. The patient states he drinks 5 beers a day. The

patient also thinks that he has lost weight last week due to not feeling well. The patient is sent to

radiology for a left lateral decubitus radiograph and then sent for a CT scan for better imaging.


1.What are the differential diagnoses? Explain.

The differential diagnoses of this patient are pleuritis, myocardial infarction, a pleural

effusion related to heart failure, pneumonia, pulmonary embolism, malignancy, or cirrhosis. The

first differential diagnosis is pleuritis. Pleuritis is suspected when patients complain of sharp

localized pain that is increased by movement, breathing, coughing, or sneezing (Chesnett et al.,

2014). When a pleural effusion is present on a chest radiograph, further diagnostic criteria

should be completed (Chesnutt et al., 2014). The patient experiences pain inflammation of the

pleural cavity. Typically, pleuritis is caused by pneumonia or a bacterial respiratory infection

(Chesnutt et al., 2014). A myocardial infarction is highly unlikely, primarily due to the fact that

the cardiac biomarkers are not elevated and the EKG does not show any ST-elevated depression.

The patient does have a cardiac history, but the shortness of breath appears to be coming from

some other pathology (Kollef & Isakow, 2012).

The most common pleural effusion etiology comes from patients with heart failure.

Pleural effusions from heart failure result in 90% of all transudative pleural effusions (Chesnutt

et al., 2014). In patients with heart failure, there is increased hydrostatic pressure in the lungs

causing pleural effusions. Patients with heart failure typically have bilateral effusions, but the

patient in this case has a unilateral effusion. The chest radiograph reveals that the patient does

not have cardiomegaly, notable in someone with heart failure. The proBNP is mildly elevated,

possibly linking the effusion to heart failure, but other etiology is suspected (Chesnutt et al.,

2014). A transthoracic echocardiogram may be ordered to distinguish the patient’s ejection

fraction and risk for pleural effusions related to heart failure (Chesnett et al., 2014).

Another differential diagnosis is a pulmonary embolus causing the chest discomfort,

shortness of breath, and pleural effusion. In a patient with a pulmonary embolism, the effusion is


typically exudative in nature (Hooper, Lee, & Maskell, 2010). Pleural effusions may be

ipsilateral, contralateral, or bilateral relative to the embolus (Hooper, Lee, & Maskell, 2010).

Though the patient is at risk for a pulmonary embolus due to the atrial fibrillation, the patient’s

electrocardiogram shows no signs of a new right bundle branch. The description of the patient’s

pain, onset of symptoms, and the co-morbidities create the possibility of another diagnosis

(Chesnutt et al., 2014).

Exudative pleural effusions in patients arise from pneumonia or an empyema (Chesnutt et

al., 2014). In this case study, the patient is without fever, cough, or an increased white blood cell

count. Though an exudative effusion can be ruled out using a gram stain and cytology from the

pleural fluid, it is unlikely based on the patient physical’s examination and social history.

In patients with malignant pleural effusions, the pleura have increased permeability

causing impairment of pleural fluid through the lymphatic system. Malignant effusions are

typically large and can be a challenge to eradicate with a thoracentesis alone (Kollef & Isakow,

2012). Common causes for malignant tumors are lung cancer, breast cancer, lymphoma, and

cancer of the gastrointestinal or genitourinary systems (Kollef & Isakow, 2012). The patient is a

smoker and drinks alcohol daily, placing him at increased risk for malignancy. The patient also

states that he has lost weight due to not feeling well. It is possible the patient has a malignant

pleural effusion. Further testing, such as a thoracentesis, is necessary to conclude a malignant

etiology.

Patients who develop cirrhosis have an increased risk for developing pleural effusions. A

patient may present with ascites on examination, often leading the practitioner to suspect a

pleural effusion related to cirrhosis (Chesnutt et al., 2014). However, patients with heart failure

may also present with ascites making the differentiation challenging. In a patient with cirrhosis,


the effusion is seen on the right side and is typically large (Chesnutt et al., 2014). Peritoneal

fluid moves across small openings into the pleural space causing the pleural effusion (Light,

2012). In this case, a hepatic hydrothorax is a possibility due to the patient’s excessive alcohol

intake. The patient does not have ascites on examination, although this does not automatically

rule out cirrhosis being the underlying problem. Further testing such as a thoracentesis can help

diagnose the type of pleural effusion the patient has (Kollef & Isakow, 2012; Chesnutt et al.,

2014).

2. What are the criteria in performing a thoracentesis?

In a patient with a pleural effusion, the decision to perform a thoracentesis is made

through specific symptomology and clinical findings. When a pleural effusion is suspected on

physical examination, a chest radiograph should be obtained. If the suspected area is shifting the

heart to the opposite side, then a pleural effusion is suspected (Parks & Bechara, 2012). If the

heart has not shifted, then atelectasis can be inferred. An imaged lateral decubitus radiograph

should be taken to view the thickness of the fluid (Kollef & Isakow, 2012). The criteria for

performing a thoracentesis include effusions greater than one centimeter on a lateral decubitus

radiograph, increased effusion despite antibiotic therapy, a continued unilateral effusion with

tachycardia or fever, and the presence of a loculated effusion on a computed tomography (CT)

scan of chest radiograph (Parks & Bechara, 2012). Other indications for a thoracentesis include

an air-fluid level in the pleural space, a rapid change in size of the effusion, and concern that an

empyema is developing (Kollef & Isakow, 2012).

There are contraindications to a thoracentesis procedure for a patient (Parks & Bechara,

2012). First, patients may not have a thoracentesis if the platelet count is less than 50,000 mm3

(Parks & Bechara, 2012). Second, patients taking aspirin or anti-platelet therapy such as


Clopidogrel must stop taking medications five days prior to the procedure (Parks & Bechara,

2012). Third, it is a safety measure that a patient’s INR levels should be < 1.5 seconds prior to

the thoracentesis. With patients taking warfarin, if a thoracentesis is warranted, fresh frozen

plasma can be given to counteract warfarin’s effects (Parks & Bechara, 2012). Finally, a patient

who is hemodynamically unstable (i.e. a patient with hypotension and tachycardia) should not be

considered for a thoracentesis until vital signs remain stable and the patient can be positioned for

proper aspiration of the fluid (Parks & Bechara, 2012).

3. Explain Light’s Criteria and other criteria for diagnosing a pleural effusion.

After the pleural fluid is obtained from the thoracentesis or biopsy, the ACNP considers

criteria to differentiate what type of pleural effusion the patient has. Light’s Criteria are used to

differentiate a transudative pleural fluid from an exudative pleural effusion. Light’s Criteria

have a sensitivity of 97.9% (Kollef & Isakow, 2012). Transudative pleural fluid occurs without

disease to the pleura. Effusions due to congestive heart failure, cirrhosis, and myexedema are

examples of transudative effusions (Kollef & Isakow, 2012). Exudative effusions are caused by

the lymphatic system’s inability to clear fluid from the pleural space (Chesnutt et al., 2014).

Examples of exudative effusions are pneumonia, empyema, hemothorax, malignancy, and a PE

(Kollef & Isakow, 2012; Chesnutt et al., 2014).

Richard Light first published the Light Criteria in 1989 after a number of years studying

pleural fluid (Light, 2013). To this day, the criteria are used when differentiating exudative

effusions from transudative effusions. In a patient suspected to have a transudative effusion,

pleural fluid will present a serum protein ratio <0.5, serum lactate dehydrogenase (LDH) ratio

<0.6, and the pleural fluid LDH will be less than two-thirds of the upper limit of the normal

serum LDH (Kollef & Isakow, 2012). The patient must present with all three findings in order to


diagnose a transudative effusion (Kollef & Isakow, 2012). A patient suspected to have an

exudative effusion can present with one of the clinical findings: serum protein ratio > 0.5, a

serum LDH ration >0.6, and a pleural fluid LDH less than two-thirds of the upper limit of the

normal serum LDH (Kollef & Isakow, 2012, p. 356).

Though Light’s Criteria is helpful in the diagnosis of a specific pleural effusion, falsely

classified effusions have been seen in up to 25% of cases (Light, 2013). At times, patients may

meet criteria for exudative effusions by a small margin. In cases where a transudative effusion is

highly suspected as compared to a patient’s testing positive for a exudative effusion, other

laboratory work should be completed in order make an appropriate diagnosis (Light, 2013).

First, if a patient has a protein gradient of greater than 3.1g/dL, the patient most likely has a

transudative effusion (Light, 2013). Second, an albumin gradient may be measured to rule on a

diagnosis of a transudative effusion or a hepatic hydrothorax. An albumin gradient of greater

than 1.2 g/dL is another rule in diagnosis of transudative effusion (Light, 2013). A pro-BNP

level can also be obtained in a situation where the pleural effusion is suspected as a result from

heart failure (Light, 2012).

Light’s Criteria are a great indicator to the type of pleural fluid the ACNP is treating.

Other laboratory work can also be measured in order to obtain a more accurate diagnosis. From

the pleural fluid, the ACNP can measure a white blood cell count, glucose level, pH of the fluid,

and test the fluid on a gram stain (Light, 2012). If neutrophil infiltrates are not present within the

pleural fluid, one can conclude the pleural effusion is due to malignancy, a pulmonary embolism,

or pancreatitis (Suratt, 2003). The presence of mononuclear cells in the pleural fluid reveals

malignancy, pleuritis, tuberculosis, or pulmonary embolism (Suratt, 2003). Greater than 50% of

small lymphocytes present in the pleural fluid is almost always secondary to tuberculosis or


cancer (Suratt, 2003). Fluid eosinophilia of greater than 10% in patients can suggest trauma,

drug induced pleuritis, or asbestos related effusion (Suratt, 2003).

Because of decreased perfusion across the pleural membrane and increased glucose

utilization in the pleural membrane, blood glucose may be decreased in the pleural fluid in

comparison to the patient’s serum blood glucose (Suratt, 2003). Pleural glucose levels of <60

mg/dL are present in malignancy, tuberculosis, pneumonia, empyema, pulmonary embolism, and

hemothorax type effusions (Suratt, 2003). Pleural effusions with glucose levels less than 60

mg/dL are typically present in unfortunate circumstances such as a misplaced central line (Suratt,

2003).

A gram-stain and cytology of the pleural fluid in a patient should also be taken. A

positive gram stain is suggestive of empyema etiology (Suratt, 2003). A gram-stain is helpful in

excluding the presence of a pleural infection in a patient who already has pleural disease (Suratt,

2003). Cytology from the pleural fluid should be sent to rule out malignancy. If lung cancer is

suspected warranting cytology, the diagnosis of a malignancy falls between 40% and 87%

(Suratt, 2003). If malignancy is still suspected in the presence of a negative cytology, a biopsy

or bronchoscopy may be completed for further evaluation (Suratt, 2003).

Finally, the pH of the pleural fluid is a good indicator of the patient’s type of effusion. In

a patient with a pH less than 7.2, one can suspect an exudative etiology (Suratt, 2003). Another

aspect to testing the pH level is it aids in establishing the extent of a pleural malignancy. A

patient with a low pH in the presence of a malignancy shows substantial pleural disease and

indicates a poor chance for survival (Suratt 2003).

4. What therapies can be done for patients with pleural effusions?


Depending on the kind of pleural effusion the patient presents with determines the course

of action the ACNP will take in order to treat the patient. Recognition of the underlying cause is

most important when treating the pleural effusion. Different sources for the effusion call for

different treatment.

In the case of a patient suspected of having a pleural effusion as a result of pulmonary

embolus, a CT scan should be obtained in order to rule in the diagnosis. Once the pulmonary

embolus has been diagnosed, anti-coagulation such as intravenous heparin or subcutaneous low

molecular weight heparin should be initiated in order to treat the pulmonary embolus (Kollef &

Isakow, 2012). By treating the underlying pulmonary embolus, the patient’s pleural effusion

should subside (Chesnutt et al., 2014). In the state of Ohio, an ACNP with a certificate to

prescribe can prescribe heparin (Ohio Board of Nursing, 2014).

In a patient with congestive heart failure, the ACNP may observe the pleural effusion

while administering medications that decrease fluid around the lungs. Medications such as

intravenous diuretics or intravenous vasodilators may help with decreasing hydrostatic pressure

and therefore pull fluid from the pleural space back into the vasculature in order decrease the

effusion (Chesnutt et al., 2014). In a patient with heart failure it is recommended to first observe

the pleural effusion during initial therapy and then address a possible thoracentesis if the pleural

effusion does not decrease with treatment of the underlying cause (Chesnutt et al., 2014; Kollef

& Isakow, 2012). In the state of Ohio, the ACNP with a certificate to prescribe can prescribe

diuretics such furosemide (Ohio Board of Nursing, 2014).

Once the patient meets the criteria for a thoracentesis (i.e. effusion of unknown etiology,

fever with a long-standing effusion, air-fluid level in the pleural space, change in size of the

effusion, or concern of a growing empyema) evaluation of the pleural fluid must be completed in


order to determine the next steps (Kollef & Isakow, 2012, p. 111). If the fluid removed is bloody

or purulent, such as with a hemothorax or empyema respectively, a chest tube insertion on a

patient is recommended (Kollef & Isakow, 2012). An empyema is difficult to treat, as it is

infected fluid in the pleural space (Hyeon, 2011). Placement of a small or large drainage

catheter, often called a pigtail drain, is done and an allowance of up to 1500 mL of drained

pleural fluid is appropriate (Hyeon, 2011). A chest radiograph is then performed in order to view

the decrease in pleural effusion and to rule out a hemothorax from the procedure (Hyeon, 2011).

If the daily volume that is extracted from the chest tube is less than 50 mL or the follow up chest

radiograph shows a re-expanded lung, the ACNP can consider removing the chest tube (Hyeon,

2011).

For a patient with a malignant pleural effusion where palliation is needed, a tunneled

catheter, often times called a pleurx catheter, is placed (Hyeon, 2011). A pleurx catheter remains

placed long term. Once the catheter is in place and sutured to the skin, the catheter is attached to

a suction bottle where up to 1500 mL of pleural fluid may be removed at a time. Patients with

malignant pleural effusions have had up to 91% relief of symptoms with the pleurx catheter

placement (Hyeon, 2011).

Patients with a hepatic hydrothorax are treated with diuretics, fluid restrictions, and

repetitive thoracentesis (Gulati, Mullen, & Magrey, 2010). Hepatic vein pressure gradients are

measured via catheterizations (Gulati, Mullen, & Magrey, 2010). Ultimately, a patient with a

hepatic hydrothorax would need a transplant (Gulati, Mullen, & Magrey, 2010). A transjugular

intrahepatic portosystemic shunt (TIPS) may be inserted in the attempt to remove pleural fluid

and is also available for symptom management. Unfortunately the mortality rate becomes as

high as 68% (Gulati, Mullen, & Magrey, 2010).


A patient with reoccurring exudative pleural effusions thought to be malignant in nature

may need a thoracoscopy (Hooper, Lee, & Maskell, 2010). A thoracoscopy is completed when

pleural fluid is inconclusive from the thoracentesis. A thoracoscopy can offer a better view of

the lung parenchyma and biopsy the area of the lung if needed. The sensitivity of a thoracoscopy

is 92% (Hooper, Lee, & Maskell, 2010). Video-assisted thoracoscopy, betters known as a VAT

procedure, is done under general anesthetic by a thoracic surgeon in order to remove the pleural

effusion caused by malignancy or empyema (Hooper, Lee, & Maskell, 2010). The surgeon may

introduce talc to obliterate the viscera and pleura in order for the effusion to cease accumulating

(Hooper, Lee, & Maskell, 2010). Talc at the end of a VAT procedure results in up a 90%

pleurodesis success rate (Hooper, Lee, & Maskell, 2010). There are many therapies for pleural

effusions. All therapies have a purpose. However, it is always important to note that it is best to

treat the underlying cause first, and then progress to the procedural and surgical aspects (Hooper,

Lee, & Maskell, 2010).


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