1. What is a solitary pulmonary nodule?

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A solitary pulmonary nodule or “coin lesion” is < 3 cm and is discrete on chest radiograph. It is usually surrounded by lung parenchyma.

2. What causes a solitary pulmonary nodule?

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The most common causes of a pulmonary nodule are either neoplastic (carcinoma) or infectious (granuloma). Pulmonary nodules may also represent lung abscess, pulmonary infarction, arteriovenous malformations, resolving pneumonia, pulmonary sequestration, hamartoma, and others. As a general rule of thumb, likelihood of malignancy is proportionate to the patient’s age. Thus, whereas lung cancer is rare (although it does occur) in 30-year-old individuals, in 50-year-old smokers, the chances of malignancy may be as high as 50-60%.

3. How does a solitary pulmonary nodule present?

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Typically, a solitary nodule is picked up incidentally on routine chest radiograph. In several large series, more than 75% of lesions were surprise findings on routine chest radiograph. Fewer than 25% of patients had symptoms referable to the lung. Solitary nodules are now seen on other sensitive imaging tests such as helical computed tomography (CT).

4. How frequently does a solitary pulmonary nodule represent metastatic disease?

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Fewer than 10% of solitary nodules represent metastatic disease. Accordingly, an extensive workup for a primary site of cancer other than the lung is not indicated.

5. Can a tissue sample be obtained by fluoroscopic or CT-guided needle biopsy?

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Yes, but the results do not change the treatment. If the needle biopsy tissue indicates cancer, the nodule must be removed. If the needle biopsy is negative for cancer, the nodule must still be removed. Positron emission tomography (PET) is 90% sensitive in identifying malignant tumors.

6. Are radiographic findings important?

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Only relatively. The resolution of modern CT scanners allows the best identification of characteristics that suggest cancer:

1. Indistinct or irregular spiculated borders of the nodule.
2. The larger the nodule, the more likely it is to be malignant.
3. Calcification in the nodule generally is associated with benign disease (the opposite of breast cancer). Specifically, whereas central, diffuse, or laminated calcifications are typical of a granuloma, calcifications with more dense and irregular “popcorn” patterns are associated with hamartomas. Unfortunately, eccentric foci of calcium or small flecks of calcium may be found in malignant lesions.
4. Nodules can be studied using a CT scanner by measuring their change in relative radiodensity after injection of contrast. This information improves the accuracy of predicting the presence of malignancy.

KEY POINTS: SOLITARY PULMONARY NODULE

1. A solitary pulmonary nodule or “coin lesion” is < 3 cm and is discrete on chest radiograph.
2. The most common causes of a pulmonary nodule are either neoplastic or infectious.
3. If the lesion proves to be cancer, anatomic lobectomy is the procedure of choice.

7. What social or clinical findings suggest that a nodule is malignant rather than benign?

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Unfortunately, none of the findings is sufficiently sensitive or specific to influence the work-up. Both increasing age and a long smoking history predispose patients to lung cancer. Winston Churchill should have had lung cancer, but he did not. Thus, the fact that the patient is the president of the spelunking club (histoplasmosis), has a sister who raises pigeons (cryptococcosis), grew up in the Ohio River Valley (histoplasmosis), works as sexton for a dog cemetery (blastomycosis), or just took a hiking trip through the San Joaquin Valley (coccidioidomycosis) is interesting associated history but does not affect the work-up of a solitary pulmonary nodule.

8. What is the most valuable bit of historic data?

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The most valuable is an old chest radiograph. If the nodule is new, it is more likely to be malignant, whereas if the nodule has not changed in the past 2 years, it is less likely to be malignant. Unfortunately, even this observation is not absolute.

9. If a patient presents with a treated prior malignancy and a new solitary pulmonary nodule, is it safe to assume that the new nodule represents metastatic disease?

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No. Even in patients with known prior malignancies, < 50% of new pulmonary nodules are metastatic. Thus, the work-up should proceed exactly as for any other patient with a new solitary pulmonary nodule.

10. How should a solitary pulmonary nodule be evaluated?

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A complete travel and occupational history is interesting but does not affect the evaluation. Because of the peripheral location of most nodules, bronchoscopy has a diagnostic yield of < 50%. Even in the best hands, sputum cytology has a low yield. CT scanning is recommended because it can identify other potentially metastatic nodules and delineate the status of mediastinal lymph nodes. As indicated previously, percutaneous needle biopsy has a diagnostic yield of approximately 80% but rarely alters the subsequent management. PET scanning may suggest cancer with accuracy.
The mainstay of management in patients who can tolerate surgery is resection of the nodule, usually by lobectomy if cancer is suspected, for diagnosis by either a minimally invasive thoracoscopy approach or a limited thoracotomy.

11. If the lesion proves to be cancer, what is the appropriate surgical therapy?

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Although several series have suggested that wedge excision of the nodule is sufficient, an anatomic lobectomy remains the procedure of choice. This can often be accomplished by a video-assisted approach. A solitary nodule that turns out to be cancer should be early-stage disease and has a 65% 5-year survival rate if there are no notable metastases. Unfortunately, the recurrence rate even for stage I tumors or a small nodule is 30% over 5 years. Recurrences are split between local and distant.

References
WEB SITE
http://www.acssurgery.com
BIBLIOGRAPHY
1. Dewey TM, Mack MJ: Lung cancer: Surgical approaches and incisions. Chest Surg Clin North Am 10:803-820, 2000.
2. Ginsberg RJ, Rubinstein LV: Randomized trial of lobectomy versus limited resection for T1 N0 non-small cell lung cancer. Lung Cancer Study Group. Ann Thorac Surg 60:615-622, 1995. Medline Similar articles Full article
3. Khouri NF, Meziane MA, Zerhouni EA, et al: The solitary pulmonary nodule: Assessment, diagnosis and management. Chest 91:128-133, 1987. Medline Similar articles
4. Miller DL, Rowland CM, Deschamps C, et al: Surgical treatment of non-small cell lung cancer 1 cm or less in diameter. Ann Thorac Surg 73:1541-1545, 2002.
5. Nesbitt J, Putnam JB Jr, Walsh GL, et al: Survival in early stage non-small cell lung cancer. Ann Thorac Surg 60:466-472, 1995. Medline Similar articles Full article
6. Walsh GL, Pisters KM, Stevens C: Treatment of stage I lung cancer. Chest Surg Clin North Am 10:17-38, 2001.

1. What is the prevalence of thyroid nodules and cancer?

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Thyroid nodules increase throughout life. Nodules are four times more common in females than in males, and 50% of 50-year-old women have a palpable nodule. After exposure to radiation, nodules develop at approximately 2% annually, reaching a peak at 25 years. Nodules are 10 times more frequent in glands examined by ultrasound, at surgery, or at autopsy. Fewer than 50% of thyroid nodules that appear solitary on physical examination are truly solitary.
Each year in the United States, there are approximately 15,000 new cases and 1000 deaths due to thyroid cancer. Up to 35% of thyroid glands examined at autopsy contain occult papillary cancer (< 1.0 cm).

2. What is the importance of the distinction between solitary and multiple thyroid nodules?

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Traditionally, multiple thyroid nodules were considered benign and solitary thyroid nodules malignant. However, multiple series suggest that a dominant nodule in a multinodular gland carries the same risk of cancer as a solitary nodule (5%).

3. What is the differential diagnosis of thyroid nodules?

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* Adenoma
o Macrofollicular (colloid)
o Microfollicular
o Embryonal
o Hurthle cell
* Carcinoma
o Papillary
o Follicular
o Medullary
o Anaplastic
o Lymphoma
o Metastatic
* Cyst
* Nodular goiter with a dominant nodule
* Other
o Inflammatory diseases (e.g., Hashimoto’s thyroiditis)
o Developmental abnormalities

4. What features of the history and physical examination indicate a higher risk of cancer?

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Nodules occurring at the extremes of age are more likely to be cancerous, particularly in males. Rapid growth and local invasion raise the possibility of malignancy, but associated symptoms (e.g., hoarseness, dysphagia) are uncommon. A history of radiation exposure increases the frequency of both benign and malignant nodules. A family history of medullary or papillary thyroid cancer or Gardner’s syndrome (i.e., familial polyposis) increases the risk of cancer.
Cancer is more often found in patients with firm, solitary nodules. Fixation to adjacent structures, vocal cord paralysis, and enlarged lymph nodes also are associated with an increased risk of malignancy.

5. What is the proper laboratory evaluation of a patient with a thyroid nodule?

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The only biochemical test that is routinely needed is a serum thyroid-stimulating hormone (TSH) concentration to identify patients with unsuspected hyperthyroidism. In patients with suspected medullary thyroid carcinoma (MTC), serum calcitonin should be measured. In patients with known medullary carcinoma, serum calcium levels and 24-hour urine collection for assessment of catecholamines and their metabolic products should be done to exclude multiple endocrine neoplasia (MEN II) before thyroidectomy. Patients with MTC should have lymphocyte-derived DNA analysis for ret proto-oncogene mutations.

6. Which single test best predicts the need for surgical intervention?

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The single best test to predict the need for surgery is fine-needle aspiration (FNA). If an adequate specimen is obtained, the three possible results are benign (70%), suspicious (15%), and malignant (5%). FNA is most reliable for the diagnosis of papillary carcinoma and in patients with medullary and anaplastic cancer. It is least reliable in distinguishing benign from malignant follicular and Hurthle cell neoplasms. The overall accuracy exceeds 95% in experienced hands. When FNA reveals cancer, it is 97% correct (3% false-positive rate); when it indicates a benign nodule, cancer is present in 4% of cases (4% false-negative rate). When the FNA is suspicious, 30% of nodules are malignant.

7. What other tests may be useful in the evaluation of a thyroid nodule?

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Thyroid radionuclide studies with isotopes of either iodine (most common) or technetium often are performed but cannot reliably differentiate malignant from benign nodules. Scans may be useful in patients with indeterminate FNA results and TSH < 1.5 μIU/mL because hyperfunctioning nodules are almost always benign.
Ultrasound categorizes nodules as cystic, solid, or mixed and is the best measure of the size of a nodule. Ultrasound can be used to determine the presence of other nodules in a patient with a solitary nodule on physical examination. It is particularly useful to follow the size of a nodule. Similar to radionuclide scans, ultrasound cannot distinguish malignant from benign nodules; thus, it is not routinely used in the evaluation of a nodule.

8. Should a solitary thyroid nodule be suppressed with thyroxine for 3-6 months to determine whether it is benign or malignant?

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Most nodules change very little over the short term. In one series, 13% of nodules decreased in size, 22% disappeared, 46% did not change, and 19% enlarged. Studies of thyroxine therapy suggest that drug treatment is not superior to placebo in patients with solitary nodules. Most nodules do not change in size, 30% decrease in size, and a few increase in size. Thus, the response to thyroxine is not a reliable indicator of malignancy.

9. What are the types and distribution of thyroid cancer?

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10. What are the axioms of thyroid surgery?

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* A meticulously dry operative field must be maintained.
* Tissue in the region of the recurrent laryngeal nerve should not be cut or clamped until the nerve is definitively identified.
* Every parathyroid gland should be treated as if it were the last functioning gland.
* If malignancy is suspected, the entire operation should be done as if the lesion were cancer.

KEY POINTS: THYROID NODULES

1. Thyroid nodules are more common in females than in males.
2. The only biochemical test that is routinely needed is a serum thyroid-stimulating hormone concentration to identify patients with unsuspected hyperthyroidism.
3. The single best test to predict the need for surgery is fine-needle aspiration.
4. Thyroid carcinoma should be treated by near-total or total thyroidectomy except in young patients with small, well-differentiated tumors (≤ 1 cm) and no evidence of lymph node or extrathyroidal disease. In such cases lobectomy and isthmusectomy are adequate therapy.

11. What is the minimal extent of thyroidectomy for a solitary thyroid nodule?

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The goal of surgery is to remove all foci of neoplastic tissue and any palpable cervical adenopathy. With the exception of small lesions in the thyroid isthmus, the minimal procedure for suspected malignancy should be lobectomy, including the isthmus (as a diagnostic biopsy). Enucleation is to be avoided. Frozen section is accurate for papillary, medullary, and anaplastic carcinoma. Frozen section is no more accurate than FNA for follicular and Hurthle cell carcinoma. Functioning “toxic” nodules may be resected by a partial lobectomy because they are usually benign. If the lesion is large, a lobectomy is preferred.

12. What is the most common form of thyroiditis in nodules?

Show answer
Hashimoto’s thyroiditis, subacute thyroiditis, and Reidel struma (rare). These conditions usually do not require surgery. Thyroidectomy is indicated for compressive symptoms or when cancer cannot be excluded.

13. What is the surgical therapy for thyroid carcinoma?

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Thyroid carcinoma should be treated by near-total or total thyroidectomy except in young patients with small, well-differentiated tumors (≤ 1 cm) and no evidence of lymph node or extrathyroidal disease. In such cases, lobectomy with resection of the isthmus is adequate therapy. Near-total thyroidectomy eliminates multifocal cancer in the thyroid, allows postoperative radioiodine for the diagnosis and therapy of metastatic disease, decreases the risk of local-regional recurrence, and improves the accuracy of serum thyroglobulin as a marker for persistent or recurrent disease. Enlarged cervical lymph nodes should be removed and examined by frozen section. If metastatic cancer is identified, a neck dissection is performed. “Berry picking” results in an increased rate of regional recurrence and should be avoided in favor of anatomic dissections.
Because medullary thyroid cancer is not responsive to radioiodine or levothyroxine, a total thyroidectomy should be performed. A central neck dissection is mandatory to evaluate metastatic disease. If the central nodes are positive for cancer on frozen section, an ipsilateral modified neck dissection is performed. The contralateral neck may be observed.
Surgery for anaplastic carcinoma is palliative and usually is limited to debulking and tracheostomy for relief of compressive symptoms.

14. Describe the arterial supply and venous drainage of the thyroid.

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The blood supply to the thyroid gland comes from the superior and inferior thyroid arteries. Occasionally, a midline thyroid imma artery arises from the aortic arch. The superior thyroid artery is the first branch of the external carotid artery. The inferior thyroid artery arises from the thyrocervical trunk.
The three major veins are the superior, middle, and inferior thyroid veins. The superior and middle thyroid veins drain into the internal jugular vein, and the inferior vein drains into the innominate vein.

15. Describe the anatomy of the recurrent laryngeal nerves.

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The right recurrent laryngeal nerve (RLN) arises from the vagus and loops around the right subclavian artery. The left vagus nerve gives off the left RLN and loops around the aorta. The RLNs run obliquely through the neck, usually in the tracheoesophageal groove. Low in the neck, the nerves are more lateral and course medially as they ascend. The right nerve runs more obliquely than the left. Occasionally, the RLN may branch before entering the larynx, usually on the left side. The motor fibers are usually in the most medial branch. In 1% of cases, the right RLN is not recurrent and enters the neck from a lateral and superior direction.

16. What defect results from injury to the RLN?

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Injury to a single RLN results in a paralyzed vocal cord, which causes a weak, hoarse voice. Patients also have abnormal swallowing and problems with aspiration. Injury to both nerves causes paralysis of both cords and obstruction of airflow. This situation necessitates a tracheostomy. RLN injury occurs in 1% of thyroidectomies.

17. Describe the anatomy of the superior laryngeal nerve and the defect that occurs with its injury.

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The superior laryngeal nerve gives off the external laryngeal nerve, which runs medial to the superior pole vessels to enter the cricothyroid muscle. This motor nerve (i.e., Amelita Galli-Curci nerve) increases tension of the vocal cords, allowing for high notes. The internal laryngeal nerve provides the sensory innervation to the posterior pharynx. It lies superior to the thyroid cartilage. Injury to the nerve leads to a weak, low voice that lacks resonance. Patients may also have problems with aspiration.

18. What is the other major complication of thyroidectomy?

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Permanent hypoparathyroidism occurs in 1% of patients who have had thyroidectomies.

19. What is the postoperative therapy for well-differentiated thyroid carcinoma?

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Patients with risk factors should be treated with postoperative radioiodine (I-131). Risk factors include older age (> 45 years old), male gender, tumor size, direct local invasion, nodal spread, and distant disease. All patients with well-differentiated thyroid cancer should be treated with levothyroxine (Synthroid) to suppress serum levels of TSH (0.2-0.5 μU/mL). This three-component therapy (i.e., surgery, I-131, levothyroxine) results in the lowest recurrence rate.

20. How should a patient be followed after therapy for well-differentiated thyroid carcinoma?

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In young, low-risk patients, physical examination of the neck is done every 6 months for 2 years and then yearly thereafter. In high-risk patients, close follow-up includes repeat neck examination in addition to assessment of serum thyroglobulin (Tg) levels, diagnostic radioiodine scans, and cervical ultrasound. Assessment of the serum Tg and scanning depends on the state of the serum TSH. In order to fully evaluate for recurrent disease, the patient should be taken off thyroxine or given recombinent TSH (Thyrogen).
Patients with recurrent cervical disease by palpation or ultrasound should have repeat surgery if the procedure can be performed with low morbidity. After removal of gross disease, patients should be treated with radioiodine. Distant disease should be treated with radioiodine if the metastases take up iodine.

References
WEB SITE
http://www.acssurgery.com
BIBLIOGRAPHY
1. Cady B: Presidential address: Beyond risk groups-a new look at differentiated thyroid cancer. Surgery 124:947-957, 1998. Medline Similar articles
2. Duren M, Siperstein AE, Shen W, et al: Value of stimulated serum thyroglobulin levels for detecting persistent or recurrent differentiated thyroid cancer in high- and low-risk patients. Surgery 126:13-19, 1999. Medline Similar articles Full article
3. Frilling A, Tecklenborg K, Gorges R, et al: Preoperative diagnostic value of [(18)F] fluorodeoxyglucose positron emission tomography in patients with radioiodine-negative recurrent well-differentiated thyroid carcinoma. Ann Surg 234:804-811, 2001. Medline Similar articles Full article
4. Haugen BR, Ridgway EC, McLaughlin BA, McDermott MT: Clinical comparison of whole-body radioiodine scan and serum thyroglobulin after stimulation with recombinant human thyrotropin. Thyroid 12:37-43, 2002.
5. Hay ID, Grant CS, Bergstralh EJ, et al: Unilateral total lobectomy: is it sufficient surgical treatment for patients with AMES low-risk papillary thyroid carcinoma? Surgery 124:958-964, 1998. Full article
6. Moley JF, DeBenedetti MK: Patterns of nodal metastases in palpable medullary thyroid carcinoma: Recommendations for extent of node dissection. Ann Surg 229:880-887, 1999. Medline
7. Rodriguez GJ, Balsalobre MD, Pomares F, et al: Prophylactic thyroidectomy in MEN 2A syndrome: Experience in a single center. J Am Coll Surg 195:159-166, 2002.
8. Singer PA, Cooper DS, Daniels GH, et al: Treatment guidelines for patients with thyroid nodules and well-differentiated thyroid cancer. American Thyroid Association. Arch Intern Med 156:2165-2172, 1996. Medline Similar articles Full article
9. Sivanandan R, Soo KC: Pattern of cervical lymph node metastases from papillary carcinoma of the thyroid. Br J Surg 88:1241-1244, 2001. Medline
10. Stojadinovic A, Hoos A, Ghossein RA, et al: Hurthle cell carcinoma: A 60-year experience. Ann Surg Oncol 9:197-203, 2002. Full article
11. Stojadinovic A, Shaha AR, Orlikoff RF, et al: Prospective functional voice assessment in patients undergoing thyroid surgery. Ann Surg 236:823-832, 2002. Medline Similar articles Full article
12. Udelsman R, Westra WH, Donovan PI, et al: Randomized prospective evaluation of frozen-section analysis for follicular neoplasms of the thyroid. Ann Surg 233:716-722, 2001.

1. What is pulmonary insufficiency?

how answer
The alveolar-capillary surface of the lung is the size of a singles tennis court. The purpose of the lung is to match alveolar ventilation (Va) to blood flow (Q). Mismatching leads to pulmonary insufficiency.

2. How is Va/Q mismatching characterized?

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Shunt: decreased ventilation relative to regional blood flow; pulmonary arterial (unoxygenated) blood “shunts” by hypoventilated alveoli
Dead space: decreased pulmonary regional blood flow relative to ventilation

3. How much energy is expended in the work of breathing?

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A healthy medical student expends about 3% of total oxygen consumption (energy use) on work of breathing. After injury, particularly a big burn, patients may increase fractional energy expenditure of breathing to 20% of their total energy use.

4. Which surgical incisions most significantly compromise a patient’s vital capacity?

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Intuitively an extremity incision or injury influences vital capacity least, followed sequentially by a lower abdominal incision, median sternotomy, thoracotomy, and upper abdominal incision. An upper abdominal incision is worse than a thoracotomy!

5. Is a chest radiograph helpful in assessing respiratory failure?

Show answer
Yes but the radiograph must be interpreted carefully. It can be difficult to standardize x-ray technique, especially in an intensive care unit.

6. What should you look for on the chest radiograph of a patient with impending respiratory failure?

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1. Are both lungs fully expanded?
2. Are there localized areas of infiltrate, atelectasis, or consolidation?
3. Are there generalized areas of infiltrate, atelectasis, or consolidation?
4. Are the endotracheal and other tubes in proper position?

7. Why is the local versus generalized distinction important in assessing respiratory failure?

Show answer
A local process may be produced by tumor or aspiration, and both are diagnosed and treated by bronchoscopy. Generalized multilobar infiltrates are more likely to represent a diffuse alveolar-capillary leak syndrome, such as adult respiratory distress syndrome (ARDS).

8. What is ARDS?

Show answer
A diffuse, multilobar capillary transudation of fluid into the pulmonary interstitium that dissociates the normal concordance of ventilation (Va) with lung perfusion (Q).

9. What governs fluid flux across pulmonary capillaries into the interstitium of the lung?

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Starling initially described the balance between intravascular hydrostatic pressure (Pc), which tends to push fluid out of the capillaries, and colloid oncotic pressure (COP), which sucks fluid back in across the capillary endothelial barrier (K):

Fluid flux = 5 K(Pc – COP)

10. What causes ARDS?

Show answer
Anything that increases lung dysfunction by promoting wet lung:

1. Heart failure backs up pulmonary intravascular Pc, forcing fluid into the pulmonary interstitium.
2. Malnutrition and liver failure decrease plasma protein and COP. Fluid is not sucked back out of the lung (if the total protein and albumin are low).
3. Sepsis may break down the capillary endothelial barrier (K), permitting water and protein to leak into the lung.

KEY POINTS: CLINICAL FEATURES OF ARDS

1. Severe hypoxemia refractory to increased inspired oxygen concentration
2. Diffuse pulmonary infiltrates
3. Low lung compliance
4. Large V/Q mismatch

11. Explain high-pressure versus low-pressure ARDS.

Show answer
Purists appropriately note that lung congestion resulting from high intravascular hydrostatic pressure secondary to heart failure is really not primary respiratory distress syndrome. If the pulmonary capillary wedge pressure (PCWP) is > 18 mmHg, the diagnosis is high-pressure pulmonary edema (not ARDS). A patient with pure mitral stenosis may have (high-pressure) lung congestion, whereas a malnourished patient may develop (low-pressure) lung congestion; neither of these is, strictly speaking, ARDS, although patients with ARDS frequently have components of both.

12. What is a normal COP?

Show answer
22 mmHg.

13. How is COP calculated?

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Of COP, 75% normally is created by serum albumin along with globulins and fibrinogen:

COP = 2.1 (total protein)

If an osmotically active molecule such as hetastarch is infused, this calculation is fouled up.

14. Define low-pressure ARDS.

Show answer
Low-pressure ARDS is a redundant term. To make the diagnosis of ARDS, the PCWP must be <18 mmHg. Pure ARDS exists only if the PCWP is > 4 mmHg less than the COP.

15. How can the pulmonary capillaries leak if the COP exceeds the PCWP?

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The current concept involves a septic expression of neutrophil CD11 and CD18 adhesion receptors, which stick to pulmonary vascular endothelial intercellular adhesion molecules. Septic stimuli provoke the adherent neutrophils to release intravascular proteases and oxygen radicals. Resultant endovascular damage breaks down the capillary endothelial barrier, permitting the lung leak-even at low hydrostatic pressure.

16. What is a Lasix sandwich?

Show answer
Many surgeons, when their backs are against the wall, give 25 g of albumin followed in 20 minutes by 20 mg of furosemide (Lasix) IV. They reason that the albumin pulls fluid out of the water-logged lung and the Lasix promotes diuresis to rid the patient of extra water. This therapeutic concept probably works only in patients who are not very sick. The sicker the patient, the faster the infused albumin leaks and equilibrates across the damaged endovascular endothelial barrier. Little water is sucked out of the sick lung in preparation for diuresis.

17. List the goals of therapy for ARDS.

Show answer

1. Reduce lung edema (typically with a diuretic).
2. Reduce oxygen toxicity (inspired oxygen concentration < 60% is safe).
3. Limit lung barotrauma (avoid peak inspiratory pressure in > 40 cm H2O).
4. Promote matching of Va and Q; frequently positive end-expiratory pressure (PEEP) is useful.
5. Maintain systemic oxygen delivery (arterial oxygen content x cardiac output).

18. What governs the distribution of lung perfusion (Q)?

Show answer
Mostly gravity. The dependent portions of the lung always are better perfused.

19. Discuss hypoxic pulmonary vasoconstriction (HPV).

Show answer
Most students believe that after dedicating the entire second year of medical school to pheochromocytoma and HPV, both entities may be safely forgotten. At least in the case of HPV, this is not true. A patient who has just undergone carotid endarterectomy illustrates the relevance of HPV. As the patient awakens from anesthesia, the blood pressure is 220/120 mmHg and arterial PO2 with 100% oxygen is 500 mmHg. So that the patient will not blow the carotid anastomosis, the surgeon urgently infuses nitroprusside. In 20 minutes, the blood pressure is 120/80 mmHg, but PO2 (still with 100% oxygen) has dropped to 125 mmHg!
Did the lab technician screw up the blood gas analysis? No-this is an example of the clinical significance of HPV, which directs pulmonary arteriolar delivery of deoxygenated blood toward ventilated alveoli and away from poorly ventilated lung regions. The patient was using HPV to attain a PO2 of 500 mmHg. All antihypertensive agents (e.g., nitroprusside) and most general anesthetics block HPV. The PO2 increment from 125 to 500 mmHg is due to HPV. HPV steered perfusion toward ventilated areas of the lung.
20. What governs the distribution of ventilation in lung? Show answer
KEY POINTS: THERAPEUTIC GOALS IN ARDS

1. Reduce lung edema
2. Reduce oxygen toxicity (FiO2 < 60%)
3. Minimize barotraumas (keep peak inspiratory pressure < 40 cm H2O)
4. PEEP to promote V/Q matching
5. Maintain systemic oxygen delivery (arterial oxygen content x cardiac output)

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A large pleural pressure gradient (more negative at the top of the lung by 20 cm H2O) squeezes gas primarily out of the dependent lung during each exhaled breath. The regional compliance of dependent lung is much better than that of lung apex, which still is distended with gas at the end of exhalation. The usual approach is to perfuse and ventilate dependent lung preferentially.

21. How does ARDS compromise lung function?

Show answer
The trachea is held open with cartilaginous rings, but terminal bronchioles are not. Wet lung collapses the terminal bronchioles, trapping distal alveolar gas. Persistent perfusion of these poorly ventilated regions is a shunt that results in hypoxia.

22. How long does it take for pulmonary arterial (deoxygenated) blood to equilibrate completely with trapped (poorly oxygenated) alveolar gas?

Show answer
About three fourths of a second. After that, no more oxygen is added, and no more CO2 is eliminated from the perfusing blood. Terminal bronchiolar closure producing trapped alveolar gas is bad.

23. What is the therapy for terminal airways closure and resultant shunt secondary to the wet lung of ARDS?

Show answer
PEEP should hold open terminal bronchioles, promoting ventilation of previously trapped alveoli and minimizing the shunt.

24. When may the patient come off mechanical ventilation and be extubated safely?

Show answer
The patient should be sufficiently alert to protect his or her airway, require an inspired oxygen concentration no greater than FiO2 = 0.4, and be comfortable breathing on a T-piece (without mechanical ventilation) for 60 minutes at a respiratory rate < 20 and a minute ventilation < 10 L/min. The patient should be able to generate a negative inspiratory force > -20 cm H2O. Finally, after 1 hour on the T-piece, oxygenation should provide a hemoglobin saturation > 85% without respiratory acidosis (see Chapter 6).

25. What is nitric oxide (NO)?

Show answer
NO is synthesized in vascular endothelial cells by constitutive nitric oxide synthase (cNOS) and inducible NOS (iNOS). Intuitively, inhaled NO should diffuse across ventilated alveoli to increase regional perfusion and improve matching of Va/Q.

26. Does inhaled NO work in ARDS?

Show answer
Almost 24 randomized controlled clinical trials have assessed the therapeutic efficacy of inhaled NO. Although systemic oxygenation and pulmonary hypertension improve transiently, ventilator time and ultimate survival are not influenced. Just say NO.

References
WEB SITES

1. http://www.ardsnet.org
2. http://www.nlm.nih.gov/medlineplus/ency/article/000103.htm

BIBLIOGRAPHY
1. Bartlett R: Pulmonary Insufficiency. New York, American College of Surgeons, Surgery WebMd Corporation, 2002.
2. Davidson TA, Caldwell ES, Curtis JR, et al: Reduced quality of life in survivors of acute respiratory distress syndrome compared with critically ill control patients. JAMA 281:354-360, 1999.
3. Gust R, McCarthy TJ, Kozlowski J, et al: Response to inhaled nitric oxide in acute lung injury depends on distribution of pulmonary blood flow prior to its administration. Am J Respir Crit Care Med 159:563-570, 1999.
4. Pesenti A, Fumagalli R: PEEP: Blood gas cosmetics or a therapy for ARDS? Crit Care Med 27:253-254, 1999.

1. What does a catheter in the central venous circulation measure?

Show answer
All intrathoracic veins have nearly the same pressure. A catheter in the central venous circulation (anywhere) measures this central venous pressure (CVP) (or right atrial pressure). CVP, plus a little right atrial “kick,” pushes blood into the right ventricle. This right ventricular “filling pressure” is also termed preload.

2. What does a pulmonary artery (PA) catheter measure?

Show answer
A PA catheter (Swan-Ganz catheter) is threaded through the central venous circulation out into the PA. The catheter has three ports-one at the tip and side ports at 4 cm from the tip (the “VIP port”) and 29 cm from the tip (the “CVP port”). With inflation of the balloon at the distal catheter tip and subsequent occlusion of a pulmonary capillary vessel, the transducer at the tip of the catheter “sees” only a static column of blood between it and the left atrium. This pulmonary capillary wedge pressure approximates left atrial pressure or left ventricular filling pressure or LV preload.
When pulmonary vascular resistance is normal, PA diastolic pressure can be used as a substitute for wedge or left atrial pressure. It is not necessary in this circumstance to inflate the balloon to estimate the wedge pressure. This spares the patient the risk of PA rupture from balloon inflation (another advantage is that you do not need to get up to replace the Swan-Ganz catheter when the balloon breaks-usually at 2 a.m.).
A PA catheter can measure blood pressure at three points:

1. The level of the superior vena cava (CVP)
2. The PA (with the balloon deflated)
3. The pulmonary venous pressure/left atrial pressure (with the balloon inflated)

Other important parameters, most importantly cardiac output and mixed venous oxygen saturation, can be measured or calculated based on numbers derived from the PA catheter (see questions 9 and 10).

3. Discuss the complications of central venous catheters and PA catheters.

Show answer
Immediate complications are pneumothorax (2%); inadvertent arterial cannulation (2%); catheter malposition (7%); and, more rarely, air embolism, hemothorax, chylothorax, arrhythmia, brachial plexus injury, vocal cord paralysis, and death (each substantially less frequent than 1%).4 Additionally, “floating” a hard PA catheter across the tricuspid valve and through the right ventricular outflow tract holds the potential for ventricular tachycardia (and if you “nudge” the atrioventricular node, you can provoke complete heart block).
Delayed complications are thrombosis (33% by radiographic studies) and less commonly bacteremia, endocarditis, or clavicular osteomyelitis. Fibrin forms on the catheter within hours of insertion, and the incidence of vessel thrombosis increases with time. PA-related bloodstream infections occur in 4.8 cases per 1000 catheter-days.2 This is roughly equivalent to one bloodstream infection among 100 patients with a catheter in place for 2 days. In autopsy series (clearly not healthy patients), the incidence of infective endocarditis is usually < 2% but increases dramatically with increasing insertion duration.2

4. What are the relative contraindications to percutaneous subclavian or internal jugular venous catheterization?

Show answer
In a patient who is anticoagulated or who has a platelet count < 50,000, it is typically safer to place a central venous line by peripheral cutdown. Inadvertent arterial puncture is tolerated fairly well unless the patient is coagulopathic. A patient with hyperinflated lungs (chronic obstructive pulmonary disease) is more likely to have a pneumothorax during catheter placement.

5. How do you percutaneously place a sheath for PA catheter placement?

Show answer

1. Place the patient in mild head-down (Trendelenburg) position and turn the head toward the contralateral side.
2. Using sterile technique and after administering local anesthesia, insert an 18-G needle on a 10-mL syringe at the point where the deltopectoral groove abuts the clavicle and pointing just north of the suprasternal notch. Hugging the undersurface of the clavicle, apply gentle suction with the syringe. When you hit the vein, dark (nonpulsatile) blood easily flows back into the syringe.
3. Remove the syringe, and insert a soft, flexible wire through the 18-G needle.
4. Remove the needle, leaving the flexible wire in place.
5. Slide a plastic sheath (with the dilator inside) over the guidewire. Remove the wire and the dilator, leaving the sheath in place (if the sheath bleeds profusely, you are in the right place). Aspirate the catheter fully to evacuate all air and flush with saline (Figure 12-1).
6. A chest x-ray must be obtained to confirm proper position and exclude pneumothorax and hemothorax.

Figure 12-1 Catheter placement by percutaneous subclavian vein puncture.

6. As a PA catheter passes through the central venous circulation, what do the pressure waveforms look like?

Show answer
See Figure 12-2.

Figure 12-2 Pressure waveforms after insertion of a Swan-Ganz catheter.

7. What is the value of the CVP and PA pressure?

Show answer
Starling’s law states that (up to a point) increasing end-diastolic volume (preload) increases stroke volume (volume of blood ejected during systole, which is multiplied by heart rate to yield cardiac output). Clinically, we cannot measure end-diastolic volume, so filling pressures are used as a surrogate.
CVP is an estimate of the pressure with which blood flows into the right side of the heart. This number does not reflect left-sided filling pressures. As stated earlier, PA diastolic or wedge pressures allow a better estimate of left-sided filling pressure.

8. Name other parameters that can be measured or calculated with use of a PA catheter.

Show answer
Cardiac output, venous oxygen saturation, pulmonary and systemic vascular resistance.

9. How is cardiac output measured?

There are two ways to use a PA catheter to calculate cardiac output:

1. The technique of thermodilution, in which a volume (10 mL) of saline with known temperature (108°C) is injected into the proximal port of a PA catheter. A temperature probe at the distal catheter tip measures the change in temperature of blood from the time when the cold saline was injected and the time that it passes by the probe. The precise volume and temperature of the injectate allow calculation of the amount of blood passing by the probe, which is a measure of cardiac output. Because cardiac output changes by 15% during the respiratory cycle, injection should be synchronized with end-expiration. A left-to-right intracardiac shunt adds warm blood to the cold saline bolus, giving a falsely elevated measurement of cardiac output.
2. The Fick principle, which relates cardiac output to venous oxygen saturation (see question 11).

10. How is the oxygen content of blood calculated?

Show answer
An oximetric PA catheter has a fiberoptic monitor at its distal tip that continuously measures hemoglobin saturation [So2 (%)]. The catheter tip in the PA measures mixed venous blood (Svo2) oxygenation. After 24 hours of placement, the catheter becomes covered with fibrin, and measurements become less reliable.
The amount of oxygen in blood (Cao2) comprises that portion dissolved in blood (almost nothing) and that portion attached to hemoglobin (lots).
The amount dissolved is calculated by:

O2 dissolved = 0.003 x PaO2

The amount attached to hemoglobin is calculated by:

O2 attached = 1.38 x [Hb] x SaO2

For example, if hemoglobin = 12 g/dL, Pao2 = 60 mmHg, and Sao2 = 90%, then Cao2 = (0.003 × 60) + (1.38 × 12 × 0.90) = 15.08 mL oxygen/100 mL blood. Dissolved oxygen usually comprises only a small percentage of Cao2 (< 1% in this example). Clinically, it is excluded from calculations (see Chapter 6).

11. How is the oxygen content of the blood used?

Show answer
Assuming normal parameters of hemoglobin = 15 g/dL, Sao2 = 96%, and Svo2 = 75%, the difference in oxygen content between the arterial circulation and the venous circulation (A-Vo2) is 4.35 vol%. For every 100 mL of blood that travels around the body, the tissues extract 4.35 mL of oxygen. The normal range for the A-Vo2 is 3-5 vol%.
The Fick principle uses this A-Vo2 to determine cardiac output. Nonstressed patients typically consume oxygen at the rate of 125 mL/min/m2. This is really a “wild guess” because we do not usually determine A-VO2 unless a patient is stressed. By measuring the A-Vo2, we can determine the oxygen contribution for each 100 mL of blood that travels around the body. If the measured A-Vo2 difference = 4.35 mL of oxygen, every 100 mL of cardiac output contributes 4.35 mL to the Vo2 of 250 mL (for a person who is 2 m2, or 2 × 125 mL/min/m2). A total of 5.75 L of blood must travel around the patient’s body each minute to meet the oxygen requirement. By “assuming” Vo2 (typically a big assumption) and by calculating the A-VO2, one can approximate cardiac output.

12. Explain the significance of the Svo2.

Show answer
This is a “poor man’s” cardiac output measure. In a patient with a fixed metabolic rate (or stable oxygen consumption), as cardiac output increases (delivering more blood/min and more oxygen/min), the patient extracts less oxygen per 100 mL of blood peripherally, and more oxygen per 100 mL returns to the right side of the heart (as your patient gets healthier, Svo2 rises). Conversely, as cardiac output decreases (delivering less oxygen/min peripherally to meet fixed demand), the patient extracts more oxygen per 100 mL of blood. Returning venous blood contains less oxygen, and Svo2 decreases. Knowing the the differential diagnosis of a falling Svo2 is important: (1) progressive anemia, (2) cardiac failure, (3) decreasing arterial saturation, and (4) increased basal metabolic rate. The differential diagnosis of a rising Svo2 is (1) sepsis, (2) left-to-right intracardiac shunt, (3) left-to-right peripheral shunt (dialysis access), and (4) inadvertent wedging of the pulmonary artery catheter. The other more gratifying possibility is that your patient is improving in response to your therapy!

KEY POINTS: Svo2 TRENDS

1. “Poor man’s” estimation of cardic output
2. Decreased Svo2: progressive anemia, cardiac failure, decreasing arterial saturation, increased basal metabolic rate
3. Increased Svo2: sepsis, cyanide toxicity, left-to-right intracardiac shunt, left-to-right peripheral shunt, inadvertent wedging of PA catheter

13. How do you determine the systemic (peripheral) vascular resistance (SVR)?

Show answer

SVR = [(MAP - CVP)/CO] x 80
where SVR = systemic vascular resistance (dyne • sec/cm-5), MAP = mean arterial blood pressure (mmHg), CVP = central venous pressure (mmHg), and CO = cardiac output (L/min).
Normal SVR is 800-1200 dyne • sec/cm-5. Multiplying by 80 corrects SVR values from Wood units (mmHg/L/min) to standard metric units (dyne • sec/cm-5).

14. How is a PA catheter used to evaluate shock?

Show answer
Management of the patient in shock requires knowledge of intracardiac “filling” pressures (CVP, PA pressure), cardiac ouput, SVR, and Svo2. Prompt PA catheter placement guides therapy (see Chapter 4 and Table 12-1).
Hypovolemic shock. Right and left filling pressures (CVP and wedge/PA pressures) are low, as are cardiac output and Svo2. SVR is high. The diagnosis is confirmed when volume repletion with rising filling pressure is associated with increased cardiac output, normalization of system pressure, and decreased SVR.
Table 12-1. PA CATHETER EVALUATION OF SHOCK

Cardiogenic shock. Shock despite adequate filling pressures means that the pump is failing. Cardiac output and SvO2 are low. If SVR is high, infuse dobutamine, 5 μg/kg/min, to stimulate the heart and reduce SVR. If SVR is low, infuse epinephrine, 0.05 μg/kg/min, to stimulate the heart and increase SVR.
Septic shock. The hallmarks of septic shock are normal or low-normal filling pressure, supranormal cardiac output, high Svo2, and low SVR (< 600 dyne • sec/cm-5). Treatment requires fluid resuscitation and systemic vasoconstriction while the underlying cause (e.g., abdominal abscess) is treated.

15. What is the evidence supporting the use of a PA catheter?

Show answer
There is no definitive evidence in support of PA catheterization. A prospective trial of > 5700 patients with various disease processes (mostly medical patients) revealed that patients who underwent PA catheterization had higher 30-day mortality, higher hospital costs, and longer intensive care unit length of stay.1
Regardless, we recommend PA catheterization3 for patients with cardiogenic shock, unexplained shock, or unexplained acidosis; all patients undergoing peripheral vascular surgery; and high-risk patients undergoing aortic surgery. Traumatically injured patients, patients with respiratory failure, and critically ill pediatric patients may benefit as well. If you cannot determine what the patient’s volume status is, insert a PA catheter.

16. Do central venous catheters or PA catheters need to be changed on a regular basis?

Show answer
In accordance with Centers for Disease Control guidelines, central venous catheters do not need to be replaced routinely if the exit wounds are dressed properly and sterilized routinely. PA catheters should be changed every 5 days to minimize risks of thrombus and infection.
When catheter-related infection is documented, a new catheter must be placed at a different location. Removed catheters in the setting of bacteremia are always sent for culture.

References
WEB SITES

1. http://www.acssurgery.com/abstracts/acs/acs0606.htm
2. http://www.acpmedicine.com/abstracts/sam/med1401.htm

BIBLIOGRAPHY
1. Connors AF, Speroff T, Dawson NV, et al: The effectiveness of right heart catheterization in the initial care of critically ill patients. JAMA 276:889-897, 1996. Medline Similar articles Full article
2. Mermel LA, Maki DG: Infectious complications of Swan-Ganz pulmonary artery catheters. Am J Respir Crit Care Med 149:1020-1036, 1994. Medline Similar articles
3. Pulmonary Artery Consensus Conference Participants: Pulmonary artery consensus conference: Consensus statement. Crit Care Med 25:910-925, 1997.
4. Ruesch S, Walder B, Tramer MR: Complications of central venous catheters: Internal jugular versus subclavian access: A systematic review. Crit Care Med 30:454-460, 2002. Medline Similar articles Full article

1. Define sudden cardiac death.

Sudden ventricular fibrillation (VF) or pulseless electrical activity (PEA). Acute coronary ischemia and preexisting cardiac disease are the most common causes. VF is becoming less common.

2. What is the predominant determinant of successful cardiopulmonary resuscitation (CPR)?

Show answer
Time to restoration of spontaneous circulation, which itself is a function of the time to effective chest compression and time to defibrillation of VF. The chance of a good outcome decreases by 10% per minute. Successful outcomes are more likely if CPR is initiated promptly and if preexisting hypothermia is present.

3. What are the ABCs?

Show answer
Airway, breathing, and circulation. But things have changed. There are now three recognized phases of CPR: electrical, mechanical, and metabolic.

1. The electrical phase lasts about 5 minutes-during that phase, only immediate electrical cardioversion may be required.
2. The mechanical phase lasts 5 to 10 minutes after onset of arrest-during this phase, a few minutes of chest compression are required before cardioversion.
3. The metabolic phase begins at 10 minutes postarrest. During this phase, pressor and antiarrhythmic drugs are required.

4. How do you electrically cardiovert (shock) a patient?

Show answer
Gel pads now are more common than hand-held paddles. If you are using paddles, place electrolyte (conductive) gel on them. Place one pad or paddle in the right subclavicular area and the other in the midaxillary line at the level of the eighth intercostal space (over the apex of the heart). If you are using a biphasic defibrillator, the fist shock should be only 100 J. With monophasic defibrillators, start at 200 J. If the patient remains in VF, rapidly increase the output to the maximum the machine allows. Take care to confirm that everyone (including you) is clear before delivering a shock.
5. Is there an immediate need for an airway? Show answer
No. Defibrillation and chest compression should be initiated first. Waiting for intubation to be completed before initiation of these interventions is one of the most common mistakes in advanced life support. Children, in whom primary respiratory arrest is more common, are an exception. Restoration of ventilation in children often reveals that pulselessness was severe shock, not cardiac arrest.

6. How do you establish an airway-even in a patient with suspected neck injury?

Show answer
The three basic maneuvers are head tilt, chin tilt, and jaw thrust. In an unconscious patient, the jaw muscles relax. The jaw thrust subluxes the mandible, pulling the tongue and epiglottis anteriorly off the upper airway (with minimal cervical hyperextension).
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7. Is endotracheal intubation mandatory?

Show answer
No.

* Mouth-to-mouth ventilation delivers 16% inspired oxygen.
* Bag-mask ventilation delivers 21% oxygen.
* Bag-mask ventilation with an oxygen supply can deliver close to 100% oxygen.

8. Name the advantages of endotracheal intubation. Show answer
A relatively secure airway. Mouth-to-mouth or bag-mask can deliver significant amounts of air to the stomach. Gastric distention impairs diaphragmatic movement and may predispose to aspiration.

9. Does an endotracheal tube (even with the cuff up) prevent aspiration?

Show answer
No. If you place a couple of drops of methylene blue on the tongue of an intubated patient, you can suction “blue” from the other end of the tube (beyond the cuff) within 90 seconds.

10. Which size endotracheal tube should you use?

Show answer
Select a tube with an internal diameter equal to the width of the patient’s little finger. For a 70-kg adult, a 7.5-mm tube is fine. Do not delay ventilation trying to place a large endotracheal tube. Adequate ventilation can be achieved through smaller tubes.

11. How do you know if the endotracheal tube is in the proper position?

Show answer

1. Listen to both lung fields.
2. Observe symmetric chest excursion with each tidal breath.
3. Listen over the epigastrium (you don’t want to hear gurgles from the stomach).

These physical findings are not fully reliable, however. In patients with spontaneous circulation, it is now standard to confirm tube placement with end-tidal CO2 (ET-CO2) measurement. In cardiac arrest, even ET-CO2 may be unreliable. You should confirm tube position as soon as possible by chest x-ray.

12. Which is preferred-oral or nasal intubation?

Show answer
Oral intubation. You can watch the tube pass directly through the vocal cords, ensuring proper placement. Nasal intubation is a blind technique, relatively contraindicated in patients with maxillofacial trauma (because of the risk of intracranial placement of the tube through an anterior fossa fracture) and in patients with known or suspected coagulopathy (because nasal mucosa is well vascularized, intubation may cause major epistaxis). Oral endotracheal intubation with “in-line” neck stabilization is preferred even in patients with suspected neck injury.

13. What is the role of an esophageal obturator airway (EOA)?

Show answer
None. At present, the EOA is not indicated because alternative techniques (mask or endotracheal tube) are safer and more effective.

14. What should be your first consideration if you are unable to ventilate or intubate a patient?

Show answer
Foreign body airway obstruction. Attempt to visualize the foreign body directly, and remove it with either suction or Magill forceps.

15. Explain the proper method of external chest compression.

Show answer
Place the patient on a firm surface-typically the floor or on a backboard. The rescuer should be positioned beside the patient’s chest. Both hands are placed just above the xiphoid-sternal junction. Keep your arms straight and your shoulders directly over the patient’s sternum. The compression depth should be 4-5 cm. Use the weight of your upper body to achieve adequate depth of compression. Perform 15 compressions followed by 2 ventilations at a rate of 100 compressions/minute.
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16. What are the essentials of external chest compressions?

Show answer
Even performed properly, external chest compression produces only a fraction of normal vital organ blood flow. Coronary blood flow occurs only during the release phase. Most providors do not use adequate force-make sure that the chest is compressed at least 2 inches in adults. Interruption in chest compression (to check the ECG rhythm or pulse) significantly reduces the efficacy of CPR.

17. What are the complications of external chest compressions?

Show answer
Complications are common but not important. Rib and sternal fractures occur 80% of the time. Major cardiac or pericardial injuries (lacerations) are rare. Bone marrow and fat emboli are common (80% in one series). Do not let fear of complication interfere with effective chest compression.

18. What are the indicators that effective CPR is being performed?

Show answer
Real-time indicators of vital organ perfusion are lacking. Effective CPR and pressor drugs should cause the VF waveform amplitude to increase-so called coarsening. Improved cerebral perfusion may result in gasping. During CPR, ET-CO2 > 15 mmHg predicts return of spontaneous circulation. Switch chest compression providers if the ET-CO2 begins to fall because this may indicate fatigue of the rescuer.

19. Is the central line the best access to the circulation?

Show answer
Yes. Large volumes of fluid can be delivered to the venous system more quickly, however, via large-bore peripheral venous catheters. A 14G, 5-cm catheter (peripheral) can deliver twice the flow of a 16G, 20-cm catheter (central). Central line placement may be associated with significant complications, including pneumothorax, air embolus, and arterial puncture. In hypo-volemic patients, in whom central veins are collapsed and peripheral veins are constricted, venous cannulation can be difficult.

20. Does a central line offer therapeutic and diagnostic advantages?

Show answer
Yes. A central line permits bolus administration of drugs to the right side of the heart. Identification of a high central venous pressure may indicate the need to treat reversible causes of PEA, such as cardiac tamponade or tension pneumothorax.

21. Is it necessary to monitor arterial blood gases during resuscitation?

Show answer
No. After you have an adequate airway and presumably are delivering 100% oxygen, you don’t care what the arterial PO2 is because you can do nothing about it. If possible, you may confirm the adequacy of oxygenation on the arterial side through an early arterial blood gas. Then you should focus on the adequacy of chest compression.

22. Which is preferred-colloid or crystalloid resuscitation fluid?

Show answer
Colloid advocates claim that the big molecules remain in the intravascular space and are more effective in elevating blood volume. Crystalloid advocates state that capillaries leak albumin, especially in the shock state. Resuscitation with crystalloid is clearly safe. Given its availability, low cost, and safety, crystalloid (lactated Ringer’s solution) is the choice for initial fluid resuscitation. When true cardiac arrest has occurred, however, volume is of little importance.

23. In a patient exhibiting asystole, bradycardia, PEA, or fine fibrillation, what is your primary goal?

Show answer
Adequate vital organ perfusion, especially to the coronary arteries. Done properly, CPR may cause PEA to progress to stable hemodynamics or VF to become “coarse enough” for successful countershock.
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24. Summarize the reversible causes and treatment of PEA.

Show answer
PEA is an orderly electrical rhythm in the absence of detectable arterial pulses. The potentially correctable situations that commonly cause electromechanical dissociation (EMD) are:

1. Tension pneumothorax (diagnosis: hyperresonant chest, decreased breath sounds), treated by decompressing the pleural space on the side of the collapsed lung
2. Pericardial tamponade (diagnosis: Beck’s triad-distant heart sounds, distended neck veins/elevated central venous pressure, and hypotension), treated with pericardiocentesis
3. Hypovolemia, treated with volume replacement
4. Pulmonary embolism, treated with fibrinolysis
5. Pump failure secondary to massive myocardial infarction, treated with fibrinolysis or mechanical assistance (intra-aortic balloon pump)
6. Hyperkalemia, treated with calcium and bicarbonate

KEY POINTS: REVERSIBLE CAUSES OF PEA

1. Tension pneumothorax
2. Pericardial tamponade
3. Hypovolemia
4. Pulmonary embolism
5. Pump failure
6. Hyperkalemia

25. Is clinical PEA always full cardiac arrest?

Show answer
PEA is a heterogeneous entity with hemodynamics ranging from full cardiac arrest through normal blood pressure. Confirm true cardiac arrest as early as possible through echocardiography or placement of an arterial catheter.

26. Name the most common cause of cardiac arrest in the perioperative period.

Show answer
Although the incidence of VF is increased in the perioperative period, PEA secondary to potentially reversible insults is more common at this time.

27. List the drugs commonly used during resuscitation and the appropriate dosages.

Show answer
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1. Oxygen: to reverse hypoxia, always provide 100% oxygen initially.
2. Epinephrine: α- and β-adrenergic agonist. IV dose is 5-10 mL of 1:10,000 solution. Because of the short duration of action, a repeat dose may be necessary after 5 minutes. Epinephrine is inactivated by alkali; do not mix with bicarbonate solutions. Although it enhances myocardial performance, epinephrine greatly increases myocardial oxygen demand. Ventilate!
3. Vasopressin: antidiuretic hormone-a new first-line pressor during cardiac arrest. Administer one time as a bolus of 40 U.
4. Amiodarone: first-line, broad-spectrum antidysrhythmic possibly useful in treating VF/ventricular tachycardia (VT) cardiac arrest and atrial arrhythmias. It is active at cardiac sodium, potassium, and calcium channels and has a- and b-adrenergic blocking properties. In cardiac arrest, it is administered as a 300-mg rapid IV infusion. Amiodarone may cause hypotension and bradycardia; a pressor drug, such as epinephrine or dopamine, should be readily available or already administered.
5. Atropine: parasympatholytic (vagolytic) agent that increases the discharge rate of the sinus node. Atropine is useful in treating sinus bradycardia associated with hemodynamic compromise. An IV dose of 0.5 mg is repeated at 5-minute intervals until a desirable rate is achieved (at least 60 beats/min). Increased heart rate increases myocardial oxygen demand; atropine should be used only if the bradycardia causes hemodynamic compromise (heart rate, 60 beats/min).
6. Dopamine: catecholamine precursor of norepinephrine active at dopaminergic receptors. Stimulates the heart and vasoconstricts (high dose) the periphery. Use as a vasopressor to treat hypotension secondary to bradycardia or decreased peripheral vasomotor tone. Dosage should be adjusted based on clinical end points starting at 2-5 μg/kg/min up to 20 μg/kg/min. The principal toxicity, seen with prolonged dosages > 10 μg/kg/min, is splanchnic and systemic vasoconstriction with resultant injury.
7. Dobutamine: synthetic catecholamine that is a cardiac b-receptor agonist used to treat cardiogenic shock. It increases cardiac contractility. Reflex peripheral vasodilation may require combination with a pressor drug, such as dopamine. Dosage should be adjusted based on clinical end points starting at 5 μg/kg/min up to 20 μg/kg/min.
8. Sodium bicarbonate (NaHCO3): no longer commonly used in cardiac arrest; in shock, it is used to reverse acidosis (hypoxia-induced anaerobic metabolism leads to acid accumulation). The initial dose is 1 mEq/kg. One ampule (50 mL) contains 50 mEq of sodium bicarbonate. Bicarbonate combines with hydrogen ions to form CO2 and water; adequate ventilation is required for bicarbonate therapy to be fully effective. Overzealous use of bicarbonate may result in hypernatremia/hyperosmolality (each HCO3- is accompanied by a sodium ion).
9. Magnesium: effective in treating drug-induced torsades de pointes or VT. Administer 1-2 g IV over 3-5 minutes. May cause hypotension.
10. Calcium chloride or gluconate: positive inotropic agent. Calcium ions bind to troponin (the cardiomyocyte-specific calcium regulatory protein used to diagnose an acute myocardial infarction), which enhances the formation of cross-bridges between muscle contractile filaments with resultant fiber shortening. Dose is calcium chloride (or gluconate), 500 mg IV push. Do not mix with bicarbonate because it will precipitate.
11. Lidocaine: local anesthetic that suppresses ventricular arrhythmias (automatic and reentrant; see Chapter 3). An IV bolus of 1 mg/kg is followed by IV infusion at 2-4 mg/min. An additional IV bolus can be given at 10 minutes after initial dose if arrhythmias persist. Amiodarone is accepted as a preferred agent for treatment of arrhythmias.
12. Adenosine: a naturally occurring vasodilating hormone that is synthesized by vascular endothelial cells and dramatically slows artrioventricular (AV) nodal conduction. It is useful in the therapy of supraventricular tachyarrhythmias. Dose is 6 mg or 12 mg injected in a rapid IV bolus (which may be repeated several times). The half-life of IV adenosine is only 12 seconds. Measurable systemic hypotension occurs in < 2% of patients because adenosine is metabolized before it reaches the systemic vessels.
13. Verapamil: slow-channel calcium blocker used to block the AV node and to treat paroxysmal supraventricular tachycardia that causes hemodynamic compromise. Dose is 0.1 mg/kg. Dilute drug with 10 mL of saline, and infuse 1 mL/min until the supraventricular tachycardia either breaks or blocks. Repeat dose after 30 minutes if not effective. The drug reduces systemic vascular resistance and may cause hypotension.

28. What measures should be considered postresuscitation to improve the chances of a good outcome?

Show answer
Laboratory and clinical data support use of mild hypothermia (34°C for 24 hours)in patients who remain comatose after resuscitation from cardiac arrest. Hypotension or causes of increased cerebral oxygen use (e.g., as seizures or fever) should be treated aggressively.

References
WEB SITE
http://www.americanheart.org/presenter.jhtml?identifier=10000056#P
BIBLIOGRAPHY
Harken AH: Cardiac dysrhythmias. In Wilmore DW, Cheung L, Harken AH, et al (eds): Scientific American Surgery. New York, Scientific American, 1999.

13. Is HLA (human leukocyte) matching still important?

Show answer
It is somewhat important. Historically, HLA matching was an important consideration when matching cadaver kidneys to recipients. With today’s improved immunosuppressive agents, many transplant surgeons believe that HLA matching is no longer critical. Six antigen match kidneys are still shared nationally and do enjoy some improvement in long-term graft survival. Donor organ quality remains the primary determinant in how well the transplanted organ functions. For example, a poorly matched living-donor kidney will still usually outlast a well-matched cadaveric kidney.

14. Does pancreas transplantation halt the progression of diabetic disease?

Show answer
This is still unproven. Logically, we would expect it to. Regression of neuropathy and eye dysfunction has been reported. Recently, long-term recipients have exhibited some regression of microscopic nephropathy.

15. Are islet cell transplants the answer in the future?

Show answer
Probably, although this has been frustratingly slow to achieve. Recent protocols using new immunosuppressive regimens and new islet cell isolation techniques have shown promise, but long-term data are still not widely available. The process requires that isolated islet cells be extracted from a donor pancreas. These cells are then injected into the portal vein, lodge in the liver, and produce insulin. Theoretically, patients achieve the benefit of a pancreas transplant without the surgical risk.

References
WEB SITE
http://www.transplantation-soc.org
BIBLIOGRAPHY
1. Bartlett ST: Laparoscopic donor nephrectomy after seven years. Am J Transpl 2:896-897, 2002. Full article
2. Donovitch G: Handbook of Kidney Transplantation, 3rd ed. Philadelphia, Lippincott Williams & Wilkins, 2001.
3. Fioretto P, Steffes MW, Sutherland DER, et al: Reversal of lesions of diabetic nephropathy after pancreas transplantation. N Engl J Med 339:69-75, 1998. Medline Similar articles Full article
4. Morris JP: Kidney Transplantation: Principles and Practice, 5th ed. Philadelphia, W.B. Saunders, 2001.

1. What are the goals of hand repair?

Show answer
Functional considerations override cosmesis in the treatment of hand trauma. There are no minor hand injuries. Initial diagnosis and management determine the final result; expert secondary repair cannot overcome primary errors in diagnosis or decision making.

2. What determines the final outcome of a hand injury?

Show answer
It is determined by minimal sacrifice of tissue and primary healing accomplished by early wound closure. Minimization of scar tissue by control of edema, prevention of infection, early wound closure, and vigorous physical therapy produce the optimal functional outcome.

3. What factors influence treatment of hand trauma?

Show answer
Mechanism, location, and timing of injury; hand dominance; occupation; age; and general health of the patient.

4. How common are occupational hand injuries?

Show answer
Hand injuries result in more days lost from work than any other type of occupational injury.

5. What are the essentials of examination of the hand?

Show answer
Inspection of position, color, and temperature often reveals the injury. Location suggests possible injury to underlying structures. Motor, sensory, and Doppler ultrasonic examination are confirmatory. All injuries must be radiographed, and surgical exploration provides the definitive diagnosis.

6. How and where should hand injuries be explored?

Show answer
Hand wounds should be explored under tourniquet control with adequate analgesia using delicate instruments in a well-lighted surgery suite. Visual magnification is usually mandatory.

7. How is emergency hemostasis of injured hands achieved?

Show answer
In the acute setting (outside the operating suite), no tourniquet should be applied, and there should be no blind clamping of any structures. Hemostasis may be achieved by elevation of the extremity and with direct compression of the wound. This approach prevents injury to delicate underlying structures that are tough to see.

8. How are fingertip injuries treated?

Show answer
If < 1 cm of pulp is disrupted, the wound will heal spontaneously with daily cleansing and dressing with nonadherent, moist gauze. Larger defects may require a skin graft, which can often be provided by defatting the amputated piece. Bone exposure necessitates flap coverage if digital length is to be maintained. Digital nerves cannot be repaired distal to the distal interphalangeal (DIP) joint.

9. What is the classification system for fingertip amputations?

Show answer

Classification for fingertip amputations is based on the amount of remaining sensate volar skin. Although the favorably angulated amputation commonly removes some nail and bone, the volar skin is available for easy coverage. This amputation type is “favorable” for treatment by dressings only, allowing wound repair by contraction and epithelialization. The volarly angulated amputation angle is “unfavorable” for conservative management and usually requires a reconstructive procedure. (Image from Ditmars DM Jr: Fingertip and nail bed injuries. In Kasdan ML (ed): Occupational Hand and Upper Extremity Injuries and Disease. Philadelphia, Hanley & Belfus, 1991, with permission.) (See Figure 34-1.)

Figure 34-1 Fingertip amputations.

10. How are nail bed injuries repaired?

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Repair of the disruption of the germinal matrix must be meticulously approximated under magnification and the nail bed splinted, preferably with the avulsed part. Subungual hematomas should be evacuated by a hot-tipped paperclip or battery-powered electric cautery. Repair of the disruption of the sterile eponychial fold must be maintained for 3 weeks with Xeroform gauze or with the original nail. Often, nail bed disruption cannot be diagnosed without removal of the nail.

11. What is the initial management of flexor tendon?

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Flexor tendon laceration is not an emergency, and repair should not be undertaken in the emergency department. If a hand surgeon is unavailable, the wound should be copiously irrigated and sutured and prophylactic antibiotics instituted. This injury can wait for definitive repair.

12. What is the proper management of an open fracture?

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Open fractures should be cultured and then undergo copious lavage with normal saline or Ringer’s lactate. Broad-spectrum antibiotic coverage should be instituted, and the hand should be splinted in the position of function with a bulky dressing.

13. What is the proper treatment for hand infection?

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The extremity should be immobilized and elevated, and parenteral antibiotics should be given. The patient should be immediately referred for possible surgical drainage.

14. What is the proper management of human bites?

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After cleansing of the wound, a radiograph should be taken. The wound should be left open-never closed. Antibiotics should be started, and the wound should be rechecked at 24 and 48 hours. If evidence of infection is present, parenteral antibiotics should be instituted and referred for possible surgical drainage. The so-called fight bite occurs over the metacarpophalangeal (MCP) joint or proximal interphalangeal joint when a clenched fist is impaled on the front teeth of an adversary. This often inoculates the MCP joint with anaerobic streptococci. When infection is diagnosed, immediate arthrotomy and lavage should be performed.

15. How are injection injuries treated?

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Despite their innocuous appearance, injection injuries may cause profound destruction of hand structures. Any such injury requires immediate hospitalization with prompt and extensive decompression, drainage, and debridement.

KEY POINTS: CARPAL TUNNEL SYNDROME

1. Symptoms: numbness, tingling, pruritus of the palm, thumb, middle, and index fingers.
2. Mechanical cause is compression of median nerve and carpal tendons.
3. Women are affected twice as often as men; the syndrome is more common after 40 years of age.
4. Predilection for people who perform repetitive manual labor.

16. What is carpal tunnel syndrome (CTS)?

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CTS is the most common peripheral compression neuropathy; it is signaled by numbness and tingling of the hand.

17. Is CTS more common in older or younger people? Men or women?

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CTS is more common in people older than age 40 years, but an increasing number of young people with CTS have been reported in recent years, usually those whose jobs involve repetitive manual labor. Women are affected approximately twice as often as men.

18. What are the most preventable causes of deformity in hand injuries?

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Edema and infection lead to increased scarring and restricted function. Prolonged immobilization in a poor position also impairs function, as does delayed skin closure. Failure to obtain a radiograph leads to a missed diagnosis with delay in recognition of an injury.

19. What is the proper emergency department treatment of all hand injuries?

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The patient should be sedated and the wound cultured and irrigated. A thorough examination must be performed and a sterile compression dressing placed. The upper extremity should be splinted, tetanus prophylaxis should be administered, and broad-spectrum antibiotic coverage should be instituted for crush avulsion or heavily contaminated wounds. Radiographs of the hand should always be obtained.

20. What are the guidelines for replantation of an amputated finger?

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There are no absolute guidelines. A microsurgeon who is a member of a replantation team should be consulted. If replantation is planned, parts should not be immersed directly in water or put directly on ice or dry ice. The part should be copiously irrigated, wrapped in a moist sponge, and placed in a sterile plastic container; the plastic container should be placed in an ice-water slurry for transport.

References
WEB SITE

* http://www.ninds.nih.gov
o Search: carpal tunnel

BIBLIOGRAPHY
1. Dunn R, Watson S: Suturing versus conservative management of hand lacerations. Hand lacerations should be explored before conservative treatment. Comment on Br Med J 325(7359):299, 2002. Br Med J 325(7372):1113, 2002.

2. Hansen TB, Carstensen O: Hand injuries in agricultural accidents. J Hand Surg 24B:190-192, 1999.
3. Irvine AJ: Suturing versus conservative management of hand lacerations. Incisions are not lacerations. Comment on Br Med J 325(7359):299, 2002. Br Med J 325(7372):1113, 2002; author reply 325(7372):1113, 2002.
4. Lee SJ, Montgomery K: Athletic hand injuries. Orthop Clin North Am 33:547-554, 2002. Medline Similar articles Full article
5. McAuliffe JA: Hand care in the new millennium: Surgeons’ perspective. J Hand Ther 12:178-181, 1999. Medline Similar articles
6. Riaz M, Hill C, Khan K, Small JO: Long-term outcome of early active mobilization following flexor tendon repair in zone 2. J Hand Surg 24B:157-160, 1999.
7. Taras JS, Lamb MJ: Treatment of flexor tendon injuries: Surgeons’ perspective. J Hand Ther 12:141-148, 1999. Medline Similar articles
8. Van der Molen AB, Matloub HS, Dzwierzynski W, Sanger JR: The hand injury severity scoring system and workers’ compensation cases in Wisconsin, USA. J Hand Surg 24B:184-186, 1999.

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