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Anorectal Disease. Pilonidal Sinus Disease

admin — Thu, 09 Jul 2009 07:32:17 +0000

PILONIDAL SINUS DISEASE

29. What is the most common clinical presentation of a pilonidal sinus?

Show answer
Pain and swelling in the sacrococcygeal region, which typically are associated with a (sometimes several) chronic draining sinus tract.

30. Is pilonidal disease acquired or congenital?

Show answer
Acquired. Hair follicles in the midline sacrococcygeal area enlarge and become infected, resulting in an abscess.

31. How is acute pilonidal abscess treated?

Show answer
Incision and drainage (like a fistula in ano, it is necessary to excise the whole tract).

32. What is the definitive therapy for pilonidal disease?

Show answer
Excision of the entire pilonidal cavity and associated sinus tracts down to the fascia with primary or delayed closure.

33. What theory explains the rarity of pilonidal disease after age 40 years?

Show answer
Changes in body habitus.

References
BIBLIOGRAPHY
1. Beck DE, Wexner SD (eds): Fundamentals of Anorectal Surgery. Philadelphia, W.B. Saunders, 1998.
2. Cho DV: Endosonographic criteria for an internal opening of fistula-in-ano. Dis Colon Rectum 42:515-518, 1999.
3. Cintron JR, Park JJ, Orsay CP, et al: Repair of fistulas-in ano using fibrin adhesive: Long-term follow-up. Dis Colon Rectum 43:944-949, 2000. Medline Similar articles
4. Corman ML: Anal fistula. In Corman ML: Colon and Rectal Surgery, 4th ed. Philadelphia, Lippincott-Raven, 1998, pp 238-271.
5. Hodgkin W: Pilonidal sinus disease. J Wound Care 7:481-483, 1998. Medline Similar articles
6. Law WL, Chu KW: Triple rubber band ligation for hemorrhoids: Prospective randomized trial of local anesthetic injection. Dis Colon Rectum 42:363-366, 1999. Medline Similar articles
7. Park JJ, Cintron JR, Orsay CP, et al: Repair of chronic anorectal fistulae using commercial fibrin sealant. Arch Surg 135:166-169, 2000.
8. Sentovich SM: Fibrin glue for all anal fistulas. J Gastrointest Surg 5:158-161, 2001. Medline Similar articles Full article

Congenital Cysts & Sinuses Of The Neck

admin — Mon, 13 Jul 2009 18:44:41 +0000

88 CONGENITAL CYSTS AND SINUSES OF THE NECK
Frederick M. Karrer M.D., Denis D. Bensard M.D.

1. What are branchial cleft anomalies?

Show answer
Cysts, sinuses, and fistulas that result from incomplete obliteration of the first, second, or third branchial clefts, and are present in early fetal development.

2. Which anomaly is the most common?

Show answer
Second branchial cleft anomalies are by far the most common, presenting near the mid- to upper border of the sternocleidomastoid (SCM) muscle. First branchial remnants are less common and third clefts are quite rare. (See Table 88-1.)
Table 88-1. BRANCHIAL CLEFT ANOMALIES

Branchial Cleft	Internal Opening	Exterior Opening	Frequency
First	External auditory canal	Angle of the jaw	8%
Second	Tonsillar fossa	Anterior border of the SCM	> 90%
Third	Piriform sinus	Suprasternal notch	< 1%

3. How do patients with branchial cleft anomalies present?

Show answer
Those with complete fistulas or sinuses present with intermittent drainage of a mucoid fluid on the neck. Patients with cysts usually present later with a mass (sterile or infected). Complete surgical excision is the treatment of choice.

4. What are the major operative hazards of branchial cleft remnant excision?

Show answer
The second branchial cleft tracts through the bifurcation of the carotid artery. The facial nerve is in close proximity to the first branchial cleft fistula. The superior laryngeal nerve and the recurrent laryngeal nerve are both at risk in dissection of a third branchial cleft.

5. What is a thyroglossal duct cyst?

Show answer
A thyroglossal duct cyst is the most common congenital cyst found in the neck. It is caused by failure of normal obliteration of the migration tract of the thyroid gland. Embryologically, the thyroid descends from the base of the tongue (foramen caecum) to its normal location in the low anterior neck.

6. How do patients with thyroglossal duct cysts present?

Show answer
They present with a paramidline mass in the upper neck; if infected, they may present with fever, tenderness, and erythema.

KEY POINTS: CONGENITAL CYSTS AND SINUSES OF THE NECK

1. The most common brachial cleft anomaly is the second brachial cleft anomaly presenting near the mid- to upper border or the sternocleidomastoid muscle.
2. A thyroglossal duct cyst is the most common congenital cyst found in the neck.
3. A cystic hygroma is a congenital lymphatic malformation that is benign an usually presents as a soft mass in the lateral neck.

7. How are thyroglossal duct cysts treated?

Show answer
The best treatment is complete excision of the cyst, along with the tract. Because embryologically the thyroid descends before formation of the hyoid cartilage, the tract may pass right through the hyoid. Therefore, complete tract removal requires excision of the central portion of the hyoid and dissection up to the base of the tongue (i.e., the Sistrunk procedure).

8. What is a cystic hygroma?

Show answer
A cystic hygroma is a congenital lymphatic malformation with a predilection for the neck. It is a benign lesion that usually presents as a soft mass in the lateral neck. Excision is often challenging because the lymph cysts do not respect the fascial planes and often intertwine with the neurovascular structures in the neck. Near-total excision is the treatment of choice.

References
BIBLIOGRAPHY
1. Alqahtani A, Nguyen LT, Flageole H, et al: 25 years experience with lymphangioma in children. J Pediatr Surg 34:1164-1168, 1999. Medline Similar articles Full article
2. Brown RL, Azizkhan RG: Pediatric head and neck lesions. Pediatr Clin North Am 45:889-905, 1998. Medline Similar articles
3. Kang L, Chang CH, Yu CH, et al: Prenatal detection of cystic hygroma using three-dimensional ultrasound. Ultrasound Med Biol 28:719, 2002. Medline Similar articles
4. Organ GM, Organ CH Jr: Thyroid gland and surgery of the thyroglossal duct: Exercise in applied embryology. World J Surg 24:886-890, 2000.
5. Smith CD: Cysts and sinuses of the neck. In O’Neill JA, Rowe MI, Grosfeld JL, et al (eds): Pediatric Surgery, 5th ed. St. Louis, Mosby, 1998, pp 757-771.
6. Telander RL, Filston HC: Review of head and neck lesions in infancy and childhood. Surg Clin North Am 72:1429-1447, 1992. Medline Similar articles

Queries 5

admin — Mon, 21 Sep 2009 06:21:43 +0000

Queries 3

admin — Fri, 14 Aug 2009 18:10:27 +0000

CAROTID DISEASE

admin — Fri, 10 Jul 2009 07:46:48 +0000

70 CAROTID DISEASE
Rao Gutta M.D., B. Timothy Baxter M.D.

1. What diseases affect the carotid arteries?

Show answer
Atherosclerosis is by far the most common (accounting for 90% of lesions in the Western world). The carotid also can be affected by fibromuscular dysplasia, inflammatory arteriopathies (e.g., Takayasu’s arteritis), extrinsic compression (e.g., neoplasm), and trauma.

2. What are the most common symptoms of carotid artery disease?

Show answer

* Transient ischemic attack (TIA)
* Reversible ischemic neurologic deficit (RIND)
* Cerebrovascular accident (CVA)
* Amaurosis fugax

3. Define TIA, RIND, and CVA.

Show answer
These clinical terms describe a spectrum of cerebral ischemic syndromes. A TIA is a neurologic deficit that lasts < 24 hours. Most TIAs last only 15-30 seconds. RIND lasts longer than 24 hours and completely resolves within 1 week (usually within 3 days). CVA, or acute stroke, is a stable neurologic deficit that may show gradual improvement over a long period.

4. Define amaurosis fugax.

Show answer
It is an episode of transient (minutes to hours) monocular blindness, often likened to a window shade pulled across the eye. It is caused by decreased blood flow through or embolization into the ophthalmic artery.

5. What are Hollenhorst plaques?

Show answer
They are bright yellow plaques of cholesterol, usually at a branch point in the retinal vessels, that have embolized from the carotid bifurcation. Clinically, this finding indicates that the atheromatous plaque in the carotid is quite friable. Further embolization may occur with manipulation at the time of surgery.

6. What mechanisms produce neurologic deficits?

Show answer

* Embolization from atherosclerotic arteries or the heart
* Reduced blood flow
* Occlusive disease with thrombosis
* Intracranial hemorrhage

7. What is the natural history of a TIA?

Show answer
The natural history of a TIA is defined by the pathology of the ipsilateral carotid artery. In patients with severe stenosis (> 70%), the risk of ipsilateral stroke within 24 months is 26%. For those with moderate disease (50-69%), the risk is 22% at 5 years. With minimal stenosis (< 30%), the risk is 1% at 3 years (see Required Reading in Chapter 1).

8. What is the effect of aspirin on TIAs?

Show answer
Acetylsalicylic acid is a cyclooxygenase inhibitor that decreases platelet stickiness and lowers the incidence of both TIAs and stroke.

9. What does a carotid bruit signify?

Show answer
Unfortunately, a carotid bruit is a general marker for atherosclerosis and is specific for very little; it is more predictive of a cardiac event than a neurologic event. Although a carotid bruit indicates increased risk of neurologic events, it is just as likely to occur on the contralateral side as on the side of the bruit.

10. Does the sound of a bruit correlate with the degree of stenosis?

Show answer
No. As a stenosis progresses, the bruit should actually diminish and disappear as flow decreases.

11. What test should be ordered to evaluate a cervical bruit?

Show answer
Duplex scanning.

12. When is surgery indicated for symptomatic carotid artery disease?

Show answer
Surgery is strongly indicated for symptomatic carotid artery disease associated with > 70% stenosis. The absolute risk reduction of stroke is 17% at 2 years. Recent data also suggest a smaller benefit in patients with symptomatic stenoses of 50-69% (6.5% risk reduction at 5 years). Patients with stenosis of < 50% do not benefit from surgery.
KEY POINTS: CAROTID DISEASE

1. The symptoms of carotid disease include transient ischemic attack, reversible ischemic neurologic deficit, cerebrovascular accident, and amaurosis fugax.
2. A carotid bruit is a general marker for atherosclerosis and is specific for very little; it is more predictive of a cardiac event than a neurologic event.
3. Surgery is strongly indicated for symptomatic carotid artery disease associated with > 70% stenosis.

13. Should a patient with asymptomatic stenosis undergo surgery?

Show answer
The absolute reduction in risk of stroke is 6% over a 5-year period in asymptomatic patients with > 60% stenosis who undergo carotid endarterectomy (CEA) plus aspirin versus patients treated with aspirin alone (5.1% versus 11%). Thus, CEA should be performed for asymptomatic carotid disease when the patient is expected to live at least 3 years and when the CEA can be performed with a combined stroke and mortality rate of < 3%.

14. What are the complications of carotid endarterectomy?

Show answer

* TIA or stroke (approximately 2%)
* Hematoma
* Cranial nerve injury
* Hypertension
* Hypotension

15. Which cranial nerves (CNs) may be injured during CEA? What are the clinical signs of injury?

* Facial nerve (CN VII): injury to the marginal mandibular branch may cause droop of the ipsilateral corner of the mouth
* Glossopharyngeal nerve (CN IX): difficulty in swallowing both solids and liquids
* Vagus nerve (CN X): hoarseness, loss of effective cough
* Superior laryngeal nerve (branch of the vagus): voice fatigue, loss of high-pitch phonation
* Hypoglossal nerve (CN XII): deviation of the tongue to the ipsilateral side, difficulty with speech and chewing

16. What is the danger of wound hematoma after surgery?

Show answer
The main danger is airway compromise, which may necessitate emergent decompression by opening of the wound. Whether vacuum drains prevent this complication is not clear.

17. What are the possible causes of postoperative hypertension?

Show answer

* Denervation of the carotid sinus
* Cerebral rennin, norepinephrine production, or both
* Preexisting hypertension
* Central neurologic deficit

18. When do neurologic events occur during CEA?

Show answer

* Dissection: dislodgement of material from the arterial wall with embolization
* Clamping: ischemic infarct
* Postoperatively: intimal flap, reperfusion, external carotid artery clot

19. What is a shunt? When is it used?

Show answer
A shunt is a small plastic tube that diverts blood flow around the surgically opened carotid artery while endarterectomy is performed. A shunt is used to ensure adequate cerebral blood flow and to avoid intraoperative cerebral ischemia. Many surgeons routinely use shunts, but others use them selectively, if at all. The decision to use a shunt is based on intraoperative assessment, including temporary clamping of the carotid under local anesthesia, measurement of stump pressure, intraoperative electroencephalography, or transcranial Doppler. None of these methods is 100% accurate.

20. What is stump pressure?

Show answer
Stump pressure is the back pressure of the internal carotid artery after clamping. It is used to assess the adequacy of cerebral perfusion. The “safe” pressure varies from author to author, but is probably around 40 mmHg.

21. Does stenosis recur after carotid endarterectomy?

Show answer
Yes. The reported incidence has been quite variable and ranges from < 2% to as much as 36%. During the first 24 months after operation, restenosis is thought to be secondary to myointimal hyperplasia. Beyond this time, it is caused by progression of disease (atherosclerosis). The incidence is lower when the arteriotomy is closed with a vein patch angioplasty.

22. What is the most common complication associated with reoperation endarterectomy?

Show answer
Cranial nerve injury (reported incidence = 2-20%). Most injuries are transient, however.
23. In which layer of the artery is the carotid endarterectomy performed? Show answer
The outer layers of the tunica media.

24. What anatomic landmark is useful in identifying the level of the carotid artery bifurcation?

Show answer
The facial vein.

25. How many branches of the internal carotid artery are located in the neck?

Show answer
None.

26. When the internal carotid artery is occluded, which branches of the external carotid artery form collaterals and reestablish circulation in the circle of Willis?

Show answer
The periorbital branches of the external carotid artery form communications with the ophthalmic artery, a branch of the internal carotid.

27. What are the functions of the carotid sinus and the carotid body?

Show answer
Both are located at the carotid bifurcation and are innervated by the glossopharyngeal and vagus nerves, respectively. The function of the carotid sinus is regulation of blood pressure. Hypertension stimulates efferent impulses to the vasomotor center in the medulla, inhibiting sympathetic tone and increasing vagal tone. The carotid body regulates respiratory drive and acid-base status via chemoreceptors. It also induces bradycardia when manipulated (this is your target during carotid massage for cardiac dysrhythmias).

28. When was the first successful surgical procedure of the extracranial carotid artery performed? Who is credited with it?

Show answer
In 1954 by Eastcott.

Evaluation & Treatment Of Cardiac Dysrhythmias

admin — Mon, 06 Jul 2009 19:31:33 +0000

3 EVALUATION AND TREATMENT OF CARDIAC DYSRHYTHMIAS
Alden H. Harken M.D.

1. Are cardiac dysrhythmias and cardiac arrhythmias the same?

Show answer
Yes. Some purists will tell you that an arrhythmia can be only the absence of a cardiac rhythm. But these are the same purists who use the word iatrogenic to mean “caused by a physician,” when, of course, the only thing that can truly be “iatrogenic” is a physician’s parents.

2. Are all cardiac dysrhythmias clinically important?

Show answer
Most are not. Many of us have isolated premature ventricular contractions (PVCs) or premature ventricular depolarizations (PVDs) all the time. Superbly conditioned athletes frequently exhibit resting heart rates in the 30s. A clinically important cardiac dysrhythmia is a rhythm that bothers the patient. As a rule, if the patient’s ventricular rate is 60-100 beats/min (regardless of mechanism), cardiac rhythm is not a problem.

3. State the goals in the treatment of cardiac dysrhythmias.

Show answer
Primary goal: to control ventricular rate between 60 and 100 beats/min
Secondary goal: to maintain sinus rhythm

4. How important is sinus rhythm?

Show answer
It depends on the patient’s ventricular function. Induction of atrial fibrillation in a medical student volunteer causes no measurable hemodynamic effect. Your ventricular compliance is so good that you do not need an atrial “kick” to fill the ventricle completely. Conversely, the worse (the stiffer) the patient’s heart, the more you should try to maintain sinus rhythm. We observed a patient with a 7% left ventricular ejection fraction whose cardiac output decreased by 40% when he spontaneously developed atrial fibrillation.

5. Do you need to be ankle-deep in ECG paper and personally acquainted with Drs. Mobitz, Lown, and Ganong to treat cardiac dysrhythmias in the intensive care unit (ICU)?

> Show answer
No.

6. When you are called by the ICU nurse to see a patient with an “arrhythmia,” what questions do you ask yourself?

Show answer
1. Does the patient really exhibit an arrhythmia? What is the patient doing? Is the stuff that looks like ventricular fibrillation (VF) really just the patient brushing his teeth? Or is the rhythm strip that looks like asystole really just a loose lead? If the patient does exhibit an arrhythmia, ask yourself the following questions.
2. Does the arrhythmia require intervention? Isolated PVCs usually can be ignored safely. Similarly a resting bradycardia in a triathlete is normal. This is the occasion to launch into your “2-second physical exam”-is the patient sweaty and confused or alert and happy?
3. What is a 2-second physical exam? You look into the patient’s eyes, hoping to determine whether he or she is perfusing his or her brain. If the patient looks back at you, you have some time. If the patient requires therapy, ask yourself the following questions.
4. How soon is therapy required? At this point, the patient becomes (paradoxically) irrelevant. The most robust indicator dictating velocity of intervention is not how sick the patient is, but how frightened you are. The dean may have had his carotid arteries firmly ligated years ago. Conversely, to match the surgical residency of your choice, you need to be firing on a lot more cylinders than the dean. You must determine rapidly whether delay in therapy is likely to put the patient at risk. If the cardiac arrhythmia is likely to inflict psychopathologic (hypoxemic) consequences not only on the patient but also, by extension, on his or her extended (societal) family, you should be frightened. If you are frightened, you must ask yourself:
5. What is the safest and most effective therapy?

7. If the patient requires antiarrhythmic therapy, what is the safest and most effective strategy?

Show answer
Therapy for cardiac arrhythmias is simple and comprises three comprehensible concepts:

1. If the patient is hemodynamically unstable (the sole determinant of instability is whether you are frightened), cardiovert with 360 J. (For lower energy, see Chapter 2.)
2. If the patient has a wide-complex tachycardia, cardiovert with 360 J.
3. If the patient has a narrow-complex tachycardia, infuse an atrioventricular (AV) nodal blocker IV. If at any time the patient becomes unstable, proceed with cardioversion.

8. In assessing a cardiac impulse, how do you distinguish supraventricular from ventricular origin?

Show answer
Supraventricular origin: When an impulse originates above the AV node (supraventricular), it can access the ventricles only through the AV node. The AV node connects with the endocardial Purkinje system, which conducts impulses rapidly (2-3 m/sec). A supraventricular impulse activates the ventricles rapidly (< 0.08 sec, 80 msec, or two little boxes on the ECG paper), producing a narrow-complex beat.
Ventricular origin: When an impulse originates directly from an ectopic site on the ventricle, it takes longer to access the high-speed Purkinje system. A ventricular impulse activates the entire ventricular mass slowly (< 0.08 sec, 80 msec, or two little boxes on the ECG paper), producing a wide-complex beat. (See Figure 3-1.)

Figure 3-1 Wide complex beats are of ventricular origin. Narrow complex beats are of supraventricular origin.

9. Extra credit: Correlate the ECG with cardiomyocyte membrane ion flux.

Show answer
See Figure 3-2.

10. Do all wide-complex beats derive from the ventricles?

Show answer
No, but most do. An impulse of supraventricular origin that is conducted with aberrancy through the ventricle can take enough time to make it a wide-complex beat. In one study, 89% of 100 patients presenting to an emergency department with a wide-complex tachycardia eventually proved to exhibit ventricular tachycardia, whereas 11% were diagnosed with supraventricular tachycardia with aberrancy.

Figure 3-2 Typical action potential of a cardiac myocyte, the ionic shifts responsible for each phase, and correlation with the surface ECG. A, Phase 0 = rapid depolarization, characterized by rapid influx of sodium (Na+) through the voltage-gated Na+ channels. B, Phase 1 = brief repolarization, characterized by transient influx of chloride (Cl-). C, Phase 2 = plateau phase, characterized by a rapid rise in calcium (Ca2+) permeability through L-type Ca2+ channels. Phase 3 = repolarization with potassium (K+) exiting the cell. D, Slow depolarization of pacemaker cells caused by slow influx of Na+ (From Meldrum DR, Cleveland JC, Sheridan BC, et al: Cardiac surgical implications of calcium dyshomeostasis in the heart. Ann Thorac Surg 61:1273-1280, 1996, with permission.)

11. What do you do if you cannot tell whether a ventricular complex is wide or narrow?

Show answer
Acutely and transiently (for 5 seconds) block the AV node by giving 6 mg of adenosine IV; if the ventricular complex persists, it is ventricular. If the ventricular complex stops, it was supraventricular.

12. To prevent lots of supraventricular impulses from getting to the ventricles, how do you block the AV node pharmacologically?

Show answer
In seconds: give 6 mg adenosine IV push.
In minutes: draw up 10 mg verapamil (calcium channel blocker) in 10 mL of saline and give 1 mL/min IV.
In hours: put 0.5 mg digoxin in 100 mL of Ringer’s lactate and infuse by IV drip over 30 minutes.

KEY POINTS: CHARACTERIZATION OF CARDIAC DYSRHYTHMIAS

1. Supraventricular origin: when an impulse originates above the AV node, it can access the ventricles only through the AV node to reach the Purkinje system, which conducts and activates the ventricles rapidly, producing a narrow-complex beat (< 2 small boxes on ECG).
2. Ventricular origin: when an impulse originates from an ectopic site on the ventricle, it takes longer to access the high-speed Purkinje system. A ventricular impulse activates the entire mass, slowly producing a wide-complex beat (> 2 small boxes on ECG).
3. Not all wide-complex beats are ventricular in origin.
4. To distinguish ventricular from supraventricular tachycardia, transiently block AV node with adenosine IVP. If ventricular complex persists, it is ventricular tachycardia; if the complex stops, it is supraventricular tachycardia.

13. Why give digoxin?

Show answer
Digoxin is an effective AV nodal blocker, but it makes cardiomyocytes more excitable. By giving digoxin, you make supraventricular impulses more likely; but by blocking the AV node, you render these impulses less dangerous.

14. Why infuse digoxin over 30-60 minutes IV?

Show answer
Studies indicate that a big pulse of digoxin (IV push) concentrates in the myocardium, making the myocytes hyperexcitable. Digoxin infused more slowly avoids this problem.

15. List the steps in calling a dysrhythmia by name.

Show answer

* Bradycardia: < 60 beats/min
* Tachycardia: 100-250 beats/min
* Flutter: atrial or ventricular rate 250-400 beats/min
* Fibrillation: atrial or ventricular rate > 400 beats/min

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.

Cardiopulmonary Resuscitation

admin — Mon, 06 Jul 2009 19:02:23 +0000

2 CARDIOPULMONARY RESUSCITATION
Norman A. Paradis M.D., Alden H. Harken M.D.

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.

Venous Disease

admin — Fri, 10 Jul 2009 08:18:04 +0000

72 VENOUS DISEASE
Thomas A. Whitehill M.D., Mark Nehler M.D.

1. Where does deep venous thrombosis (DVT) originate?

Show answer
More than 95% of DVTs develop in the deep veins of the lower extremities; the majority originate in the valve sinuses of the calf veins.

2. What is the usual source of a pulmonary embolus?

Show answer
Calf vein thrombosis may propagate proximally into the deep venous system to involve the popliteal, femoral, or iliac veins (or a combination of veins). These proximal DVTs are the culprits in > 90% of pulmonary emboli.

3. What is Virchow’s triad?

Show answer
(1) Hypercoagulability, (2) disruption of an intact venous intimal lining, and (3) stasis of venous blood flow. In most patients with DVT, at least two of these three components are operative.

4. What are the major hypercoagulable syndromes (thrombophilia)?

Show answer
Factor V Leiden mutation, antithrombin III deficiency, protein C deficiency, protein S deficiency, dysfibrinogenemia, lupus anticoagulant, antiphospholipid syndrome, prothrombin 20210A mutation, and abnormalities of fibrinolysis are the major examples. The most common is the factor V Leiden mutation (i.e., activated protein C resistance).

5. What causes venous intimal injury?

Show answer
Venous intimal changes may be secondary to vein wall trauma, infection, inflammation, indwelling catheters, or surgery. Venodilation during anesthesia and surgery may produce microscopic intimal tears as well as stasis. The injured venous intima initiates the release of thromboplastic substances that can activate the coagulation cascade.

6. What causes stasis of venous blood flow?

Show answer
Venostasis is common in surgical patients; it occurs during anesthesia, after certain types of trauma, and with perioperative immobility.

7. What are the usual clinical risk factors for DVT?

Show answer
Risk factors include malignancy (especially pancreatic, genitourinary, stomach, lung, colon, and breast cancer), age older than 40 years, female gender, obesity, history of venous thrombosis or pulmonary embolism, major surgical procedures, pregnancy, limited mobility, hypercoagulable state, and trauma.

8. What signs and symptoms suggest DVT? How can DVT be accurately diagnosed?

Show answer
The signs and symptoms are calf or thigh pain, tenderness, increased skin temperature, swelling, or superficial venous dilatation. None of these signs is specific for DVT. Even the well-known Homan’s sign (i.e., calf pain with dorsiflexion of the foot) is unreliable; its accuracy is only 50%. Doppler ultrasound examination (duplex scanning) detects DVT proximal to the calf veins with > 95% accuracy; unfortunately, it is not as sensitive in detecting calf vein DVT. Ascending venography is still the reference standard.

9. Is there any value to D-dimer testing?

Show answer
Measurement of D-dimer cross-linked fibrin degradation products (FDPs), formed by the action of plasmin on cross-linked fibrin, has been proposed as an alternative to initial noninvasive testing. A sensitivity of 96.8% and a specificity of 35.2% have been reported for the enzyme-linked immunosorbent assay (ELISA) test, making it theoretically possible to limit noninvasive testing to those with positive D-dimer testing. Unfortunately, the ELISA test is time consuming and impractical as a screening test. More rapid (1 hour) ELISA assays are now available. Prospective evaluation of the safety of withholding anticoagulation therapy in patients who are D-dimer negative has been limited. False-positive results are a problem in patients with malignancy, infection, or recent surgery.

10. What methods of perioperative DVT prophylaxis should be used? In which surgical patients?

Show answer
Perioperative DVT prophylaxis is strongly recommended in all high-risk patients who are older than age 40 years and undergoing major general or orthopedic procedures. In general surgical patients, well-applied prophylactic measures decrease the relative risk of DVT by 67%. The best prophylaxis for DVT includes pre- and postoperative walking. Intermittent pneumatic compression stockings and some form of heparin therapy (low-dose unfractionated heparin [LDUH] or low molecular weight heparin [LMWH]) are recommended as the patient’s risk profile increases.
KEY POINTS: VENOUS DISEASE

1. More than 95% of deep vein thromboses (DVTs) develop in the deep veins of the lower extremities; the majority originate in the valve sinuses of the calf veins.
2. Virchow’s triad consists of hypercoagulability, disruption of an intact venous intimal lining, and stasis of venous blood flow.
3. The best prophylaxis for DVT includes pre- and postoperative walking.

11. How does heparin work?

Show answer
Heparin binds to antithrombin III (ATIII), rendering it more active. Low-dose heparin (5000 U administered subcutaneously every 8-12 hours until the patient is fully ambulatory) activates ATIII, inhibits platelet aggregation, and decreases the availability of thrombin.

12. What is LMWH?

Show answer
LMWH is a fragment of heparin produced by chemical breakdown. It exerts its anticoagulation effect by binding with ATIII and inhibiting several coagulation enzymes, principally factor Xa. It has a longer half-life than standard preparation heparin and can be administered once daily. LMWH gives a more predictable anticoagulant response at high doses and thus can be administered without monitoring (it is not necessary to follow the partial thromboplastin time).

13. Should the placement of an inferior vena cava (IVC) filter ever be considered?

Show answer
In patients with a documented, recurrent pulmonary embolism while taking adequate anticoagulation therapy or with an absolute contraindication to anticoagulation, an IVC filter can be placed to prevent embolization or propagation of clot to the lungs. A significant rate of recurrent DVT has been associated with IVC filters.

14. What are the characteristics of chronic venous insufficiency and postphlebitic syndrome?

Show answer
The primary characteristic is venous valvular incompetence with distal ambulatory venous hypertension. After DVT, involved venous segments eventually recanalize to some degree. However, their delicate valves remain scarred or trapped by residual organized thrombus. The loss of valvular function disables the venomotor pump. The vein walls become thicker and less compliant, increasing resistance to proximal blood flow. These factors result in distal venous hypertension. Protein-rich fluids, fibrin, and red blood cells are extravasated and deposited through large pores in the distended microcirculation during periods of venous hypertension. This process leads to inflammation, scarring, fibrosis of the subcutaneous tissues, and discoloration by hemosiderin deposition (”brawny” edema). The resultant inflammatory reaction, scarring, and interstitial edema create a further barrier to capillary flow and diffusion of oxygen; adequate nutrition to the skin is inhibited. These changes may lead to tissue atrophy and ulceration (i.e., venous stasis ulcer).

15. Do all patients with DVT develop postphlebitic syndrome?

Show answer
No. Recent epidemiologic studies suggest that the incidence of venous ulceration is about 5%. As many as one in five post-DVT patients have absolutely no symptoms and maintain normal noninvasive vascular test data. The median time for the appearance of a first venous stasis ulcer is 2.5 years. Of interest, 50% of patients with venous ulcers have no history of DVT (probably because of previous asymptomatic calf vein DVT).

16. How are patients with postphlebitic syndrome treated?

Show answer
With proper patient education and compliance, postphlebitic stasis sequelae can be controlled by nonoperative means in well over 90% of patients, particularly if no residual venous outflow obstruction complicates valvular incompetence. Nonoperative treatment consists of graded elastic compression stockings (or Unna boots) to retard swelling and periodic leg elevation during the day. Patients must be taught to elevate their legs above the heart (”toes above your nose”) at regular intervals (e.g., 10-15 minutes every 2 hours). Compliance is critical.

17. Distinguish between phlegmasia alba dolens and phlegmasia cerulea dolens.

Show answer
Iliofemoral venous thrombosis is characterized by unilateral pain and edema of an entire lower extremity, discoloration, and groin tenderness. A total of 75% of the cases of iliofemoral venous thrombosis occur on the left side, presumably because of compression of the left common iliac vein by the overlying right common iliac artery (May-Thurner syndrome). In phlegmasia alba dolens (literally, painful white swelling), the leg becomes pale and white. Arterial pulses remain normal. Progressive thrombosis may occur with propagation proximally or distally and into neighboring tributaries. The entire leg becomes both edematous and mottled or cyanotic. This stage is called phlegmasia cerulea dolens (literally, painful purple swelling). When venous outflow is seriously impeded, arterial inflow may be reduced secondarily by as much as 30%. Limb loss is a serious concern; aggressive management (i.e., venous thrombectomy, catheter-directed lytic therapy, or both) is necessary.

18. What is venous claudication?

Show answer
When venous recanalization fails to occur after iliofemoral venous thrombosis, venous collaterals develop to bypass the obstruction to venous outflow. These collaterals usually suffice while the patient is at rest. However, leg exercise induces increased arterial inflow, which may exceed the capacity of the venous collateral bed and result in progressive venous hypertension. The pressure buildup in the venous system results in calf pain commonly described as tight, heavy, or bursting (venous claudication). Relief is obtained with rest and elevation but is not as prompt as with arterial claudication.

19. How can one distinguish primary varicose veins from secondary varicose veins?

Show answer
Primary varicose veins result from uncomplicated saphenofemoral venous valvular incompetence and have a greater saphenous distribution, positive tourniquet test result, no stasis sequelae (dermatitis or ulceration), and no morning ankle edema (lymphedema).
Secondary varicose veins are most commonly a consequence of deep and perforator venous incompetence secondary to postphlebitic syndrome.

20. Why do people develop primary varicose veins?

Show answer
The most common cause is congenital absence of venous valves proximal to the saphenofemoral junction. There are normally no valves in the vena cava or common iliac veins and only an occasional valve in the external iliac veins. Thus, the sentinel valve in the common femoral vein just above the saphenofemoral junction is of critical importance. However, anatomic studies reveal that this valve is absent on one or the other side in 30% of patients.

21. How, when, and in whom should varicose veins be treated?

Show answer
Varicose veins that cause discomfort or serious cosmetic embarrassment require treatment. Better results are obtained with early treatment before continuous retrograde pressure and flow down the superficial system and into communicating perforating veins (whenever the patient is standing) cause secondary, irreversible perforator incompetence. High saphenous vein ligation at an early stage can arrest progression of this gravitational process. The distal varicosities can be managed by selective surgical stripping, sclerotherapy, or both.

References
WEB SITE
http://www.acssurgery.com
BIBLIOGRAPHY
1. Clarke-Pearson DL, Dodge RK, Synan I, et al: Venous thromboembolism prophylaxis: Patients at high risk to fail intermittent pneumatic compression. Obstet Gynecol 101:157-163, 2003. Medline Similar articles Full article
2. Franks PJ, Sharp EJ, Moffatt CJ: Risk factors for leg ulcer recurrence: A randomized trial of two types of compression stockings. Age Ageing 24:490-494, 1995. Medline Similar articles
3. Gallix BP, Achard-Lichere C, Dauzat M, et al: Flow-independent magnetic resonance venography of the calf. J Magn Reson Imaging 17:421-426, 2003. Medline Similar articles Full article
4. Geerts W, Heit JA, Clagett GP, et al: Prevention of venous thromboembolism. Chest 119:132s-175s, 2001. Medline Similar articles
5. Ginsberg JS: Management of venous thromboembolism. N Engl J Med 335:1816-1828, 1996. Medline Similar articles Full article
6. Janssen MC, Wollersheim H, Verbruggen B, et al: Rapid D-dimer assays to exclude deep venous thrombosis and pulmonary embolism: Current status and new developments. Semin Thromb Hemost 24:393-400, 1998. Medline Similar articles
7. Philbrick JT, Heim S: The d-dimer test for deep venous thrombosis: Gold standards and bias in negative predictive value. Clin Chem 49:570-574, 2003. Medline Similar articles Full article
8. Sorensen HT, Mellemkjaer L, Steffensen FH, et al: The risk of a diagnosis of cancer after primary deep venous thrombosis or pulmonary embolism. N Engl J Med 338:1169-1173, 1998.

Top 100 Secrets

admin — Thu, 09 Jul 2009 18:49:39 +0000

These secrets are 100 of the top board alerts. They summarize the concepts, principles, and most salient details of surgical practice.

Clinical determinants of brain death are the loss of the
papillary, corneal, oculovestibular, oculocephalic, oropharyngeal, and
respiratory reflexes for > 6 hours. The patient should also undergo
an apnea test, in which the pCO₂ is allowed to rise to at
least 60 mmHg without coexistent hypoxia. The patient should be
observed for the absence of spontaneous breathing.
The estimated risks of HBV, HCV, and HIV transmission by
blood transfusion in the United States are 1 in 205,000 for HBV, 1 in
1,935,000 for HCV, and 1 in 2,135,000 for HIV.
The most common location of an undescended testicle is the
inguinal canal.
The most common solid renal mass in infancy is a congenital
mesoblastic nephroma and in childhood a Wilms’ tumor.
Ogilvie’s syndrome is acute massive dilatation of the cecum
and the ascending and transverse colon without organic obstruction.
The best screening method for prostate cancer is digital
rectal exam combined with serum prostate-specific antigen.
The most common histologic type of bladder cancer is
transitional cell carcinoma.
Carcinoma in situ of the bladder is treated with
immunotherapy with intravesical bacillus Calmette-Guérin.
Localized renal cell carcinoma is treated with surgery
(radical nephrectomy).
The most common cause of male infertility is varicocele.
The most common nonbacterial cause of pneumonia in
transplant patients is cytomegalovirus.
Chimerism is leukocyte sharing between the graft and the
recipient so that the graft becomes a genetic composite of both the
donor and the recipient.
OKT3 is a mouse monoclonal antibody that binds to and
blocks the T-cell CD3 receptor.
The most common disease requiring liver transplant is
hepatitis C.
Cystic hygroma is a congenital malformation with a
predilection for the neck. It is a benign lesion that usually presents
as a soft mass in the lateral neck.
In neuroblastomas, age at presentation is the major
prognostic factor. Children younger than 1 year have an overall
survival rate > 70%, whereas the survival rate for children older
than 1 year is < 35%.
The most feared complication of diaphragmatic hernia is
persistent fetal circulation.
The three most common variants of tracheoesophageal fistula
are (1) proximal esophageal atresia with distal tracheoesophageal
fistula, (2) isolated esophageal atresia, and (3) tracheo-esophageal
fistula with esophageal atresia.
Atresia can occur anywhere in the GI tract: duodenal (50%),
jejunoileal (45%), or colonic (5%). Duodenal atresia arises from
failure of recanalization during the 8th-10th week of gestation;
jejunoileal and colonic atresia are caused by an in utero mesenteric
vascular accident.
The types of aortic dissection are ascending (type A)
dissection, which involves only the ascending or both the ascending and
descending aorta, and descending dissection (type B), which involves
only the descending aorta.
A solitary pulmonary nodule is < 3 cm and is discrete on
chest radiograph. It is usually surrounded by lung parenchyma.
Mediastinal staging is indicated in patients with apparent
or documented lung cancer who have (1) known lung cancer with
mediastinal nodes > 1 cm accessible by cervical mediastinal
exploration, as assessed by CT scan; (2) adenocarcinoma of the lung and
multiple mediastinal lymph nodes < 1 cm; (3) central or large (>

5 cm) lung cancers with mediastinal lymph nodes < 1 cm; and (4) lung
cancer with risk of thoracotomy and lung resection.
The most common causes of aortic stenosis are now
congenital anomalies and calcific (degenerative) disease.
In mitral regurgitation, the left ventricle ejects blood
via two routes: (1) antegrade, through the aortic valve, or (2)
retrograde, through the mitral valve. The amount of each stroke volume
ejected retrograde into the left atrium is the regurgitant fraction. To
compensate for the regurgitant fraction, the left ventricle must
increase its total stroke volume. This ultimately produces volume
overload of the left ventricle and leads to ventricular dysfunction.
The indications for CABG are (1) left main coronary artery
stenosis; (2) three-vessel coronary artery disease (70% stenosis) with
depressed left ventricular (LV) function or two-vessel coronary artery
disease (CAD) with proximal left anterior descending (LAD) involvement;
and (3) angina despite aggressive medical therapy.
Hibernating myocardium is improved by CABG. Myocardial
hibernation refers to the reversible myocardial contractile function
associated with a decrease in coronary flow in the setting of preserved
myocardial viability. Some patients with global systolic dysfunction
exhibit dramatic improvement in myocardial contractility after CABG.
The surgical treatment of ulcerative colitis is total
colectomy with ileoanal pouch anastomosis.
Dieulafoy’s ulcer is a gastric vascular malformation with
an exposed submucosal artery, usually within 2-5 cm of the
gastroesophageal junction. It presents with painless hematemesis, often
massive.
The role of blind subtotal colectomy in the management of
massive lower gastrointestinal bleeding is limited to a small group of
patients in whom a specific bleeding source cannot be identified. The
procedure is associated with a 16% mortality rate.
Colorectal polyps < 2 cm have a 2% risk of containing
cancer, 2 cm polyps have a 10% risk, and polyps > 2 cm have a cancer
risk of 40%. Sixty percent of villous polyps are > 2 cm, and 77% of
tubular polyps are < 1 cm at the time of discovery.
Patients with colorectal cancer with lymph node involvement
(Dukes’ C) should receive chemotherapy postoperatively to treat
micrometastases.
Goodsall’s rule states the location of the internal opening
of an anorectal fistula is based on the position of the external
opening. An external opening posterior to a line drawn transversely
across the perineum originates from an internal opening in the
posterior midline. An external opening, anterior to this line,
originates from the nearest anal crypt in a radial direction.
Incarcerated inguinal hernia: structures in the hernia sac
still have a good blood supply but are stuck in the sac because of
adhesions or a narrow neck of the hernia sac. Strangulated inguinal
hernia: hernia structures have a compromised blood supply because of
anatomic constriction at the neck of the hernia.
Chvostek’s sign is spasm of the facial muscles caused by
tapping the facial nerve trunk. Trousseau’s sign is carpal spasm
elicited by occlusion of the brachial artery for 3 minutes with a blood
pressure cuff.
The two surgical options for Graves’ disease are subtotal
thyroidectomy or near-total thyroidectomy.
The only biochemical test that is routinely needed to
identify patients with unsuspected hyperthyroidism is serum
thyroid-stimulating hormone concentration.
The surgically correctable causes of hypertension are
renovascular hypertension, pheochromocytoma, Cushing’s syndrome,
primary hyperaldosteronism, coarctation of the aorta, and unilateral
renal parenchymal disease.
The “triple negative test” or “diagnostic triad” for
diagnosing a palpable breast mass includes physical examination, breast
imaging, and biopsy.
Chest wall radiation is indicated after mastectomy in
patients with greater than 5 cm primary cancers, positive mastectomy
margins, or more than four positive lymph nodes, all of which are
associated with heightened locoregional recurrence rates.
Sentinel lymph nodes are the first stop for tumor cells
metastasizing through lymphatics from the primary tumor.
The most common site of origin of subungual melanomas is
the great toe. Amputation at or proximal to the metatarsal phalangeal
joint and regional sentinel lymph node biopsy are advised by most
authors.
Ramus marginalis mandibularis, the lowest branch of the
nerve that innervates the depressor muscles of the lower lip, is the
most commonly injured facial nerve branch during parotidectomy.
Waldeyer’s ring is the mucosa of the posterior oropharynx
covering a bed of lymphatic tissue that aggregates to form the
palatine, lingual, pharyngeal, and tubal tonsils. These structures form
a ring around the pharyngeal wall. This may be the site of primary or
metastatic tumor.
A patient in whom the head and neck examination is
completely normal but FNA of a cervical node reveals squamous cancer
should have examination of the mouth, pharynx, larynx, esophagus, and
tracheobronchial tree under anesthesia (triple endoscopy). If nothing
is seen, blind biopsy of the nasopharynx, tonsils, base of tongue, and
pyriform sinuses should be done at the same sitting.
The microorganisms implicated in atherosclerosis include Chlamydia
pneumoniae, Helicobacter pylori, streptococci, and Bacillus
typhosus.
The cumulative 10-year amputation rate for claudication is
10%.
The absolute reduction in risk of stroke is 6% over a
5-year period in asymptomatic patients with > 60% stenosis who
undergo carotid endarterectomy plus aspirin versus patients treated
with aspirin alone (5.1% versus 11%).
Abdominal aortic aneurysm’s average expansion rate is 0.4
cm/year.
Heparin binds to antithrombin III, rendering it more
active.
The patient with suspected intermittent claudication should
initially be evaluated by obtaining ankle brachial index or segmental
limb pressures at rest.
Shock is suboptimal consumption of O₂ and
excretion of CO₂ at the cellular level.
Nitric oxide is synthesized in vascular endothelial cells
by constitutive nitric oxide synthase and inducible NOS, using arginine
as the substrate.
Saliva has the hightest potassium concentration (20 mEq),
followed by gastric secretions (10 mEq), then pancreatic and duodenal
secretions (5 mEq).
Basal caloric expenditure = 25 kcal/kg/day with a
requirement of approximately 1 g protein/kg/day.
6.25 g of protein contains 1 g of nitrogen.
Dextrose has 3.4 kcal/g, protein 4 kcal/g, fat 9 kcal/g
(20% lipid solution delivers 2 kcal/mL).
Maximal glucose infusion rates in parenteral formulas
should not exceed 5 mg/kg/min.
Refeeding syndrome occurs in moderately to severely
malnourished patients (e.g., chronic alcoholism or anorexia nervosa)
who, upon presentation with a large nutrient load, develop clinically
significant decreases in serum phosphorus, potassium, calcium, and
magnesium levels. Hyperglycemia is common secondary to blunted insulin
secretion. ATP production is mitigated, and the classic presentation is
respiratory failure.
Glutamine is the most common amino acid found in muscle and
plasma. Levels decrease after surgery and physiologic stress. Glutamine
serves as a substrate for rapidly replicating cells (interestingly, it
is also the number one metabolic substrate for neoplastic cells),
maintains the integrity and function of the intestinal barrier, and
protects against free radical damage by maintaing GSH levels. Glutamine
is unstable in IV form unless linked as a dipeptide.
Fever is caused by activated macrophages that release
interleukin-1, tumor necrosis factor, and interferon in response to
bacteria and endotoxin. The result is a resetting of the hypothalamic
thermoregulatory center.
Cardiac output = heart rate x stroke volume; normal CO is
5-6 L/min.
SVR = [(MAP - CVP)/CO] x 80; normal SVR is 800-1200
dyne.sec/cm^-5.
Hypovolemic shock: low CVP and PCWP, low CO and SVO₂,
high SVR.
Cardiogenic shock: high CVP and PCWP, low CO and SVO₂,
variable SVR.
Septic shock: low or normal CVP and PCWP, high CO
initially, high SVO₂, low SVR.
Kehr’s sign is concurrent LUQ and left shoulder pain,
indicating diaphragmatic irritation from a ruptured spleen or
subdiaphragmatic abscess. Anatomically, the diaphragm and the back of
the left shoulder enjoy parallel innervation.
Rebound tenderness implies peritoneal inflammation and
irritation not simply abdominal tenderness.
The 5 Ws of post-operative fever are wound
(infection), water (UTI), wind (atelectasis,
pneumonia), walking (thrombophlebitis), and wonder
drugs (drug fevers).
Cricothyroidotomy should not be performed in
patients < 12 years old or any patient with suspected direct
laryngeal trauma or tracheal disruption.
The radial (wrist) pulse estimates SBP > 80 mmHg;
femoral (groin) pulse estimates SBP > 70 mmHg; and carotid (neck)
pulse estimates SBP > 60 mmHg.
A general rule for crystalloid infusion to replace blood
loss is a 3:1 ratio of isotonic crystalloid to blood.
Raccoon eyes (periorbital ecchymosis) and Battle’s sign
(mastoid ecchymosis) are clinical indicators of basilar skull fracture.
CPP = MAP – ICP. Some debate exists on the minimum
allowable CPP, but consensus indicates that a cerebral perfusion
pressure of 50-70 mmHg is necessary.
Violation of the platysma defines a penetrating neck wound.
Tension pneumothorax is air accumulation in the pleural
space eliciting increased intrathoracic pressure and resulting in a
kinking of the SVC and IVC that compromises venous return to heart.
The most common site of thoracic aortic injury in blunt
trauma is just distal to the take-off of the left subclavian artery.
The most common manifestation of blunt myocardial injury is
arrhythmia.
Indications for thoracotomy in a stable patient with
hemothorax include an immediate tube thoracostomy output of > 1500
mL and ongoing bleeding of 250 mL/h for 4 consective hours.
Beck’s triad is hypotension, distended neck veins, and
muffled heart sounds.
The hepatic artery supplies approximately 30% of blood flow
to the liver while the portal vein supplies the remaining 70%. The
oxygen delivery, however, is similar for both at 50%.
The Pringle maneuver is a manual occlusion of the
hepatoduodenal ligament to interrupt blood flow to the liver.
Splenectomy significantly decreases IgM levels.
90% of trauma fatalities due to pelvic fractures are due to
venous bleeding and bone oozing; only 10% of fatal pelvic bleeding from
blunt trauma is arterial (most common site is superior gluteal artery).
Intraperitoneal bladder rupture from blunt trauma:
operative management; extraperitoneal rupture: observant management.
Pseudoaneurysm is a disruption of the arterial wall leading
to a pulsatile hematoma contained by fibrous connective tissue (but not
all three arterial wall layers, which defines a true aneurysm).
The earliest sign of lower extremity compartment syndrome
is neurologic in the distribution of the peroneal nerve with numbness
in the first dorsal webspace and weak dorsiflexion.
Posterior knee dislocations are associated with popliteal
artery injuries and are an indication for angiography.
Management of suspected navicular fracture despite negative
radiography is short-arm cast and repeat x-ray in 2 weeks; at high risk
for avascular necrosis.
Parkland formula: lactated Ringer’s at 4 mL/kg x %TBSA
(second- and third-degree only) of burn. Infuse 50% of volume in first
8 hours and the remaining 50% over the subsequent 16 hours.
The metabolic rate peaks at 2.5 times the basal metabolic
rate in severe burns > 50% TBSA.
Gallstones and alcohol abuse are the two main causes of
acute pancreatitis.
Alcohol abuse accounts for 75% of cases of chronic
pancreatitis.
Isolated gastric varices and hypersplenism indicate splenic
vein thrombosis and are an indication for splenectomy.
The treatment for gallstone pancreatitis is cholecystectomy
and intraoperative cholangiogram during the same hospital stay once the
pancreatitis has subsided.
Proton pump inhibitors irreversibly inhibit the parietal
cell hydrogen ion pump.
Definitive treatment of alkaline reflux gastritis after a
Billroth II includes a Roux-en-Y gastro-jejunostomy from a 40-cm
efferent jejunal limb.
Cushing’s ulcer is a stress ulcer found in critically ill
patients with central nervous system injury. It is typically single and
deep, with a tendency to perforate.
Curling’s ulcer is a stress ulcer found in critically ill
patients with burn injuries.
Marginal ulcer is an ulcer found near the margin of
gastroenteric anastomosis, usually on the small bowel side.
The most common cause of small bowel obstructions is
adhesive disease; the second most common cause is hernias.

Neck Masses

admin — Thu, 09 Jul 2009 18:31:09 +0000

67 NECK MASSES
Nathan W. Pearlman M.D.

1. What causes lumps in the neck?

Show answer
Enlarged lymph nodes, benign or malignant tumors, congenital abnormalities, and normal anatomy.

2. Can neck masses be part of normal anatomy?

Show answer
Yes. In some patients, the neck mass is nothing more than a submaxillary gland or omohyoid muscle that has become prominent with aging and loss of surrounding fat. This finding usually is apparent if the other side of the neck is carefully examined.

3. A 34-year-old man presents with a 2-3-cm mass just below the angle of the mandible. What are the likely causes?

Nonspecific lymphadenopathy	Branchial cleft cyst
Infectious mononucleosis	Submaxillary or parotid gland tumor
Intraoral infection	Lymphoma
Carotid body tumor	Metastatic carcinoma

4. Doesn’t this patient seem awfully young for metastatic cancer?

Show answer
Yes, but it still occurs in this age group, particularly thyroid, tongue, and nasopharyngeal cancer.

5. This is a long list. Is there any way to narrow it?

Show answer

* Inflammatory nodes and nodes of mononucleosis are mildly tender, relatively soft, bilateral (one side may be more symptomatic than the other) of recent onset. They generally are < 3 cm in diameter, the patient usually reports a history of a systemic illness, and the skin over the tender nodes is normal.
* Lymphadenopathy caused by intraoral infection is also of recent onset but exquisitely painful, indurated, and unilateral; the overlying skin is often erythematous.
* Carotid body tumors may be tender and unilateral but are long standing, more rubbery than infectious nodes, and cannot be separated from the carotid pulse.
* A branchial cleft cyst is unilateral, relatively soft, nontender, and long standing; it also transilluminates.
* Nodes of lymphoma are nontender and have the consistency of the submaxillary gland. They may be unilateral or bilateral and of recent onset or several months' duration. In addition, signs of systemic illness may or may not be present.
* Submaxillary or parotid tumors are rubbery and nontender and occupy the position of the contralateral gland.
* Lymphadenopathy caused by metastatic cancer is hard, nontender, and often larger than 3-4 cm.
* Tuberculosis can mimic all of these conditions.

6. Why not just remove the mass or lymph node and see what it is?

Show answer
Open biopsy can unduly complicate further management when it is the initial diagnostic maneuver. If lymphoma or an unusual infection is present but not suspected, the node may be mishandled when sent to the pathology or microbiology departments. If metastatic cancer is the problem, the scar tissue created by the biopsy may be difficult to distinguish from tumor on computed tomography (CT) or magnetic resonance imaging (MRI), leading to inaccurate staging. The scar also may resemble cancer at subsequent surgery, potentially resulting in a larger operation than originally needed. A better choice for histologic diagnosis is fine-needle aspiration (FNA), which is 95% accurate and avoids the problems of open biopsy.

7. A complete head and neck examination shows nothing abnormal, but FNA of the node reveals squamous cancer. What should be done next?

Show answer
Examination of mouth, pharynx, larynx, esophagus, and tracheobronchial tree under anesthesia (triple endoscopy) should be done. If nothing is seen, blind biopsy of the nasopharynx, tonsils, base of tongue, and pyriform sinuses should be done at the same sitting.
KEY POINTS: DIFFERENTIAL DIAGNOSIS OF NECK MASSES

1. Enlarged lymph nodes
2. Benign or malignant tumors
3. Congenital abnormalities
4. Normal anatomy (e.g., submaxillary gland or omohyoid muscle that has become prominent with age)

8. Isn’t this a bit much?

Show answer
No. The squamous cancer came from somewhere, and the most likely site is somewhere in the region (e.g., mouth, pharynx). In approximately 15% of patients, the primary tumor is detected at triple endoscopy when it cannot be found on office examination, and another 10% of patients are found to have a synchronous second primary tumor elsewhere in the aerodigestive tract.

9. Why not just start with triple endoscopy and skip all the other folderol?

Show answer
Examination with the patient awake provides information about tongue and laryngeal function that cannot be obtained when the patient is asleep, and treatment planning depends on such knowledge. In addition, examination under anesthesia may be a blind search because of collapse of the tongue and pharynx, unless directed by findings while the patient is awake.

10. Should CT scan or MRI be used?

Show answer
Both modalities may provide information about areas difficult to evaluate by physical examination, such as the base of the skull, and are helpful in staging if cancer is present. However, they do not replace the measures already outlined.

11. We do all that and still can’t find a primary tumor. What now?

Show answer
Two options exist. Most surgeons would treat the patient with a functional or modified radical neck dissection and postoperative irradiation to the neck and likely site of the primary tumor. Alternatively, one may proceed with irradiation alone to the neck and likely primary site, with neck dissection at a later date if the enlarged node or nodes persist after treatment.

12. What if the primary tumor never shows up? Does this influence prognosis?

Show answer
No. Prognosis is determined by the presence of metastatic neck disease, not by whether a small primary tumor is or is not found.

13. If the mass or enlarged node is in the posterior triangle of the neck, is the work-up still the same?

Show answer
Yes. Although most oral or pharyngeal tumors spread first to nodes in the anterior triangle, it is not uncommon for naso- or hypopharyngeal tumors, thyroid cancers, and lymphomas to present as enlarged nodes in the posterior triangle.

14. What if FNA of the node reveals only lymphocytes or shows adenocarcinoma?

Show answer
The presence of lymphocytes most likely represents inflammation or lymphoma; however, if the “node” is just below the ear lobe, it may be a Warthin’s tumor (cystadenoma-lymphomatosa) of the parotid. Adenocarcinoma found on FNA usually indicates metastases from thyroid cancer or a primary site below the clavicles, but it may mean salivary gland cancer if the “node” lies high in the anterior triangle. If only lymphocytes are present, excision of the node may be reasonable, as long as it was clearly not in the parotid or submaxillary gland. In the latter case, one should proceed with a parotidectomy or submaxillary gland excision.

15. Lumps in the neck are common, and relatively few patients have cancer. Isn’t this a cost-ineffective approach?

Show answer
No. Most patients with lumps in the neck have benign, self-limiting conditions, which should be apparent on the initial history and physical examination. If there is a question, FNA can be done. Only rarely is removal of the mass indicated for diagnosis or treatment.
On the other hand, if neck lumps are routinely excised to facilitate the work-up (or to see what they are), the physician will constantly be surprised by what is found (e.g., metastatic cancer, lymphoma, tuberculosis). The work-up outlined above will then have to be undertaken anyway-and in a field dirtied by the biopsy. Such a course is not cost effective but, in fact, is a waste of time and resources.

References
WEB SITE
http://www.acssurgery.com
BIBLIOGRAPHY
1. Attie JN, Setzon M, Klein I: Thyroid cancer presenting as an enlarged cervical lymph node. Am J Surg 166:428-430, 1993. Medline Similar articles
2. Lee NK, Byers RM, Abbruzzese JL, Wolfe P: Metastatic adenocarcinoma to the neck from an unknown primary source. Am J Surg 162:306-309, 1991. Medline Similar articles Full article
3. Rice DH, Spiro RH: Metastatic carcinoma of the neck, primary unknown. In Current Concepts in Head and Neck Cancer. Atlanta, American Cancer Society, 1989, pp 126-133. Full article
4. Tarantino DR, McHenry CR, Strickland T, Khiyami A: The role of the fine-needle aspiration biopsy and flow cytometry in the evaluation of persistent neck adenopathy. Am J Surg 176:413-417, 1998. Medline Similar articles Full article