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I. Nissen

360˚ wrap (left crus approach) used when medical management for GERD

fails, severe esophageal injury (ulcer, stricture, or Barrett’s)

- Procedure of choice for patients with normal esophageal motility

- Advantage of direct and early view of short gastrics, spleen

II. Operative -Position: low lithotomy -Surgery: Dissect out left crus and greater curvature. Take down short gastrics

to mobilize fundus. Mobilize left crus and right crus. Open lesser omentum. Preserve anterior and posterior vagi (both contained by wrap). Reapproximate crura posteriorly. Heavy permanent sutures allow passage of 52F bougie. Wrap created length of 2.5-3cm and anchor to esophagus and bilateral crus at hiatus. Anchor anteriorly and posteriorly.

III. Complications -3 – 10% of patients

A. Operative

-Pneumothorax – most common: 5 – 8%. Violation of pleural space by CO2. No need to evacuate gas. Lung will usually expand without incident. Supplemental O2, repeat CXR 2h after operation.

-Gastric/Esophageal Injuries – less common: <1%. Result of overaggressive tissue manipulation or passage of bougie. May be repaired with suture or automatic stapler if identified at time of surgery. If injury not seen at operation, patient will likely need second operation to repair viscus unless the leak is small and contained.

- Liver/Spleen – reported rarely. Careful retraction of left lobe of liver will prevent significant laceration and subcapsular hematomas. Splenic injury usually results from dissection of fundus and greater curvature.

B. Post-operative

-Bloating – complaint of bloating in 30% of patients, <4% after 2 months. Difficulty belching secondary to wrap. Vagal trauma may lead to delayed gastric emptying. Patients have tendency to swallow saliva (unconscious effort to relieve symptoms of reflux) and with this a significant amount of air.

- Dysphagia – 20% of patients. Due to dissection of hiatus or suture placement and handling of esophagus will cause some edema. dysphagia is usually short-lived. If the wrap is too tight, unlikely to resolve without dilation.

Barrett’s Esophagus

-premalignant condition in which abnormal columnar epithelium replaces the

stratified squamous epithelium that normally lines the distal esophagus -most severe histologic consequence of chronic gastroesophageal reflux -predisposes to the development of adenocarcinoma of the esophagus

Epidemiology- usually discovered during endoscopy -mean age of diagnosis is 55 years; 3M>F -can affect children, but rarely before age 5 (and thus supports an acquired

condition vs. a congenital one) -10-15% Barrett’s are found during endoscopy for symptoms of GERD -uncommon in African Americans and Asians -prevalence in Hispanics is similar to Caucasians -prevalence in the general population is variable -risk factors: male, white, smoker

Clinical Features- columnar metaplasia in Barrett’s esophagus causes no symptoms -most patients are seen initially for symptoms of GERD (heartburn, regurgitation, dysphagia) -GERD associated with Barrett’s esophagus is frequently complicated by esophageal ulceration/perforation, stricture, shortening and hemorrhage -histologically, 3 different types of columnar epithelia in Barrett’s: -specialized intestinal metaplasia (villiform surface and intestinal-type

crypts lined by mucous-secreting columnar cells and goblet cells -gastric fundic-type epithelium -junctional-type epithelium

-specialized intestinal metaplasia is the most common, and likely associated with dysplasia and carcinoma

Diagnosis- sensitivity of endoscopy in detecting Barrett’s is related to the length of

involved mucosa (long segment Barrett’s) -overall reliability of endoscopy for detection of Barrett’s is ~ 80% -controversy regarding diagnostic criteria for Barrett’s (no reproducible anatomic

landmarks that clearly delimit the esophagus-GEJ or squamocolumnar junction)

-3 terms describing the specialized intestinal metaplasia in the esophagus: -long segment Barrett’s (range 2-5 cm, but 3 cm is the accepted cutoff) -short segment Barrett’s (less than 3 cm), more prevalent -junctional intestinal metaplasia (squamocolumnar junction=GEJ)

-long segment has a higher risk of dysplasia and adenocarcinoma

Treatment- endoscopic surveillance is the current recommendation -reflux control with antireflux procedure to prevent mucosal damage prn -if confirmed high grade dysplasia or cancer, esophagectomy is recommended -other procedures with less success: laser ablation, photodynamic therapy,

mucosectomy, argon plasma coagulation

1. What is the differential diagnosis of a solitary lung mass in a middle aged smoker?

Schwartz’s Principles of Surgery – 8th Ed. (2005)

In nonselected patient populations, a new solitary pulmonary nodule observed on a chest radiograph has a 20 to 40% likelihood of being malignant, with the risk approximating 50% or higher for smokers. The remaining causes of pulmonary nodules are numerous benign conditions. Infectious granulomas arising from a variety of organisms account for 70 to 80% of this type of solitary nodule; hamartomas are the next most common single cause, accounting for about 10%. The differential diagnosis of a solitary pulmonary nodule should include a broad variety of congenital, neoplastic, inflammatory, vascular, and traumatic disorders. The initial assessment of a pulmonary nodule should proceed from a clinical history and physical examination. Risk factors for malignancy include a history of smoking, prior neoplastic disease, hemoptysis, and age over 35 years.

1. What is the CPIS (clinical pulmonary infection score) for diagnosing ventilator associated pneumonia?

ACS Surgery: Principles & Practice (2006)

The CPIS quantifies a number of clinical findings suggestive of pneumonia—temperature, WBC count, tracheal secretions, tracheal cultures, oxygenation, chest x-rays, and the presence of and progression of infiltrates on x-rays—in an attempt to diagnose pneumonia noninvasively.

LoadingA CPIS higher than 6 is associated with a high likelihood of pneumonia, and there is a clear correlation between a high CPIS and a high concentration of bacteria found with invasive culture techniques. The main use of the CPIS is as a method of defining the probability of pneumonia in a given patient that is more objective than clinical judgment alone. A patient with a low CPIS probably need not be treated for pneumonia, whereas one with a high CPIS is likely to benefit from invasive culturing, followed by rapid institution of broad-spectrum antibiotic therapy. The main drawbacks of the CPIS are (1) that all of its elements are weighted equally (for example, the presence of an infiltrate is given the same weight as a WBC count of 11,000/mm³, even though it is substantially more suggestive of pneumonia) and (2) that assessment of chest x-rays and sputum production is necessarily subjective, meaning that an equivocal CPIS could lead to an inappropriate treatment decision.

1. What are the causes of a spontaneous pneumothorax?

Schwartz’s Principles of Surgery – 8th Ed. (2005)

Spontaneous pneumothorax is secondary to intrinsic abnormalities of the lung, and the most common cause is rupture of an apical subpleural bleb. The cause of these blebs is unknown, but they occur more frequently in smokers and males, and they tend to predominate in young postadolescent males with a tall thin body habitus.
Other causes are emphysema (rupture of a bleb or bulla), cystic fibrosis, AIDS, metastatic cancer (especially sarcoma), asthma, lung abscess, and occasionally lung cancer. Management of pneumothorax in these circumstances is often tied to therapy of the specific disease process; in uncomplicated cases a simple thorascopic bleb resection and pleurodesis will suffice; more complicated cases or recurrences post pleurodesis may involve tumor resection, thoracoscopic pleurectomy, or talc pleurodesis.

1. What is the minimal amount of FEV₁ a patient would need for postoperative lung function? Why is this so?

Townsend: Sabiston Textbook of Surgery, 17th ed.

Pulmonary function testing measures the lung volumes and mechanical properties of lung elasticity, recoil, and compliance. It also evaluates gas exchange functions. Occasionally, the combined measurement of the cardiorespiratory axis serves as a more appropriate study to assess the patient’s physiologic reserve. The predicted postoperative forced expiratory volume in 1 second (FEV₁) is the most common and important predictor of postoperative pulmonary reserve. Typically, this should be greater than 0.8 L. FEV₁ may be expressed as an actual value, such as 0.9 L/sec, or as a percentage, such as 68% of that predicted. The predicted value is based on height and weight in normal patients. In addition, FEV₁ of less than 0.8 L/min suggests an increased risk of postoperative pulmonary morbidity. Patients with an FEV₁ of less than 0.5 liter have the greatest risk of postoperative pulmonary complications. [NB this is likely due to poor coughing ability postop]

1. How does non-small cell lung cancer present?

Schwartz’s Principles of Surgery – 8th Ed. (2005)

Tumors in the NSCLC group include squamous cell carcinoma, adenocarcinoma (including bronchoalveolar carcinoma), and large-cell carcinoma. Although they differ in appearance histologically, their clinical behavior and treatment is similar. As such, they are usefully thought of as a uniform group.

Squamous cell carcinoma is primarily located centrally and arises in the major bronchi, often causing the typical symptoms of centrally-located tumors, such as hemoptysis, bronchial obstruction with atelectasis, dyspnea, and pneumonia. Central necrosis is frequent and may lead to the radiographic findings of a cavity (possibly with an air-fluid level). Such cavities may become infected, with resultant abscess formation.

In contradistinction to squamous cell carcinoma, adenocarcinoma is most often a peripherally-based tumor, thus it is frequently discovered incidentally on routine chest radiographs. Symptoms of chest wall invasion or malignant pleural effusions dominate. Bronchoalveolar carcinoma and large-cell carcinoma share similar characteristics with squamous cell and adenocarcinoma.

1. What is the most common etiology and location of a lung abscess?

Schwartz’s Principles of Surgery – 8th Ed. (2005)

Lung abscess is the result of a lower respiratory tract infection only by organisms that cause necrosis. Microorganisms gain access to the respiratory tract via inhalation of aerosolized particles, aspiration of oropharyngeal secretions, or hematogenous spread from distant sites. Direct extension from a contiguous site is less frequent. Most primary lung abscesses are suppurative bacterial infections secondary to aspiration. Normal oropharyngeal secretions contain many more Streptococcus species and more anaerobes (about 10⁸ organisms/mL) than aerobes (about 10⁷ organisms/mL). Pneumonia that follows from aspiration, with or without abscess development, is typically polymicrobial. An average of two to four isolates present in large numbers have been cultured from lung abscesses sampled percutaneously. Overall, at least 50% of these infections are caused by purely anaerobic bacteria, 25% are caused by mixed aerobes and anaerobes, and 25% or fewer are caused by aerobes only.

1. What are three causes of hemopytsis?

Townsend: Sabiston Textbook of Surgery, 17th ed.

• Lung cancer
• Lung abscess
• Cavitary aspergillosis
• Tuberculosis
• Bronchiectasis
• Swan-Ganz catheterization
• Cystic fibrosis
• Broncholithiasis
• Foreign body
• Transbronchial lung biopsy
• Tuberculosis

1. Discuss the management of empyema. What is the timing of surgery?

Townsend: Sabiston Textbook of Surgery, 17th ed.

Treatment of empyema is dependent on its phase but involves the identification and systemic treatment (antibiotics) of the causative organism and complete drainage of the pleural space. In the acute and early fibrinopurulent phases, complete thoracentesis can be both diagnostic and therapeutic if the effusion is drained entirely. The prior administration of antibiotics may lead to a sterile tap, but Gram stain, cell count , chemistries (protein, LDH, amylase, and glucose), and pH (<7.3) all can be useful in making the diagnosis.

Tube thoracostomy may be indicated for pleural drainage if thoracentesis fails or the empyema has progressed beyond its earliest stages. Chest tube insertion, however, can be ineffective if the empyema has become loculated or organized. VATS empyema drainage with early pleural débridement has the added advantage of more complete pleural drainage by visualizing and breaking down loculations. Occasionally, radiologically guided catheter drainage can be a useful adjunct to these surgical procedures. Thoracotomy with débridement or formal decortication in later-stage empyema is reserved for treatment failures with persistent sepsis.

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1. What are the stages of hemorrhagic shock?

Trauma – 5th Ed. (2004),

The clinical and physiologic response to hemorrhage has been classified according to the magnitude of volume loss. Loss of up to 15% of the circulating volume (700 to 750 mL for a 70-kg patient) may produce little in terms of obvious symptoms while loss of up to 30% of the circulating volume (1.5 L) may result in mild tachycardia, tachypnea, and anxiety. Hypotension, marked tachycardia (pulse > 110 to 120 beats/min) and confusion may not be evident until more than 30% of the blood volume has been lost, while loss of 40% of circulating volume (2 L) is immediately life-threatening. Young healthy patients with vigorous compensatory mechanisms may tolerate larger volumes of blood loss while manifesting fewer clinical signs despite significant peripheral hypoperfusion being present. These patients may maintain a near-normal blood pressure until a precipitous cardiovascular collapse occurs. Elderly patients may be taking medications that either promote bleeding (warfarin, aspirin) or mask the compensatory response to hypovolemia (beta blockers). In addition, atherosclerotic vascular disease, diminished cardiac compliance with age, inability to elevate heart rate or cardiac contractility in response to hemorrhage, and overall decline in physiologic reserve decrease the elderly patient’s ability to tolerate hemorrhage.

1. What are the hemodynamic changes associated with septic shock?

Current Critical Care Diagnosis & Treatment – 2nd Ed. (2003)

The distinguishing hemodynamic features of septic shock are elevated cardiac output, decreased systemic vascular resistance, and decreased blood pressure. Tachycardia is partially responsible for maintaining the blood pressure. [NB the ventricles become dilated so as to increase output according to the Frank-starling curve, this is how the heart compensates for the myocardial depression that septic mediators often cause]. More recent investigations have shown that cardiac output remains elevated until decreased output develops as a preterminal event. A normal or elevated mixed venous oxygen saturation and decreased arterial-venous oxygen content difference is present.

1. What are the hemodynamic changes associated with cardiogenic shock?

Schwartz’s Principles of Surgery – 8th Ed. (2005)

Emergency Medicine: A Comprehensive Study Guide – 6th Ed.

Hemodynamic criteria include sustained hypotension, reduced cardiac index (< 2.2 L/min per square meter), and elevated pulmonary artery wedge pressure (> 15 mm Hg). Clinical signs of cardiogenic shock include evidence of poor CO with tissue hypoperfusion (hypotension, mental status changes, cool mottled skin) and evidence of volume overload (jugular venous distention, rales, and an S₃ gallop).

1. What are the hemodynamic changes associated with hypovolemic shock?

Harrison’s Principles of Internal Medicine – 16th Ed. (2005)

Reduced cardiac output and a compensatory sympathetic mediated response characterized by tachycardia and elevated systemic vascular resistance.

1. A 30 y.o. pt. arrives s/p fall from a tree. He is noted to be hypotensive on arrival. Invasive hemodynamic monitoring shows him to have a CVP of 1 mm Hg (nl 2-8 mm Hg), a cardiac output of 3 L/min (nl 4-6 L/min), an SVR of 450 dyne/sec/cm-5 (nl 900-1200 dyne/sec/cm-5), and a mixed venous oxygen saturation of 55% (nl 70-80%). Characterize his shock state.

Schwartz’s Principles of Surgery – 8th Ed. (2005)

Neurogenic Shock – Loss of vasoconstrictor impulses results in increased vascular capacitance, decreased venous return, and decreased cardiac output. Neurogenic shock is usually secondary to spinal cord injuries from vertebral body fractures of the cervical or high thoracic region that disrupt sympathetic regulation of peripheral vascular tone. Rarely, a spinal cord injury without bony fracture, such as an epidural hematoma impinging on the spinal cord, can produce neurogenic shock. Sympathetic input to the heart, which normally increases heart rate and cardiac contractility, and input to the adrenal medulla, which increases catecholamine release, may also be disrupted, preventing the typical reflex tachycardia that occurs with hypovolemia. Acute spinal cord injury results in activation of multiple secondary injury mechanisms: (1) vascular compromise to the spinal cord with loss of autoregulation, vasospasm, and thrombosis, (2) loss of cellular membrane integrity and impaired energy metabolism, and (3) neurotransmitter accumulation and release of free radicals. Importantly, hypotension contributes to the worsening of acute spinal cord injury as the result of further reduction in blood flow to the spinal cord. Management of acute spinal cord injury with attention to blood pressure control, oxygenation, and hemodynamics, essentially optimizing perfusion of an already ischemic spinal cord, seems to result in improved neurologic outcome. Patients with hypotension from spinal cord injury are best monitored in an intensive care unit, and carefully followed for evidence of cardiac or respiratory dysfunction.

1. When should a pulmonary artery wedge pressure be recorded? Is it any different in a ventilated versus a non-ventilated patient?

Emedicine

The timing of PCWP measurement is critical because intrathoracic pressures can vary widely with inspiration and expiration and are transmitted to the pulmonary vasculature. During spontaneous inspiration, the intrathoracic pressures decrease (more negative); during expiration, intrathoracic pressures increase (more positive). Positive pressure ventilation (eg, in an intubated patient) reverses this situation. To minimize the effect of the respiratory cycle on intrathoracic pressures, measurements are obtained at end-expiration, when intrathoracic pressure is closest to zero. [NB this is the same in ventilated and non-ventilated patients. The difference is how the pressure tracing looks].

1. What are some indications for placement of a pulmonary artery catheter?

Emedicine, Uptodate.com – Swan-Ganz catheterization: Indications and complications.

No study has definitively demonstrated improved outcome in critically ill patients managed using pulmonary artery catheters. Thus, the accepted indications for pulmonary artery catheterization have been generated largely on the basis of expert opinion. Fundamentally, the decision to place a Swan-Ganz catheter should be based on a specific question regarding a patient’s hemodynamic status that cannot be satisfactorily answered by clinical or noninvasive assessment; if the answer could change management, then placement of the catheter is indicated [NB remember this principle for the ABSITE!] Common indications are listed

· Diagnosis of shock states

· Differentiation of high- versus low-pressure pulmonary edema

· Diagnosis of primary pulmonary hypertension (PPH)

· Diagnosis of valvular disease, intracardiac shunts, cardiac tamponade, and pulmonary embolus (PE)

· Monitoring and management of complicated AMI

· Assessing hemodynamic response to therapies

· Management of multiorgan system failure and/or severe burns

· Management of hemodynamic instability after cardiac surgery

· Assessment of response to treatment in patients with PPH (Primary pulmonary hypertension)

1. What are some indicators of endpoints of resuscitation? What are their benefits

and drawbacks?

Schwartz’s Principles of Surgery – 8th Ed. (2005)

Lactate – Elevated serum lactate is an indirect measure of the oxygen debt, and therefore an approximation of the magnitude and duration of the severity of shock. The admission lactate level, highest lactate level, and time interval to normalize the serum lactate are important prognostic indicators for survival.

Base deficit - Base deficit can be stratified into mild (3 to 5), moderate (6 to 14) and severe (≥15) categories, with a trend toward higher mortality with worsening base deficit in patients with trauma. Both the magnitude of the perfusion deficit as indicated by the base deficit and the time required to correct it are major factors determining outcome in shock. [NB Both lactate and base deficit are global measures of perfusion, and thus may miss regional hypoperfusion. They may be confounded by underlying organ dysfunction as well, and may not fully reflect the oxygen debt of underlying tissue. Nevertheless, they are useful indetermining both response and mortality]

Gastric tonometry – Goal-directed human studies, with gastric mucosal pH (pHi) as an endpoint in resuscitation, have shown normalization of pHi to correlate with improved outcome in several studies, and with contradictory findings in other studies. Utility of pHi as a singular endpoint in the resuscitation of critically-ill patients remains controversial.

Tissue pH, oxygen, carbon dioxide levels – Tissue probes with optical sensors have been used to measure tissue pH and partial pressure of oxygen and carbon dioxide in subcutaneous sites, muscle, and the bladder. These probes may utilize transcutaneous methodology with Clark electrodes or direct percutaneous probes. The percutaneous probes can be inserted through an 18-gauge catheter and hold promise as continuous monitors of tissue perfusion.

Near infrared spectroscopy – Trauma patients with decoupled oxyhemoglobin and cytochrome a,a₃ have redox dysfunction and have been shown to have a higher incidence of organ failure (89 vs. 13%). Not widely used in clinical practice

1. How do you calculate oxygen delivery? Systemic vascular resistance?

Current Critical Care Diagnosis & Treatment – 2nd Ed. (2003)

The delivery of oxygen is dependent upon the quantity of oxygen present in the blood and the cardiac output. The oxygen content, is calculated as follows:

. Multiply by cardiac output to get oxygen delivery. The last term is often negligible.

Systemic Vascular resistance is calculated as follows:

1. Where on the EKG tracing should the CVP be measured? Where should the pulmonary artery wedge pressure be measured?

1. What is the blood supply of the stomach:

a. Celiac trunk: left gastric, hepatic, and splenic arteries.

b. Right gastric artery branch of the gastroduodenal artery or common hepatic artery /

c. Right gastroepiploic artery branch of the gastroduodenal artery branch of the common hepatic artery.

d. Left gastroepiploic artery branch of the splenic artery.

2. What is the location of the maximal parietal mass In the stomach?

Body followed by the fundus.

3. What is the criminal nerve of Grassi?

It is a branch of the right (posterior) vagal trunk that enters the fundus. Called this because sometimes overlooked in a vagotomy leading to recurrence of ulcer.

4. What are the various types of vagotomies and the physiology on the stomach?

a. Truncal vagotomy: division ot the right and left vagal trunks at the level of the esophagus ((level at the diaphragm hiatus).

b. Selective vagotomy: divides the nerves of Latarjet preserves the celiac and hepatic trunks.

c. Highly selective vagotomy: divides individual fibers, preserves the crow’s foot.

d. Vagal denervaton: all forms increases emptying of liquids (vagally mediated receptive relaxation and accommodation of the stomach is lost, leading to increase gastric pressure.

e. Complete vagotomy (complete or selective) decreases the emptying of solids.

f. Highly selective vagotomy normal emptying of solids, normal or increase emptying of liquids.

5. What is the treatment of a perforated gastric ulcer:

a. Patient is hemodynamically unstable: exploratory laparotomy, Graham patch, will requires biopsy of the ulcer.

b. Hemodynamically stable patient: Graham patch and highly selective vagotomy if patient has already received PPI therapy, biopsy the ulcer.

6. Treatment of a perforated duodenal ulcer? Graham patch.

7. What are the endoscopic signs that show increase risk of rebleeding?

a. Visible vessel in the clot.

b. Gross bleeding

c. Adherent clot without oozing

8. How to you treat intractable bile gastritis following Billroth II?

Conversion to a Roux-en-Y gastrojejunostomy with an afferent limb of 60 cm distal to the original gastrojejunostomy.

9. How do you treat gastric Maltoma:

Treat for H. Pylori 970 to 100%} regress if it does not may need chemotherapy (CHOP).

10. How do you treat gastric GIST tumor?

Surgical therapy The role of surgery in the treatment of a GIST is to resect the tumor with grossly negative margins and an intact pseudocapsule. Lymph node involvement is rare with GISTs, and thus, no effort is made to perform ELND. The tumor must be handled with care to prevent intra-abdominal rupture. Formal gastric resection is rarely required: as a rule, it is indicated only for lesions in close proximity to the pylorus or the esophagogastric junction.

Nonsurgical therapy If the tumor has metastasized or has advanced locally to the point where surgical therapy would result in excessive morbidity, the patient is treated with the tyrosine kinase inhibitor imatinibmesylate. (Gleevac) Imatinib is a selective inhibitor of a family of protein kinases that includes the KIT-receptor tyrosine kinase, which is expressed in the majority of GISTs. Originally indicated for the treatment of chronic myelocytic leukemia, imatinib was approved for the treatment of KIT-positive GIST in 2002, when phase II clinical trials documented sustained objective responses in a majority of patients with advanced unresectable or metastatic GIST. Patients with borderline resectable lesions should be treated with imatinib until they exhibit a maximal response as documented by CT and positron emission tomography (PET); surgery may then be undertaken to resect any residual foci of disease. Similarly, whereas patients with metastatic disease are unlikely to manifest a complete response to imatinib therapy, they should be periodically reevaluated and considered for resection should surgical treatment become technically feasible.

After an R0 resection of a GIST, no adjuvant therapy is indicated unless the patient is participating in a clinical trial. The American College of Surgeons Oncology Group is currently conducting two trials of imatinib in the postoperative setting. A phase II trial (Z9000) of imatinib, 400 mg/day, for patients with high-risk GIST, has reached accrual, and a phase III trial (Z9001) comparing 1 year of imatinib, 400 mg/day, with placebo in patients with intermediate-risk GIST is currently under way.

Gastric Carcinoid

11. What is the treatment choice for a 35 cm old female with BMI of 55 and associated co-morbilities such as DM and HTN?

Long limb gastric bypass surgery.

12. What are the indications for bariatric surgery? (data from 1991 NIH consensus conference)

a. BMI35-40 with significant obesity related comorbidities such as diabetes, sleep apnea, hypertension or degenerative joint disease

b. BMI equal or greater than 40.

13. What are the risk factors for gastric cancer?

a. Previous gastric resection.

b. Nitrosamines.

c. Smoked fumes.

d. Menetrier’s disease

e. Pernicious anemia.

f. Adenomatous polyps.

g. Blood type A.

h. Atrophic gastritis.

14. How to you treat early gastric cancer?

The current recommendation (at least according to the gurus who write ACS Surgery 2006) is to perform a subtotal gastrectomy with Billroth II reconstruction for tumors of the distal stomach, a total gastrectomy with Roux-en-Y esophagojejunostomy for most cancers of the fundus and the proximal stomach and either a transthoracic esophagogastrectomy or a transhiatal esophagogastrectomy with gastric interposition for tumors of the esophagogastric junction and the cardia. This assumes the lesion is resectable. Although there is conflicting evidence regarding the utility of an extended lyphadenectomy (the so-called D2 resection), most American surgeons do a good D1 nodal dissection taking the perigastric lymph nodes on the greater and lesser curves of the stomach.

15.How do you classify gastric volvulus:

According to the axis around which the stomach rotates, gastric volvulus is classified as follows:

a. Organoaxial: The stomach rotates around an axis that connects the gastroesophageal junction and the pylorus. The antrum rotates in opposite direction to the fundus of the stomach. This is the most common type in both children and adults and is usually associated with diaphragmatic defects. Strangulation and necrosis commonly occur with this type and have been reported in 5-28% of cases.

b. Mesentericoaxial The axis bisects both the lesser and greater curvatures. The antrum rotates anteriorly and superiorly so that the posterior surface of the stomach lies anteriorly. The rotation is usually incomplete and occurs intermittently. Vascular compromise is uncommon. Patients with this type usually present without diaphragmatic defects and usually have chronic symptoms.

c. Combined This is a rare form in which the stomach twists both mesentericoaxially and organoaxially. This form is usually observed in patients with chronic volvulus.

ABSITE Review

1. Describe the technique of gaining control of the renal vessels prior to exploring a perirenal hematoma.

Trauma – 5th Ed. (2004)

Access to the kidneys and ureters is generally obtained by reflecting the colon on either side medially and exposing Gerota’s fascial envelope. While modern descriptions of exposing the injured kidney often involve a discussion of first obtaining vascular control of the renal vessels prior to entering the perirenal hematoma, the important element in this practice is achieving access to the pedicle such that atraumatic vascular clamping can be achieved if significant bleeding is encountered. This can be accomplished through individually dissecting and “looping” the renal vessels through an incision in the posterior peritoneum over the aorta (which can allow access to either the left or right-sided artery and the left-sided vein) or by first reflecting the colon on the side of injury and then obtaining vascular control or access to the pedicle.

1. Describe the technique of renorrhaphy.

Trauma – 5th Ed. (2004)

If renal reconstruction is planned, several steps are generally followed. Following evacuation of the hematoma, the kidney is carefully examined to identify lacerated vessels, the open collecting system, and devitalized parencyhyma. Large areas of lacerated, devitalized parenchyma are excised sharply, with smaller vessels controlled with an absorbable 3-0 or 4-0 suture. In general, an absorbable suture is utilized for intrarenal suturing, as a permanent suture may create a nidus for stone formation if in contact with the collecting system. If adequate closure of the collecting system is achieved, there is no need for stenting or a nephrostomy. If repair of the collecting system is tenuous or incomplete, placement of an internal stent (complemented by a bladder catheter) or a nephrostomy tube may decrease the risk of postoperative urinary extravasation and the formation of a urinoma.

1. What are some indications for a partial nephrectomy?

Smith’s General Urology – 16th Ed. (2004)

Partial nephrectomy is performed in patients with renal lesions and risk for postoperative renal insufficiency (anatomically solitary kidney, bilateral lesions, significant preoperative renal insufficiency) or risk factors for future renal disease [NB in the ABSITE, diabetes has been a classic indicator of this]. In trauma where significant injury has occurred to a specific pole, partial nephrectomy is warranted.

1. How would you treat a gunshot wound to the ureter that completely transected it approx. 5 cm from the renal pelvis?

Smith’s General Urology – 16th Ed. (2004)

Prompt treatment of ureteral injuries is required. If the injury is not recognized until 7-10 days after the event and no infection, abscess, or other complications exist, immediate reexploration and repair are indicated. Proximal urinary drainage by percutaneous nephrostomy or formal nephrostomy should be considered if the injury is recognized late or if the patient has significant complications that make immediate reconstruction unsatisfactory. The goals of ureteral repair are to achieve complete debridement, a tension-free spatulated anastomosis, watertight closure, ureteral stenting (in selected cases), and retroperitoneal drainage.

Lower Ureteral Injuries
Injuries to the lower third of the ureter allow several options in management. The procedure of choice is reimplantation into the bladder combined with a psoas-hitch procedure to minimize tension on the ureteral anastomosis. An antireflux procedure should be done when possible. Primary ureteroureterostomy can be used in lower-third injuries if the ureter can be mobilized without tension. The ureter is usually long enough for this type of anastomosis. A bladder tube flap can be used when the ureter is shorter. Transureteroureterostomy may be used in lower-third injuries if extensive urinoma and pelvic infection have developed (such as missed ureteral injury). This procedure allows anastomosis and reconstruction in an area away from the pathologic processes.

Midureteral Injuries
Midureteral injuries usually result from external violence and are best repaired by primary ureteroureterostomy or transureteroureterostomy.

Upper Ureteral Injuries
Injuries to the upper third of the ureter are best managed by primary ureteroureterostomy. If there is extensive loss of the ureter, autotransplantation of the kidney can be done as well as bowel replacement of the ureter.

Stenting
Most anastomoses after repair of ureteral injury should be stented. The preferred technique is to insert a silicone internal stent through the anastomosis before closure. These stents have a J memory curve on each end to prevent their migration in the postoperative period. After 3-4 weeks of healing, stents can be endoscopically removed from the bladder. The advantages of internal stenting are maintenance of a straight ureter with a constant caliber during early healing, the presence of a conduit for urine during healing, prevention of urinary extravasation, maintenance of urinary diversion, and easy removal.

1. How does an amniotic fluid embolism present?

Trauma – 5th Ed. (2004)

History: AFE usually occurs during labor but has occurred during abortion, abdominal trauma, and amnioinfusion.

A woman in the late stages of labor becomes acutely dyspneic with hypotension; she may experience seizures quickly followed by cardiac arrest. Massive DIC­associated hemorrhage follows and then death. Most patients die within an hour of onset.

Physical: In case reports, patients are described as developing acute shortness of breath, sometimes with a cough, followed by severe hypotension. The following signs and symptoms are indicative of possible AFE:

·Hypotension: Blood pressure may drop significantly with loss of diastolic

measurement.

·Dyspnea: Labored breathing and tachypnea may occur.

·Seizure: The patient may experience tonic-clonic seizures.

·Cough: This is usually a manifestation of dyspnea.

·Cyanosis: As hypoxia/hypoxemia progresses, circumoral and peripheral cyanosis and changes in mucous membranes may manifest.

·Fetal bradycardia: In response to the hypoxic insult, fetal heart rate may drop to less than 110 beats per minute (bpm). If this drop lasts for 10 minutes or more, it is a bradycardia. A rate of 60 bpm or less over 3-5 minutes may indicate a terminal bradycardia.

·Pulmonary edema: This is usually identified on chest radiograph.

·Cardiac arrest

·Uterine atony: Uterine atony usually results in excessive bleeding after delivery. Failure of the uterus to become firm with bimanual massage is diagnostic.

1. What are the indications for a c-section following trauma?

Trauma – 5th Ed. (2004)

Specific indications for cesarean section during celiotomy include maternal shock and pregnancy near term, threat to life from exsanguination from any cause, mechanical limitation for maternal repair, irreparable uterine injury, instability in a potentially viable fetus, unstable thoracolumbar spine injury, and maternal death.

1. What are the presenting signs & symptoms of pelvic inflammatory disease? What common surgical diagnoses can this medical entity mimic?

Schwartz’s Principles of Surgery – 8th Ed. (2005)

The classic signs include fever, lower abdominal pain with pelvic tenderness, and purulent vaginal discharge. Some patients, however, will have minimal or absent symptomatology, particularly in the presence of a chlamydial infection. The lack of symptoms does not preclude pelvic inflammatory disease and tubal damage. Those patients who present with an acute illness must be studied thoroughly to rule out the possibility of acute appendicitis, ectopic pregnancy, gastrointestinal obstruction or perforation, and urinary stones. Control and Prevention (COC) has adopted an approach to maximize diagnosis by using minimal criteria and by urging providers to maintain a low threshold for diagnosis and empiric treatment.

·Minimum criteria for the diagnosis of PID are listed below. Institute empiric treatment of PID when a patient has all of the following minimal clinical criteria in the absence of an established cause other than PID:

a Lower abdominal tenderness on palpation a Adnexal tenderness

a Cervical motion tenderness

·Additional criteria, especially in women with more severe clinical signs, can be used to increase the specificity of the diagnosis.

Oral temperature more than 38.3°C (101°F)

Abnormal cervical or vaginal discharge

Elevated erythrocyte sedimentation rate (ESR) a Elevated C-reactive protein

Laboratory documentation of cervical infection with N gonorrhoeae or C trachomatis.

1. Contrast prerenal causes with intrinsic causes of acute renal failure: What is the urine sodium in the two disorders? What would the FENA be?

Current Critical Care Diagnosis & Treatment – 2nd Ed. (2003)

ACS Surgery: Principles & Practice (2006)

Pre-renal ARF: The term prerenal typically indicates that the kidney is malfunctioning predominantly as a result not of reasons intrinsic to the kidney but of systemic factors, which, through variable mechanisms, can alter renal blood flow (RBF) or intraglomerular hemodynamics and result in a decrease in GFR.
Although both serum creatinine and urea nitrogen increase, low tubular flow results in increased reabsorption of urea. Therefore, the serum BUN:creatinine ratio increases usually to > 20:1. Because renal tubular function is normal in early prerenal azotemia, avid sodium reabsorption in the face of volume depletion causes FE_Na to be very low, usually less than 1%. Urinary sediment is usually normal except for the finding of a few granular casts; white blood cells and red and white cell casts are absent. Common systemic causes of ARF include a low cardiac output state (e.g., myocardial infarction, tamponade, or valvular disease), cardiac surgery, major vascular surgery, trauma with hypovolemia, shock of any type (anaphylactic, hemorrhagic, or hypovolemic), hemodynamic instability associated with surgery, hepatic failure, increased intra-abdominal pressure, intra-abdominal hypertension, and rhabdomyolysis.

Parenchymal ARF: The term parenchymal ARF is used to define a syndrome in which the principal source of damage is within the kidney and in which typical structural changes can be seen on microscopy. Nephrotoxic drugs are a particularly important cause of paren chymal ARF, especially in hospitalized patients. Specific causes include; glomerulonephritis, vasculitis, renovascular disease (renal artery or vein occlusion; malignant hypertension), exposure to toxins, either endogenous (myoglobin; hemoglobin; uric acid), exogenous (radiocontrast media; antimicrobials; chemotherapeutic agents; immunosuppressive agents; ethylene glycol), interstitial nephritis (from antimicrobials, diuretics, malignancy, or infection), tubular deposition, obstruction (from bilateral cortical necrosis, multiple myeloma, or amyloidosis), renal allograft rejection and Trauma.

Test	Result in Prerenal ARF	Result in parenchymal ARF
Urine sediment	Normal	Epithelial casts
Specific gravity	> 1.020	< 1.020
UNa	< 10 mEq/L	> 20 mEq/L
FENa	< 1%	> 1%
Urinary osmolality	> 500 mOsm/kg H2O	< 300 mOsm/kg H2O
UCr/PCr ratio	> 40	< 10
Plasma urea/creatinine ratio	High	Normal

1. What is the initial management of oliguria?

Schwartz’s Principles of Surgery – 8th Ed. (2005)

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Low urine output (oliguria) is initially evaluated by examining the patient and flushing the Foley catheter using sterile technique. When this fails to produce the desired response, it is reasonable to administer an intravenous fluid challenge with a crystalloid fluid bolus of 500 to 1000 mL. However, the immediate postoperative patient must be examined and have recent vital signs recorded with total intake and output tabulated, as well as urinary electrolytes measured. A hemoglobin and hematocrit level should be checked immediately. Patients in compensated shock from acute blood loss may manifest anemia and end-organ malperfusion as oliguria alone. If there is any question of a possible shock state, central hemodynamic monitoring is appropriate.

Visit the ABSITE Review Course with practice questions at www.ClinicalReview.com/ABSITE.php

1. What are the characteristics of primary wound healing?

a. Primary wound healing or healing by first intention occurs within hours of repairing a full­thickness surgical incision. . The edges of the wound are approximated and held together with sutures, tape or tissue adhesives. This surgical insult raesults in the mortality of a minimal number of cellular constituents. Wound closes with minimal intervention.

b. First intention wound healing is the most desirable. Most surgical wounds heal by first intention if the wound is not contaminated, dead spaces are closed, tissue is handled gently, hemostasis is achieved, and the tissues are approximated accurately.

2. What is meant by healing by secondary intention?

a. Wound closes by contraction and reepithelialization. [NB Remember the role of the myofibroblasts].

b. Wounds heal by secondary intention if there are post-operative complications such as: infection, wound dehiscence, excessive scar, or excessive drainage. If sutures were used prior to the development of the complication, they are removed and the wound is allowed to heal by forming granulation tissue from the bottom of the wound outward. If an infection is present when the surgical procedure takes place, the surgeon may not attempt any suturing of the wound, and allow the wound to head by secondary intention. This type of healing takes much longer than healing by first intention.

3. What is tertiary healing?

The last type of wound healing is by third intention. When granulation tissue has developed along the edges of a wound the surgeon may use large retention type sutures to assist in healing. Third intention healing is used when there is gross infection, or after tissue has been lost due to traumatic injury or surgical debridement. The use of skin grafts or free flaps may be necessary to effect healing.

4. Name the stages or phases of wound healing

a. The wound healing process has 3 phases. They are the inflammatory phase, the proliferative phase, and the maturational phase, also known as scar remodeling.

i. The inflammatory phase (days 1 to 10) is characterized by hemostasis and inflammation. Collagen exposed during wound formation activates the clotting cascade (both the intrinsic and extrinsic pathways), initiating the inflammatory phase. After injury to tissue occurs, the cell membranes, damaged from the wound formation, release thromboxane A2 and prostaglandin 2-alpha, potent vasoconstrictors. This initial response helps to limit hemorrhage. After a short period, capillary vasodilatation occurs secondary to local histamine release, and the cells of inflammation are able to migrate to the wound bed. The timeline for cell migration in a normal wound healing process is predictable. Cells involved in this phases are PMNs, macrophages; epithelialization 1-2 mm/day. Platelets, the first response cell, release multiple chemokines, including epidermal growth factor (EGF), fibronectin, fibrinogen, histamine, platelet-derived growth factor (PDGF), serotonin, and von Willebrand factor. These factors help stabilize the wound through clot formation. These mediators act to control bleeding and limit the extent of injury. Platelet degranulation also activates the complement cascade, specifically C5a, which is a potent chemoattractant for neutrophils. The inflammatory phase continues, and more immune response cells migrate to the wound. The second response cell to migrate to the wound, the neutrophil, is responsible for debris scavenging, complement-mediated opsonization of bacteria, and bacteria destruction via oxidative burst mechanisms (ie, superoxide and hydrogen peroxide formation). The neutrophils kill bacteria and decontaminate the wound from foreign debris. The next cells present in the wound are the leukocytes and the macrophages (monocytes). The macrophage, referred to as the orchestrator, is essential for wound healing. Numerous enzymes and cytokines are secreted by the macrophage. These include collagenases, which debride the wound; interleukins and tumor necrosis factor (TNF), which stimulate fibroblasts (produce collagen) and promote angiogenesis; and transforming growth factor (TGF), which stimulates keratinocytes. This step marks the transition into the process of tissue reconstruction, ie, the proliferative phase.

ii. - The second stage of wound healing is the proliferative phase (5 days to 3 weeks). Epithelialization, angiogenesis, granulation tissue formation, and collagen deposition are the principal steps in this anabolic portion of wound healing. Epithelialization occurs early in wound repair. If the basement membrane remains intact, the epithelial cells migrate upwards in the normal pattem. This is equivalent to a first-degree skin bum. The epithelial progenitor cells remain intact below the wound, and the normal layers of epidermis are restored in 2-3 days. If the basement membrane has been destroyed, similar to a second­ or third-degree bum, then the wound is re-epithelialized from the normal cells in the periphery and from the skin appendages, if intact (eg, hair follicles, sweat glands). Angiogenesis, stimulated by TNF-alpha, is marked by endothelial cell migration and capillary formation. The new capillaries deliver nutrients to the wound and help maintain the granulation tissue bed. The migration of capillaries into the wound bed is critical for proper wound healing. The granulation phase and tissue deposition require nutrients supplied by the capillaries, and failure for this to occur results in a chronically unhealed wound. Mechanisms for modifying angiogenesis are under study and have significant potential to improve the healing process. The final part of the proliferative phase is granulation tissue formation. Fibroblasts differentiate and produce ground substance and then collagen. The ground substance is deposited into the wound bed; collagen is then deposited as the wound undergoes the final phase of repair. Many different cytokines are involved in the proliferative phase of wound repair. The steps and the exact mechanism of control have not been elucidated. Some of the cytokines include PDGF, insulin-like growth factor (IGF), and EGF. All are necessary for collagen formation.

iii. The final phase of wound healing is the maturational phase (3 weeks to 1 year). The wound undergoes contraction, ultimately resulting in a smaller amount of apparent scar tissue. The entire process is a dynamic continuum with an overlap of each phase and continued remodeling. The wound reaches maximal strength at one year, with a tensile strength that is 30% of normal skin. Collagen deposition continues for a prolonged period, but the net increase in collagen deposition plateaus after 21 days. Type three collagen replaced with type I; decreased vascularity. Collagen cross-linking occurs. Peripheral nerves regenerate at 1 mm/day.

5. Name local factors that influence wound healing?

a. Mechanical injury.

b. Infection.

c. Edema.

d. Ischemia/necrotic tissue.

e. Topical agents.

f. Ionizing radiation.

g. Low oxygen tension.

h. Foreign bodies.

6. Name some general principals in the management of clean wound?

a. Moist environment (avoid desiccation).

b. Oxygen delivery: optimal fluids, no smoking, pain control, arterial reconstruction,

c. supplemental oxygen.

d. Avoid edema: leg elevation, compression

e. Remove necrotic tissue,.

7. What are the general factors that influence wound healing:

a. Age.

b. Nutrition.

c. Metabolic diseases.

d. Trauma.

e. Immunosuppression. Steroid use is a well known inhibitor of wound healing. There is data that suggests the effects of steroids can be reversed by the application of Vitamin A.

f. Connective tissue disorders.

g. Smoking.

8. What is a contaminated wound:

a. Fresh, traumatic wound.

b. Gross spillage of gastrointestinal contents in the abdomen.

c. Mayor break in sterile technique.

d. Incision through an inflammed tissue.

It is generally not advisable to primarily close contaminated wounds. One option for their management is the delayed primary closure, in which the wound is dressed open with an occlusive dressing and then closed in 3-5 days if there is no sign of invasive infection. Otherwise tertiary closure, debride and irrigate wound and initiate dressing changes with antibacterial cream until bacterial count is less than 10⁵ / g tissue then proceed with closure. (ACS Surgery 2006)

9. How does one manage the contaminated chronic wounds:

The first principle in managing chronic wounds is to diagnose and treat any underlying circulatory disease. The second principle is never to allow open wounds to dry (ie, use moist dressings). Moist dressings may also relieve pain. A third principle is to control any infection with systemic antibiotics. Topical barriers to infection are useful but not always necessary. A fourth principle is to recognize that chronically scarred tissue is usually poorly perfused. Debridement of unhealthy tissue, often followed by skin grafting, may be required for healing. A fifth principle is to reduce autonomic vasoconstriction by means of warmth, moisture, pain relief, or pharmacologic vasodilation medications. The use of various wound preparations may be helpful in this situation

10. What are fibroblasts?

Fibroblasts are mesenchymal cells that secrete the collagen and proteoglycans of the connective tissue matrix that weld wound edges together. They assume high-molecular-weight polymeric forms and become the physical basis of wound strength.

11. Name some of the newer advances in wound dressings.

Some novel approaches to wound management have been developed since the latter part of the 1990s. One such approach involves the use of skin substitutes, such as Alloderm, Integra, and Apligraf. Alloderm and Integra contain only dermal elements, whereas Apligraf and others contain cellular components, including epithelium. The cellular elements most likely do not remain in the wound for long, but they are thought to provide cytokines that may stimulate the healing process in the short term. Hydrocolloids and negative pressure dressings, such as the wound VAC are other slick techniques that may improve wound healing.

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1. Describe the work up of a solitary breast mass in a 50 year old female.

2. Treatment of inflammatory breast cancer?

3. What are the contraindications to sentinel node biopsy?

4. What are common chemotherapeutic agents to treat breast cancer? What is herceptin?

5. What is the workup for unilateral bloody breast discharge?

6. How would you treat a solitary cyst in a perimenopausal woman?

7. What are the common pathogens that cause breast abscess?

8. How are the following benign breast lesions treated?

- Fibroadenoma in a young woman?

- Unilateral gynecomastia in a young male?

- Firm unilateral mass in an elderly male?