Mcq Salad 011

Recurrent volvulus of the stomach into the chest is a serious condition that can lead to incar– ceration and gangrene. Every attempt should be made to repair this diaphragmatic hernia.

The presentation itself should alert the clini– cian to the possibility of a pneumothorax (Fig 4–3). This condition is seen quite frequently with patients that are thin and tall. This lady presents with a catamenial pneumothorax syndrome.Figure 4–3.Spontaneous pneumothorax on right side. (Reproduced, with permission, from Doherty GM: Current Surgical Diagnosis and Treatment, 12th ed. 349. McGraw–Hill, 2006.)

This is the first documented pneumothorax on this patient. The treatment of choice is inser– tion of a chest tube. If the air leak persists forAnswers: 40–58 95more than 3 days or if she develops a recur– rence after discharge, a thoracoscopy, resection of bullae and pleurodesis becomes the treat– ment of choice.

The decision to operate in patients with aortic stenosis is based on transvalvular gradient. 50–mm gradient is termed critical aortic stenosis and the valve should be replaced in a symptomatic patient.

Congestive heart failure. In patients with aortic stenosis, risk factors include a history of agina, stroke or TIAs, and a history of conges– tive heart failure, which indicates a compro– mised left ventricle. Of the three, congestive heart failure is the factor which is the greatest risk factor for patients undergoing surgery.

Aortic insufficiency. This is the murmur of a patient with aortic insufficiency. Typically, these patients will be well compensated at rest but will have decreased cardiac output with exercise. These patients should be operated on.

Aortic dissection. This describes a patient with Marfan syndrome, who are typically at risk for aortic dissection. With dissection you may preserve right radial pulse but lose femoral pulses. (C) Adenocarcinoma, originated from islands of Barrett’s esophagus, is today the most common cancer of the esophagus in the United States.

D

C

B

D

C

C

B

B

D

C

b tumours less than 2 cm in size require no further therapy other than appendicectomy

d carcinoid syndrome arises when hepatic metastases\nhave occurred

e synchronous carcinoid tumour in the distal ileum may\nbe present

b regular surveillance with flexible sigmoidoscopy

c enrolment in a familial adenomatous polyposis registry

d identification of presymptomatic carrier by molecular genetic testing

c most affected individuals develop polyps by the age of 10 years

d desmoid tumour is an association

e all affected patients will develop colorectal carcinomas with time

b colonic bleeding

c purulent peritonitis

d colovaginal fistula doesn't cause colon ca

b iritis

c sacroileitis

d sclerosing cholangitis

b erythema nodosum

c toxic megacolon

e response to mesalazine

The incidence of reinfarction is increased in patients undergoing intrathoracic or intra-abdominal procedures lasting longer than three hours. The site of surgery or anesthetic technique have not been shown to change the incidence of reinfarction if the procedure is less than three hours in duration. Patients with known three-vessel or left main coronary artery disease are at increased risk, while those who have undergone prior coronary artery bypass grafting are of substantially decreased risk of reinfarction. Prophylactic therapy with beta blockers, calcium channel agents, and nitrates has not been proven beneficial; however, withdrawal of these agents has been associated with perioperative ischemia, myocardial infarction, and death. CHF is the single most important factor predicting postoperative cardiac morbidity. Rhythm disturbances, particularly frequent premature ventricular beats, more than five beats/minute, are also independently associated with an increased risk of perioperative cardiac complications.

Patients with significant pulmonary diseases require special anesthetic techniques. Obstructive pulmonary disease can either be chronic (COPD) or acute (asthma). In either case, the reversible component of obstruction should be reversed prior to elective surgery. In patients with reactive airway disease, the endotracheal tube may induce severe bronchospasm. Even in patients who are well treated preoperatively, reactive bronchospasm may complicate anesthetic induction and emergence from anesthesia. The principal method used to prevent or diminish this “foreign body” induced bronchospasm is intubation of the patient at a deep level of anesthesia when reflexes are blunted. The classic way of managing a patient with severe asthma is to induce with an agent that produces bronchodilatation and to ventilate the patient with an inhalation agent until deeply anesthetized prior to laryngoscopy and intubation. The patient should be extubated while spontaneously ventilating, but with the inhalation agent still in effect, bringing the patient to consciousness while ventilating by mask.Because of the potential adverse effects of systemic narcotics on respiratory drive, the use of epidural narcotics and local anesthetics for postoperative pain control has become very popular. These techniques allow the patient to be extubated earlier, and patients with intrathoracic and upper abdominal surgery, help restore pulmonary function toward preoperative values. Preoperative use of intermittent positive pressure breathing has not been demonstrated to decrease the incidence of postoperative pulmonary complications.

Narcotics and synthetic analogues belong in the class of drugs called opioids. Narcotics produce profound analgesia and respiratory depression. They have no amnesic properties, no myocardial depressive effects, and no muscle relaxant properties. Narcotics may produce significant hemodynamic effects indirectly through the release of histamine and/or blunting of the patient’s sympathetic vascular tone due to analgesic properties. Acutely injured patients may be hypovolemic and in pain, with high sympathetic tone and peripheral resistance. Therefore, such patients can experience a dramatic drop in systemic blood pressure with minimal doses of opioids. All opioids can be reversed with naloxone. Naloxone reversal, however, can be dangerous because the agent acutely reverses not only the analgesic effects of the opioid but also analgesics effects of native opioids. Naloxone treatment has been associated with acute pulmonary edema and myocardial ischemia and should not be used electively to reverse the effects of narcotic. Propofol is a lipid-soluble substitute isopropyl phenol non-narcotic agent that produces rapid induction of anesthesia followed by awakening in four to eight minutes

The technique of patient-controlled analgesia is based on investigations that small intravenous bolus doses of narcotic on demand can provide patients with improved pain relief at the same or less total narcotic dose. The system requires some degree of sophistication and a conscious patient who has been instructed in the technique. Numerous studies have demonstrated that PCA is as safe as conventional IM medication. The patient can be restricted from receiving excessive agents via setting a lockout interval duration of several minutes during which time a dose of narcotic cannot be successfully administered. In addition, limits to the total hourly dose can be set.

Twenty-four percent of patients experience a post-anesthetic care unit complication. Nausea, vomiting and airway support comprise 70% of these complications. The need to maintain airway support is by far the most common respiratory complication. Hypothermia has a deleterious effect on altering drug metabolism and delaying recovery. Nausea and vomiting are rarely unifactorial and cause considerable discomfort to the patient. There is little evidence to favor one anesthetic or anesthetic technique over another. Nitrous oxide does not appear to increase incidence of nausea in well documented studies. The new serotonin antagonist, odansetron, has been shown in several studies to be superior to other agents as a perioperative antiemetic agent.Perioperative myocardial ischemia is an extremely important complication but difficult to recognize. Diagnosis is complicated by the fact that only 10—30% of patients suffering documented myocardial infarction will have pain and that postoperative EKG changes are often nonspecific. One must therefore look for secondary indications of on-going ischemia such as hypotension, arrhythmias, elevated filling pressures, or postoperative oliguria.

Pulse oximetry continuously, noninvasively and inexpensively provides arterial hemoglobin saturation and peripheral pulse determination. It must be remembered, however, that a pulse oximeter measures oxygen saturation and not arterial oxygen tension (PaO2). The PaO2 must drop below 80 mm Hg before any significant change in oxygen saturation will occur. End tidal CO2 monitoring reflects metabolism (the production of CO2), circulation (blood flow to the lungs), and ventilation (respiratory rate in an intact ventilatory circuit). It can be used as a surveillance monitor for both the respiratory circuit and the cardiovascular system. Any acute decrease in cardiac output will decrease output to the lung and increase alveolar dead space, causing an acute drop in end tidal CO2.Hemodynamic stability can be monitored in a variety of methods, the most basic of which is systemic arterial blood pressure measure. Intermittent, noninvasive measure of systemic blood pressure with an oscillometric blood pressure cuff has become the standard in the operating room with an accuracy equal to that of clinical measurement by auscultation. When tighter control is required in patients with significant hypertension, serious heart disease, or in patients who may suffer acute blood loss, invasive arterial monitoring is employed. In patients with left ventricular dysfunction who are undergoing extended surgical procedures with significant fluid shifts and potential blood loss, central venous pressure monitoring is frequently used, with pulmonary arterial catheter monitoring reserved for more critically ill patients and for those with significant left ventricular dysfunction

Anesthetic agents effectively obtund or completely block nearly all physiologic protective mechanisms, therefore, there is an associated risk even without a surgical procedure. Fortunately, with the advent of newer agents and monitoring techniques, it is estimated the mortality due to anesthesia alone has decreased from approximately 1:10,000 in the 1950s to as low as 1:100,000 or less for healthy patients today. It has been estimated that between 50–75% of anesthetic-related deaths are due to human error and are preventable. The most common problems associated with adverse outcomes are related to the airway: inadequate ventilation, unrecognized esophageal intubation, unrecognized extubation, and unrecognized disconnection from the ventilator.

The history of myocardial infarction is an important risk factor for general anesthesia. Large retrospective studies have found that the incidence of reinfarction is related to the time elapsed since the previous myocardial infarction. The incidence of reinfarction appears to stabilize at approximately 1% after six months, with the highest rate of reinfarction occurring in the first three months after the infarct. Mortality from reinfarction, for patients undergoing non-cardiac surgery, has been reported to be between 20–50% and usually occurs within the first 48 hours after surgery. Invasive hemodynamic monitoring with pulmonary artery catheters and aggressive pharmacologic intervention has been demonstrated to reduce reinfarction rates.

Local anesthetics constitute a class of drugs which produce temporary blockage of nerve conduction by binding to neuronal sodium channels. Adverse consequences associated with the use of local anesthetics fall into three categories: acute central nervous system toxicity due to excessive plasma concentration, hemodynamic and respiratory consequences due to excessive conduction block of the sympathetic or motor nerves, and allergic reactions. Whenever a local anesthetic has been injected, there may be inadvertent intravascular injection or an overdose of the drug due to rapid uptake from the tissues. All may produce seizures. Complications can be minimized by aspirating prior to injection to avoid intravascular injection and limiting the doses to the safe range. When local anesthetics are administered for a spinal or epidural block, there will be a progressive blockade of the sympathetic nervous system which will produce systemic vasodilatation. If the block travels along the thoracolumbar region, a sympathetic blockade will result in profound systemic vasodilatation and bradycardia with resultant hypotension.Local anesthetics are divided into two groups: esters and amides. Most commonly used agents, the amides, include lidocaine and bupivacaine. Lidocaine is noted for a fast onset of action but a short duration whereas bupivacaine has a slower onset with the duration lasting for four to 12 hours. The addition of epinephrine (100 µg) will lower the toxicity and increase the duration of the local anesthetic.

Neuromuscular blocking agents can be classified as depolarizing or nondepolarizing inhibitors of the neurotransmitter, acetylcholine at the neuromuscular junction. The only noncompetitive inhibitor employed clinically is succinylcholine. This drug rapidly binds to the neuromuscular junction and produces depolarization, clinically obvious as fine muscle fasciculations occurring approximately 60 seconds after injection. All other clinically useful muscle relaxants are termed competitive inhibitors and do cause depolarization when they attach to the neuromuscular junction. Since these agents compete with acetylcholine, the block produced is in direct proportion to the concentration of the agent relative to the concentration of acetylcholine. If the concentration ratio is low enough, competitive relaxants can be “reversed” if the concentration of acetylcholine is artificially elevated. Increase of acetylcholine concentration can be achieved by giving a drug which blocks metabolism of anticholinesterase (neostigmine).Nondepolarizing relaxants are frequently used in critically ill patients who are difficult to manage otherwise during prolonged periods of mechanical ventilation. It is imperative that these drugs be given in conjunction with analgesics and amnesic agents, since neuromuscular blocking agents have no analgesic or amnestic properties and only prevent motion of voluntary muscles. Patients may therefore be totally aware and in pain and unable to communicate. All muscles of the body do not have equal sensitivity in muscle relaxants. The diaphragm is both resistant to neuromuscular blockade while the neck and pharyngeal muscles that support the airway are most sensitive. It is possible for an intubated patient to spontaneously ventilate and even to produce a large negative inspiratory force and yet have complete airway obstruction when extubated due to effects of residual muscle relaxants on upper airway muscles. The definitive clinical test for complete reversal of neuromuscular blockade is the ability of the patient to sustain a head lift from the bed for five seconds.

Renal failure is the primary cause of hypermagnesemia. Because of the kidneys ability to excrete large magnesium loads, hypermagnesemia rarely occurs if renal function remains normal. Because the kidneys are able to conserve magnesium well in states of magnesium depletion, hypomagnesemia rarely occurs from poor intake alone. The combination of low intake and increased gastrointestinal loss may lead to hypomagnesemia. Prolonged periods of intravenous fluid replacement without magnesium replacement and the chronic use of loop diuretics or other medications such as cyclosporine or aminoglycosides can also result in hypomagnesemia. Deficiencies of magnesium may present signs and symptoms similar to hypocalcemia. Hypomagnesemia may be treated by the oral administration of magnesium however large doses frequently leads to diarrhea. Correction of major deficits is therefore best managed by intravenous administration of magnesium sulfate at a dose of 50 to 100 mEq/d.

A primary decrease in PCO2 resulting in an increase extracellular pH is referred to as respiratory alkalosis. Hyperventilation and the ensuing fall in PCO2 may be secondary to hypoxia, reflux simulation from decreased pulmonary compliance, drugs, mechanical ventilation, and other causes. The two most common causes of hypoxia resulting in respiratory alkalosis are pulmonary disease and exposure to high altitudes. Renal compensation for respiratory alkalosis is not achieved by increasing excretion of bicarbonate but by decreasing net acid excretion, primarily through the reduction in ammonia excretion and increases in organic anion excretion. Chronic respiratory alkalosis is generally asymptomatic. Acute respiratory alkalosis may cause sensations of breathlessness, dizziness, and nervousness and can result in circumoral and extremity parathesias, altered levels of consciousness, and tetany. These signs are related to decreased cerebral blood flow secondary to decreased PCO2 and decreased ionized calcium concentration secondary to increased blood pH. In acute symptomatic respiratory alkalosis rebreathing, by breathing in and out of a paper bag, can temporarily relieve the symptoms.

The major cardiovascular effects of acute metabolic acidosis are peripheral arteriolar dilitation, decreased cardiac contractility, and central venous constriction. These may lead to cardiovascular collapse and pulmonary edema. Catecholamine secretion is stimulated by metabolic acidosis and in mild cases, heart rate may be increased. In addition to these cardiovascular effects, metabolic acidosis may also affect oxygen delivery by shifting the oxygen-hemoglobin disassociation curve to the right.

Chronic volume deficits may be manifested by decreased skin turgor, weight loss, sunken eyes, hypothermia, oliguria, orthostatic hypotension and tachycardia. Serum BUN and creatinine may be elevated, with a high BUN/creatinine ratio. The hematocrit may be elevated as well. Plasma sodium is not an indicator of intravascular volume, and if the loses have been isotonic, plasma sodium concentration remains normal. Fluid resuscitation for hypovolemia is initiated with an isotonic solution such as lactated Ringer’s solution. Urine flow in critically ill patients is monitored with an indwelling Foley catheter, with the goal of a urine output 0.5mL/kg/h desirable.

A number of electrolytes solutions are available for parenteral administration. Lactated Ringer’s solution is a physiologic solution containing many of the electrolytes found in plasma. The disadvantage of this solution is the relatively low sodium content (130 mEq/L) as compared to plasma. Hyponatremia can occur with extended use of lactated Ringer’s solution. Isotonic saline (0.9% or normal saline) contains 154 mEq of both sodium and chloride. The excess of both sodium and chloride can lead to electrolyte and acid-base disturbances. Infusion of large volumes of 0.9% saline can lead to total body sodium overload and hyperchloremia. The less-concentrated saline solutions are hypo-osmotic and have excess free water. In addition, 0.2% saline solution is hypotonic with respect to plasma and can result in red blood cell lysis if rapidly infused. For this reason, 5% dextrose is added to these solutions to increase the tonicity. Plasma expanders are commonly used in surgical patients. Plasma protein solutions such as 5% and 25% albumin act initially by increasing plasma oncotic pressures. Abnormalities in microvascular permeability such as those found in the pulmonary circulation in adult respiratory distress syndrome, in regional circulatory bed burns or infections, and in the systemic circulation in sepsis, may result in extravasation of these proteins into the interstitial space. About half of all exogenously administered albumin eventually ends up in the extravascular space. The half life of exogenously administered albumin is about 11 days.

Fluid therapy during the postoperative period should be tailored to each patient and depends on the adequacy of patient’s volume status at the completion of the operative procedure, as well as ongoing fluid losses. Maintenance fluid should be supplemented by replacement of the additional fluids needed to replace the ongoing third space loss as well as losses from various tubes and drains. In general, isotonic solution should be used for volume resuscitation during the early postoperative period. It is best not to give potassium supplements during this period unless they are specifically required as indicated by serum electrolyte measurements. Monitoring fluid status during the postoperative period is best accomplished by careful monitoring of vital signs, urine output, and central venous pressure, if necessary. Urine output is maintained at a level greater than 0.5 mL/kg/h. A urine specific gravity of greater than 1.010 to 1.012 indicates that urine is being concentrated and the patient may not be receiving adequate hydration.

The impaired ability of the kidney to excrete acid and hence generate bicarbonate may be secondary to a decrease in the number of functioning nephrons and is termed uremic acidosis or renal tubular acidosis. Renal tubular acidosis, which can occur both in acute and chronic renal failure, is primarily caused by reduction in ammonia excretion secondary to a reduction in the number of functioning proximal tubular cells. In addition, decreased proximal tubular bicarbonate reabsorption contributes to the development of acidosis. Although the onset of uremic acidosis is related to declining renal function, its appearance may be influenced by diet-dependent protein and organic anion ingestion. Renal tubular acidosis may be classified as distal or proximal, depending on the primary site of the renal tubular defect leading to acidosis. In renal tubular acidosis with hyperkalemia, the mechanism is decreased luminal negativity secondary to impaired sodium reabsorption. In distal renal tubular acidosis with hypokalemia, mechanisms including increased tubular permeability with backleak of secreted H+ into the tubular cell and reduced H+ pump activity are proposed mechanisms.