Latent hypocalcemia can be diagnosed by tapping on the facial nerve to elicit Chvostek sign or by inflating a sphygmomanometer to 20 mmHg above systolic pressure generic 200 mg avanafil amex erectile dysfunction meds at gnc, which produces radial and ulnar nerve ischemia and causes carpal spasm known as Trousseau sign buy 200mg avanafil mastercard erectile dysfunction causes tiredness. The differential diagnosis of hypocalcemia can be approached by addressing four issues: age of the patient order avanafil 200 mg amex erectile dysfunction caused by vasectomy, serum phosphate concentration, general clinical status, and duration of hypocalcemia. An otherwise healthy patient with chronic hypocalcemia probably is hypoparathyroid. In renal insufficiency, reduced phosphorus excretion results in hyperphosphatemia, which downregulates the 1α-hydroxylase responsible for the renal conversion of calcidiol to calcitriol. This, in combination with decreased production of calcitriol secondary to reduced renal mass, causes reduced intestinal absorption of calcium and hypocalcemia. The definitive treatment of hypocalcemia necessitates identification and treatment of the underlying cause (Table 16-21). Hypocalcemia resulting from hypomagnesemia or hyperphosphatemia is treated by repletion of magnesium or removal of phosphate. Treatment of a patient who has tetany and hyperphosphatemia requires coordination of therapy to avoid the consequences of metastatic soft-tissue calcification. Potassium and other electrolytes should be measured and abnormalities should be corrected. Hyperkalemia and hypomagnesemia potentiate hypocalcemia-induced cardiac and neuromuscular irritability. In contrast, hypokalemia protects against hypocalcemic tetany; therefore, correction of hypokalemia without correction of hypocalcemia may provoke tetany. For instance, in most patients after cardiac surgery, administration of calcium only increases blood pressure and actually attenuates the β-adrenergic effects of epinephrine. Therefore, calcium infusions should be of limited value in surgical patients unless there is demonstrable evidence of ionized hypocalcemia. Calcium salts appear to confer no benefit to patients already receiving inotropic or vasoactive agents. The cornerstone of therapy for confirmed, symptomatic, ionized hypocalcemia ([Ca2+] < 0. In patients who have severe hypocalcemia or hypocalcemic symptoms, calcium should be administered intravenously. In emergency situations, in an averaged-sized adult, the “rule of 10s” advises infusion of 10 mL of 10% calcium gluconate (93 mg elemental calcium) over 10 minutes, followed by a continuous infusion of elemental calcium, 0. Calcium salts should be diluted in 50 to 100 mL D W (to limit venous irritation and thrombosis), should not be mixed5 with bicarbonate (to prevent precipitation), and must be given cautiously to digitalized patients because calcium increases the toxicity of digoxin. During calcium replacement, clinicians should monitor serum calcium, magnesium, phosphate, potassium, and creatinine. Urinary calcium should be monitored in an attempt to avoid hypercalciuria (>5 mg/kg/24 hr) and urinary tract stone formation. Although the principal effect of vitamin D is to increase enteric calcium absorption, osseous calcium resorption is also enhanced. When rapid changes in dosage are anticipated or an immediate effect is required (e. Because the effect of vitamin D is not regulated, the dosages of calcium and vitamin D should be adjusted to raise the serum calcium into the low normal range. Adverse reactions to calcium and vitamin D include hypercalcemia and hypercalciuria. If hypercalcemia develops, calcium and vitamin D should be discontinued and appropriate therapy given. The toxic effects of vitamin D metabolites persist in proportion to their biologic half-lives (ergocalciferol, 20 to 60 days; dihydrotachysterol, 5 to 15 days; calcitriol, 2 to 10 days). In hypoalbuminemic patients, total serum calcium can be estimated (albeit inaccurately) by assuming an increase of 0. Severe hypercalcemia (total serum calcium > 13 mg/dL) is associated with more severe neuromyopathic 1061 symptoms, including muscle weakness, depression, impaired memory, emotional lability, lethargy, stupor, and coma. The cardiovascular effects of hypercalcemia include hypertension, arrhythmias, heart block, cardiac arrest, and digitalis sensitivity. Skeletal disease may occur secondary to direct osteolysis or humoral bone resorption. In response to hypovolemia, renal tubular reabsorption of sodium enhances renal calcium reabsorption. Effective treatment of severe hypercalcemia is necessary to prevent progressive dehydration and renal failure leading to further increases in total serum calcium, because volume depletion exacerbates hypercalcemia. Clinically, hypercalcemia most commonly results from an excess of bone resorption over bone formation, usually secondary to malignant disease, hyperparathyroidism, hypocalciuric hypercalcemia, thyrotoxicosis, immobilization, and granulomatous diseases. Granulomatous diseases produce hypercalciuria and hypercalcemia because of conversion by granulomatous tissue of calcidiol to calcitriol. Malignancy may produce hypercalcemia through either bone destruction or secretion by malignant tissue of hormones that promote hypercalcemia. Factors that promote hypercalcemia may be offset by coexisting disorders, such as pancreatitis, sepsis, or hyperphosphatemia, that cause hypocalcemia. Although definitive treatment of hypercalcemia requires correction of underlying causes, temporizing therapy may be necessary to avoid complications and to relieve symptoms. General supportive treatment includes hydration, correction of associated electrolyte abnormalities, removal of offending drugs, dietary calcium restriction, and increased physical activity. During saline infusion and forced diuresis, careful monitoring of cardiopulmonary status and electrolytes, especially magnesium and potassium, is required. Intensive diuresis and saline administration can achieve net calcium excretion rates of 2,000 to 4,000 mg/24 hr, a rate eight times greater than saline alone, but still less than the 6,000 mg every 8 hours that can be removed by hemodialysis. Bone resorption, the primary cause of hypercalcemia, can be minimized by increasing physical activity and initiating drug therapy with bisphosphonates, calcitonin, glucocorticoids, or calcimetrics. Bisphosphonates are the principal drugs for the management of hypercalcemia mediated by osteoclastic bone resorption. Risedronate has been associated with less gastrointestinal morbidity than alendronate. Although calcitonin is relatively nontoxic, more than 25% of patients may not respond. Thus, calcitonin is unsuitable as a first-line drug during life-threatening hypercalcemia. Glucocorticoids rarely improve hypercalcemia secondary to malignancy or hyperparathyroidism. Control of hypercalcemia associated with malignancy usually requires control of the underlying cancer. With the first agent, cinacalcet, recently released for clinical use in the United States and others undergoing clinical trials, calcimimetic agents also reduce inorganic phosphate concentration (Pi) and the calcium × phosphate product. Because the risk of extraskeletal calcification of organs such as the kidneys and myocardium is less if phosphates are given orally, the intravenous route should be reserved for patients with life-threatening hypercalcemia and those in whom other measures have failed. Phosphate Physiologic Role Phosphorus, in the form of inorganic phosphate (Pi), is distributed in similar concentrations throughout the intracellular and the extracellular fluids. Of total body phosphorus, 90% exists in bone, 10% is intracellular, and the remainder, less than 1%, is found in the extracellular fluid. Phosphate circulates as the free ion (55%), complexed ion (33%), and in a protein-bound form (12%).
Latency generic avanafil 200 mg online where to buy erectile dysfunction pump, usually measured in milliseconds order genuine avanafil on-line erectile dysfunction doctor cape town, refers to the delay in peak signal following stimulation and reflects transit time along the neural pathway cheap 200 mg avanafil fast delivery erectile dysfunction pills nz. This modality is especially useful for monitoring the integrity of the peripheral nerves, dorsal columns of the spinal cord, the brainstem, the subcortex, and the sensory cortex of the brain. Since sensory tracts decussate at the brainstem before proceeding through the thalamus and up to the sensory cortex, stimuli are recorded on the contralateral scalp. They may also be useful during neurovascular brain35 surgery to ensure sufficient perfusion to the somatosensory cortex during procedures that may put this cortex at risk, such as cerebral aneurysm clipping. Stimulation may be performed magnetically or electrically, with the latter being the more common method. Indirect electrical stimulation of the motor cortex, via scalp electrodes, is performed, usually in a single pulse or train of pulses that travels caudad and depolarizes the upper motor neurons in the spinal cord, summating in the ventral horn. From here, the signal travels to the α-motor neurons via the internuncial pathways, descending to the motor endplates, where muscle movement related to an action potential can be measured. Although there is no formal definition of “significant changes” that warrant concern for altered neural pathway function, a decrease in amplitude of 50% is considered “significant” as is a need to increase the stimulation intensity required to maintain a reproducible signal. If there is disruption of the bony pedicle, and hence contact or near-contact between the screw and neural elements, the amount of current necessary to stimulate the corresponding nerve root will be much less than if the pedicle were intact. Thousands of signals are averaged, yielding a typical waveform consisting of six waves. Retraction on the cerebellum may prolong the44 latency of the tracing between waves I and V. A bright stimulus is applied to the eyes using special goggles or contact lenses, and responses are recorded from scalp electrodes. Robust signals can, however, usually be obtained in neurologically intact patients with up to 0. Nitrous oxide has more of a depressant effect on signal amplitude rather than latency. Lastly, it is important to note that these anesthetic effects are much less prominent with regard to subcortical, cervical, and peripheral signal acquisition, as these areas are much more resistant to the inhibitory effects of anesthesia. Hence, it is wise to avoid muscle relaxation or reverse the effects of muscle relaxants prior to pedicle screw testing or cranial nerve identification. Small increases in latency can be seen with deep inhalational or intravenous anesthesia. Notably, cold irrigation fluids at the brainstem will also cause some increases in interwave latencies. The ultrasound probe emits a high-frequency sound wave that reflects off red blood cells and returns to the probe at a different frequency determined by the Doppler Effect. Specifically, the velocity of blood cells relative to the ultrasound probe will cause a change in the frequency of ultrasound waves that are reflected back to the probe. This “Doppler shift” is proportional to the velocity of blood and the sign (positive or negative) of the Doppler shift is determined by direction of blood flow. Positive (increase in frequency) occurs when blood is moving toward the probe and negative (decrease in frequency) occurs when blood is moving away from the probe. Flow velocity that is greater than expected can indicate stenosis, emboli, or vasospasm. This distinction is significant as decreased arterial diameter will lead to an increased blood flow velocity but a decrease in blood flow volume. Specifically, the presence of characteristic Lundberg waves can provide valuable information about the state of the brain. Although invasive modalities allow for actual57 pressure measurement, they have associated risks (described later). Also, a ventriculostomy can be used to deliver drugs, such as antibiotics and thrombolytic agents. Most notably, infection is a great risk, since the intraventricular drain pierces the meninges and brain parenchyma. The first is a microtransducer system attached to a flexible wire, and the second is a fiberoptic system with a pressure transducer at its tip. Both systems require a hollow screw to be inserted in the skull, whereby the wire or fiberoptic cables can traverse the brain parenchyma. These systems rely on a small bolt that is threaded through a burr hole in the skull, with the tip placed 1 mm beneath the dura. They are unacceptably inaccurate, however, reflecting only the epidural space and not the entire intracranial compartment. Cerebral Oxygenation and Metabolism Monitors Other devices used to monitor the homeostasis of the brain, including its oxygenation and metabolism, are available but may not be commonly employed in the clinical setting. Jugular bulb venous oximetry is the most common of these techniques and involves a fiberoptic catheter placed in a retrograde fashion into the internal jugular vein. The catheter is advanced cephalad beyond the common facial vein and into the jugular bulb that lies at the skull base. Proper placement entails x-ray confirmation of the catheter tip at the level of the mastoid process. Other metabolites that can be measured from this source include lactate and glucose concentrations. Measurement can be accomplished by serial sampling but this method only gives information about the status of the brain at single points in time. Brain tissue oxygen monitors measure the partial pressure of oxygen (PbtO ) in a portion of brain2 interstitium 15 to 20 mm wide, directly and invasively, via a Clark-type electrode. PbtO values reflect the balance2 2 between oxygen supply and demand in the region of brain surrounding the electrode. Generally, values below 20 mmHg in2 pathologic brain states are considered significant and may portend secondary injury to otherwise healthy brain tissue. A filamentous catheter is placed into the brain parenchyma, consisting of outer and inner tubes and a semipermeable membrane at its tip. At the tip of the catheter, metabolites in the extracellular fluid are driven by a concentration gradient into the outer tubing and are eventually collected into a microvial. This solution is then analyzed for its metabolite contents and their concentrations, including glucose, pyruvate, lactate, glutamate, and glycerol. Clinical correlation, with attention to the location of the catheter tip and comparison of values over time, is required. Although glucose, pyruvate, and lactate concentrations are measures of adequate aerobic metabolism, glutamate and glycerol levels represent ischemic neuronal stress and cell membrane degradation, respectively. For example, measurement of values obtained from regions of brain remote from the site of brain injury might indicate minimal, if any, abnormality. Therefore, microdialysis and measurement of oxygen partial pressure is best obtained from locations where “at risk” brain exists. Lastly, cerebral oximetry has become more prevalent in the clinical setting recently. A decrease of at least 20% from baseline values is considered significant hypoxia, though definitive data in this regard do not exist.
Serious conditions such as intracranial aneurysms cheap avanafil 100mg visa erectile dysfunction caused by nicotine, cardiac valvular disease purchase cheap avanafil what is erectile dysfunction wiki answers, and pheochromocytoma present rarely during pregnancy and may not require surgical intervention until postpartum order 50 mg avanafil with visa erectile dysfunction diabetes causes. Treatment of an incompetent cervix (cervical cerclage) typically occurs in early pregnancy or midpregnancy. The goal for treating patients undergoing nonobstetric operative procedures is the same as with any patient; safe perioperative care. This goal is complicated by the need to consider the well-being of both mother and fetus. That said, surgical outcomes in pregnant patients are similar to nonpregnant patients. Miscarriage and rate of birth defects are not significantly different when compared to the general obstetric population. Gastric emptying is essentially normal in the first two trimesters, but is prolonged in the third. Gastroesophageal sphincter tone is decreased after 20 weeks, thus caution regarding the unprotected airway is essential. The effects of altered physiology during pregnancy are not limited23 to general anesthesia. There is an increased effect of local anesthetics during pregnancy; thus, the amount of local anesthetic administered should be reduced by 25% to 30% during any stage of pregnancy. However, most of the critical organogenesis occurs in the first trimester (days 13 to 60). Although many commonly used anesthetics are teratogenic at high doses in animals, few, if any, studies support teratogenic effects of anesthetic or sedative medications in the doses used for human anesthesia care. Medicinal doses of benzodiazepines are safe when needed to treat perioperative anxiety. Nitrous oxide has also been suggested to be teratogenic in animals when administered for prolonged periods (1 to 2 days). Although teratogenesis has been seen only in animals under extreme conditions, not likely to be reproduced in clinical care, some believe that nitrous oxide use is contraindicated in the first two trimesters. One of the largest studies regarding reproductive outcome after surgery 2911 during pregnancy is a Swedish registry review covering the years 1973 to 1981. The results of this study are reassuring in that there was no increased incidence of congenital anomalies or stillbirths among infants exposed in utero to maternal surgery and anesthesia. However, in this group, there was an increased frequency of very low and low birth weights, and of deaths within 168 hours after delivery. The reasons for this are unclear and are not related to any specific type of operation. The authors postulated that the maternal illness itself might have been a major contributor to adverse neonatal outcome. Recent studies showing accelerated neuronal cell death in immature rat brain exposed to anesthetics raise concerns regarding use of general anesthetics. Further human studies are also inconclusive regarding anesthesia exposure in utero or in early childhood. Alkalosis also shifts the oxyhemoglobin dissociation curve, resulting in the release of less oxygen to the fetus at the placenta. Maternal hypotension leads to a reduction in uterine blood flow and thus fetal hypoxia. Uterine hypertension, as occurs with increased uterine irritability, will also decrease uterine blood flow. To summarize, elective surgery should be delayed until the patient is no longer pregnant and she has returned to her nonpregnant physiologic state (approximately 2 to 6 weeks postpartum). Procedures that can be scheduled with some flexibility but cannot be delayed until postpartum are best scheduled in the second trimester. This lessens the risk for teratogenicity (first-trimester medication administration) or preterm labor (greater risk in the third trimester) (Fig. If emergency surgery is required, there is no data to suggest that any well-conducted anesthetic is preferred over another, provided oxygenation and blood pressure are maintained and hyperventilation is avoided. Despite this statement, regional anesthesia should be considered as it minimizes fetal exposure to medications. Left uterine displacement should be used during the second and third trimesters, and aspiration prophylaxis should be administered to all pregnant patients after approximately 20 weeks of gestation. The possibility of pregnancy should be considered in all female surgical patients of reproductive age. On the basis of the maternal and fetal hazards already described, the following approach to anesthesia is suggested (Fig. Anesthesiologists and surgeons should obtain consultation from an obstetrician before performing nonobstetric surgery in pregnancy. The patient’s apprehension should be allayed as much as possible by personal reassurance during the preanesthetic visit and by adequate sedation and premedication. A nonparticulate antacid (15 to 30 mL), should be administered within half an hour before induction of anesthesia. Beginning in the second trimester, uterine displacement must be maintained at all times. Hypotension related to spinal or epidural anesthesia should be prevented as much as possible by rapid intravenous infusion of crystalloid solution during induction of anesthesia. If the mother becomes hypotensive, ephedrine or phenylephrine should be promptly administered intravenously. The risk of aspiration should be minimized by application of cricoid pressure and rapid tracheal intubation with a cuffed tube. To reduce fetal hazard, particularly during the first trimester, it appears preferable to choose drugs with a long history of safety. These drugs include thiopental, morphine, meperidine, muscle relaxants, and low concentrations of nitrous oxide. The decision to monitor the fetus should be made in conjunction with the obstetrician based on the severity of maternal disease, the potential for fetal jeopardy, whether the fetus is viable, and whether a physician able to perform a cesarean delivery plans to be immediately available. Uterine tone may also be monitored with an external tocodynamometer if the uterus reaches the umbilicus or above. Monitoring uterine activity should be continued after the operation, 2913 and tocolytic agents may be required. Figure 41-11 Recommendations for management of parturients and surgical procedures. Increased levels of procoagulants and reduced levels of inhibitors during pregnancy induce a hypercoagulable state, combined with a reactive fibrinolysis. Changes in hemostasis activity during delivery and the immediate postpartum period. Changes in electrophoretic patterns of plasma proteins 2914 through the cycle and following delivery. Early pregnancy changes in hemodynamics and volume homeostasis are consecutive adjustments triggered by a primary fall in systemic vascular tone. Effect of lateral tilt angle on the volume of the abdominal aorta and inferior vena cava in pregnant and nonpregnant women determined by magnetic resonance imaging.
In laparoscopic bariatric surgery generic 200 mg avanafil free shipping erectile dysfunction and diabetes ppt, high volume loading (10 mL/kg/h) compared to low volume loading (4 mL/kg/h) of Ringer’s lactate resulted in similar rates of oliguria with no difference in renal dysfunction cheap avanafil 100mg on line medicare approved erectile dysfunction pump. Steep Trendelenburg positioning may result in more craniofacial edema and airway compromise cheap avanafil 100mg amex impotence at 52,104 which might be ameliorated with intraoperative fluid restriction. A change to steep reverse Trendelenburg position during laparoscopic surgery for morbidly obese patients, compared to healthy normal weight patients, induces a significant change in pulse pressure variation, suggesting a low preload state and a need for rapid volume loading. Furthermore, they occur almost five times more often during blind abdominal entry than during the laparoscopic phase of the surgery. Abdominal entry away from the midline puts other vessels at risk, such as the superior and inferior mesenteric arteries, epigastric artery, and other small vessels of the abdominal wall. Vessels proximal to the site of surgical dissection are at increased risk of injury, such as the cystic and hepatic artery during laparoscopic cholecystectomy, and the dorsal vein complex during robotic prostatectomy. Though frank bleeding may be seen during a major vascular injury, most significant bleeding events during laparoscopy remain occult, requiring clinicians to have a high level of suspicion throughout the procedure. The anesthesiologist should be prepared for immediate surgical conversion to an open laparotomy to control severe bleeding, while managing possible hemodynamic instability due to hemorrhagic shock. Intraoperative testing and interpretation of hematocrit as an assessment of acute blood loss anemia should be performed cautiously, given the confounding effects of preoperative hematocrit collection, active bleeding, and intravascular dilution from crystalloid infusion. Transfusion triggers should be made on an individual basis, taking into account severity of bleeding, hemodynamics, and the patient’s coexisting diseases. Preoperative requirement for type and screen testing for laparoscopy continues to be defined. Gastrointestinal and urological structures can be injured during both the abdominal entry and the intra-abdominal portion of laparoscopic surgery. Because most intestinal injuries go unrecognized, the risk of postoperative intra-abdominal sepsis is high, making it a common cause of death related to laparoscopy. Deflation of the stomach with an orogastric tube should be routinely performed to minimize the risk of gastric injury during left upper quadrant trocar insertion. Bladder perforation and ureter ligation or transection are also possible during laparoscopy and may present with low urine output, hematuria, and, rarely, pneumaturia. Postoperative hemodynamic instability or unexpected gross hematuria should trigger immediate suspicion of occult injury. Consultation 3163 with the surgeon and critical care specialist may be warranted postoperatively. Cardiopulmonary Acute cardiovascular complications associated with laparoscopy include hypertension, hypotension, dysrhythmias, and rarely cardiac arrest. Hypotension can sometimes be the result of a low cardiac output from vagal stimulation and impaired venous return during insufflation. Preload can be further reduced during positive pressure ventilation and steep reverse Trendelenburg positioning. This effect may further impact preload in patients with pulmonary hypertension or right ventricular failure. A vagal-mediated cardiovascular reflex triggered by peritoneal stretching can induce bradyarrhythmias, which can range from sinus bradycardia to more life-threatening nodal rhythms. Profound vasovagal reaction to rapid peritoneal distention during insufflation has been implicated in acute cardiovascular collapse and cardiac arrest. Acute hypertension is often transient, and may be ameliorated by adjusting the depth of anesthesia. Conversion to open laparotomy or termination of surgery may be indicated if there is recurrent hypotension. Refractory hypotension may require immediate abdominal decompression, return to neutral patient position, and exploration of occult life-threatening conditions, such as severe bleeding or capnothorax. Pulmonary complications that develop during laparoscopy can present as acute hypercarbic (Table 44-6) and hypoxemic (Table 44-7) events. Treatment of hypoxemia should be swift, focusing on confirming O delivery and endotracheal tube positioning. Immediate2 3164 pneumoperitoneum release, 100% O ventilation, and neutral positioning2 should be instituted for refractory hypoxia. Risk factors for the development of subcutaneous emphysema include longer operative times (i. Unexplained sudden or persistent hypercarbia or acute hypotension may be early signs of subcutaneous emphysema or capnothorax, respectively. If2 concerns for persistent or recurrent hypercarbia from subcutaneous emphysema exist during the postoperative recovery, clinicians should maintain oxygen therapy and monitor for somnolence and acute respiratory acidosis by arterial blood gas. Cervical emphysema should be evaluated with a chest x-ray and the airway should be evaluated for signs of obstruction. Capnothorax Carbon dioxide gas accumulation within the pleural space is called capnothorax. Tension capnothorax may occur from uncontrolled pressurization of the thoracic cavity, leading to an increase in intrathoracic pressure, mediastinal shift, decreased venous return, and subsequent right ventricular compression—a potentially life-threatening condition. Risk factors for capnothorax are similar to those for subcutaneous emphysema; however, greater risk exists during procedures near the diaphragm. Physical exam findings may include reduced breath sounds bilaterally or unilaterally, as well as reduced chest excursion. Transthoracic echocardiography is increasingly being used to assess lung pathology, including intraoperative pneumothorax. Close observation is usually adequate for healthy patients with minimal physiologic derangements. The hemodynamic unstable patient should be supported with fluids or vasoactive agents while the capnothorax is reabsorbed. In severe cases, emergent needle decompression or chest tube insertion may be necessary intraoperatively. If tension capnothorax and hemodynamic instability recur after reinsufflation, termination of laparoscopy and conversion to an open surgical procedure may be indicated. Severe capnomediastinum and capnopericardium may be associated with severe hemodynamic instability due to excessive pressure of large mediastinal vascular structures and cardiac chambers. Fatalities from suspected gas embolism occurred in seven patients in a retrospective review of 500,000 closed-entry laparoscopies, over three decades. According to several case-series, the risk of gas embolism during laparoscopic major hepatectomy may be less than 1. Round ligament transection and2 broad ligament dissection during laparoscopic hysterectomy have resulted in gas embolisms. In the2 animal model, laparoscopic hepatectomies in the reverse Trendelenburg position preferentially resulted in venous gas embolisms. Diagnosis is usually dependent on the constellation of clinical signs associated with gas emboli. If deemed necessary, the patient may be placed in Trendelenburg2 with a left lateral decubitus position to help minimize the severity of right ventricular air lock. Figure 44-2 Venous air embolism of the right atrium visible with transesophageal echocardiographic monitoring. Patient Shifting and Falls Extreme positioning and potential for injury are common in laparoscopic procedures, particularly in robot-assisted laparoscopy. Patients undergoing laparoscopy in steep reverse Trendelenburg and steep Trendelenburg are at risk of unexpectedly shifting down or up on the operating room table.