Aurogra

By T. Thorus. Lincoln Christian College and Seminary. 2019.

This “gas trapping” occurs when high airway resistance lengthens the time required to exhale completely order aurogra online, or if improper inspiration/expiration ratios or high ventilatory rates are used during mechanical ventilation purchase aurogra master card. Increased Carbon Dioxide Production Carbon dioxide production varies directly with metabolic rate best 100mg aurogra, body temperature generic 100mg aurogra overnight delivery, and substrate availability. Inadequate Postoperative Oxygenation Systemic arterial partial pressure of oxygen (PaO ) is the best indicator of2 pulmonary oxygen transfer from alveolar gas to pulmonary capillary blood. Arterial hemoglobin saturation monitored by pulse oximetry yields less information on alveolar-arterial gradients and is not helpful in assessing impact of hemoglobin dissociation curve shifts or carboxyhemoglobin. Adequate arterial oxygenation does not mean that cardiac output, arterial perfusion pressure, or distribution of blood flow will maintain tissue oxygenation. Sepsis, hypotension, anemia, or hemoglobin dissociation abnormalities can generate tissue ischemia despite adequate oxygenation. In postoperative patients, the acceptable lower limit for PaO varies with2 3880 individual patient characteristics. A PaO below 65 to 70 mmHg causes2 significant hemoglobin desaturation, although tissue oxygen delivery might be maintained at lower levels. Maintaining PaO between 80 and 100 mmHg2 (saturation 93% to 97%) ensures adequate oxygen availability. Little benefit is derived from elevating PaO above 110 mmHg because hemoglobin is2 saturated and the amount of additional oxygen dissolved in plasma is negligible. Distribution of Ventilation Loss of dependent lung volume commonly causes V·/Q· mismatching and hypoxemia. Reduced ventilation in dependent lung is particularly damaging47 because gravity directs pulmonary blood flow to dependent areas. Right upper lobe collapse secondary to partial right main stem intubation is a frequently overlooked cause. During one-lung anesthesia, the weight of unsupported mediastinal contents, pressure from abdominal contents on the dependent diaphragm, and lung compression all reduce dependent lung volume. Gravity and lymphatic obstruction promote interstitial fluid accumulation and further V·/Q· mismatching. This “down lung syndrome” may appear as unilateral pulmonary edema on the chest film. Postoperatively, acute pulmonary edema from overhydration, ventricular dysfunction, airway obstruction, or increased capillary permeability (e. Small airway occlusion from compression, retained secretions, or aspiration leads to distal hypoventilation and hypoxemia, as does main stem intubation. If possible, patients should recover in a semisitting or reverse Trendelenburg position to reduce abdominal pressure on the diaphragms. Intubation for delivery of noninvasive ventilation does not mandate positive-pressure ventilation. In postoperative2 patients, position affects oxygenation if gravity forces blood flow to areas with reduced ventilation. For example, placing a poorly ventilated lung in a dependent position can reduce PaO. When possible, avoid placing an atelectatic or diseased lung in a dependent position. Placing poorly ventilated parenchyma in a nondependent position could improve V·/Q· matching, but positioning a diseased lung in an “up” position may promote drainage of purulent material into the unaffected lung. Hypoventilation must be severe to cause hypoxemia based on the alveolar gas equation, and can be completely masked by even small amounts of supplemental oxygen administration. Complete apnea or airway obstruction by a foreign body, soft-tissue edema, or laryngospasm as well as very high small airway resistance all lead to rapid depletion of alveolar oxygen, and preclude effective ventilation. Volume displacement of oxygen could also occur during severe hypercarbia in a patient breathing ambient air, although acidemia is often a greater problem. If arterial oxygen content decreases 3883 or tissue extraction increases, P O falls. The lower the P O in blood that is2 2 shunted or flows through low V·/Q· units, the greater the reduction of PaO. In postoperative patients, shivering, infection, and hypermetabolism lower P O by increasing peripheral oxygen extraction. Low cardiac output2 and hypotension also lower P O by decreasing tissue oxygen delivery. Figure 54-3 SpO versus postanesthesia care unit time in patients spontaneously2 ventilating in room air after general anesthesia (Group 1, 0 to 1 year of age; group 2, 1 to 3 years; group 3, 3 to 14 years; group 4, 14 to 58 years). A comparative study of early postoperative hypoxemia in infants, children, and adults undergoing elective plastic surgery. This obstruction in turn interrupts sleep patterns, resulting in daytime 3884 hypersomnolence, decreased ability to concentrate, increased irritability, as well as aggressive and distractible behavior in children. The airway obstruction may cause episodic oxygen desaturation, hypercarbia, and possibly lead to cardiac dysfunction. These numbers51 are likely to increase as the population ages and become increasingly obese. Postoperative management concerns include analgesia, oxygenation, patient positioning, and monitoring. Regional anesthesia with minimal sedation is best for recovery versus increased use of opioids. Positioning should be used to minimize the patient’s ability to obstruct the airway, which can be limited based on the type of surgery. With regard to monitoring, there is agreement among the consultants on the task force that pulse oximetry should be used until the patient’s oxygen saturation remains above 90% on room air while sleeping. Anemia Preoperative hematocrit and intraoperative hemorrhage determine a patient’s red cell mass and oxygen-carrying capacity after surgery. The hematocrit at which oxygen delivery becomes insufficient to match tissue needs varies with cardiac reserve, oxygen consumption, hemoglobin dissociation, PaO , and2 3885 blood flow distribution. Of course, this level of hemoglobin may be too low to be an appropriate transfusion trigger. However, it does illustrate the large excess of hemoglobin available to meet metabolic O demands. Each patient has a minimum hematocrit below which2 tissues use inefficient anaerobic metabolism, generating a lactic acidemia. Patients with vascular disease are at increased risk of vital organ ischemia as hematocrit falls. It is well accepted now that patients who are stable, not bleeding, and euvolemic can tolerate a hemoglobin of 6. Transfusion may be of some benefit between 6 and 8 g/dL and it is rarely useful above 10 g/dL. Furthermore, transfusion of red cells to assist in weaning a patient from the ventilator has been shown to make the weaning process prolonged and/or make it far more difficult to discontinue mechanical ventilation. Table 54-3 Common Oxygen Delivery Systems with Correlating O Flow Rates to2 Delivered FiO Ranges2 Supplemental Oxygen The incidence of hypoxemia in postoperative patients is high. One cannot predict which54 patients will become hypoxemic or when hypoxemia will occur. Patients with 3886 lung disease or obesity, those recovering from thoracic or upper abdominal procedures, and those with preoperative hypoxemia are at increased risk. Supplemental oxygen6 does not address underlying causes of hypoxemia in postoperative patients, its use does not guarantee that hypoxemia will not occur, and it is likely to mask hypoventilation. Although oxygen might cause minor mucosal drying,56 routine humidification is of little benefit unless intubation bypasses natural humidification. Pulmonary morbidity from perioperative aspiration varies with the type and volume of the aspirate. Although aspiration of gastric contents is most widely feared, surgical patients also experience other aspiration syndromes. Aspiration of clear oral secretions during induction, face mask ventilation, or emergence is common and usually insignificant. Cough, mild tracheal irritation, or transient laryngospasm are immediate sequelae, although large- volume aspiration predisposes to infection, small airway obstruction, or pulmonary edema. Aspiration of blood secondary to trauma, epistaxis, or airway surgery generates marked changes on the chest radiograph that are out of proportion with clinical signs.

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The microbiome is the ecological community of microorganisms that reside in the whole body buy 100mg aurogra fast delivery. The most intensively studied branch is the gut microbiome which consists of 40 trillion microbes generic 100mg aurogra overnight delivery, as many cells as we have in our bodies [82] purchase aurogra amex. Within 6 h of the onset of sepsis [83] generic aurogra 100mg line, the microbiome is converted into the “pathobiome” [84, 85] which is highlighted by (a) a loss of microbial diversity, (b) dominance of pathogenic micro- organisms, and (c) alterations in bacteria present to become more virulent [86, 87]. Together, these induce extremely low microbial diversity which is associated with worse outcomes in sepsis patients [84–86]. Each of these has been demon- strated to improve patient-centric outcomes such as ventilator-associated pneumo- nia, diarrhea, and mortality. However, our understanding of the microbiome is still very much in the nascent stage. The road ahead will allow us to understand our inner microbial community on a cellular and subcellular level and how to potentially modulate this community in a precision manner to improve outcomes in a more targeted, mechanistic method. Historically, many trials have attempted to decrease the pro-infammatory response in sepsis. While this approach has often been successful in preclinical trials of inbred mice when the precise time of onset of sepsis is known, they have generally been unsuccessful in septic patients [96]. This can lead to secondary infection in the immunosuppressive stage of sepsis, which is a common cause of late death in sepsis [104, 105]. Notably, co-inhibitor blockade is associated with improved survival in multiple preclinical models of sepsis. While clinical trials examining co-inhibitory blockade in septic patients are just beginning to enroll patients, immune augmentation represents an attractive strategy in the future for sepsis. Further, a better understanding of a patient’s immune status (pro- infammatory, anti-infammatory, exhausted, immunosuppressed, etc. Sixteen (53%) of the 30 patients survived, 73% in group 1, 60% in group 2, and 36% in group 3. Survival correlated well with age less than 50 and the absence of multiple organ failure. The authors emphasized that the technique was easy to perform, avoiding many of the pitfalls previously reported. They pointed out that the absorbable polyglycolic acid (Dexon®) was found superior to the nonabsorbable polypropylene mesh. In 1989, this group presented their second series to the Eastern Association for the Surgery of Trauma and published it in 1990 [16]. Some kept the abdomen closed in between procedures; others used various closure techniques such as retention sutures, slide fasteners, zippers, and Velcro adhesive sheets or towel clips. In 1993, the Surgical Infection Society carried out a prospective, open, consecutive, nonrandomized trial to examine management 1 Open Abdomen: Historical Notes 7 techniques and outcome in severe peritonitis [18]. There was no signifcant difference in mortality between patients treated with a “closed abdomen technique” (31% mortal- ity) and those treated with variations of the “open abdomen” technique (44% mor- tality). Factors indicative of progressive or persistent organ failure during early postoperative follow-up were shown to be the best indicators for ongoing infection and were associated with posi- tive fndings at relaparotomy [20]. Planned relaparotomy did not, therefore, lose its indication for selected patients. A majority of these patients were being seen at the end of their physiologic reserve, a situation called “physio- logic exhaustion. This truly heralded a new era in the management of the most severely injured and ill patients. Specifcally, the practice of supranormal oxygen delivery as an endpoint of adequacy of resuscitation, even though debunked by two prospective trials [23, 24], meant excessive crystalloid and colloid infusion. Group 1 consisted of 47 patients who received mesh at initial celiotomy, and group 2, 26 patients who received mesh at a subsequent celiotomy. These two groups were sta- tistically similar in demographics, injury severity, and mortality. However, group 2, compared with group 1, had a signifcantly higher incidence of postoperative abdominal compartment syndrome (35 versus 0%), necrotizing fasciitis (39 versus 0%), intra-abdominal abscess/peritonitis (35 versus 4%), and enterocutaneous fs- tula (23 versus 11%) (p < 0. Ivatury and associates [31] had been studying patients with catastrophic pene- trating trauma undergoing damage control procedures from 1992 to 1996. Further advances were also realized through the efforts of a remarkable group of clinical researchers interested in the subject. The efforts of anticipation of the complication, measures of prophylaxis, and earlier recognition and intervention all soon bore fruits: fewer organ failures and better survival. They also documented that abdominal decompression does not prevent return to gainful employment and should not be considered a permanently disabling condition. Another study [45] surveyed Dutch surgeons with a literature-based and expert consensus survey. A similar lack of application of defnitions and guidelines was reported among German pediatric intensivists [47] and Australian critical care nurses [48]. In most of the existing treatment strategies, the abdomen needed to be closed within a window of 5–7 days for a high chance of fascial closure. In those initial years, two important and highly morbid complications of this approach were frequent: abdominal wall hernia and enteroatmospheric fs- tula [49–54]. Many different techniques have been introduced during the past 10 years [49], but there were no controlled trials. Initially a nonabsorbable mesh (polypro- pylene) was used but soon fell out of favor because of the rigidity, propensity to cavuse bowel fstula when it came into contact with bowel, and also subsequent fragmentation. Furthermore, it often required a diffcult reoperation to excise it from the wound. Absorbable mesh soon became popular, initially polyglycolic acid (Dexon®) and later Vicryl®. They got absorbed and incorpo- rated into the granulation tissue covering the open abdomen. The Wittmann Patch consists of hook-and-loop (Velcro®-like) sheets that are pressed together to form a secure closure and peeled apart for abdominal reentry. As abdominal swelling decreases, the fascial edges are pulled closer together and excess patch material is trimmed. When the two fascial edges are close enough, the remaining patch material is removed, and the abdominal wall is closed by suturing fas- cia to fascia. Brock in 1995 [58] and Barker in 2007 [59] pioneered the concept of using a vacuum drainage of the free peritoneal fuid by suction catheters. The open abdo- men was covered by a fenestrated polyethylene sheet between the abdominal vis- cera and the anterior parietal peritoneum; a moist, surgical towel over the sheet with two suction drains; and an adhesive drape over the entire wound which is airtight. As soon as the drains were connected to wall suction, the entire apparatus would “collapse,” evacuating the peritoneal fuid and blood. The importance of a rigid protocol and a standardized approach were illustrated by several reports [60–63] with a fascial closure rate of 88–100%, even as late as 9–21 days after the frst laparotomy. It was simi- lar in design to the previous system with the addition of six foam extensions radially situated on the visceral protective layer. A nonadherent fenestrated polyurethane sheet separates the bowel from abdominal wall and helps remove fuid. On study days 1, 2, 3, 7, and 28, blood and peritoneal fuid were analyzed for cytokines. The cumulative incidence of fascial closure at 90 days was similar between groups. It is as follows: “Grade I, without adherence between the bowel and abdominal wall or fxity of the abdominal wall (lateralization), subdivided as 1A, clean; 1B, contaminated; and 1C, with enteric leak. An enteric leak controlled by closure, exteriorization into a stoma, or a permanent enterocutaneous fstula is considered clean. They recruited 572 patients from 14 American College of Surgeons-verifed Level I trauma centers. Subsequent results from this group [75, 76] included predictors of enterocutaneous, enteroatmospheric fstulae and intra-abdominal sepsis. Surgeons should be aware of the pathophysiology of severe intra-abdominal sepsis and always keep in mind the option of using open abdomen to be able to use it in the right patient at the right time” [78]. The most common indications for operation were perforated viscus/free air (20%), mesenteric ischemia (17%), peritonitis (16%), and gastrointestinal hem- orrhage (12%).

Afferent input to the hypothalamus from the warm peripheral compartment counteracts conflicting input from the cooling central compartment buy aurogra 100mg overnight delivery, thus delaying the initiation of compensatory thermoregulation order aurogra 100 mg with amex. In the absence of reliable temperature monitoring discount aurogra 100 mg on-line, it is possible that the first indication of hypothermia would be the onset of shivering generic 100 mg aurogra mastercard, by which time considerable central cooling may have occurred. Furthermore, the method that was most frequently used to monitor temperature may not accurately reflect core temperature, the most important determinant of thermoregulatory response and perioperative morbidity. The accuracy of these devices for perioperative temperature monitoring remains controversial; they do not reliably detect malignant hyperthermia and are not sufficiently accurate for fever screening purposes in children. Patients will frequently complain of feeling too warm when covered by heavy drapes. Although malignant hyperthermia is rare during monitored anesthesia care, hyperthermia is still possible as a result of thyroid storm or malignant neuroleptic syndrome. The subjective sensation of hyperthermia may also be the first indicator of important adverse events in evolution such as hypoxia, hypercarbia, cerebral ischemia, local anesthetic toxicity, and myocardial ischemia. Sedation monitoring is attractive because of the potential to titrate drugs more accurately, avoiding the adverse effects of both over- and underdosing. Conventional assessment involves patient stimulation at frequent intervals to determine the level of consciousness, requires patient cooperation, and is subject to testing fatigue. However, the inability to recall a nonnoxious stimulus such as a picture, as used in the previously mentioned studies, may not necessarily correspond to amnesia to noxious events such as surgical stimulation. Table 30-8 Observer’s Assessment of Alertness/Sedation Scale Preparedness to Recognize and Treat Local Anesthetic Toxicity Monitored anesthesia care is often provided in the context of regional or local anesthetic techniques. It is vitally important that the anesthesiologist responsible for the patient have a high index of suspicion and be fully prepared to recognize and treat local anesthetic toxicity immediately (see Chapter 22). This point deserves special emphasis, particularly in view of the fact that monitored anesthesia care is often provided to the elderly or debilitated patient who has been deemed “unfit” for general anesthesia; these are the patients most likely to suffer adverse reactions to local anesthetic drugs. Even if the anesthesiologist does not perform the block personally, he 2081 or she is in a unique position to fulfill an important “preventive” role by advising the surgeon about the most appropriate volume, concentration, and type of local anesthetic drug or technique to be used. Systemic local anesthetic toxicity occurs when plasma concentrations of drug are excessively high. Plasma concentrations will increase when the rate of entry of drug into the circulation exceeds the rate of drug clearance from the circulation. The clinically recognizable effects of local anesthetics on the central nervous system are concentration dependent. At low concentrations, sedation and numbness of the tongue and circumoral tissues and a metallic taste are prominent features. As concentrations increase, restlessness, vertigo, tinnitus, and difficulty focusing may occur. Higher concentrations result in slurred speech and skeletal muscle twitching, which often herald the onset of tonic–clonic seizures. The conduct of monitored anesthesia care may modify the individual’s response to the potentially toxic effects of local anesthetic administration and adversely affect the margin of safety of a regional or local technique. For example, a patient with compromised cardiovascular function may experience a further decline in cardiac output during sedation. The resultant reduction in hepatic blood flow will reduce the clearance of local anesthetics that are metabolized by the liver and have a high hepatic extraction ratio, thereby increasing the likelihood of achieving toxic plasma concentrations. A patient receiving sedation may experience respiratory depression and a subsequent increase in arterial carbon dioxide concentration. By increasing cerebral blood flow, hypercarbia will increase the amount of local anesthetic that is delivered to the brain, thereby increasing the potential for neurotoxicity. By reducing neuronal axoplasmic pH, hypercarbia increases the intracellular concentration of the charged, active form of local anesthetic, thus also increasing its toxicity. In addition, hypercarbia, acidosis, and hypoxia all markedly potentiate the cardiovascular toxicity of local anesthetics. Furthermore, the administration of sedative–hypnotic drugs may interfere with the patient’s ability to communicate the symptoms of impending neurotoxicity. However, the anticonvulsant properties of benzodiazepines and barbiturates may attenuate the seizures associated with neurotoxicity. In both of these circumstances, it is possible that the symptoms of cardiotoxicity will be the first evidence that an adverse reaction has occurred. Thus, appropriate treatment is delayed or inadvertent intravascular injection is continued because of the absence of any clinical evidence of neurotoxicity. Cardiovascular toxicity usually occurs at a higher plasma concentration than neurotoxicity, but when it does occur, it is usually much more difficult to manage than neurotoxicity. Although cardiotoxicity is usually preceded by neurotoxicity, it may on occasion be the initial presenting feature. Deep sedation is occasionally delivered by trained specialists, including emergency department physicians and intensivists. The specific reasons for nonanesthesiologist involvement differ from institution to institution and from case to case and include convenience, availability, and scheduling issues; perceived lack of anesthesiologist availability; perceived increased cost; and a perceived lack of benefit concerning patient satisfaction and safety when sedation and analgesia are provided by anesthesiologists. Despite our frequent noninvolvement in these cases, anesthesiologists are indirectly involved in the care of these patients by being required to participate in the development of institutional policies and procedures for sedation and analgesia, as mandated by the Joint Commission. The practice guidelines emphasize that sedation and analgesia represent a continuum of sedation wherein patients can easily pass into a level of sedation deeper than intended. This statement contains a chart representing the clinical progression along this continuum (Table 30- 9). The importance of continuous patient monitoring is discussed—in particular, the response of the patient to commands as a guide to the level of sedation. The appropriate monitoring of ventilation, oxygenation, and hemodynamics is also discussed, and recommendations are made for the contemporaneous recording of these parameters. The task force strongly suggests that an individual other than the person performing the therapeutic or diagnostic procedure be available to monitor the patient’s comfort and physiologic status. Specific educational objectives include the potentiation of sedative-induced respiratory depression by concomitantly administered opioids, adequate time intervals between doses of sedative/analgesics to avoid cumulative over-dosage, and familiarity with sedative/analgesic antagonists. At least one person with Basic Life Support training should be available during moderate sedation, with immediate availability (1 to 5 minutes) of personnel trained in Advanced Life Support. This individual should have the ability to recognize airway obstruction, establish an airway, and maintain oxygenation and ventilation. The practice guidelines recommend that appropriate patient- size emergency equipment be readily available, specifically including equipment for establishing an airway and delivering positive pressure ventilation with supplemental oxygen, emergency resuscitation drugs, and a working defibrillator. Adequate postprocedure recovery care with appropriate monitoring must be provided until discharge. Controversy exists regarding the level of training required for nonanesthesiologists to be credentialed to provide moderate and deep sedation. These “anesthesia” services must be provided by: A qualified anesthesiologist; a doctor of medicine or osteopathy, a dentist, oral surgeon, or podiatrist who is qualified to administer anesthesia under state law; an appropriately supervised Certified Registered Nurse Anesthetist or Anesthesia Assistant, all who are separate from the practitioner performing the procedure. Failure to follow these recommendations could put patients at increased risk of significant injury or death. These devices integrate patient monitoring variables with the programmed delivery of propofol. The manufacturer of this system required that it should only be used in facilities where an anesthesia professional is immediately available to assist or consult as needed. However, the device worked in conjunction with a single administered dose of fentanyl given 3 minutes prior to the start of a propofol infusion in an attempt to yield some analgesic effect. After a maintenance infusion rate escalation, further increases were limited by a 3-minute lockout period. There were several safety mechanisms in place to ensure both adequate depth of sedation, and prevention of oversedation. An automated responsiveness monitor actuated by the patient assessed his/her responsiveness by requiring interaction with a hand-held device when prompted by vibratory or auditory stimulation. Oxygen delivery was also automatically titrated as determined by oxygen saturation measurement. There were alarm systems to alert the provider to low respiratory rate, low oxygen saturation or apnea events. Monitored anesthesia care presents an opportunity for our patients to observe us at work.

In light of this purchase 100 mg aurogra overnight delivery, ophthalmic ultrasound has been proposed as a safe purchase generic aurogra line, real-time safe aurogra 100 mg, point-of-care means by which to assess intracranial pressure and cerebrovascular hemodynamics purchase aurogra discount, through assessment of the optic nerve sheath diameter and Doppler properties of the ophthal- mic artery , respectively. The ophthalmic artery represents an accessible surrogate for the smaller caliber intracerebral vessels, which is the likely level at which hemodynamic changes occur in preeclampsia. Reference ranges for a number of Doppler indices in this vessel have been published [7, 8], although it is the “peak ratio”—the ratio between the frst peak diastolic velocity and the peak systolic velocity—that is considered to be the most sensitive measure of hemodynamic change in this context. Further research is required to confrm the potential clinical applicability of these imaging modalities. The latter has been defned as a drop of at least a 50 cm/s from the maximum diastolic velocity but is often assessed subjectively [10]. In the frst trimester, the uterine artery Doppler waveform commonly demonstrates an early diastolic notch (46–64% of nor- mal gestations) and low end-diastolic velocities [11]. This phenomenon is secondary to a fall in resistance in uterine vessels following trophoblastic invasion. Similarly, notching disappears between 20 and 26 weeks’ gestation due to an increase in uterine artery compliance [12]. Abnormal maternal vascular tone is associ- ated with persistent early diastolic notching in the second trimes- ter. Reference ranges for uterine artery Doppler parameters have been established in various populations [13–17] using the techniques described below. The examiner’s hand may rest on the bridge of the patient’s nose or on her fore- head to control and minimize the degree of pressure on the eye. Using B-mode imaging, set the feld depth to encompass the globe and the retro-orbital space, with the focus set to the latter. Using color Doppler, identify the ophthalmic artery by its direction of fow (toward the probe) and pulsatility. Ophthalmic artery Doppler analysis: A window into the cerebrovasculature of women with preeclampsia. Apply pulsed wave Doppler, with the sample volume placed around 15 mm behind the optic disc, medial to the optic nerve; the sample volume should be 2 mm in length. Keep the insonation angle at <20°, and set the high-pass flter to its minimum value. Standard Doppler indices may be calculated automatically by the ultrasound machine, although the peak ratio will require man- ual measurement of the frst diastolic peak velocity. Measurements have been shown not to differ between the right and left eyes, vali- dating unilateral assessment [20]. Place electronic calipers across the optic nerve sheath 3 mm behind the globe, perpendicular to the optic 4 Stefan C. Optic nerve ultrasound for the detection of elevated intracranial pressure in the hypertensive patient. Assess the diameter in two planes—transverse and sagittal, the latter requiring rotation of the probe by 90°. The aver- age of the two measurements represents the mean optic nerve sheath diameter if one eye is assessed, whereas if both eyes are examined, the four measurements may be averaged for a single mean sheath diameter. In multiple pregnancies, the uterine artery impedance measurements appear to be lower, but studies of uterine artery Doppler screening in this subgroup are limited [23, 24]. Overall, uterine artery Doppler is more accurate for prediction of pre- eclampsia in the second trimester than in the frst, but the test does not perform adequately in isolation in any trimester to be used clinically [25, 26]. The screening performance of uterine artery Doppler analysis is improved when performed as part of a multiparametric model incorporating maternal characteristics and serum biomarkers [27–29]. First-Trimester Uterine Artery Doppler Analysis in the Prediction of Later Pregnancy Complications. Firstly, obtain a midsagittal section of the uterus and cervical canal and move the trans- ducer laterally until the paracervical vessels are visualized. The uterine arteries are seen as aliasing vessels along the side of the cervix when color fow Doppler is applied. Using pulsed wave Doppler, obtain fow velocity waveforms from the ascending branch of the uterine artery at the point closest to the internal os, with the Doppler sampling gate set at 2 mm. In order to achieve the highest systolic and end-diastolic velocities, use the smallest angle of insonation (<30°). An alternate transabdominal technique involves Doppler insonation of the uterine artery at the level of its apparent 6 Stefan C. First-Trimester Uterine Artery Doppler Analysis in the Prediction of Later Pregnancy Complications. Position the transducer approximately 2–3 cm inside the iliac crests, then direct it toward the pelvis and the lateral side of the uterus. Apply pulsed wave Doppler approximately 1 cm above the point at which the uterine artery crosses over the external iliac artery [30]. The site of uterine artery crossover with the external iliac artery can be harder to locate with a smaller uterus in the frst trimester, whereas the frst technique-measuring uterine artery Doppler at the level of the internal cervical os is achievable in most cases. Place the transducer in the anterior vaginal fornix and obtain a sagittal section of the cervix. Move the vaginal transducer laterally until the paracervical vascular plexus is Diagnostic Imaging: Ultrasound 7 seen. Identify the uterine artery with color Doppler at the level of the cervico-corporeal junction. Take measurements with pulsed wave Doppler at this point before the uterine artery branches into the arcuate arteries [30]. Transabdominal technique: The technique is similar to the Assessment in the Second aforementioned transabdominal method in the frst trimester. Trimester Place pulsed wave Doppler 1 cm downstream from the cross- over point of the uterine artery and external iliac artery [30]. Using color Doppler, identify the uterine artery at the level of the internal cervical os. Altman D, Carroli G, Duley L, Farrell B, J Ultrasound Med 28(5):563–569 Moodley J, Neilson J, Smith D (2002) Do 9. The Magpie into the cerebrovasculature of women with Trial: a randomised placebo-controlled trial. Campbell S, Bewley S, Cohen-Overbeek T F (2013) Stroke during pregnancy and pre- (1987) Investigation of the uteroplacental cir- eclampsia. Dubourg J, Javouhey E, Geeraerts T, Messerer Development of uterine artery compliance in M, Kassai B (2011) Ultrasonography of optic pregnancy as detected by Doppler ultrasound. Intensive Care Med 37(7):1059– Costa Fda S (2013) Reference range of uterine 1068. Comparison of two different sites of measure- eclampsia and fetal growth restriction in twin ment for transabdominal uterine artery pregnancies at 23 weeks of gestation by trans- Doppler velocimetry at 11-13 weeks. Rizzo G, Arduini D, Romanini C (1993) Uterine lines: use of Doppler ultrasonography in artery Doppler velocity waveforms in twin preg- obstetrics. The diagnosis of preeclampsia is currently based on nonspecifc crite- ria including blood pressure, proteinuria, and subjective patient symptomatology. These parameters are late, end-organ effects of disease [3–7], and they display poor test accuracy for prediction of adverse outcomes. Measurements for these biomarkers can be performed quickly allowing rapid bedside results. These platforms are becoming fea- sible to use in an everyday clinical context as part of the diagnostic workup for patients with suspected preeclampsia, given their rela- tive ease of use and quick turnaround time for results. The plat- forms available have been validated in numerous studies in the diagnosis of preeclampsia [15–17, 20–23]. We have used this platform within our department recently to test retrospectively collected frozen patient serum for the purpose of research into the prediction of preeclampsia at midgestation. The system consists of the analyser, which performs all functions required for fully automated sample and assay process- ing, and a control unit, which controls the analyser through the user software. The Cobas® e 411 analyser was designed for both quantitative and qualitative in vitro determination of analytes in body fuids using a wide vari- ety of tests, with a throughput of approximately 85 tests per hour. The Cobas® e 411 analyser is a discrete unit, which can be placed on a benchtop in the laboratory. All assay reagent, calibrator, and control information can be automatically entered into the software through the use of bar- codes and e-barcodes. Data transmission to and from the analyser, result evaluation, documentation, and quality control are performed automatically by the software.

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