Timothy Witham, M.D.

• Director, the Johns Hopkins Neurosurgery Spinal Fusion Laboratory
• Professor of Neurosurgery

https://www.hopkinsmedicine.org/profiles/results/directory/profile/0020144/timothy-witham

The amount of blood flowing through the shunt can be quantified by measuring oxygen saturations in various locations in the venous system and the right heart ("oxygen saturation run") prostate cancer younger men purchase eulexin 250mg mastercard. The samples need to be acquired with the patient breathing room air or a gas mixture containing no more than a maximum of 30% oxygen ( to minimize the amount of dissolved oxygen in the blood) androgen hormone pregnancy purchase 250 mg eulexin with mastercard. Regurgitant orifice area >40 mm2 has been associated with a poor prognosis and is considered a strong indication for surgery androgen hormone zyklus discount eulexin 250mg mastercard. Eventually cardiac output begins to decline prostate cancer survival rate buy eulexin on line amex, resulting in worsening functional limitation mens health report order eulexin 250mg line. Decreased ejection fraction (<60%) is a negative prognostic sign and is considered a strong indication for mitral valve surgery prostate cancer jamaica order 250 mg eulexin with visa. The continuity equation produces a reliable and accurate estimate of the mitral valve area. The Gorlin formula is then used to convert hemodynamic data to an estimate of the mitral valve area. Later, chronic pulmonary venous hypertension can result in pulmonary arteriolar constriction and hypertrophy, which can lead to irreversible pulmonary arterial hypertension. When there are incongruous findings on the echocardiogram, many patients are referred for hemodynamic assessment in the cardiac catheterization laboratory. This is dependent on accurate measurement of the systolic ejection period and corresponding pressure waveforms and is inherently inaccurate at low cardiac outputs. This scenario is often encountered in patients with aortic root dilatation and/or bicuspid aortic valve. The left ventricular volume is usually reduced and the hypertrophy is asymmetric involving the interventricular septum in 70% of cases. The degree of obstruction increases during systole, when the ventricle contracts and the asymmetric septum moves toward the outflow tract. The initial spike occurs during the early phase of systole, when there is minimal obstruction. Hemodynamic tracings from a patient with restrictive cardiomyopathy showing rapid X and Y descents with the classic W or M sign in the atrial tracing (A) and a rapid rise and plateau of ventricular diastolic pressures (square root sign; B). Note the decrease in aortic pulse pressure after a premature ventricular contraction (Brockenbrough sign). It can be further classified as myocardial or endomyocardial based on the mechanism of disease. Atrial pressure tracings can show a quick X and Y descent from the rapid early filling. The rapid early filling of the ventricle along with the reduced compliance results in a sudden and sharp rise in ventricular pressure during early diastole. Diastolic filling of the ventricle is then curtailed as the pressure in the ventricle rapidly approaches atrial pressures. The visceral pericardium is a mesothelial monolayer that is adherent to the epicardium and reflected back on itself at the level of the great vessels. In the potential space that exists between these two layers there is normally 5 to 50 cc of serous fluid. The normal pericardium serves three primary functions: it fixes the heart within the mediastinum, limits the spread of adjacent infections, and limits acute cardiac distention during sudden increases in intracardiac volumes. Cardiac Tamponade the primary hemodynamic pathophysiologic process in the development of tamponade is increased pericardial pressure that impairs diastolic filling. Normal pericardial pressure is zero; any increase can have hemodynamic consequences. The pericardium is a relatively noncompliant structure and thus the relationship between pericardial pressure and volume is nonlinear. Pericardial pressure rises exponentially as pericardial volume increases after a certain threshold is reached. Factors that influence the development of hemodynamic compromise in the setting of a pericardial effusion include the rate at which the fluid accumulates, the amount of pericardial fluid, the compliance of the pericardium, the size of the pericardial space, and ventricular compliance. Left and right ventricular hypertrophy renders the heart more resistant to elevated pericardial pressures. The hemodynamic effects of increased pericardial pressure occur on a spectrum and cardiac tamponade can be divided in to three phases. As pericardial fluid continues to accumulate and pericardial pressure rises, pulmonary capillary wedge pressure begins to rise and external compression of both left and right ventricles is present (phase 2). End diastolic pressures throughout the cardiac chambers are elevated and within 5 mm Hg of each other. While stroke volume is diminished, compensatory tachycardia attempts to maintain cardiac output. In patients with tamponade, a relatively larger amount of cardiac filling occurs following ventricular contraction as ventricular volume transiently falls, enabling atrial expansion and filling. In contrast to constrictive pericarditis, pericardial pressure varies with intrathoracic pressure in tamponade. While it is normal to have a drop in systolic blood Constrictive Pericarditis Constrictive pericarditis is characterized by a dense, fibrous thickening of the pericardium that adheres to and encases the myocardium resulting in impaired diastolic ventricular filling. The clinical presentation is generally that of rightsided heart failure and may resemble restrictive cardiomyopathy, cirrhosis, or cor pulmonale, among other conditions. In constrictive pericarditis, the stiff pericardium limits expansion of the cardiac chambers which can fill only by compressing other chambers and thus the diastolic pressures equalize. In severe constrictive pericarditis, intrathoracic pressure is not communicated to intrapericardial space. Pulsus paradoxus is minimal or absent in rigid constrictive pericarditis because ventricular filling is not affected by intrathoracic pressure. Ventricular systolic discordance is thought by some to be the most specific hemodynamic sign of constrictive pericarditis. Pulsus paradoxus may not be present in patients with tamponade and acute aortic regurgitation. Effusive-Constrictive Pericarditis Effusive-constrictive pericarditis is an uncommon syndrome characterized by constriction of the heart by the visceral pericardium in the presence of a tense pericardial effusion. The majority of patients diagnosed with effusive-constrictive pericarditis will progress to chronic constriction, but a proportion of those with idiopathic disease may have only temporary cardiac constriction and then go on to eventual full resolution. As in both constrictive pericarditis and cardiac tamponade, the expansion of the cardiac chambers during diastole is limited and there is elevation and equalization of diastolic pressures in the atria and ventricles. Prior to drainage of the effusion, the hemodynamic findings most resemble cardiac tamponade with a preserved X descent and an absent or attenuated Y descent on the right atrial pressure tracing. Once the effusion has been drained, constrictive physiology predominates with return and exaggeration of the Y descent leading to a classic M- or W-shaped configuration of the right atrial pressure waveform. The ventricular pressure tracings demonstrate the square root sign due to rapid ventricular filling in early diastole. Measurements are taken after maximal hyperemia has been achieved with the administration of intracoronary adenosine. This can result in equalization of the diastolic pressures typical of constrictive physiology. This knowledge of coronary physiology is essential in determining whether or not to perform percutaneous coronary intervention on coronary lesions. Fractional Flow Reserve One major limitation of standard angiographic techniques is the inability to assess coronary physiology. Coronary flow reserve is reduced with epicardial artery stenosis, microvascular disease, or both. However, there are two major limitations: inter- and intra-observer variabilities of visual evaluation and discrepancies between the angiographic severity of the lesion and the actual degree of underlying atherosclerosis. Furthermore, the rate of hard endpoint (composite of acute myocardial infarction and cardiac death) was only 3. Large arteries include left main trunk and three major coronary arteries and their branches. As most large arteries run over the epicardial surface of the heart, these are called as epicardial arteries. These arteries do not create significant resistance to coronary blood flow and are also called as conductance vessels. These microvessels take most of the coronary vascular resistance, and are called as resistance vessels. They can modulate the vascular tone and resistance under various physiologic and pharmacological conditions to control the myocardial blood flow. Prearteriolar vessels (100-500 m) are responsive to flow and pressure changes, and their function is to maintain the pressure in a narrow range at the origin of arterioles when coronary perfusion flow or pressure changes. Intramural arterioles (<100 m) are the main part of the metabolic regulation of coronary blood flow. When oxygen consumption increases, arterioles are dilated and vascular resistance is reduced in response to myocardial metabolites. This induces the dilatation of other vessels by the increase in flow and shear stress. Maximum vasodilation Flow Rest Coronary Blood Flow and Concept of Coronary Flow Reserve Coronary arterial blood flow occurs predominantly during diastole, and the systolic component at hyperemia is less than 25% of total flow. The myocardial oxygen demand is much higher than other organs even in the resting condition, and coronary capillary density is also higher to meet the high oxygen demand. Nevertheless, the oxygen extraction by the myocardium is much higher than the other organs and reaches near maximum. The oxygen saturation of coronary sinus venous blood is only about 20-30% (renal vein: 85%). Therefore, coronary circulation can meet the increasing oxygen demand mainly by increasing coronary blood flow. Resting coronary blood flow can be maintained at a relatively constant level under various coronary perfusion pressures in the range of from 40 to 130 mm Hg through the mechanism of autoregulation. The concept of coronary flow reserve was developed to describe the flow increase in response to an increase in oxygen demand. Schematic illustration of coronary pressure-flow relation at rest and at maximal vasodilatation. To measure the coronary flow reserve in a catheterization laboratory, pharmacologic stimuli that can minimize the vascular resistance and induce maximal coronary blood flow are needed. Various routes and drugs are currently being used to induce maximal hyperemia (Table 38-1). Intracoronary bolus administration of adenosine is a simple and safe way to induce maximal hyperemia. The peak effect occurs in less than 10 seconds and the duration of action is less than 20 seconds. Although the resting coronary flow can be maintained until 80-90% diameter stenosis of the epicardial coronary artery, coronary flow reserve is reduced as the portion of vasodilatory reserve is already used to maintain normal coronary flow. In patients with microvascular disease, coronary flow reserve is decreased due to the decrease in maximal coronary blood flow. Arterial and distal coronary pressure changes in a patient with coronary artery disease during continuous infusion of adenosine. Maximal hyperemia corresponds with maximum trans-stenotic pressure gradient and minimal distal coronary pressure. Steady state maximum coronary hyperemia is maintained by continuous infusion of adenosine. Papaverine was considered the gold standard for induction of hyperemia as this drug can induce long maximal hyperemic plateau with bolus administration. However, its use is decreasing due to the potential risk of ventricular arrhythmia. Determination of the mechanism of stent restenosis and to enable selection of appropriate therapy. Evaluation of coronary obstruction at a location difficult to image by angiography in a patient with a suspected flow-limiting stenosis. Assessment of a suboptimal angiographic result after percutaneous coronary intervention. Establishment of the presence and distribution of coronary calcium in patients for whom adjunctive rotational atherectomy is contemplated. Determination of plaque location and circumferential distribution for guidance of directional coronary atherectomy. However, there are two major limitations: inter- and intra-observer variability of visual evaluation and discrepancies between the angiographic severity of the lesion; and the actual degree of underlying atherosclerosis. Although the quantitative coronary angiography has reduced its limitations, it cannot completely overcome the limitation of twodimensional angiographic analysis. Therefore, additional procedures are required in lesions with ambiguous or questionable angiographic findings. Intravascular ultrasound is commonly used in such conditions and can give detailed three-dimensional information on both the lumen and vessel. Pressure- and flow-derived indexes are also frequently used to evaluate the physiologic significance of lesions in both epicardial artery and microvasculature. Coronary pressure or Doppler velocimetry may also be useful as an alternative to performing noninvasive functional testing to determine whether an intervention is warranted. The mechanical system has a single transducer, which can rotate at the speed of 1800 rpm, while the solid state system has multiple, cylindrically arrayed transducer elements that can be activated sequentially. When performed by an experienced operator, the risk of this invasive imaging procedure is very low. The most frequent complication is transient coronary artery spasm, but this event usually responds well to the intracoronary nitroglycerin. In some of the normal subjects, only a monolayer structure is observed due to very thin medial layer. Intimal thickness increases with age, and normal thickness in adults is considered to be >250-500 m. Average thickness of media in normal coronary arteries is about 200 m and becomes thinner with the progression of atherosclerosis.

The combination of a positive indium antimyosin scan and nonventricular dilation is significantly predictive of a positive myocardial biopsy prostate cancer vitamin d generic eulexin 250 mg with visa. Gallium scanning can also be utilized in myocarditis mens health 60 day transformation 250mg eulexin with amex, however androgen nuclear hormone receptor purchase eulexin 250mg otc, it only detects myocardial inflammation and is nonspecific for myocarditis prostate cancer nursing diagnosis discount 250 mg eulexin with amex. Myocardial Imaging Echocardiography this imaging modality has been routinely utilized to evaluate patients with suspected myocarditis prostate cancer x-ray cheap eulexin generic. Findings on echocardiography include possible chamber dilation as well as regional hypertrophy and wall motion abnormalities prostate defense buy eulexin 250 mg otc. Identification of pericardial effusion, a marker of general inflammation, is reported in 32 to 57% of myocarditis patients. Myocardial tissue in myocarditis has a myriad of histopathological changes, including changes in membrane permeability, tissue edema and inflammation, and necrosis as well as fibrosis. Other imaging protocols such as double and triple inversion recovery turbo spin recovery sequences provide excellent contrast between regional edema and normal myocardium. Quantitative assessment of signal abnormality can be performed in comparison to adjacent normal myocardium or skeletal muscle (global edema). In those patients with active myocarditis, regional edema was found in 36% of the patients. In the absence of late gadolinium uptake, edema likely represents reversible myocardial injury. T1 weight fast spin-echo imaging with gadolinium infusion is useful in detecting tissue changes in myocarditis. Early gadolinium enhancement indicates hyperemia and capillary leakage that occurs in the active inflammatory state. An inversion pulse sequence is used to highlight the late gadolinium uptake as well as decrease the normal myocardial signal. Clinical and pathological studies give support to the use of late gadolinium enhancement as a gold standard for high specificity in the detection of irreversible myocardial injury. This likely is related to the size of the inflammatory changes as well as the reversibility of some myocarditis lesions. The subepicardium region is typically highlighted with gadolinium; however, this can have a transmural extension. Typical, subepicardial involvement is not isolated, thus distinguishing it from ischemia-mediated injury. Gadolinium uptake tends to localize in the inferolateral segments; however, anteroseptal areas can have involvement. Also, uptake in the basal septum may represent fusion of the right ventricular moderator band to the intraventricular septum. It was found that focal myocardial enhancement in areas of regional wall motion abnormalities was present in 10 of 12 patients with suspected or biopsy proven myocarditis. Thus, these findings strongly support a diagnosis of myocarditis and can be utilized in clinical evaluation of myocarditis. It is generally recommended that at least two of the three findings be positive for the diagnosis of myocarditis: (1) regional or global increased signal intensity in T2 weighted images, (2) increased early gadolinium enhancement between myocardium over skeletal muscle in T1 weight images, and 3) at least one focal lesion with nonischemic regional distribution in inversion recovery-prepared late-gadolinium enhanced T1-weighted images. It is interesting that if patients with fulminant myocarditis can recover from the initial insult of cytokine release and hemodynamic collapse, then the survival is ~90% at a decade. Giant cell myocarditis patients have the worst overall prognosis with medial survival of 6 months, and many are listed for transplantation. Chronic active myocarditis patients have a relatively poor prognosis with a mortality of 20% at 1 year and 56% at 4. Five-year survival rates in the Mayo Clinic observational study were similar at 50%. Normal chamber size on echo, resolution of myocarditis on follow-up biopsy, and viral negative biopsy appear to predict a better outcome. Animal data are available and suggest the following: (1) Aerobic exercise soon after onset of cardiac symptoms should be avoided based on exercise intervention in rats that had increased mortality, (2) use of candesartan improved survival in a murine model of myocarditis, and (3) pathologic data and ventricular dimensions improved after treatment with carteolol for coxsackie virus B myocarditis. Arrhythmias can be seen in patients with acute myocarditis; however, treatment is often supportive as they often resolve in the recovery phase. However, even in the setting of acute phase, management may need to be aggressive and could include temporary pacemakers for symptomatic bradycardia or complete heart block. Amiodarone or an implantable cardioverter defibrillator may be needed for symptomatic or sustained ventricular arrhythmias. Immunosuppressive and Antiviral Treatment Treatment with immunosuppressive medications such as corticosteroids, cyclosporine, or immune globulin has been considered for the management of myocarditis and for the related cardiomyopathy. There have been a number of observational trials that have supported the immunosuppressive agents, however, the randomized trials performed to evaluate the actual utility and efficacy of these agents have yielded less than supportive evidence for these agents, including no significant change in mortality in most of these trials. However, this was not sustained over 6 to 9 months and there was no mortality benefit. The Myocarditis Treatment Trial randomized 111 patients with biopsy-verified myocarditis to placebo or prednisone plus cyclosporine or azathioprine. Of note, only 16% of the patients were noted to have pathologic features of myocarditis on biopsy. Observational data support mechanical support in regard to benefit in the acute stage (improve wall stress and geometry and reduce cytokine burden) as well as long-term survival. It appears that inflammation in cardiomyopathy may be the marker for response from immunosuppressive therapy. It is interesting that a small study of lymphocytic myocarditis with all patients treated with either azathioprine or prednisone found that circulating cardiac autoantibodies were seen in responders and a biopsy-positive viral genome was seen in nonresponders at 1 year. There are two possible approaches to immune therapy that involve physical modification. Immune adsorption therapy attempts to remove cardiac depressant factors (cytokines, antibodies, etc. The irradiation may induce apoptosis in the white blood cells and suppress activity of immune cells. At a mean follow-up of 10 months, there was no significant difference in the two groups (placebo vs. Additional randomized, controlled trials will be needed to further examine the utility of inflammatory marker-guided therapy. Agents such as interferon appear promising but also need further supportive evidence. Antiviral treatment has been mainly investigated in animal models and small human case series. The presence of a viral genome on biopsy has been associated with a progressive course of heart failure, death, and transplantation. Ribavirin and interferon alfa treatment reduced myocarditis severity and death in a murine myocarditis model. As the onset of symptoms is often delayed in acute myocarditis from initial viral infection, treatment would likely be less beneficial. However, in those patients with chronic, dilated cardiomyopathy, treatment with interferon resulted in viral clearance and improvement in left ventricular function. Additional treatment trials are needed in such patients to warrant recommendation of antiviral treatment in this setting. The 5-year mortality for patients with symptomatic heart failure approaches 50% and may be as high as 80% at 1 year for the end-stage patients. Over the past four decades, cardiac transplantation has become the preferred therapy for select patients with end-stage heart disease. Approximately 2,400 heart transplants are performed annually in the United States. Critical to the success of heart transplantation are the continual investigational efforts to optimize immunosuppressive regimens. Improvements in immunosuppression, donor procurement, surgical techniques, and posttransplant care have resulted in a substantial decrease in acute allograft rejection, which had previously significantly limited survival of transplant recipients. Thus, heart transplant recipients can now expect excellent quantity and quality of life. Conditional half-life = time to 50% survival for those recipients surviving the 1st year posttransplantation. The transplant half-life (the time at which 50% of those transplanted remain alive, or median survival) for the entire cohort of adult and pediatric heart recipients is currently 10 years, with a half-life of 13 years for those surviving the 1st year. The most common indication for heart transplantation is intractable heart failure. Angina alone is often not considered an indication for transplantation in the absence of heart failure, since it is not clear if the survival of such patients is improved with heart transplantation. Thus, it is essential to determine if patients are truly refractory to maximal medical therapy, which may require referral to an advanced heart failure center. At an advanced heart failure center, evaluation may include tailored therapy with pulmonary arterial catheterization for optimization of filling pressures and cardiac output, high-risk revascularization of coronary artery disease, or specialized therapies, such as ablation of ventricular tachycardia, before consideration of heart transplantation. Contraindications There are two major areas of contraindication for heart transplantation: medical and social/psychological. The extensive evaluation process is designed to identify any contraindication, outlined in detail below and listed in Table 64-1. Age In general, patients should be considered for heart transplantation if they are 70 years of age or younger, since advances in posttransplant care have shown that survival in the older age group is comparable to that of younger transplant recipients. Patients older than 70 years have also been reported to have acceptable outcome, but careful consideration of associated comorbidities is essential. Malignancy Active neoplasm excluding nonmelanoma skin cancer is an absolute contraindication to heart transplantation due to limited survival rates. In general, heart transplant recipients with cancers that have been in remission for more than 5 years or that are low-grade, such as prostate cancer, are often acceptable. Pulmonary Hypertension Right heart failure contributes to morbidity and mortality after heart transplantation, related to preoperative pulmonary hypertension. Thus, assessment of invasive hemodynamics is an essential part of the transplant evaluation. Diabetes Diabetes that is uncontrolled or associated with end-organ damage (proliferative retinopathy, severe neuropathy, nephropathy, peripheral vascular disease) is often considered a contraindication to transplantation. At our institution, patients will ideally achieve control with a hemoglobin A1c under 7. Renal Dysfunction Renal dysfunction is no longer considered an absolute contraindication to heart transplantation, unless the renal dysfunction is due solely to diabetes, since in this situation, it is a sign of poorly controlled diabetes with end-organ damage. If the renal dysfunction is related to poor cardiac function, it may improve posttransplant, and for some patients, dual heart-kidney transplantation is a consideration. Obesity Obese patients have a greater risk of poor wound healing, infections, and pulmonary complications after cardiac surgery, although the data for outcomes in heart transplant recipients are less clear. Peripheral Vascular Disease There is little consensus on the role of cerebrovascular and peripheral vascular disease in heart transplant candidates. It is clear that clinically severe disease that is not amenable to revascularization is an absolute contraindication. However, asymptomatic disease, which can be addressed prior to transplantation, may be considered in the overall context of other risk factors. Chagas disease, although uncommon in the United Status, is a common indication for transplantation in South America, and reactivation of disease can occur. The decision to proceed with transplantation in these situations must be made in collaboration with an infectious disease specialist well-versed in transplantation. Substance Use Active tobacco smoking is a relative contraindication to heart transplantation, and smoking during the previous 6 months before transplant is a risk factor for poor outcomes. At our institution, we require patients to achieve abstinence from tobacco smoking for 6 months, documented by urine cotinine screens, prior to listing for transplantation. Addiction to alcohol or illicit drugs is an absolute contraindication, as it suggests that these patients will have poor compliance after transplantation, and 6 months abstinence with participation in counseling programs is often required. This assessment may be difficult to make in the critically ill patient in whom transplantation cannot be delayed for 6 months. The next tier is Status 1B for the following situations: (1) continuous intravenous inotropic support with one agent and no pulmonary artery catheter in place or (2) a ventricular assist device beyond the first 30 days without a device-related complication. The rest of patients, essentially ambulatory end-stage patients, fall under Status 2 listing. Wait Time the average wait time for a heart transplant varies by region, medical urgency status, blood type, and size. The shortest wait would be for a Status 1A patient who is small and non-O blood type, whereas the longest wait would be for a Status 2 patient who is large and blood type O. An assessment of the wait time to transplantation often factors in to the decision to place a ventricular assist device as a bridge to transplant. For a failing patient, a ventricular assist device may be considered if the anticipated wait time is long. Alternate List the major limiting factor in heart transplantation is supply of donor hearts. Based on this, our program began the use of nonstandard donor hearts often used for higher risk recipients, resulting in the creation of two recipient lists. The concept of the alternate list is to match donor and recipient risk, with a resulting expansion of both the donor and recipient pools. Criteria for the alternate recipient list include those factors that would otherwise preclude transplant: advanced age (usually older than 70 years), moderate renal insufficiency, retransplantation, or peripheral vascular disease. Alternate, or nonstandard, donors are considered to be those with known coronary disease (often requiring revascularization before transplant), high-risk behavior, and hepatitis seropositivity and who are older than 55 years of age. The use of these donor hearts has increased the number of heart transplant operations being performed. In our program, older or nonstandard donor hearts have been used for alternate recipients for the past 15 years, with similar long-term survival and transplant coronary artery disease between older and younger donors. Psychosocial Evaluation Patients must be able to demonstrate the ability to comply with medications and follow-up after transplantation, which includes social support with a dedicated caregiver and transportation after transplant. This is a critical issue, and patients have been denied transplantation due to lack of demonstrated compliance and social support.

Homeostasis of cardiopulmonary androgen hormone wiki cheap 250mg eulexin with amex, endocrine prostate cancer 2015 discount 250mg eulexin, and other somatic systems requires a committed critical care team prostate removal and sexual health purchase discount eulexin on line, but can yield a bright outcome in the midst of tragedy androgen hormone yaki generic 250 mg eulexin otc. An obstetrical code is a situation in which a physician is essentially called upon to save two lives in less than 5 minutes prostate seed implant order 250mg eulexin mastercard. Understanding the pathophysiology prostate 3 biopsies order 250 mg eulexin otc, and preparing ahead of time-on an individual and institutional level-are the keys to providing the best chance for the mother and the baby to survive. Task Force on Scandinavian Therapeutic Hypothermia Guidelines, Clinical Practice Committee Scandinavian Society of Anaesthesiology and Intensive care Medicine. Scandinavian clinical practice guidelines for therapeutic hypothermia and postresuscitation care after cardiac arrest. Unstable signs include altered mental status, ongoing chest pain, hypotension or other signs of shock Note: rate-related symptoms uncommon if heart rate <150/min Wide (0. The rate of fetal mortality after trauma is significant (3%-38% after blunt abdominal trauma), and fetal loss can occur without significant maternal injury. Thus, all pregnant women should be evaluated after trauma, even in the setting of a minor incident. Pregnant women are hospitalized for injuries more commonly than many physicians realize. When compared to nonpregnant trauma patients, pregnant women are younger, less severely injured, and more likely to be African American or Hispanic. Twenty percent of pregnant trauma patients tested positive for drugs or alcohol in one study. In one series, 19%-24% of trauma patients delivered when they required hospitalization for an injury. Motor vehicle crashes account for two-thirds of trauma during pregnancy overall, a fact that is not surprising when one reviews trends in automobile use. The average number of miles driven annually by women of reproductive age increased from 3721 to 8258 during 1975 to 2001. Pregnant women have similar rates of using seat belts (14%) and seat position (70% driver) as nonpregnant women. Nonetheless, it is estimated that the rate of fetal death due to motor vehicle crashes now exceeds infant death by a factor of 7. Blunt trauma most often results from motor vehicle crashes, falls, pedestrian injuries, and assaults are other sources of blunt trauma. The uterus is protected within the pelvis until 12 weeks, so chances of injury are limited. After 20 weeks, the fundal height (in centimeters) corresponds to weeks of gestation. The bladder is displaced upward as the uterus grows, making it an intra-abdominal organ vulnerable to injury. The uterine wall becomes thinner and the relative amount of amniotic fluid decreases with advancing gestation; these changes contribute to the possibility of adverse placental or fetal effects. Gunshot wounds are more common, but the risk of death is decreased in pregnant women compared with nonpregnant women. The gravid uterus provides protection to abdominal organs, so wounds are less likely to cause bowel or vascular injury. However, upper abdominal wounds can be associated with complex bowel injuries in late pregnancy, since the bowel is displaced. Gunshot wounds to the abdomen may enter the uterus and cause fetal injury in up to 70% of cases, with a high fetal mortality rate (40%-65%). Pelvic fracture represents a serious injury, often with hypovolemic shock due to retroperitoneal or intraabdominal hemorrhage. Pelvic fracture alone is not a contraindication to vaginal delivery, but severely dislocated or unstable fractures may be a reason to consider cesarean as the route of delivery. This is likely related to an increased severity of hemorrhage and relative difficulty in diagnosing intra-abdominal pathology. Uncommon types of maternal injuries reported in published literature include thoracic aorta rupture or liver rupture. In rare instances, severe burns, electrical injury, or spinal cord injury can affect pregnancy-the patient should be treated in the same fashion as a nonpregnant individual. Regardless of the type of maternal injury, a variety of adverse sequelae have been reported. Trauma can affect pregnancy outcomes via direct uteroplacental injury, or may be a marker for behavioral risk factors; thus, both short- and long-term complications are possible. Fetal Death A 3-year study of fetal death certificates from 16 states identified 240 fetal deaths due to maternal trauma (3. Motor vehicle crashes accounted for 82% of cases, with firearms and falls accounting for 6% and 3% of cases, respectively. The risk of fetal or infant death is strongly influenced by gestational age at delivery. Other important clinical risk factors include prolonged maternal hypotension or hypoxemia, abruption, uterine rupture, and direct uterine trauma. However, uninjured pregnant women experiencing trauma are also at risk for preterm labor and placental abruption (relative risks of 7. The worst outcomes are seen among women who deliver during the initial trauma hospitalization. Complications in such cases include maternal death, fetal death, uterine rupture, or abruption. Women with prenatal injury (but not delivery) also are at risk for adverse outcomes at delivery, including abruption, preterm labor, and maternal death. Preterm contractions are common among third trimester trauma patients (25%), but these resolve spontaneously in 90%. It is important to monitor women carefully during the remainder of their pregnancy even after the initial trauma episode. Placental abruption is one of the most common complications of blunt abdominal trauma. Typical signs and symptoms include vaginal bleeding, painful contractions, and fetal distress. However, the clinical presentation can be subtle in cases where there is concealed hemorrhage. Historical risk markers include low education level, nonwhite race, lack of seat belt use, and high-speed collision. The risk of abruption is 1% to 5% after minor trauma, but up to 40% to 50% after severe injury. The clinical consequences can be severe, such as fetal death due to acute hemorrhage, fetal hydrops, and maternal sensitization to RhD or other minor antigens. Fortunately, the mean fetal blood loss is typically low, with 98% of cases less than 30 mL. Seventy five percent of cases involve the fundal region of the uterus, and fetal death is common. Among cases of uterine rupture after trauma, maternal death was seen in 10%- much higher than for cases of uterine rupture due to other causes. Clinical features include uterine pain or tenderness, non-reassuring fetal heart rate pattern, abdominal distension, peritoneal signs, and vital sign changes from minimal tachycardia to hypovolemic shock. Cases of uterine rupture with fetal death and fetal spinal fracture have been reported, even with seat belts. Persons able to perform neonatal resuscitation, as well as delivery and neonatal equipment, should be immediately available. Physical examination for the pregnant trauma patient should include all elements as in nonpregnant women, with additional attention to items pertaining to pregnancy. It is important to stabilize the mother first, and then turn attention to the pregnancy and fetus. E-Expose the Remove all clothing; inspect the patient entire body for wounds or ecchymoses. If indicated, arterial blood gas testing should be done if respiratory function is compromised. Be aware that "normal ranges" for laboratory results are based on nonpregnant persons. The arterial pH is increased along with decreased serum bicarbonate level and arterial Pco2. In fact, the most sensitive laboratory indicator of abruption is a decreased fibrinogen content. Secondary Assessment After initial stabilization, evaluate for specific maternal injuries and assess fetal well-being. Adjunctive laboratory tests focus on injury patterns related to the mechanism of injury, patient complaints, or suspicious findings on exam. A secondary survey includes an early vaginal and rectal examination, with attention to dilation and effacement of the cervix. If vaginal bleeding is present in the second or third trimester, cervical examination should be deferred until sonography excludes placenta previa. Gestational age can be initially estimated by fundal height, and is confirmed by bedside ultrasound. External fetal monitoring should be performed on patients at viability or greater, typically 23 weeks and beyond. Among women with contractions every 10 minutes or more, the risk of abruption is 20%. Imaging Studies It is important to obtain quick, reliable imaging in the setting of maternal trauma. Do not avoid or delay necessary exams due to concerns about fetal radiation exposure. Ultrasonic features of placental abruption can be variable, and it plays a limited role in making a diagnosis. Acute hemorrhage is difficult to confirm, since blood has an echotexture similar to myometrium, but retroplacental lucencies may be seen days after abruption. After initial sonogram, 96% of gravid trauma patients required no tests using ionizing radiation, in one study. Theoretical fetal risks of ionizing radiation to the fetus include excess cases of childhood cancer (mainly leukemia), with an estimated risk of 1 in 2000. The potential for congenital anomalies, growth restriction, or mental retardation requires at least 200 mGy of exposure during organogenesis or the fetal period. Most patients can be reassured that the potential fetal risk after a typical trauma evaluation is negligible. This test reliably detects severe fetal anemia, which can cause fetal hydrops or death. Sonographic features of hydrops include placentomegaly, subcutaneous edema, fetal ascites, and pleural or pericardial effusion. Tetanus Prophylaxis Tetanus is a rare, potentially fatal disease caused by the anaerobe Clostridium tetani. Wounds that are crushed, devitalized, or contaminated with dirt or rust are considered to be tetanus-prone. Open fractures, punctures, and abscesses are also associated, but severity of the wound does not determine the risk. If a vaccination history is unknown, tetanus toxoid can be considered when convenient. There are several modifications for pregnant patients, which may improve the effectiveness of resuscitation. It is important to secure the airway early, using continuous cricoid pressure before and during intubation attempts. Although vasopressors decrease uterine blood flow, there are no alternative agents or regimens. Consider potentially reversible causes of cardiac arrest when approaching the gravid patient. In addition to the same causes seen in nonpregnant patients, other factors may include excess magnesium sulfate, preeclampsia/ eclampsia, acute coronary syndromes, aortic dissection, pulmonary embolism, stroke, amniotic fluid embolism, trauma, and drug overdose. With respect to defibrillations, there are no modifications in dose or pad position. It is important to remove any fetal or uterine monitors prior to delivering a shock. Cesarean delivery has been shown to be life-saving for fetuses at viability or beyond. Gestational age and the interval from cardiac arrest to delivery determine the chance of survival and the risk for neurological impairment. A retrospective review of 61 cases indicated 93% of surviving infants were born within 15 minutes of death, with most survivors (70%) delivered by 5 minutes. Cesarean delivery not only plays a role in saving the life of the fetus, but may improve resuscitation efforts for the mother. Mechanisms for improving maternal outcome after emergency cesarean include relieving vena cava compression and improving thoracic compliance. In one series of 38 perimortem cesareans (with 34 surviving infants), 20 cases were due to "resuscitatable" causes. Important elements of standardized care plans include establishing the viability and gestational age of pregnancy, and triaging women in to risk categories based on injury and obstetrical characteristics.

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