A second factor to consider in assessing the hemodynamic consequences of a particular arrhythmia is loss of the atrial contribution to ventricular preload order generic rhinocort online. However buy rhinocort online from canada, as many patients who do not develop fibrillation have such “warning arrhythmias” as those who do generic 100 mcg rhinocort with visa. The previous practice of prophylactic suppression of ventricular premature beats with antiarrhythmic drugs is not indicated and may actually increase the risk for fatal bradycardic and asystolic 1 events. Accelerated Idioventricular Rhythm An accelerated idioventricular rhythm typically occurs during the first 2 days, with about equal frequency in anterior and inferior infarctions. Accelerated idioventricular rhythm often follows when successful reperfusion has been established with fibrinolytic therapy. Ventricular Tachycardia and Ventricular Fibrillation A leading hypothesis for a major mechanism of ventricular arrhythmias in the acute phase of coronary 133 occlusion is reentry caused by inhomogeneity of the electrical characteristics of ischemic myocardium (Fig. The cellular electrophysiologic mechanisms for reperfusion arrhythmias appear to include washout of various ions such as lactate and potassium and toxic substances that have accumulated in the ischemic zone. As noted earlier, magnesium should be repleted to achieve a serum level of 2 mEq/L. After reversion to sinus rhythm, every effort should be made to correct any underlying abnormalities, such as hypoxia, hypotension, acid-base or electrolyte disturbances, or digitalis excess. Urgent revascularization is warranted if ventricular arrhythmias are ongoing and caused by ischemia. The use of extended antiarrhythmic therapy, such as amiodarone or lidocaine, is discussed in Chapters 36 and 39. Thus the acute 1 mortality rate in patients with sinus bradycardia appears similar to that in those without this arrhythmia. Management Isolated sinus bradycardia, unaccompanied by hypotension or ventricular ectopy, should be observed rather than treated. These agents should be stopped only if a higher-degree block or hemodynamic impairment occurs. If the block is a manifestation of excessive vagotonia and is associated with sinus bradycardia and hypotension, administration of atropine, as already outlined, may be helpful. Continued electrocardiographic monitoring is important in such patients in view of the possible progression to higher degrees of block. Temporary pacing systems are almost never needed in the management of this arrhythmia. Complete heart block in patients with inferior infarction usually 133 develops gradually, often progressing from a first-degree or type I second-degree block. Pacing is indicated, however, if symptoms related to a ventricular rate emerge, if ventricular arrhythmias or hypotension is present, or if pump failure develops. However, pacing protects against asystole and may protect against transient hypotension, with its attendant risks of extending the infarction and precipitating malignant ventricular tachyarrhythmias. Mortality is increased in these patients, although not as much as in those with other forms of conduction block. The posterior fascicle is larger than the anterior fascicle, and in general, a larger infarct is required to block it. Mortality is also high because of the occurrence of severe pump failure secondary to the extensive myocardial necrosis required to produce such an extensive intraventricular 1 block. All these forms are more common with large infarcts and in older patients and have a higher incidence of other accompanying arrhythmias than seen in patients without bundle branch block. This category includes patients with new bilateral (bifascicular) bundle branch block (i. Supraventricular Tachyarrhythmias (See Chapters 37 and 38) Sinus Tachycardia Sinus tachycardia is typically associated with augmented sympathetic activity and may provoke transient hypertension or hypotension. Treating sinus tachycardia caused by pain, anxiety, or fever with beta blockers is reasonable, but these agents are contraindicated in patients who are tachycardic because of pump failure. Clinicians face the critical task of distinguishing recurrent angina or infarction from nonischemic causes of discomfort that might result from infarct expansion, pericarditis, pulmonary embolism, and non–cardiac-related conditions. Diagnosis Extension of the original zone of necrosis or reinfarction into a separate myocardial zone can be a difficult diagnosis, especially within the first 24 hours after the index event. The presence of a rub and lack of responsiveness to nitroglycerin may be useful in distinguishing pericardial discomfort, but doing so on clinical grounds is frequently challenging, and diagnostic coronary angiography may be necessary to exclude acute native vessel or stent thrombosis. Prognosis Regardless of whether postinfarction angina is persistent or limited, its presence is important because of the associated higher short-term morbidity rate. Stent thrombosis can occur acutely (hours to days after stent deployment) or late (many months after stent deployment) (see Chapter 62). Pericardial Effusion and Pericarditis (See Chapter 83) Pericardial Effusion Effusions are generally detected echocardiographically, and their incidence varies with imaging modality and technique, criteria, and laboratory expertise. The reabsorption rate of a postinfarction pericardial effusion is slow, with resolution often taking several months. An effusion does not necessarily indicate pericarditis; although they may coexist, most effusions develop without other evidence of pericarditis. When tamponade does occur, it is usually 150 caused by ventricular rupture or hemorrhagic pericarditis. The pain of pericarditis may be confused with that resulting from postinfarction angina, recurrent infarction, or both. An important distinguishing feature is radiation of the pain to either trapezius ridge, a finding that is almost pathognomonic of pericarditis and rarely seen with ischemic discomfort. Additionally, the discomfort of pericarditis usually worsens during a deep inspiration but can be relieved or diminished by sitting up and leaning forward. An acute fibrinous pericarditis, pericarditis epistenocardica, occurs frequently after transmural infarction, but most patients do not report any symptoms from this process. Although transient pericardial friction rubs are relatively common within the first 48 hours in patients with transmural infarction, pain or electrocardiographic changes occur much less often. The development of a pericardial rub, however, appears to correlate with a larger infarct and greater hemodynamic compromise. Nevertheless, detection of a significant (≥1 cm) or enlarging pericardial effusion usually should indicate discontinuation of anticoagulation. Patients in whom continuation or initiation of anticoagulant therapy is strongly indicated (e. Late pericardial constriction caused by anticoagulant-induced hemopericardium has been reported. Treatment of pericardial discomfort consists of aspirin, but usually in doses higher than prescribed routinely following infarction—doses of 650 mg orally as often as every 4 hours may be necessary. Dressler Syndrome Also known as post–myocardial infarction syndrome, Dressler syndrome usually occurs 1 to 8 weeks after infarction. The wall of a true aneurysm is thinner than that of the rest of the left ventricle (eFig. Pathogenesis Aneurysm formation presumably occurs when intraventricular tension stretches the noncontracting infarcted heart muscle and thus produces expansion of the infarct, a relatively weak, thin layer of necrotic muscle, and fibrous tissue that bulges with each cardiac contraction. Aneurysms occur approximately four times more often at the apex and in the anterior wall than in the inferoposterior wall. The overlying pericardium generally adheres densely to the wall of the aneurysm, which may even become partially calcified after several years. Death in these patients is frequently sudden and presumably related to the relatively high incidence 152 of ventricular tachyarrhythmias that occur with aneurysms.
This causes an involuntary withdrawal of the feet such that there is ﬂexion at the knees and hips effective 100 mcg rhinocort. Because of the position of the child as it is placed in the water purchase cheap rhinocort online, there will be a very characteristic distribution of burns (Figure 12 order cheap rhinocort. The skin in the popliteal fossae and in the knee region is spared because the child ﬂexes its legs such that the knees project above the water and the ﬂexed thigh and calf protect the skin of the popliteal fossa. If the thigh is brought back hard against the abdomen, which is often the case, there may also be sparing of the inguinal regions. If the child is wearing a diaper and immersion is not very long, there may be some sparing of the inguinal region by the diaper. Based on the authors’ experiences, smothering is, after impulse homicides, the second most common type of homicide in infants. One closes off the child’s nose with two ﬁngers, at the same time pushing up on the lower jaw with the palm to occlude the airway. Other methods have involved placing 350 Forensic Pathology a pillow or towel over the child’s face and pressing down; pushing the face down into bed clothing, or just covering the nose and mouth with one’s hand. The true number of smotherings in infants is not known and can never be known until there is some scientiﬁc test to determine whether an indi- vidual has been smothered. The amount of force necessary to produce smoth- ering is so minor in this age group that there is virtually never evidence of trauma. The amount of time necessary to smother an infant, such that their electroencephalogram is ﬂat and there is no spontaneous respiration, has been documented at 70–90s. While most homicidal suffocation of infants is sporadic, a small num- ber of individuals, virtually all of whom are mothers, practice a lethal form of Munchausen’s syndrome by proxy, a form of child abuse in which chil- dren are brought to physicians and hospitals for induced signs and symp- toms of illnesses in conjunction with a ﬁctitious history. Thus, a child might be brought into the hospital with hypoglycemia because the mother is administering insulin or there may be blood in the urine because the mother pricks her own ﬁnger and adds blood to the child’s urine. With the more common forms of Munchausen’s, the diagnosis is usually made after a number of admissions because the symptoms and signs usually do not make sense clinically and appear bizarre. Male and female children are affected equally and, in virtually every instance, the perpetrator is the mother. The father is usually supportive of the mother, is unaware of what she is doing, and usually stands by her after she is accused. The mother and child seem to be extremely close and it is difﬁcult for the physician or social worker to realize what the mother is doing. Forensic pathologists are familiar with a much more lethal version of this entity in which the individual, again virtually always the mother, repeat- edly smothers the child into unconsciousness. Children are then either resus- citated by the parent or brought to an emergency room in a semi-moribund state, with a history of apnea, cyanosis, and losing consciousness. After admis- sion, the children are worked up extensively, with no abnormal ﬁndings. Usually, these children never have these episodes of apnea and cyanosis while in the hospital. If they do, a careful history reveals that the parents who have witnessed these attacks outside the hospital are alone with the children in the hospital room at the time the attack occurs. After discharge from the hospital, the “attacks” continue until either the diagnosis is made or the children killed. The mother gave a history of almost daily episodes of apnea, cyanosis, bradycardia, and loss of consciousness since 1 week of age. She had had multiple apneic episodes in the hospital and was found apneic, cyanotic, bradycardic, and unresponsive. On this admission, however, the physicians became suspicious and, using video equipment, were able to document the mother smothering the child by placing the palm of her right hand over the baby’s face. As awareness of this syndrome spread among pediatrians, and because of the availability of video cameras, other cases have been discovered and documented. In the second child, 6 months of age, the mother also placed a garment over the face of the child and forced its head onto the mattress. In a prior episode, which was not videotaped, but during which monitoring was being conducted, the child was found uncon- scious and cyanotic apparently after 2 min of smothering. The videotapes showed that both the children struggled violently until they lost consciousness. It took at least 70 s before electroencephalographic changes, probably associated with loss of consciousness, occurred. At 1 min, there was the appearance of a series of deep breaths occurring at a relatively slow rate with a prolonged expiratory phase, in other words, a “gasping” respiratory pattern. About this time, the electroencepha- logram showed large slow waves progressing to an isoelectric baseline indic- ative of cerebral hypoxemia. Neonaticide, Infanticide, and Child Homicide 353 The authors have encountered a number of fatal cases of Munchausen’s syndrome by proxy, such as the previously mentioned case described by Di Maio and Bernstein, where a woman was convicted of smothering her adopted child after repeated episodes of admission to the hospital for cyanosis and apnea. Other cases encountered by the authors have involved anywhere from one to three deaths. In one instance, a mother was indicted by the grand jury for smothering two chil- dren, though she was never tried for either death, because the district attorney refused to try the case. When a second sibling presented with the same history of multiple episodes of cyanosis, a video camera recorded the mother smothering the child (M. She was suspected of administering heparin, potassium chloride, and succiny1choline (alone and in various combinations) to infants and young children to precipitate a medical crisis (massive bleeding, cardiac and pulmonary arrest) so that she could resuscitate them and be viewed as a heroine. She was convicted of killing one child with succinylcholine and injuring another with heparin. Attorneys involved in the case suspected her of causing the deaths of from 15 to 30 other children. The mother admitted holding his nose, causing the child to become cyanotic and apneic. The presentation of the lethal variant of Munchausen’s cases, however, is usually the same. Repeated apneic 354 Forensic Pathology episodes in the presence of one individual (usually a parent), with the child’s becoming cyanotic and limp; resuscitation, and repeated presentation in an emergency room or hospital with numerous admissions to a hospital, at which time the child has no problems unless left alone with the parent. Unfortunately, if suspicion is not aroused, there is a possibility that this will lead to the death of the child. This concept was proposed by Stein- schneider in an article in Pediatrics in 1972. Two subsequently died of what was called the sudden infant death syndrome; three survived. One of the two was a 29- day-old female seen because of recurrent cyanotic episodes. She was admitted to the hospital at the time and discharged at the age of 25 days without a diagnosis. This pattern of admission, discharge and readmission occurred until her death at home at 79 days of age.
By 3–4 weeks after injury order 100mcg rhinocort visa, the hematoma is covered Trauma to the Skull and Brain: Craniocerebral Injuries 169 by a membrane of ﬁbrous tissue that grows inward from the edges of the clot cheap 100 mcg rhinocort with visa. By 4–5 weeks buy genuine rhinocort line, the arachnoid membrane has half the thickness of the dura, with the dural surface equal in thickness to the dura. The clot is completely liqueﬁed and hemosiderin-laden macrophages are present in the membranes. At 1–3 months, the membrane is hyalinized on both its inner and outer aspects, with large capillaries invading the clot. This goes on to eventual complete resorption, with only a residual gold-colored membrane adherent to the dura. Some individuals do not develop signiﬁcant symptoms of a subdural hematoma for weeks to months after head injury. In this entity, instead of the initial acute subdural hematoma’s becoming organized and then smaller as it is reab- sorbed, it begins to enlarge. This continues until the chronic subdural hematoma produces sufﬁcient symptomology. The victims of chronic subdural hematomas tend to be either infants younger than 6 months of age or the elderly. In the case of infants, this is due to incomplete fusion of bony plates; in the elderly, increased intracranial space due to brain atrophy. Because of the prolonged time between trauma and symptoms, in a signiﬁcant percentage of individuals with chronic subdural hematomas, no history of trauma can be elicited. The etiology of chronic subdural hematomas is generally thought to be rebleeding from thin-walled sinusoidal blood vessels in the neo-membrane of a resolving acute subdural hematoma. A small amount of bleeding may also be present, giving the ﬂuid a xanthochromic color. If the hygroma, instead of being reabsorbed, continues to grow, it can produce the same space-occupying effects as a subdural hematoma. Diffuse Axonal Injury Immediate prolonged coma unaccompanied by an intracranial mass lesion occurs in almost half of patients with severe head injuries. While, 170 Forensic Pathology theoretically, impaction of the head against a hard object is not necessary, in reality, brain injury in humans requires contact, not just acceleration or deceleration. For all practical purposes, it is the impact that starts the acceleration or deceleration injury to the brain. Diffuse axonal injury is a continuum, varying from mild brain injury and dysfunction to severe irreversible dysfunction and injury, and even death. The severity of injury is determined by the amount of acceleration or decel- eration of the brain, the time span over which it occurs, and the direction of movement. Sagittal head movement produces diffuse axonal injury of mild, or at most, moderate type. At low levels of acceleration or deceleration, there is no anatomical dis- ruption of the axons, only physiological dysfunction. As the physical force increases, there will be a progressive increase in the extent of irreversible physiological injury to axons (thus making it more likely that they will subsequently undergo degeneration) plus an increase in the amount of immediate structural disruption of axons (transaction) with immediate ces- sation of all activities. If it does, it develops 5 or 10 min after the trauma and, while it might subsequently decrease, there will always be some residue. What is clinically called concussion is thought to be a manifestation of diffuse brain injury, with no or insigniﬁcant irreparable physical injury to the brain. In the second-impact syndrome, individuals incur a minor head injury, followed by a second head injury before the symptoms of the ﬁrst have disappeared. Some axons, however, may show immediate physical disruption with cessation of func- tions. In other axons, the physiological disruption will eventually lead to degeneration. Focal hemorrhages are usually grossly visible in the corpus callosum and dorsolateral quadrant of the rostral brainstem. Gliding contusions of the gray matter of the cerebral hemispheres and hippocampi may be present. They are seen in the cerebral white matter, corpus callosum, and upper brain stem. This is because, while the initial trauma causes transection of some axons with formation of retraction balls, other axons are irreversibly injured but continue functioning for a while prior to cessation of function and degeneration. Two to three weeks after injury, the number of axon retraction balls begins to decrease and clusters of microglial cells, the most prominent lesion, appear. Severe angular accelerations over a short time period result in subdural hematomas; acceleration over a long time period, diffuse axonal injury. When diffuse axonal injury has been documented following falls, these have been falls from a considerable height. Death Due to Cerebral Concussion The authors have seen a number of deaths following blunt trauma to the head in which no, or at least insigniﬁcant, anatomical injury to the brain could be documented. The ﬁrst is illustrated by the case of an 8-year-old boy riding in the back seat of a motor vehicle that was involved in a head-on collision with another vehicle. The boy was propelled over the back seat, striking the top of his head against the wind- shield. At autopsy, there was no evidence of any injury to the scalp, skull, brain, or neck (anterior and posterior dissection). A second, similar case involved a 20-year-old man who fell 20 ft to the ground from a ladder. At autopsy, there was a small laceration of the scalp in the temporal region without fracture of the skull or gross evidence of injury to the brain. The second category of deaths involves individuals who, while acutely intoxicated with alcohol, are severely beaten about the head, usually with ﬁsts and feet (Figure 6. Analysis of vitreous humor indicates that, even if there had been prolonged survival, the blood alcohol level was never in the lethal range. The cause of death in this category of cases is posttraumatic apnea due to a combination of concussion and acute alcohol intoxication. With concussion alone, however, posttraumatic apnea is rare, brief, relatively mild and not life-threatening. Subarachnoid Hemorrhage Subarachnoid hemorrhage is the most common sequela of trauma to the head. In most cases, it is of a diffuse nature, overlying the cerebral hemispheres, with min- imal pooling on the ventral surface of the brain. Large collections of blood in the subarachnoid space of the base of the brain are more common in natural diseases than trauma, e. Hyperextension can cause bleeding because of lacerations of the basal or vertebral arteries.
Imaging of vulnerable plaques using near-infrared spectroscopy for risk stratification of atherosclerosis 100mcg rhinocort with visa. Morphometric assessment of coronary stenosis relevance with optical coherence tomography: a comparison with fractional flow reserve and intravascular ultrasound rhinocort 100mcg overnight delivery. Pathophysiology of acute coronary syndrome assessed by optical coherence tomography buy genuine rhinocort line. Assessment of culprit lesion morphology in acute myocardial infarction: ability of optical coherence tomography compared with intravascular ultrasound and coronary angioscopy. Incidence and clinical significance of poststent optical coherence tomography findings: one-year follow-up study from a multicenter registry. Delayed coverage in malapposed and side-branch struts with respect to well-apposed struts in drug-eluting stents: in vivo assessment with optical coherence tomography. Examination of the in vivo mechanisms of late drug- eluting stent thrombosis: findings from optical coherence tomography and intravascular ultrasound imaging. Incidence, predictors, morphological characteristics, and clinical outcomes of stent edge dissections detected by optical coherence tomography. Heart disease and stroke statistics—2013 update: a report from the American Heart Association. Differences in the incidence of congestive heart failure by ethnicity: the Multi-Ethnic Study of Atherosclerosis. Use of both systems in conjunction provides a reasonable framework for clinician communication and patient prognostication. Following thorough history and physical examination together with initial diagnostic testing, imaging (e. Further, the history helps to evaluate incongruent results that may emerge during the diagnostic process, and it can obviate the need for needless further testing. None of these is entirely sensitive or specific for identifying the presence of severe congestion (Table 21. Probing more deeply into the current level of activity may uncover a decline in exercise capacity that is not immediately apparent. Patients may sleep with their heads elevated to relieve dyspnea while recumbent (orthopnea); additionally, dyspnea while lying on the left side (trepopnea) may occur. The presence of Cheyne-Stokes respiration is generally indicative of an adverse prognosis. These symptoms all typically reflect pulmonary congestion, whereas a history of weight gain, increasing abdominal girth, early satiety, and the onset of edema in dependent organs (extremities or scrotum) indicate right-sided heart congestion. Unintended weight loss, often leading to cachexia, may be prominent and is a 10 major prognostic indicator. Environmental or toxic exposures, including alcohol or drug abuse, should be carefully sought. Information about the presence of comorbidities (as described later) is essential in devising management plans. The skin examination may show pallor or cyanosis resulting from underperfusion, stigmata of alcohol abuse (e. Additional findings supporting amyloidosis include deltoid muscle infiltration (leading to the “shoulder pad sign”), tongue hypertrophy, and bilateral thenar wasting from carpal tunnel syndrome. By observing or palpating the apical impulse, the examiner can rapidly determine heart size and quality of the point of maximal impulse. Tricuspid regurgitation, which is also common, can be differentiated from mitral regurgitation by the location of the murmur at the left sternal border, an increased intensity of the murmur during inspiration, and the presence of prominent “V” waves in the jugular venous waveform. Both mitral and tricuspid regurgitation murmurs may become softer as volume overload is treated, and a reduction in ventricular size (with corresponding reduction in annular diameter) improves valve coaptation and competency. The presence of a third heart sound is a crucially important finding and suggests increased ventricular filling volume; while difficult to identify, a third heart sound is highly specific for heart failure and carries a substantial prognostic meaning. Dullness to percussion and diminished breath sounds at one or both lung bases suggest the presence of a pleural effusion. Bilateral pleural effusions are most common, but when an effusion is present unilaterally, it is usually right sided, with only approximately 10% occurring exclusively on the left side. Leakage of fluid from pulmonary capillaries into the alveoli can be manifest as rales or rhonchi, and wheezing may result from reactive bronchoconstriction. It can result in an incorrect diagnosis of “obstructive airways disease exacerbation,” with consequent mistriage and incorrect therapy with bronchodilators; such 16 mismanagement may be associated with increased risk for mortality. Detecting reduced cardiac output and systemic hypoperfusion are key components of the examination. Patients with poor systemic perfusion usually have low systolic and narrow pulse pressures as well as weak and thready pulses, but this relationship is not exact. Many patients with systolic blood pressure in the range of 80 mm Hg (or even lower) may have adequate perfusion, whereas others with reduced cardiac output may maintain blood pressure in the normal range at the expense of tissue perfusion by greatly increasing systemic vascular resistance. Findings suggesting reduced cardiac output include poor mentation, reduced urine output, mottled skin, and cool extremities. Assessment for systemic congestion taken together with evaluation for reduced cardiac output may be useful to categorize patients into “dry/warm” (uncongested with normal perfusion), “wet/warm” (congested with normal perfusion, the most common combination found in decompensated heart failure), 17 “dry/cold” (uncongested but hypoperfused), and “wet/cold” (cardiogenic shock), as discussed in Chapter 24. These categories not only are prognostic, but also inform treatment decision making (Fig. Clinical assessment identifies hemodynamic profiles that predict outcomes in patients admitted with heart failure. Chest Radiography Despite advances in other imaging technologies, the chest x-ray film remains a useful component of the assessment, particularly when the clinical presentation is ambiguous. Results of chest radiography are additive to clinical variables from history and physical examination and similarly complement the results of biomarker testing. The classic chest x-ray pattern in patients with pulmonary edema is a “butterfly” pattern of interstitial and alveolar opacities bilaterally fanning out to the periphery of the lungs. Many patients, however, present with subtler findings, in which increased interstitial markings, including Kerley B lines (thin horizontal linear opacities extending to the pleural surface caused by accumulation of fluid in the interstitial space), peribronchial cuffing, and evidence of prominent upper lobe vasculature (indicating pulmonary venous hypertension) are the most prominent findings. It may provide important clues regarding incident heart failure while assisting in understanding when previously diagnosed patients experience an episode of decompensation. In the absence of a prior history of hypertension, such a finding might be caused by valvular heart disease or by hypertrophic cardiomyopathy, particularly if bizarre repolarization patterns are noted. If right ventricular hypertrophy is present, primary or secondary pulmonary hypertension should be considered. As discussed later, the natriuretic peptides may be exceedingly useful for diagnosis as well as for prognostication. Hyponatremia is associated with impaired cognitive and neuromuscular function, and when present and persistent, low sodium is strongly 20 prognostic for longer hospital stay, as well as a high risk for mortality. Despite this fact, strategies to 21 correct serum sodium levels have not been shown clearly to improve the clinical course (see Chapter 24). In addition to increasing the risk of cardiac arrhythmias, low potassium may also lead to leg cramps and muscle weakness. The causes of this “cardiorenal” syndrome are complex but include the severity of right-sided heart congestion, increased intra-abdominal pressure, and renal hypoperfusion from inadequate cardiac output.