R. Karmok. University of Advancing Technology.
Most occur in the midportion and are similar in location to those resulting from accidental trauma generic 100mg kamagra oral jelly mastercard impotence effect on relationship. Fractures of the distal ends of the clavicle are less common and are caused by sudden traction on the extremity buy kamagra oral jelly visa impotence etymology. The Shaken Baby Syndrome “If any one of them can explain it discount kamagra oral jelly uk erectile dysfunction age 30,” said Alice … “ I’ll give him sixpence. In other words, these injuries were not caused by direct-impact injuries to the head, but rather by indirect acceleration–deceleration traction stresses caused by the head’s whipping back and forth. Caffey’s paper also suffered from a number of problems in regard to his case material, e. If death occurred, autopsies were not always performed and scant mention was made of the ﬁndings. Following the initial description, as more cases of this syndrome were diagnosed and studied, injuries to the scalp and skull (contusions and fractures), explainable only by impact trauma, began to be detected in alleged cases. At autopsy, however, all 13 children had evidence of blunt head trauma: eight had soft tissue contusions and ﬁve had contusions and skull fractures. Of the seven deaths in which blunt trauma to the head was missed clinically, four presented with the classical symptoms of retinal hemorrhage, subdural hematoma, and subarachnoid hemorrhage. The other three, while having subdural hematoma and subarachnoid hemorrhage, did not have retinal hemorrhage. No way of differentiating pre-impact intracranial trauma from post- impact is given. To many observers, the “shaken impact syndrome” appears to be an attempt to explain away inconvenient observations that call into question the existence of the shaken baby syndrome itself. The way to accomplish this is by exper- imentation and repeated objective observations to exclude other possible explanations. Establishment of the validity of a hypothesis by observation is dependent on the quality of the observations and the observer. Observations might be handicapped by limitations of the senses or equipment employed. The quality of the observer is determined by training and experience but might be mod- iﬁed by prejudice and emotions. These latter qualities might cause individuals to either consciously or unconsciously distort the evidence to ﬁt a precon- ceived theory. The individual charged with injury to a child cannot be con- sidered an objective unbiased observer. Most people charged with injuring or killing a child would rather confess to or be charged with shaking a baby than slamming its head against an object or throwing it across a room like a football. Obviously, it is easier to claim as a defense ignorance of the consequences of shaking, rather than the other actions. The original observations, in which head impact was “excluded,” were almost all clinical and did not involve autopsies. Cases where the child does not die and the absence of signs of impact are based on external and radiological examinations cannot be used to substantiate the existence of this entity, as there can be extensive impact injury, such as skull fractures, without either external or radiologic evidence of trauma. Absence of external or radiological evidence of injury, in cases where massive trauma is demonstrated at autopsy, is routinely seen by all experienced forensic pathologists. One cannot blithely propose two causes for injuries in a case where one will be sufﬁcient just because this ﬁts a preexisting theory or prejudice. After each shaking episode, the occipital area of the model was impacted against either a metal bar or padded surface. The results of 69 Neonaticide, Infanticide, and Child Homicide 361 shaking tests were then compared with 60 impacts. Thus, acceleration due to impact exceeded acceleration due to shaking by a factor of nearly 50 times. As expected, impact against a padded surface was associated with signiﬁcantly smaller acceleration (mean 380. Both the magnitude of angular acceleration and the time interval of the acceleration are important biomechanical factors inﬂuencing the nature of the injuries. Large angular accelerations over short time intervals tend to result in subdural hematomas, while longer intervals are associated with diffuse axonal injury. Based on work by Thibault and Gennarelli on subhuman primates, the angular acceleration and velocity associated with shaking is below the injury range for concussion, subdural hematoma or diffuse axonal injury, while the results from the impacts are within the range. What about the rare case of traumatic intracranial bleeding in a child where there is no evidence of impact on the scalp or skull? The authors have seen numerous cases of witnessed impact involving both adults and children who subsequently died of head trauma in which there was no evidence of impact in the scalp or skull at autopsy. This observation is in agreement with the opinions of Bernard Knight, who, in his book Forensic Pathology, in discussing acute subdural hematomas, states “… blunt impacts may leave no sign in the scalp, externally or internally, and no skull fracture. This situation may well have arisen because a blunt impact upon the head of an infant, if spread over a wide area following contact with a ﬂat surface, can leave no external scalp mark, no subscalp bleeding and no fracture of the skull — yet the transmitted forces can still be sufﬁcient to cause high strain — shearing stresses within the cranial cavity leading to subdural bleeding. First, the underlying premise (the existence of the shaken baby syndrome) is unproven. Second, retinal hemorrhage occurs with other etiologies: acci- dental trauma (especially subdural hematoma); resuscitation (rarely); papilledema; in 14. Suggested are increased retinal venous pressure, extravasation of subarachnoid blood, and traction of retinal vessels at the vitreo-retinal inter- face due to angular deceleration. If the head is whipping back and forth with such velocity as to tear cerebral blood vessels and cause retinal hemorrhage, why are there no fractures of the cervical spinal column? When challenged in regard to this, the reason is said to be the suppleness (bendability) of the spine in small children. The cord should be crushed by the “supple” vertebrae shifting back and forth — or, if not crushed, at least torn or severely stretched. They concluded that the presence of epidural hemorrhage in the cervical cord area was not related to trauma, not damaging to the cord, and probably due to hemodynamic forces. Case, in a study of this phenomenon in 50 children below the age of 3 years, some of whom had been allegedly shaken, found no relationship between shaking and epidural hemorrhages. Since then, we have had no reason to change this opinion but rather to solidify it. The authors feel that head injury ascribed to shaking is due to impact of the head Unintentional Causes of Intracranial Hemorrhage While most children presenting in the ﬁrst few years of life with intracranial bleeding and retinal hemorrhage are victims of child abuse, this is not abso- lute. Typically presenting 4–6 weeks after birth, it is manifested by intracranial bleeding (subdural, subarachnoid, intracerebral) as well as bleed- ing in the skin, gastrointestinal tract and urogenital tract. In this case, because the child lived long enough to get to the hospital and survived 24 hours, hematological tests could be performed. They revealed prolonged prothrombin and partial thromboplastin times with a normal thrombin time and ﬁbrinogen levels. Severe vita- min K deﬁciency results in production of this nonfunctioning protein. This and other tests conﬁrmed the diagnosis of late-form hemorrhagic disease of the newborn.
The inside wing of the spinning aircraft is usually the ﬁrst to strike the ground buy generic kamagra oral jelly from india impotence husband, with the outside wing creating a ground scar directly opposite the scar produced by the inside wing order kamagra oral jelly online pills causes of erectile dysfunction include. While most airplane crashes impacting in spin-type accidents do nose down discount kamagra oral jelly 100mg on line erectile dysfunction drugs used, occasionally some will impact ﬂat. When a plane hits the ground while spiraling, the spiral impact pattern is created. Unlike the pattern from the spin impact, however, wreckage is spread over a relatively large, fan-shaped area. The wings may be torn from the aircraft but come to rest some distance from the fuselage. The engines usually separate from their mounts when mounted on the wing and remain near the initial point of impact. The low-speed, small-angle-of-impact accident is usually the result of a forced landing. Here, the aircraft damage is substantially less than that of a high- speed impact and individuals may survive. In the high-speed, small-angle- of-impact, there are long, fan-shaped debris patterns, with the aircraft break- ing into many pieces, the heavier parts traveling the farthest forward in the pattern of debris. As the plane begins to impact, the ﬁrst mark seen could be from the wheels if the landing gear is down, or the propellers, if the plane is a propeller aircraft. In wooded areas, the wings can be damaged by tree tops long before contacting the ground. High-speed, small-angle-of-impact accidents are essentially caused by a controlled ﬂight into the ground because of ﬂying too low. In in-ﬂight disintegration, major parts of the aircraft are scattered over a wide area without an apparent logical pattern. This type of pattern-less scattering is seen in in-ﬂight explosions, major structural failure and midair collisions. The bodies should be X-rayed for bomb fragments or fragments of the Airplane Crashes 323 plane propelled into the body by an explosion. In-Flight Fire In-ﬂight ﬁres are indicated by elevated carbon monoxide levels in the pas- sengers or crew, as well as the presence of soot downstream from the area of ﬁre damage in the aircraft. Beads of molten aluminum will also be blown downwind along the fuselage from the area of ﬁre damage. In post-crash ﬁres, there is a widespread pattern of soot and ﬁre damage without any speciﬁc distribution of soot and melted aluminum. The only unusual aspect of these crashes, compared with those involving ﬁxed-wing aircraft, is that, if a helicopter loses power or is somehow incapacitated in ﬂight (e. The resultant injuries might be more similar to those from falls rather than traditional aircraft crashes Hot-Air Balloons Hot-air ballooning is popular in some areas of the U. Contact with a power line can cause the basket to overturn, or the basket cables to be severed by the wires, or electrocution. Thus, Cherington and Mathys were able to identify only 40 such incidents from 1963–1989. Lightning can cause an accident by (1) entering the fuel compartment and igniting the fuel, (2) temporarily blinding the pilot by the bright ﬂash, or (3) disrupting the electrical system. Because of upgrad- ing of the fuel, electrical and automatic control systems, Cherington and Mathys felt that accidents caused by lightning should become even less com- mon. With the use of composite materials in airplane construction, another problem has arisen. Thus, if they are stuck by lightning, the lightning could burn a hole through the material. Manufactures are developing methods to conduct electricity from lightning strike points. Cherington M and Mathys K, Deaths and injuries as a result of lightning strikes to aircraft. These facts are often misunderstood by both the public and the medical profession. This does not detract from the fact, however, that the vast majority of these cases are of a natural etiology. The former con- dition was manifested by an “enlarged” thymus, in fact, a normal ﬁnding in infants. Interstitial pneumonitis was just as nonexistent and essentially referred to the normal hypercellular appearance of the alveolar septae of an infant. In the 1930s and early 1940s, crib deaths were often thought to be caused by suffocation from blankets, bedclothing, or mattresses. Thus, Abramson, in a paper in 1944, reported 139 deaths from suffocation during a 5-year period in New York City alone, a number greater than the total number of deaths from measles, scarlet fever, and diphtheria. Wooley pointed out that he had analyzed the atmosphere 325 326 Forensic Pathology breathed by infants covered in various manners by different types of bedding. He also attempted to induce anoxia by having the subject sleep with the nose and mouth closely pressed to pillows and mattresses. Even the smallest child, however, was capable of rolling aside to obtain a patent airway. Wooley thus concluded that the importance of suffocation as an explanation of sudden death in infancy could not be substantiated. This modiﬁcation was made so as to prevent infants placed on their sides rolling onto their stomachs. Presentation of Cases As stated previously, there are approximately 3000–4000 deaths per year in the U. While these may also be of unknown etiology, they are most probably not the result of the same conditions that cause death after a month of age. Most probably, these are disorders associated with neonatal development and adaptation to a new world. Race does not appear to be a factor, but the socioeconomic status of the family does. Most chil- dren are found dead in their cribs in the morning when their parents go to feed them. The second death by the same mother is labeled undetermined, and a more intensive investigation of the circumstances surrounding the death is conducted. The police are usually asked to interview the family, though in a discreet fashion. A third death with the same mother is thought by the authors to be homicide until proven otherwise. Allusions are made to mitochondrial disorders, fatty acid oxidation disorders etc. When autopsying the third case, one might consider saving frozen samples of skin, muscle, liver, kidney, lung, brain and heart as well as performing the most recent battery of tests for hereditary disease. Part of the toxicological screen should consist of an electrolyte exam- ination performed on the vitreous. Petechiae of the thymus, epi- cardium, and pleural surfaces of the lungs are common. There have been reports of hypertrophy and hyperplasia of the muscular media of small pulmonary arteries, right ventricular hypertrophy, and brain stem gliosis.
The high-dose strategy was associated with greater relief of dyspnea and net fluid loss at 72 hours order kamagra oral jelly in india erectile dysfunction causes and cures, although more patients in the high-dose group had a transient increase in creatinine greater than 0 purchase kamagra oral jelly cheap erectile dysfunction ed treatment. In the setting of diuretic resistance 100 mg kamagra oral jelly visa erectile dysfunction pump implant, administration of a thiazide-like diuretic that blocks the distal 89 tubule can provide significant augmentation of the diuretic effect. If hypokalemia is a persistent problem with replacement requirements, administration of a potassium-sparing diuretic, such as spironolactone or eplerenone, should be considered and may also 90 provide synergistic diuretic effects, especially at higher doses, as well as long-term beneficial effects on outcomes (see Chapter 25). In practice, however, vasodilators appear to provide symptom relief in these patients. Vasodilators can be classified as (1) predominantly venous dilators, with consequent reduction in preload; (2) arterial dilators, leading to a decrease in afterload; and (3) balanced vasodilators, with combined action on both the venous and the arterial system. These should be used with caution in patients who are preload or afterload dependent (e. These agents are potent venodilators, producing rapid decreases in pulmonary venous and ventricular filling pressures and improvement in pulmonary congestion, dyspnea, and myocardial O demand at low doses. At slightly higher doses and in the2 presence of vasoconstriction, nitrates are also arteriolar vasodilators, reducing afterload and increasing cardiac output. Nitrates are relatively selective for epicardial, compared to intramyocardial, coronary arteries, resulting in increased coronary blood flow and making them useful for patients with concomitant active myocardial ischemia. The starting dose of nitroglycerin is usually 20 µg/min with rapid uptitration occurring every 5 to 15 minutes in either 20-µg/min increments or doubling of the dose. The major limitation of organic nitrates is the tolerance that typically develops 95 within 24 hours. Symptomatic hypotension (5%) may also be noted, but generally resolves when nitrate therapy is discontinued. Given the risk of severe hypotension with potentially catastrophic consequences, the recent use of phosphodiesterase 5 inhibitors (sildenafil, tadalafil, vardenafil) should be ruled out before administration of nitrates. However, significant vasodilation of the intramyocardial vasculature has been noted, possibly producing a coronary steal phenomenon; and consequently, nitroprusside is not recommended for patients with active myocardial ischemia. The most common complaints with nitroprusside are related to the cyanide metabolite, including nausea, abdominal discomfort, dissociative feelings, and dysphoria. Cyanide rarely accumulates in patients, but impaired hepatic function and doses greater than 250 µg/min for more than 48 hours increase this risk. Cyanide levels may be measured but rarely return in a timely fashion to be useful. As with other vasodilators, nesiritide may reduce diuretic requirements, but in clinical studies, there is limited evidence for a significant direct “natriuretic” effect. Nesiritide has clear effects on hemodynamics and has limited need for frequent dose adjustments and an absence of tolerance, but its high cost and lack of clear clinical benefit beyond other, less expensive, more readily titratable agents have limited its use. The clinical effects on dyspnea were relatively modest and have generally not been regarded as clinically important compared to placebo (Fig. In this study, nesiritide had no beneficial effect on urine output or cystatin C or on any of the other secondary endpoints reflective of decongestion, renal function, or clinical outcomes, although it was associated with more symptomatic hypotension. In A, numbers above the bars indicate overall percentage of patients who reported being markedly or moderately better after receiving study treatment (i. Hypotension, at times prolonged (>2 hours) despite the relatively short (18-minute) half-life of the peptide, is more common in patients with volume depletion, and consequently, nesiritide use should be limited to those with congestive signs and symptoms. Other actions of nesiritide include neurohormonal antagonism with reduction in vasopressin, aldosterone, and sympathetic tone and alteration of intrarenal hemodynamics and glomerular filtration. Therefore, these agents are reserved for use in select situations of hypoperfusion when other interventions are inappropriate or have failed. In North American and European registries, approximately 15% and 25% of patients were treated with inotropic agents, although given the minimal supportive clinical evidence, there is marked local variability in the use of these 102 drugs. Dobutamine Dobutamine is the most commonly used positive inotrope in Europe and the United States, despite 103,104 evidence that it increases mortality. Dobutamine at doses of 1 to 2 µg/kg/min may improve renal perfusion in patients with cardiogenic shock, although higher doses (5 to 10 µg/kg/min) may be necessary for more profound hypoperfusion. Tachyphylaxis may occur with infusions of more than 24 to 48 hours, partially because of receptor desensitization. In general, dobutamine (or dopamine) is the preferred inotrope in patients with significant hypotension and in the setting of significant renal dysfunction, given the renal excretion of milrinone. Concomitant beta-blocker therapy will result in competitive antagonism of the effects of dobutamine, and higher doses of dobutamine (10 to 20 µg/kg/min) may be required to obtain the desired hemodynamic effects. The patient should be gradually weaned off dobutamine and the clinical status reevaluated with each dose adjustment. Temporary adjustments to afterload- reducing agents or diuretics may assist in weaning. As an agonist of both beta - and beta -adrenergic receptors with variable effects on the alpha receptors,1 2 dobutamine has multiple actions (see Chapter 22). At low doses, stimulation of beta and alpha receptors2 causes vasodilation, resulting in decreased aortic impedance and systemic vascular resistance with reduction in afterload and indirect increases in cardiac output. At higher doses, vasoconstriction can ensue with decreased venous capacitance and increased right atrial pressure. Dopamine In both the United States and Europe, dopamine is used as often as dobutamine, presumably as a vasoconstrictor and for its putative effects on renal vasodilation. Patients should be gradually weaned from these doses down to 3 to 5 µg/kg/min and then discontinued, to avoid potential hypotensive effects of low-dose dopamine. Low-dose dopamine (≤2 µg/kg/min) has been proposed to cause specific dilation of renal, splanchnic, and cerebral arteries, potentially increasing renal blood flow in a selective manner, as well as promoting natriuresis through direct distal tubular effects. Therefore, there appears to be no indication for low-dose dopamine therapy to improve renal function. High-dose dopamine (10 to 20 µg/kg/min) causes peripheral and pulmonary artery vasoconstriction, mediated by direct agonist effects on alpha receptors. These doses pose a significant risk of1 precipitating limb and end-organ ischemia and should be used cautiously. Epinephrine Epinephrine is a full beta receptor agonist and a potent inotropic agent with balanced vasodilator and vasoconstrictor effects. The direct effect of epinephrine on increasing inotropy independent of myocardial catecholamine stores makes epinephrine a useful agent in the treatment of transplant patients with denervated hearts. The independence of the mechanism from adrenergic receptors bypasses receptor downregulation, desensitization, and antagonism by beta blockers. In addition, this mechanism allows for synergistic effects with beta receptor agonists, such as dobutamine. Therapy may be initiated with a 25- to 75-µg/kg bolus over 10 to 20 minutes, although in clinical practice the bolus dose is usually omitted. Also because of these pharmacodynamics, patients who have had prolonged administration of milrinone may have delayed deterioration, so they should be observed for at least 48 hours after cessation. Milrinone is renally excreted, necessitating dose adjustment in the presence of renal dysfunction or substitution with dobutamine. Milrinone has many side effects, including hypotension and atrial and ventricular arrhythmias. There was no difference in the primary endpoint of days hospitalized for cardiovascular causes with 60 days, but significant increases in sustained hypotension and new atrial arrhythmias were noted in the milrinone-treated patients. Enoximone dosing is essentially one-tenth that of milrinone, with a bolus dose of 0.